The latest saturated fat study to come down the pike has been picked up by all the newspapers it seems, reinforcing one of my favorite Mark Twain quotes:

If you don’t read the newspaper, you are uninformed. If you do read the newspaper, you are misinformed.

This latest piece of whatever has followed the typical trajectory of such things. Study done, pre-publication press release, dissemination by gullible press that doesn’t have sense enough to ask the right questions, publication in scientific journal. In this case it goes to show that the gullible press is really gullible where saturated fat is concerned. No study is too moronic as long as it implicates saturated fat as a bad nutritional actor.
Let’s look at a sampling of what a number of “health and science’ outlets have to say. Medical News Today warns that meals high In saturated fat Impair “good” cholesterol’s ability to protect against clogged arteries and cautions us that

Before you bite into that burger or devour that doughnut, first chew on this: New research shows that just one meal high in saturated fat can affect the body’s ability to protect itself against some of the underlying causes of heart disease and stroke.

HealthDay asks us if we ‘need more proof that a diet high in saturated fats is bad for [our] heart[s]?’ Then informs us that ‘just a little high-saturated fat can be hard on the arteries.’
Good ol’ reliable WebMD (reliable, that is, if what you want to know is the low-fat take on things) comes through with the caveat that ‘even one fatty meal affects arteries’ and tells us that

a new study that shows eating a meal high in saturated fats, like a cheeseburger and fries, can reduce the ability of the body’s “good” HDL cholesterol to protect against clogged arteries.

And enlists the aid of an expert to help make the case

“It’s further evidence to support the need to aggressively reduce the amount of saturated fat consumed in the diet,” says researcher Stephen J. Nicholls, MBBS, PhD, PRACP, FACC, a cardiologist at The Cleveland Clinic in Ohio.

And you thought that all those letters behind someone’s name make him smart?
Reuters chimes in with ‘saturated fat impedes “good” cholesterol activity.’
What I’ve laid out is just the short list. I found this study mentioned in practically every newspaper I read from throughout the world. They were all the same. Not an ounce of questioning, but a ton of implication instead. Notice how in the above examples the reporters are so certain. There is no equivocation. In their minds saturated fat is, by God, bad for you, and that’s how they’re going to report it.
Let’s take a look at the actual study to see if it lives up to all it’s hype, let’s see if it’s worthy of all the knee jerk substantiation by the finest minds in the medical reporting world.
The study, published in the current issue of the Journal of the American College of Cardiology, looks at what happens to the arteries of subjects who consume a high-saturated-fat meal as compared to those who eat a high-polyunsaturated-fat meal.
Fourteen thin (BMI 23.6), healthy subjects (average age 29.5), after an overnight fast consumed a single meal containing primarily saturated fat or primarily polyunsaturated fat. A month later the process was repeated with the opposite diet.

The first meal contained safflower oil (fatty acid composition: 75% polyunsaturated, 13.6% monounsaturated, and 8.8% saturated fat). The second meal contained coconut oil (fatty acid composition: 89.6% saturated fat, 5.8% monounsaturated, and 1.9% polyunsaturated fat). The order of meals ingested was determined by random allocation and was blinded to the investigators.

How did they provide the saturated and polyunsaturated meals? I mean it’s hard to down a bunch of safflower oil and coconut oil all by themselves, so how did they get the subjects to eat all this fat?
Well, according to the paper

Subjects consumed 1 of 2 isocaloric meals comprising a slice of carrot cake and a milkshake containing 1 g of fat/kg of body weight.

Say what? Carrot cake and a milkshake?
Is there anything else in carrot cake and milkshakes besides fat? How about sugar and flour? Let’s see what the article says about the nutritional breakdown of the carrot cake and milkshake meal. Would you believe that it doesn’t say anything at all? Nada. Zip. Zero. Other than the fact that there is about 70 gms of fat per meal and that one meal contains 89.6% saturated fat and the other 75% polyunsaturated fat, we are provided with no nutritional information.
Never one to let researcher lack of openness stand in my way, I looked up a milkshake and carrot cake in my handy nutritional analysis program and worked backwards to calculate what else we would find in these foods along with the 70 grams of fat. Turns out that a piece of carrot cake contains about 55 grams of fat and 24 ounces of milkshake contains the other 15 grams. What else is in there along with the fat? How about 173 grams of carbohydrate, 143 grams of which is sugar. Remember, 100 grams of sugar is about a half cup, so 143 grams is almost 3/4 cup. Of sugar.
So, what we have are two meals: one high in refined carbohydrates and saturated fat, the other high in refined carbohydrates and polyunsaturated fats. In fact, both diets are higher in carbohydrates (in terms of calories) than they are in fat. Each diet contains 692 kcal of carb and 630 kcal of fat. If you add it all up, including the protein, you get a single meal containing 1426 kcal, most of which is carb.
We all know that the standard American diet, which is the high everything diet, causes problems. So, what these researchers have done is studied the standard American diet with two different types of fat. Assuming they found a difference, all they can really say is that saturated fat in combination with a ton of carbohydrates (mainly sugar) causes more problems than the same diet using polyunsaturated fat. What of value can we take away from any of these findings, assuming there are some? The researchers have used two foods that allow this kind of fat substitution and maintain their taste and mouthfeel. Any more–thanks to the food police–most foods containing saturated fat do so only because saturated fat has some cooking property that is necessary in the preparation of that particular food. Anything else is made with unsaturated fat. So, we have a study that may tell us that there is a difference between the actions of saturated fat and unsaturated fat in a giant, calorically dense meal that contains more carbohydrate than anything else. Who cares? The great unwashed masses who flock to the fast food places and chow down on ‘indulgent’ items certainly don’t care. And the study isn’t applicable to those following either low-fat or low-carb diets.
Let me get off my soap box and let’s move on. The researchers did a number of evaluations on the subjects while they were fasting, gave them the 1426 kcal cake and milkshake diet, then repeated the evaluations at 3 hours and 6 hours after the meal.
What did they look at?
The researchers looked at four different parameters. They wanted to see if the difference in fat type made a difference in blood lipid and insulin levels, if it made a difference in the way the subjects arteries reacted in a couple of different ways, and they wanted to see if the different fats made the HDL particles less anti-inflammatory.
First, looking at the difference between serum total cholesterol, LDL, HDL, triglycerides, Insulin, and non-esterified fatty acid levels after the two diets, we find that only two–total cholesterol levels and LDL levels–are different to a statistically significant degree. Both were lower after the saturated fat meal. Now most low-fat advocates believe that LDL is the single most important lipid parameter in existence, but for some reason these guys chose to not even mention the fact that in this study LDL was lower on the saturated fat diet than on the polyunsaturated fat diet. I wonder why?
Next, the researchers performed two different tests for evaluating arterial function on the subjects. One of these tests was a measurement of forearm blood flow; the other was a measurement of brachial artery (a large artery in the arm) diameter change. Both of these methods of evaluation are difficult to explain using non-technical language, but basically both work in similar ways. When blood vessels are compressed with a tourniquet for a period of time, the arteries downstream from the area of restriction receive little to no blood. When the tourniquet is released, blow flows into the artery and the artery dilates. You can press your thumb hard into the inside of your forearm and hold it for 10 seconds. When you remove your thumb, the area underneath will be white. As you watch, the area under your thumb print will become pinkish red as blood flows back into it. The more quickly blood flows back in, the better your arterial and capillary function. The two tests used in this study look at this same thing only using much more sophisticated techniques.
In one of the two tests there was a slight difference in the negative direction at the 3 hour mark with the saturated fat diet, but overall there was no statistically significant difference between the two diets in either test.
Finally, the researchers performed a complicated evaluation of HDL samples incubated with human umbilical vein endothelial cells. I’ll let them explain it.

Human umbilical vein endothelial cells were isolated and incubated with HDL samples at a concentration of 2, 4, or 8 mmol/l apoA-I in media containing 10% heat-inactivated serum for 16 h at 37°C in 5% CO2. Cells were incubated for a further 5 h in the basal or stimulated state following the addition of tumor necrosis factor-alpha (0.2 ng/ml). The cell surface expression of adhesion molecules was assessed with an enzyme-linked immunosorbent assay technique. Cellular viability was determined to be greater than 95% by trypan blue exclusion.

After incubation with the HDL collected after both the meals, there was a higher level of expression of ICAM-1 and VCAM-1 in the ‘activated’ cells incubated with the HDL from the saturated fat diet than from that from the polyunsaturated fat diet. This difference would seem to indicate that there may be a decrease in inhibition of these inflammatory molecules by the HDL from the saturated fat diet. And, although the data was difficult to determine from the paper, this difference apparently reached statistical significance. What we can’t tell from the paper is if the difference really makes any difference in the real world of arterial function. In other words, I may get a statistically greater amount of ethanol in gasoline I purchase from Mobil than I do in gas I purchase from Chevron, but does it make a difference in how my car runs? Given all this, I will readily stipulate that HDL from the subjects who ate the high-carb, high-saturated fat diet has a reduced anti-inflammatory potential as measured in incubated human umbilical vein endothelial cells compared to the other HDL. But no one can tell me what it means–if anything–in real life.
I suspect that it doesn’t mean a lot since the authors of the paper went to great lengths to play up the non-significant differences in the more direct tests. As mentioned before, there was not a single word about the differences in total cholesterol and LDL levels, which were significant.
The authors reported

A nonsignificant trend toward impairment of endothelium-dependent vascular reactivity in conduit arteries was also demonstrated after the saturated fat meal.

Hey, guys, there ain’t no such animal. Just like a woman can’t be trending toward pregnancy, there is no nonsignificant trend toward anything. It’s either significant or it isn’t. Period. Unless, of course, you’re trying to pull the wool over someone’s eyes.

There was a trend toward a greater post-prandial impairment seen after the consumption of the saturated compared with the polyunsaturated fat.

There they go again.

Although the meals had different effects on hyperemia in conduit and resistance vessels, the direction of the meal-related changes was similar in large and small vessel studies, with a trend toward a greater increase in flow after consumption of polyunsaturated fats.

And again.
Let’s see what the conclusions of this study are. First, let’s look at the conclusion in the abstract, which is the only part of this study that the vast majority of people will ever see.

Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.

Pretty darn unequivocal, I would say. These guys aren’t shy. No pussyfooting around here.
Now let’s look at the conclusions at the end of the paper, the ones someone would see who actually took the trouble to read the paper and see all the references to nonsignificant trending.

In summary, the present study raises the possibility that the differential effects of dietary fats on the anti-inflammatory potential of HDL and endothelial function may contribute to the apparent benefits of polyunsaturated over saturated diets observed in the epidemiologic literature.

Quite a difference I would say.
Now, go back and read the press reports now that you know the real story behind this study.
Once again, I’ve got to say, the anti-saturated fat bias is so pronounced that this mealy mouthed study was picked up by news services and newspapers all over the world and reported as gospel. All because the press report spun it the way they did. Well, I have to say it. The spin stops here.


  1. Is anyone surprised damage occurs when someone consumes high glycemic meals along with high levels of saturated fat? The following citations demonstrate pancreatic beta cell toxicity adversely affecting insulin secretion under such conditions:
    Endocrinology Vol. 144, No. 9 4154-4163
    Saturated Fatty Acids Synergize with Elevated Glucose to Cause Pancreatic ß­Cell Death
    Wissal El-Assaad, Jean Buteau, Marie-Line Peyot, Christopher Nolan, Raphael Roduit, Serge Hardy, Erik Joly, Ghassan Dbaibo, Lawrence Rosenberg and Marc Prentki
    Pleiotropic effects of fatty acids on pancreatic beta-cells.
    Haber EP, Ximenes HM, Procopio J, Carvalho CR, Curi R, Carpinelli AR
    J. Cell. Physiol. 194: 1?12, 2002.
    Hi Steve–
    Thanks for the citations. Is it any wonder the authors of the study I posted about didn’t provide the nutritional breakdown of the meals in question?

  2. It makes me really angry when I read “news” articles such as the ones you linked to in this post that misconstrue or mangle the real information in scientific studies. A much more valid study might have involved a third meal, one consisting of no or low carbohydrate content and high saturated fat, like a nice chunk of steak or something. Carrot cake and a milkshake? And they want to say the effects were from the FAT?
    I have to fight to keep the truth in front of me every day. I have to decide whether to talk back to “professionals” or just keep my mouth shut. In May I had a lipid profile done. I am 51 and have completed menopause in the last 12 months so I knew I might be in for an unpleasant surprise. Total was 261, HDL 32, LDL 139, triglycerides were 465. I had been staying away from trans fats, processed foods, and high fructose corn syrup, and had previously (in 1999) lost weight on a Protein Power diet, but had “fudged” and cheated my way back up to my previous weight. Only with the best foods, of course… but that would include starchy veggies and what I considered a modest amount of home-baked goodies. OK, and ice cream a bit too often.
    The nurse who snottily reported these numbers to me said I should immediately go on a low-fat, low-cholesterol diet and that the doctor would have to put me on meds in three months if my numbers didn’t improve. I wanted to say, “You thought!” as my daughter is wont to do. Instead, I said, “I’m not going to do that. I’ll handle this on my own and we’ll see what happens in three months.”
    I got out my copy of The Protein Power Lifeplan and found your blog here and read every single post, took notes, and was especially struck by the post in which you said you just can’t cheat the diet; you cannot expect to eat, was it 100 g of carbs for a woman?, per day and think you’re still going to get the benefit of a real low-carb diet. Thank you! That was a very helpful bit of information.
    I spent the next three months eating almost zero sugar, no flour, no potatoes-rice-pasta, any of that, while still having some fresh fruit every day and plenty of other wonderful farm-raised meats and veggies we get from regional farmers around here. Lost 15 pounds, but this time I wasn’t doing it for the weight. I was doing it to beat their dumb game.
    Went back in for my lipid re-take at 3 months. Total was 259, HDL was 37, LDL 192, and triglycerides 150. I was so proud of the trigylceride number. I had hoped the HDL would be over 40 and the total a bit lower (cannot figure out why they weren’t; lack of exercise perhaps?). The snotty nurse who reported the numbers to me said, “Your LDL and total are still too high. You’ll have to start the low-fat, low-cholesterol diet now. Doctor is going to put you on meds if the numbers don’t improve in 4 months.”
    She wouldn’t even tell me the triglyceride number at first. I had to ask what it was.
    I said, “I am not going to go on meds. I would like some credit for having lost 15 pounds and bringing my trigylceride number down to 150.”
    She said, “I’ll talk to the doctor about that. But the LDL number went up, and that means you just increased your risk for heart disease by 40 percent.”
    I wanted to say, “Prove it! Show me the science that says that’s true!” But instead I said, “I don’t think the LDL number is valid anyway. It was apparently derived from the other numbers.” (I had recently read one of your posts, or was it in one of the books, about how the LDL number is derived from the others and so does not actually measure LDL cholesterol.)
    She said, “I don’t know how they get that number.” I proceeded to tell her how the number is derived. She had nothing to say, just another recommendation that I go on a low-fat, low-cholesterol diet. I finally said, “Why would I want to do that? My triglycerides would go up again and I would gain all that weight back.”
    It’s so aggravating. And it makes me really sad. There’s so much good science, knowledge that would help people become more healthy and thinner too, and yet all we ever hear is fat, fat, fat.
    Anyway, I just wanted to share my story and thank you for this excellent information. I have started on a niacin supplement to help bring down the numbers for my next test, and am hoping if I can get out for a brisk walk every day that might help the HDL go up over 40.
    Hi Anne–
    It gets my bile up, too, when I read the newspaper misinformational reports about all these studies. I’m trying to do my small part in setting the record straight.
    Looks like you’re on your way to getting your lipid situation improved.
    A few facts you might find of interest…
    HDL goes up in response to fat in the diet (especially saturated fat) as well as to exercise and a little alcohol consumption.
    Fish oil and/or krill oil tend to increase HDL and decrease triglycerides.
    Niacin will help, but sustained release niacin (I don’t think it’s still around, but it may be) has been shown to cause some fairly severe liver damage. The only kind of niacin I ever recommend for patients is one of the formulations known as “no flush” niacin.
    It must be remembered that fruit (even good, fresh fruit) and vegetables contain carbohydrate, and it’s easy to be seduced by the ” healthful” benefits of such (not to mention their taste) into over consuming. Really, truly ratcheting down the carbs to the 30-50 gram per day level should reduce triglycerides to below 100 mg/dl.
    LDL is not just LDL. In other words, all LDL is not created the same. There are different particle sizes of LDL; the larger, fluffier variety are a different animal from the smaller, denser kind. The larger LDL, type A pattern, is pretty harmless, whereas the small dense LDL, type B pattern, is the kind that runs up the risk for heart disease. In virtually all studies I’ve seen and in all the patients MD and I have actually checked first hand, increasing the fat and decreasing the carbs in the diet shift the LDL from the small, dense to the larger, fluffier variety. (You might want to ask the ‘snotty nurse’ the next time around what your LDL pattern is. She, of course, won’t have a clue (it requires a special lab test that’s kind of pricey), but you’ll get that special frisson of superiority that comes from possessing more knowledge than the so-called experts.)
    Good luck in your health improvement endeavors. It isn’t easy, but the payoff is well worth it. Keep me posted.
    Thanks for writing.

  3. The nice lady at my local “ye olde vitamin/supplement” store insists krill harvesting has been found to threaten the food supply of various desirable “food fish” (ie. salmon)and is being reduced or prohibited or something. She maintains she has trouble finding sources for krill oil to sell whereas she previously had numerous supplier. Huh??
    Hi William–
    If the krill oil market is in trouble, you couldn’t prove it by the number of vendors at a natural health expo I recently attended. Everyone, it seemed, had a krill oil supplement for sale. According to Neptune Technologies, their annual harvest of krill represents and infinitesimal fraction of a percentage of the krill biomass. I’ll keep my ear to the ground to see if I can find any info and report it if I do.
    Thanks for writing.

  4. You are so right, it’s hard to read stories like Anne’s and not get angry at the suggestion of the low fat/high carb diet. I have done the same, lowered my triglycerides from over 300 to 90, raised my HDL from 30 to 60, and lowered my fasting blood sugars from the 150’s to the 80’s, all through a protein based diet and exercise. I did cut back my fruit consumption to one small serving a day(some blueberries with breakfast), eating mostly protein with salads and vegetables. I have eaten some oatmeal from time to time, but the portion is small(less than a 1/4 cup) and only once in a while.
    Having a support system is also important. My wife is supportive of my diet, and many times eats what I eat. We try to work out together when we can, many times it’s a hike or bike ride with the kids. My main source of exercise is lifting weights.
    Anyone who defies the doctors and gets the lipid profile numbers where they need to be without meds is to be congratulated, you beat the drug company system. I just turned 49, and my last lipid file done a few months ago was the best one yet!
    Hi Audley–
    Thanks for your story and congratulations!
    Losing weight–even on a low-carb diet–requires a lot of effort and vigilance. I appreciate your sharing with us how you did it.

  5. Thanks for your comment on my comment. 🙂 Yes, thanks, I knew the “no-flush” niacin was the kind to get. And I’m hoping to get some krill oil or fish oil soon (have had that on the list for a couple of weeks). I will keep you posted. I think your suggestion to ratchet down to that 30-50 gram level again is a good idea. It wouldn’t be so darned difficult to accomplish if it weren’t fresh peach, blueberry, and canteloupe season. 🙂
    But you’re so right. It’s definitely worth some work to get that payoff.
    It is tough with all the fresh stuff around. In fact, I had some fresh cantaloupe myself today, but only a single slice. MD toothpicked it with so much prosciutto that I could barely taste the cantaloupe. Of course if I were on a Dean Ornish style diet I could eat all the cantaloupe I wanted, but the prosciutto would only be a gleam in my eye. And my weight would go up, and my triglycerides would go up, and my LDL would get smaller, and…well, you get the picture.

  6. (This is a book)
    I can sympathize with the ‘snotty nurse’ of one of the previous posters. I went in for some routine blood work when I was 37. I suspected I was a T2 but wanted confirmation because I was TTC at the time. Had been doing ‘low fat high carb to no avail and was eating about 1250 cal/day. I can count and I wasn’t cheating! My lipid numbers were atrocious. Total was 240, HDL was 38 and IIRC, LDL was 190(something). Don’t remember triglycerides but don’t think they were too bad as I have always taken fish oil capsules. BS numbers were DEFINITELY T2! Nurse called with the results and told me the Dr would ‘definitely put me on a statin’. I laughed and told her we were TTC and he’d do no such thing! Went SUPER duper LC, went on metformin (even super duper LC wasn’t enough to improve my numbers as I was also 100+lbs overweight at the time).
    Fast forward 8 months, finally lost enough weight to cycle normally (as in cycles longer than 21 days), reduced my met dosage by half and voila!, got pregnant w/o fertility treatments (underwent fertility treatments for nearly a year before LC and quack RE NEVER took any glucose/insulin readings).
    Continued modified LC during pregnancy (alternated peeing on ketostix and sticking my finger and kept my fastings under 85 and my 1hr at 120ish or usually lower, stayed out of ketosis by keeping smallish ‘carbish’ (1-2g) things close at hand to bump me out but not raise my BS readings). Probably ate 50g/day. The ‘you must eat at least 100g/day’ is very individual. Only gained 16lbs (but I was still ‘overweight/obese’ when I got pg) I can’t imagine how the pregnancy would have turned out if I’d followed the ADA diet (horrors!). My daughter just turned 1 and is at the 90th+ percentile developmentally. Talking up a storm, walked unassisted at 10m, rolled over at 2.5m (both ways) /etc. Hardly ‘retarded’.
    Fell off the wagon for 3 months or so after I had her. Turned over ‘new leaf’ in Jan of this year and went in for more ‘bloodwork’ since I was about 6m post partum. Keep in mind I ‘enjoyed myself’ during Thanksgiving and Christmas/New Years! but was LC the rest of the time. Total Cholesterol levels 180. HDL 68, LDL 102. Triglycerides 64. Snotty nurse called with the results and commented ‘I see he finally got you on a statin!’. I laughed and told her I just had a baby!. IF she only knew MY diet was ~40% fat, much of that saturated and 55% protein with only about 5% carbs she’d probably have dropped dead of shock LOL.
    LC worked again, we’re expecting again the end of October. (were probably pregnant early on when I had my bloodwork!) At MY advanced age (will turn 40 the month after this little one is born). W/o fertility treatments!. I wonder just how much of the decrease in fertility in my age group over the past hundred years is related to insulin resistance and a ‘low fat’ diet?
    I shudder to think of the poor schmucks who follow the ADA diet and are on LOTS of different drugs, going so far as to even inject insulin. If I were to follow the ADA diet I can tell you right now…I’d still weigh way over 200lbs, be on all kinds of meds and still be infertile/childless. How sad :(. If I were to put on a tinfoil hat I’d suspect they want us T2’s to drop dead sometime before 65 so they don’t have to pay SS/medicare. You really gotta wonder. Instead, I got BABIES! 🙂
    Long term goal is to lose all the weight (still have about 50ish pounds to go) and see if I can LC enough to ditch the meds!
    Hi Beth–
    Thanks for the inspiring story. Keep on with your efforts and I’m sure you’ll be able to jettison your meds.
    Keep us posted.
    BTW, what does TTC stand for?

  7. I guess one could say that a scientific study touting non-significant trends is pretty unique.
    Maybe pretty unique, but more likely kind of unique. Possibly even really unique.

  8. I have been meaning to write to you for a while now, about my own cholesterol conundrum. I have been following a LC way of life for close to 2.5 years. My total cholesterol has gone up significantly, both LDL and HDL. Triglycerides have gone down. My ratios remain good, but I still worry, probably some deep seated remnants of fear from hearing the “experts” expound on the link between cholesterol and CHD.
    I am a 43 year old woman, with no family history of CHD, or diabetes. The females from both my mother’s and father’s sides have prevalent obesity in later years (most were slim when young). I had put on an extra 40 pounds over a period of about 10-12 years. Since LC, I have dropped the 40 pounds and am a trim 120-122 lbs at 5ft. 3 inches.
    Here are my numbers, for reference. The 3/04 numbers are from pre-LC and are very indicative of what they had been for the previous 15-20 years.
    3/04 7/04 11/04 3/05 6/06
    Total 215 273 294 276 352
    LDL 125 173 192 163 240
    HDL 71 69 73 92 100
    TG 94 153 146 105 62
    Total/HDL 3.0 4.0 4.0 3.0 3.5
    I started taking flush-free niacin (500mg 2X/day), probably about a year ago. I had also been taking fish oil and flax oil capsules as well as a multivitamin like Centrum or One-A-Day. After reading your Protein Power and Protein Power Lifeplan books, I switched to taking a quality multivitamin/mineral/trace elements, and Carlson’s Cod Liver Oil, still continuing to take the niacin. I had started this regime maybe a month before my last cholesterol test. Then after reading about your experience with Krill Oil and curcumin, I have added these in the last month or so (after the latest test).
    I have a biology background, and have read as many scientific articles as I can get my hands on to try and figure out if I should be worried. I believe in LC, and eating good fats, and do not believe that cholesterol is necessarily an indicator of CHD risk. I also know that higher cholesterol is protective and can contribute to longevity, particularly in women. But I don’t know if there is a limit to how much is good. One of your books says that cholesterol should be lower than 220, but shouldn’t go too low (I can’t remember what the low number is), based on scientific studies (U shaped mortality curve). This is where my concern comes in, since my cholesterol is significantly higher than 220.
    I recognize that cholesterol is a necessary component in the body, and fulfills a vital role. The way that I understand the way LDL and HDL work in the body, it seems to me that it shouldn’t matter what the number is, as long as the ratio of HDL to LDL is balanced.
    I refuse to go on statin drugs, which of course my doctor tries to get me to take. At the last appointment, I asked about the possibility of having a lipo-profile test done. The doctor didn’t know anything about it (although they are residents, so I excuse then to some extent), luckily I had brought copies of articles, and information about the test. The response was, we don’t do that test. I guess they weren’t even willing to check into having it done. The recommendation was for me to stop taking the fish oil, and have my cholesterol checked again in three months. Needless to say, I have not stopped taking the fish oil. I have tried eating less eggs and red meat, in case I have a problem with AA. But my consumption of dairy products has gone up as a result, which I am not sure is an improvement.
    My question for you is should I be worried? And if I wanted to further pursue testing for my lipo-profile, and other risk factors (like crp testing, or an artery scan to look for plaques), who should I go to, a cardiologist, endocrinologist, or other type of doctor? I work at Duke University, and don’t know if Dr. Eric Westman see patients, but wonder if he might be interested in my case. I haven’t written to him, because I am not quite sure what to say, it seems like a bit of an imposition. This is also the reason I had not written to you before now, since I know that you do not give medical advice to non-patients. I am hoping that I have asked questions that you can answer though. Any other advice would be welcome as well. I admire you and your wife, along with the other professionals out there trying to spread the word of LC, and health.
    Thanks so much.
    Hi Cathy–
    Here is what the ‘real’ data say about cholesterol. There seems to be no relation to total cholesterol and mortality in women of all ages except for women over 50. In women over 50 there appears to be some protective effect with higher cholesterol levels. And if total cholesterol is high because it is made up of a lot of HDL, who cares?
    As you know from reading this blog, I’m not a real believer in the lipid hypothesis of heart disease. Having said that, if there is any part of the whole hypothesis that I think is even part way valid it would be that HDL cholesterol is protective. And probably that small, dense LDL is more easily oxidized and may contribute to cardiovascular disease. It’s obvious that your HDL cholesterol is high, very high, in fact, so this should be protective.
    You can go to the trouble and expense (it cost about $200 the last time I checked) to get your LDL analyzed as to particle size. There have been enough studies done now showing that triglycerides are a surrogate marker for LDL particle size–high triglycerides indicate small dense LDL; low triglycerides mean large fluffy, type A, LDL–that I don’t bother with the expensive test any longer. I simply look at triglycerides, and yours are certainly low. (You could request an ApoB test, which will show how many LDL particles you have; if there aren’t very many and you have a lot of LDL, then you’ll know that the particle size is large. ApoB is a less costly lab test than the direct measurement of particle size.) Even the folks who are firm believers in the LDL-cholesterol-is-bad theory, don’t particularly fear the large type A LDL particles.
    I’m sure Eric Westman or Bill Yancey (they work together) would be interested in your case. I know them both. Tell them I suggested you contact them. They are both extremely nice and both are experienced with low-carb diets.
    Good luck. Keep me posted.

  9. Oh, I forgot to say that my blood pressure is low, 113/74, 112/68.
    I really do not have any other risk factors.
    Please feel free to post, or not post, any or all of my comments. Thanks again.
    I read this before I answered the other comment.

  10. TTC= Trying to conceive
    Yeah, I saw all those reports in the paper about the study and my very first thought was “I wonder just how much sugar/carbs were in those meals?” But when I found out that they had used carrot cake and milkshakes, I was floored, as that was even worse than I had envisioned. At any rate, as it so often does these days, my skepticism kicked in and I didn’t believe a word that was written, figured that you’d be posting on the study and that I’d wait to see what the actual body of the study revealed. As usual, it turns out to be something entirely different than advertised. Sheesh. The low-fat gospel adherents just aren’t going to give up, are they?
    Off topic here but I just have to rant a little, why are routine tests such as mammograms, etc. called “preventive medicine?” They prevent nothing and at best, will detect a problem early enough so that you can get it taken care of. True preventive medicine would mean taking care of yourself so that the problems would never have a chance to getting a start in the first place. At any rate, that term used like it is has always rankled me. Yesterday’s paper had a whole section on such tests (headline of course read “preventive medicine”) and with a run-down on each. The reason under cholesterol check said this: “Too much cholesterol can clog your blood vessels and is a major cause of heart disease.” Such statements will be far more likely to give me a heart attack than my cholesterol ever will.
    BTW, I sure can sympathize with those who constantly must battle their doctors and their staff. My husband’s primary care physician wanted to put him on a statin despite the fact that he has liver disease. I put my foot down on that one and said we were trying to keep his liver as healthy as possible, not kill it outright.
    Hi Esther–
    Sheeesh is right! Here’s your rant for everyone to see. Saves me from having to do it.
    TTC = trying to conceive? I never would have guessed.

  11. Ok, I’m back from vacation and throwing myself back into low-carb again. I cheated a bit on vacation, but only a bit. 🙂
    Two points I want to make:
    1) I have never watched my saturated fat and my HDL has gone from 45 to 82. It’s not the fat. It’s due to cutting out sugar and starches and exercising regularly.
    2) Re: Cathy’s story, that’s so sad. When my last cholesterol test came back at 214 (with all other numbers within parameters) I received a letter from my doctor telling my I needed a I need a “therapeutic lifestyle change.” Of course this “therapeutic lifestyle change” is the same old high-carbohydrate, low-fat, low-cholesterol diet, with 6-11 servings of grains, pasta, rice, cereal, crackers, and baked potatoes each day. Hahahaha! I actually laughed out loud. I’ll follow that diet when hell freezes over! I only feel sorry for all the people who could be helped with a low-carb diet who will get insulin resistance and diabetes from these high-carb guidelines. And in order to “adjust the number and size of portions to reach and stay at your healthy body weight” I would likely be constantly hungry. Who wants to live like that?
    Next to the “therapeutic lifestyle change” it says “see enclosed,” and the doctor wrote in “please read.” Enclosed is the flier that tells me to stuff myself with carbohydrates. *sigh* Why can’t I find a doctor who doesn’t push low-fat dogma?
    And guess what? At 214 with all other numbers in range and even excellent, I’m not worried.
    Getting rid of sugar and starches from my diet is the smartest thing I ever did for myself and I really think the media is so far behind the times that it’s sad.
    Hi Victoria–
    Welcome back and thanks for the commentary.

  12. Thank you, Cathy, for asking your question, and Dr Eades for your answer. I had a medical about 6 months after starting PP (about 3 years ago), and my blood figures were very close to Cathy’s. (I’m just a couple of years older at 45, and 5′ 2″, 112 lbs, having lost about 35 lbs following PP, so not that much different in size.) Needless to say, the doctor suggested that I be retested with a view to starting treatment to lower my cholesterol.
    Having read Uffe Ravnskov during my LC researches, and since all of my cholesterol ratios were good according to the guidelines in PP & PPLP, and triglycerides were low (53), I decided not to bother, but it’s sometimes hard to maintain confidence with the constant barrage of “cholesterol is bad” messages that seem to prevail even with some low carb proponents.
    Hi Janet–
    It is indeed hard to maintain confidence. That’s why I’m doing my small part to present the other side.
    I had dinner last night with a guy who, until recently, ran one of the huge scanners that does total body scans and ultrafast CT scans of the heart. He told me of a conversation about cholesterol he once had with a big time cardiologist from USC. The cardiologist asked my friend if he knew how to tell if high cholesterol levels would lead to heart disease in a patient. My friend said ‘no.’ The cardiologist said: ‘flip a coin.’ In other words, there is no correlation.
    So, it’s not just MD and me and Ravnskov who don’t think cholesterol is the problem; there are a lot of other physicians out there, too. They just don’t have the drug-underwritten soapbox.

  13. It’s so clear that it’s the sugar and fat together that it’s not even funny!
    How true, how true.

  14. Great article. I really like your blog and am looking forward to your future work.
    Thanks. I’ll try to live up to your expectations.

  15. Hi Dr. Eades,
    I thought you might be interested in my latest blood lipid results. I also asked my doctor to have the apoB test done.
    Total 296 (improved from 352)
    LDL 179 (improved from 240)
    HDL 103 (from 100)
    TG 69 (was 62)
    Total/HDL ratio 2.9 (goal <4.4, which the doctor seemed to think was the most important)
    TG/HDL ratio 0.67 (goal <2)
    apoB 112 mg/dL (reference 44-148) (3rd quartile of reference range)
    apoA-1 203 mg/dL (reference 98-210)
    apoB/apoA-1 ratio 0.55
    How would you interpret the LDL and apoB? Does this correlate to larger fluffy LDL?
    I did some reading (see reference below) and find that for apoB, I am close to the 50th percentile, between the 50th and 75th, and just above the 75th percentile depending on the research data. For apoA-1, I am above the 95th percentile.
    Also, from this reference:
    I see that an apoB concentration of 120 or greater is significantly associated with an increased risk for CAD, whereas less than 100 is indicative of low risk.
    I found out that the NMR LipoProfile (LipoScience) test now costs $98.00 (according to their web site), available through LabCorp. I guess the price has come down.
    I have started to do IF, after reading your blog post on this. I want to have a few weeks of IF, before having the LipoProfile test done. It will be interesting to see what kind of difference it might make.
    The LipoProfile web site state that LDL particle number goals are aligned with NCEP ATP III guidelines for LDL cholesterol. The main goal for LDL particle number in primary prevention is <1400 nmol/L, and in secondary prevention is <1100 nmol/L.
    I tried to calculate the nmol/L from the reported apoB 112 mg/dL, but I’m not sure I have done it correctly. Somewhere I read that the molecular weight of apoB was 550,000 g/mol. This is the number I used, but maybe that is the wrong number. I get 2036 nmol/L, which puts me in the very high category. Perhaps apoB is not exactly equivalent to LDL particle number?
    I guess I am still confused as to whether or not my lipid profile puts me at risk. I think there are so few people with lipid profiles similar to mine, that it is hard to assess what the risk might be. My doctor agreed to request the LipoProfile test, and my insurance covers the test, so maybe it will give me a better indication of my risk. My doctor and I discussed the fact that I don’t have any other risk factors, and agreed that referral to a cardiologist wasn’t necessary. He did say that the next step in treatment would be low dose statin, but he understood that I did not want to treat something that I am unsure is a risk, and with a drug I consider to be unsafe. I am currently trying to find out if there is concrete evidence that isolated elevated LDL is a risk factor. Although considering my feelings on statin drugs, I don’t know what I would do if I found that my risk is increased. Probably continue to make dietary and supplement changes. My doctor said he would request blood lipid screenings every 6 months.
    I found out that my family is fairly long lived, I had a great-grandmother that died at ~94, one grandmother died at 79, the other at 85. One grandfather is still alive at almost 87, and the other grandfather died at 88 (after having had a heart attack at 78). My father is 69, my mother 64, and neither has any heart conditions, although both are currently taking statin drugs (not surprising). But this only adds to my feeling that I am not at risk, even with elevated blood lipids.
    I did contact Eric Westman and we had a nice conversation. He gave me a recommendation for an endocrinologist, although I’m not sure I will need to/or be able to see him. But the conversation did give me a lot to think about. He asked about sharing my story with Dr. Mary Vernon, which is intriguing and flattering. He also recommended Dr. Weston A. Price’s book, Nutrition and Physical Degeneration, which I am now about half way through. Very interesting stuff.
    Thanks for everything. And sorry this is so long.
    Hi Cathy–
    Thanks for the update. Keep us posted.
    P.S. I don’t know how to calculate (without looking it up) nmol/L either, so don’t feel bad.

  16. I think this is now my 3rd comment on this post, but it’s following up on my previous comments.
    My doctor insisted I get a liver panel done because of the niacin supplement (even though it’s the no-flush and I tried to tell her the liver concern wasn’t necessary, if I understood you correctly).
    Since I was getting blood drawn anyway I asked if I could have another lipid panel done and if they could do an actual LDL test where they see what size the particles are (I’m not sure what that’s called — ILDL? VLDL?).
    I got back the results today — liver is fine, of course. And the separate LDL analysis hasn’t come back yet. But the cholesterol numbers they ran are “much worse” according to the nurse. But I don’t know. Are they?
    Previous test was at beginning of August, this one at end of September.
    Total — 259 then, 283 now
    Trigylcerides — 150 then, 137 now
    HDL — 37 then, 40 now
    LDL (derived?) — 192 then, 216 now
    Am I doing something wrong? I was very careful in my diet, ratcheting back to 30-50 grams of carbs a day. Still not much exercise, hardly any alcohol. I added a bunch of supplements: 450 mg of niacin, two Ultimate Omega fish oils, two krill oils per day. (Plus potassium, magnesium, and a multi-, but those shouldn’t affect cholesterol numbers, right?)
    I guess my real question is, should I be concerned? It will be interesting to see how the LDL breaks out. What phrase should I use to ask the nurse the right question to get me the numbers I want? Thanks so much for your time. –Anne
    Hi Anne–
    It can certainly be frustrating to work hard at dieting and find your blood values worse. In your case, however, they are not all worse. Your triglycerides came down, as they almost always do when restricting carbs, and your HDL levels went up, which typically happens when fat intake goes up.
    Your LDL levels are almost certainly derived and not actual LDL levels.
    As to what questions to ask about the LDL particle size, ask if they were small or large. Type A (large) or Type B (small).

  17. I got back the LDL analysis. The nurses (they both called me this time, thoroughly alarmed) said I must start Zocor immediately. But they could not tell me what the numbers meant on this test. They had never heard of “Type A” or “Type B.”
    In the end, since I refused to start on statins, they recommended I see a cardiologist.
    I’ve spent about an hour trying to figure out what these phrases and numbers mean on the printout they sent me, and I understand some of them but not all.
    Mayo Clinic did this analysis. Their numbers are slightly different than the ones my local clinic came up with, but the LDL is definitely different.
    Some figures were marked H to indicate High. I have noted when they marked H.
    Total 289 (H)
    Triglycerides 150
    LDL 188 (H)
    LDL Triglycerides 46
    Apolipoprotein B, P 144
    HDL 40
    VLDL Cholesterol 48 (H)
    VLDL Triglycerides 98
    Lp(a) Cholesterol 13 (H)
    … and several things were “not detected”: Beta VLD Cholesterol, Beta VLDL triglycerides, Chylomicron cholesterol, Chylomicron triglycerides, and LpX.
    Mayo’s interpretation as noted on the printout is “Mild Type II-A Hyperlipoproteinemia.” How can they tell that without having seen me or without knowing anything about my family history or my diet?
    I’ve reviewed the Cholesterol chapter in PPLP and perhaps I don’t need to check into the hospital or update my will right away. Seems that Lp(a) might be a little high, but I wonder what it was before I stopped eating so many carbs? –Anne
    Hi Anne–
    In the same way the Eskimos have 29 different words for snow, those who take the lipid hypothesis a fact have come up with a classification system that ‘defines’ particular lipid findings. Type II-A hyperlipoproteinemia is what they call it if cholesterol is high and triglycerides are normal, which is your situation. They don’t have to see you or know your diet–they make the diagnosis simply by looking at the lipid profile. Reassuring, isn’t it?
    I can’t believe they don’t know how to tell you what your LDL particle size it. From the looks of your lab, you have large LDL particles, or type A. How do I know? Your APO B is normal (APO B is a measure of the number of LDL particles) and your LDL is high, meaning that each particle has to be big. If your APO B were high and your LDL normal or low, then it would mean the particle size was smaller.

  18. Okay, I think maybe the less than and greater than signs are what is causing the problem. Here we go again, with all words.
    I finally got the NMR Lipo Profile test done. Here are my results.
    In parenthesis (and under my results in some cases) is the goal and/or ranges for each. Where it says HIGH indicates where they flagged my result as a problem.
    LDL Particle Number
    LDL-P 1899 nmol/L (less than 1000) HIGH
    Optimal less than 1000; Above optimal 1000-1299; Borderline 1300-1599; High 1600-2000; Very high greater than 2000
    Small LDL-P 163 nmol/L (less than 600)
    Low less than 600; Moderate 600-849; Borderline 850-1200; High greater than 1200
    Total Cholesterol 384 mg/dL (less than 200) HIGH
    LDL-C 283 mg/dL (less than 100) HIGH
    Optimal less than 100; Above optimal 100-129; Borderline 130-159; High 160-189; Very high greater than 189
    HDL-C 86 mg/dL (greater than or equal to 40)
    Triglycerides 75 mg/dL (less than 150)
    Metabolic Syndrome Markers
    LDL Particle Size 22.6 nm
    Small/Pattern B 18.0-20.5
    Large/Pattern A 20.6-23.0
    Large HDL-P 22.7 umol/L (greater than 3.9)
    Large VLDL-P 0.1 nmol/L (less than 5.0)
    It looks like I have Pattern A, with large LDL particle size.
    Even though I have a high number of LDL particles, I have a very low number of small LDL particles. The small LDL particles are the ones that are more likely to be oxidized, and involved in forming arterial plaques from what I understand. Also the very last number, for large VLDL-P – they say those also have a higher association with heart disease, and you can see that I have very little of that too.
    The ranges/goals they give for total cholesterol look to be the same as those used by the traditional medical establishment, so I’m not worried about the fact that they are classifying them as HIGH.
    I had been taking an OTC no-flush niacin for a while, but had stopped maybe a month or month and a half ago. I’m wondering if my HDL came down a little because of that, previously it had been up at 100/103.
    Should I be worried about the HIGH LDL-P number?
    Do you have an opinion on no-flush OTC niacin?
    Would love to hear any other suggestions or opinions.
    Hi Cathy–
    Interesting lab results.  Unfortunately I can’t really comment on them because that would be practicing medicine over the internet, which is verboten.  Also, were I to comment on your labs, I would be inundated with people sending me their labwork to evaluate.
    Many things come in to play when analyzing labs that make it more difficult than it might seem.  I don’t know how old you are, I have no idea if you are on any medications other than the no flush niacin that you had taken previously, I don’t know if you have any other medical conditions, I don’t know your family history, I don’t know if your overweight, underweight or normal weight, I don’t know your thyroid status, I don’t know a hundred different things that I would know if you were my patient and I had examined you and had taken a thorough history.
    What I can tell you is that I’ve changed my opinion on no flush niacin.  Although I used to recommend it, I’ve now come to the conclusion that the regular ‘flush’ niacin is probably better.  If I were going to give someone niacin (which I probably wouldn’t because I’m not a believer in the lipid hypothesis), it would be the regular kind.


  19. Here’s an interesting take on this study:
    Another point: since the medium-chain SFAs in coconut oil get a straight ride to the liver via the portal vein, it seems more of a stretch that they would have any effect on HDL. My understanding is that these SFAs bind directly to albumin, rather than getting carried around in lipoproteins; but that may be an oversimplification of what acutally happens.
    Hi Dave–
    Thanks for the Weston Price article.  I hadn’t read it yet.
    I’m pretty sure you’re on the money about MCT (medium chain triglycerides).  MCT are definitely taken up directly into the liver without going through the lymphatic system first, as do the longer chain triglycerides.  As I recall they do bind directly to albumin – as do free fatty acids in the circulation – and don’t get carried in the HDL.

    I don’t think either of those studies are valid or prove anything about saturated fat causing diabetes. They are test-tube studies using isolated cells and fatty acids. There is no proof that such effects will occur in the body. I have read other studies that unsaturated fats, esp safflower oil and corn oil, will cause diabetes or diabetic symptoms in-vivo. Please, Dr. Eades, don’t accept these lies that saturated fats “synergize” with carbohydrates to make them more damaging. The opposite is true. Saturated fats are the best fats. They protect the pancreas and all other organs from oxidative damage. Unsaturated, esp PUFAs, are extremely toxic and dangerous. They destroy and damage cells in-vivo. Test-tube studies don’t prove anything bad about saturated fat combined with carbohydrates. The only studies that mean anything are in-vivo studies using real foods, not cultured cells and isolated fatty acids.
    Just read the following study, for example. Saturated fats protect against diabetes and every other disease. Unsaturated fats, esp PUFAs, cause or aggravate all diseases.
    I agree with you about the virtues of saturated fats, but the study you linked to to prove your point was a study in rats, not in people. I tend to rely more heavily on studies on people to come to my conclusions.

  21. I think the results would be the same with people, because there is a consistent biochemical mechanism. The problem is that nobody would fund a study that aimed to prove saturated fat was superior in every disease context. We have to look at old studies to find the truth, as it’s being suppressed by studies like the milkshake-and-carrot-cake one. The study I cited clearly shows that pure saturated fat diets gave high protection. Rats fed a high-fat coconut oil diet, for example, had only 29% diabetes and 12% mortality from a high dose of alloxan (160 mg/kg). Rats fed high-fat corn oil diets had 100% diabetes and 90% mortality from the same dose. They attributed this to the oxidative damage of the poly-unsaturated fats.
    “A diet enriched in saturated fatty acids effectively reverses alcohol-induced necrosis, inflammation, and fibrosis despite continued alcohol consumption. The therapeutic effects of saturated fatty acids may be explained, at least in part, by reduced endotoxemia and lipid peroxidation….” (Nanji, et al., 1995, 2001)
    I agree with you about the virtues of saturated fats. I just don’t like to draw conclusions based on studies on rats because rats aren’t just furry little humans – they are an entirely different species. And what works or doesn’t work on rats doesn’t directly apply to humans. There are enough studies both new and old showing the virtues of saturated fats that we don’t have to rely on rat studies to make our point.

  22. I don’t think the newer studies are as convincing, because they are tainted with bias. These older studies clearly show it’s the PUFAs that are bad. And even MUFAs in excess are harmful, like lard. Many experiments have induced disease and pathology in animals by feeding them a high-lard diet (60%). I think we should consider all the evidence from animals and humans, not just ignore old studies, becase they used rats. Surely you are not suggesting that humans fed 60% corn and safflower oil would be healthier than those fed 60% butter and coconut oil.
    The idea that saturated fat is harmful is simply untenable and irrational, no matter what the situation. It bothered me when other readers suggested that the combination of carbs and saturated fat is what caused the damage. I disagree. I think the safflower oil diet was highly damaging, and this could be shown if you did a long-term study of total mortality.
    The modern studies are mostly short-term and they don’t look at total mortality and disease incidence, but rather “markers.” My point is that saturated fat will always be better, and it makes no sense to suggest (as Loren Cordain does) that “carbs and saturated fat” are worse than “carbs and unsaturated fat.” How is anti-oxidation worse than pro-oxidation?
    I agree with you (and disagree with Loren) on the saturated fat debate. But, if the newer studies show the benefits of saturated fat despite the bias build into them, then I figure they’re really strong.

  23. Yes, thank you for debunking this absurd study. I agree with you that they failed to show any harm from the saturated fat meal. They only looked at markers. The total cholesterol and LDL were both lower on the coconut oil, and that was the only significant finding. The rest was a “nonsignificant trend.” LOL. So, I disagree with people saying that the saturated fat was “bad” in combination with the carbs. It wasn’t bad. Eating fats with carbs may be bad, but saturated fats are always healthier, and it’s the (refined) carbs that are to blame.
    Chris Masterjohn and Anthony Colpo have also commented on this study at the Weston Price website. I don’t agree with Chris’s theory that Vitamin E may have been the problem, because (like you) I don’t see a problem. “Non-significant trends” aren’t a problem. Coconut Oil is low in Vitamin E, because it’s so highly saturated, it doesn’t need much. I see no risk from eating saturated fat at all. So it might raise LDL slightly, but it will also raise HDL, reduce C-Reactive Protein, and reduce Lipoprotein(a). Saturated fat prevents all diseases.
    Risk Factors for Alcoholic Liver Disease:
    “One important class of the risk factors is nutrition. It is well recognized that protein-calorie deficiency commonly accompanies ALD and a nutritional support to alleviate this condition has shown some beneficial effects on patients with ALD. Polyunsaturated fat (vegetable or fish oil) is known as a critical nutritional factor for induction of experimental ALD and feeding saturated fat (beef fat) results in remarkable prevention of or accelerated recovery from experimental ALD. Indeed, epidemiological studies support these observations by revealing a positive correlation of the incidence of cirrhosis in various countries with consumption per capita of polyunsaturated fatty acids, particularly linoleic acid and an inverse correlation with saturated fat. It is postulated that polyunsaturated fat accentuates alcohol-induced oxidative injury via its synergistic effect on induction of microsomal ethanol-oxidizing enzymes (e.g., cytochrome P4502E1, CYP2E1). Iron is another pro-oxidant nutrient.”
    Hi Bruce–
    Thanks for the link. I have read multiple studies showing the protective effect of saturated fat on the liver. I suspect that one of the reasons we’ve got an epidemic of fatty liver disease on our hands is that everyone is avoiding saturated fats.

  24. Hi,
    I just read the blog about how you consider high triglycerides as a marker for LDL particle size Pattern B. My husband has had two lipid profiiles within three months. The y are as follows:
    First /Second-after 3 months
    TC 240/244
    TG 88/143
    HDL 44/48
    Chol/hdl -c ratio 5.5/5.1
    LDL/hdl ratio4.0/3.5
    vldl 17/28
    LDL-P 1991/2246
    small ldl-p 1644/1917
    ldl particle size 20.3/19.7
    Also had the following tests done the second time ( after 3 months)
    LP (a) <3.0
    hs-CRP 0.2
    Homocysteine 12.69
    My question is twofold. A little background first is that my husband is 5 11′ 195 pounds, exercises walks and yoga regularly, has heart disease in family. and has blood pressure of systolic in 130-35 range and diastolic from 65-70 range.
    The triglycerides are within normal but his particle sizes are very small and he has alot of them. Is there a way to decrease increase the particle sizes and decrease the number by food and more exercise? Also, what is the best way to increase the HDL’s. Sorry, one more question does having normal lipoprotein (a) , CRP and HOmocysteine counteract or lower the other risk factors (LDL numbers and particle sizes and numbers)?
    Thanks so much.
    Hi Mary–
    In my opinion, based on many years of practice, the best way to get LDL particle size to increase is to go on a good-quality whole-food low-carbohydrate diet. The carbohydrate restriction will reduce triglycerides, increase LDL particle size, while the fat in the diet will increase HDL levels.
    Having normal Lp(a), CRP and homocysteine is certainly better than having abnormal values, but I wouldn’t say it would compensate for small, dense LDL particles.

  25. Hi again,
    I feed my husband high quality organic grass fed beef, chicken, wild fish, whole grains (brown rice, whole wheat, spelt, lots of green leafy vegetables (particularly kale), all kinds of veggies, lots of herbs (fresh cilantro, parsley, oregano, basil), spices, some fruit (not much), nuts, seeds, some sea vegetables, butter and raw cheese from organic grass fed cows and occasionally raw milk. Not your typical SAD. We use extra virgin olive oil, coconut oil, grapeseed oil and ghee as well. Once or twice a week we may go out for pizza or wings and fries but that’s about it. We also drink red wine and beer but not to an excess maybe one to two with dinner. He eats well at work soups, salads, beans, chicken, etc. with olive oil mostly. He occassionally slips in some white pasta (maybe once a month at work but no cookeis, cakes candies). We try not to eat white carbs and sugar at all. We eat more fats and proteins than carbs. Maybe once every 3 months have ice cream or a dessert. With this diet my small ldl particle number are 130 with a total of ldl-p of 1159 while my husbands are B sand 2000. Most of mine are Pattern A though. My LDL are mod. high at 157 but my ration’s is good 3.3 (chol/hdl ratio) and my ldl/hdl ratio is 2.21. My TC is 244. Do you think I should cut back on the brown rice (now at 2 x a week)and whole wheat pasta (once a week) or cut down on the cheese, protein or fat. Could it be that we swung to far the other way and his body needs more high quality carbs?
    Hi Mary–
    I can’t give specific medical/nutritional advice, but I can tell you that despite the quality of the foods you are consuming, the carb count looks kind of high. Your pancreas doesn’t really care whether your carbs come in in the form of locally-grown, organic wheat flour or store-bought, non-organic flour – it’s all carbs, and the pancreas releases the same anount of insulin. And if too many carbs come in – even organic ones – insulin resistance and hyperinsulinemia can be the end result. And too much insulin can indeed cause more small LDL particles.
    Hope this helps.

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