Thank,

Mary

Those add to the carb load.

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–

MRE

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–

MRE

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.

http://www.westonaprice.org/knowyourfats/saturated-fat-attack.html

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.”

http://www.surgery.usc.edu/divisions/hep/livernewsletter-riskfactorsforalcoholicliverdisease.html

Hi Bruce–

MRE

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.

MRE

“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)

http://raypeat.com/articles/articles/fats-degeneration.shtml

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.

MRE

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.
http://jn.nutrition.org/cgi/reprint/51/3/441.pdf

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.

MRE

http://www.westonaprice.org/knowyourfats/saturated-fat-attack.html

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.

Dave

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.

Cheers–

MRE 

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

Lipids

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.

Questions:
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.

Thanks,
Cathy

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.

Best–

MRE 

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.

Best–

MRE