Saturday, February 13, 2010

Want to improve your cholesterol profile? Replace refined carbs and sugars with saturated fat and cholesterol in your diet

An interesting study by Clifton and colleagues (1998; full reference and link at the end of this post) looked at whether LDL cholesterol particle size distribution at baseline (i.e., beginning of the study) for various people was a determinant of lipid profile changes in each of two diets – one low and the other high in fat. This study highlights a few interesting points made in a previous post, which are largely unrelated to the main goal or findings of the study, but that are supported by side findings:

- As one increases dietary cholesterol and fat consumption, particularly saturated fat, circulating HDL cholesterol increases significantly. This happens whether one is taking niacin or not, although niacin seems to help, possibly as an independent (not moderating) factor. Increasing serum vitamin D levels, which can be done through sunlight exposure and supplementation, are also known to increase circulating HDL cholesterol.

- As one increases dietary cholesterol and fat consumption, particularly saturated fat, triglycerides in the fasting state (i.e., measured after a 8-hour fast) decrease significantly, particularly on a low carbohydrate diet. Triglycerides in the fasting state are negatively correlated with HDL cholesterol; they go down as HDL cholesterol goes up. This happens whether one is taking niacin or supplementing omega 3 fats or not, although these seem to help, possibly as independent factors.

- If one increases dietary fat intake, without also decreasing carbohydrate intake (particularly in the form of refined grains and sugars), LDL cholesterol will increase. Even so, LDL particle sizes will shift to more benign forms, which are the larger forms. Not all LDL particles change to benign forms, and there seem to be some genetic factors that influence this. LDL particles larger than 26 nm in diameter simply cannot pass through the gaps in the endothelium, which is a thin layer of cells lining the interior surface of arteries, and thus do not induce plaque formation.

The study by Clifton and colleagues (1998) involved 54 men and 51 women with a wide range of lipid profiles. They first underwent a 2-week low fat period, after which they were given two liquid supplements in addition to their low fat diet, for a period of 3 weeks. One of the liquid supplements contained 31 to 40 g of fat, and 650 to 845 mg of cholesterol. The other was fat and cholesterol free.

Studies that adopt a particular diet at baseline have the advantage of departing from a uniform diet across conditions. They also typically have one common characteristic: the baseline diet reflects the beliefs of the authors about what an ideal diet is. That is not always the case, of course. If this was indeed the case here, we have a particularly interesting study, because in that case the side findings discussed below contradicted the authors’ beliefs.

The table below shows the following measures for the participants in the study: age, body mass index (BMI), waist-to-hip ratio (WHR), total cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol, and three subtypes of high-density lipoprotein (HDL) cholesterol. LDL cholesterol is the colloquially known as the “bad” type, and “HDL” as the good one (which is an oversimplification). In short, the participants were overweight, middle-aged men and women, with relatively poor lipid profiles.


At the bottom of the table is the note “P < 0.001”, following a small “a”. This essentially means that on the rows indicated by an “a”, like the “WHR” row, the difference in the averages (e.g., 0.81 for women, and 0.93 for men, in the WHR row) was significantly different from what one would expect it to be due to chance alone. More precisely, the likelihood that the difference was due to chance was lower than 0.001, or 0.1 percent, in the case of a P < 0.001. Usually a difference between averages (a.k.a. means) associated with a P < 0.05 will be considered statistically significant.

Since the LDL cholesterol concentrations (as well as other lipoprotein concentrations) are listed on the table in mmol/L, and many people receive those measures in mg/dL in blood lipid profile test reports, below is a conversion table for LDL cholesterol (from: Wikipedia).


The table below shows the dietary intake in the low and high fat diets. Note that in the high fat diet, not only is the fat intake higher, but so is the cholesterol intake. The latter is significantly higher, more than 4 times the intake in the low fat diet, and about 2.5 times the recommended daily value by the U.S. Food and Drug Administration. The total calorie intake is reported as slightly lower in the high fat diet than in the low fat diet.


Note that the largest increase was in saturated fat, followed by an almost equally large increase in monounsaturated fat. This, together with the increase in cholesterol, mimics a move to a diet where fatty meat and organs are consumed in higher quantities, with a corresponding reduction in the intake of refined carbohydrates (e.g., bread, pasta, sugar, potatoes) and lean meats.

Finally, the table below shows the changes in lipid profiles in the low and high fat diets. Note that all subtypes of HDL (or "good") cholesterol concentrations were significantly higher in the high fat diet, which is very telling, because HDL cholesterol concentrations are much better predictors of cardiovascular disease than LDL or total cholesterol concentrations. The higher the HDL cholesterol, the lower the risk of cardiovascular disease.


In the table above, we also see that triglycerides are significantly lower in the high fat diet, which is also good, because high fasting triglyceride concentrations are associated with cardiovascular disease and also insulin resistance (which is associated with diabetes).

However, the total and LDL cholesterol were also significantly higher in the high fat compared to the low fat diet. Is this as bad as it sounds? Not when we look at other factors that are not clear from the tables in the article.

One of those factors is the likely change in LDL particle size. LDL particle sizes almost always increase with significant increases in HDL; frequently going up in diameter beyond 26 nm, and thus passing the threshold beyond which an LDL particle can penetrate the endothelium and help form a plaque.

Another important factor to take into consideration is the somewhat strange decision by the authors to use the Friedewald equation to estimate the LDL concentrations in the low and high fat diets. Through the Friedewald equation, LDL is calculated as follows (where TC is total cholesterol):

    LDL = TC – HDL – Triglycerides / 5

Here is one of the problems with the Friedewald equation. Let us assume that an individual has the following lipid profile numbers: TC = 200, HDL = 50, and trigs. = 150. The calculated LDL will be 120. Let us assume that this same individual reduces trigs. to 50, from the previous 150, keeping all of the other measures constant. This is a major improvement. Yet, the calculated LDL will now be 140, and a doctor will tell this person to consider taking statins!

By the way, most people who do a blood test and get their lipid profile report also get their LDL calculated through the Friedewald equation. Usually this is indicated through a "CALC" note next to the description of the test or the calculated LDL number.

Finally, total cholesterol is not a very useful measure, because an elevated total cholesterol may be primarily reflecting an elevated HDL, which is healthy. Also, a slightly elevated total cholesterol seems to be protective, as it is associated with reduced overall mortality and also reduced mortality from cardiovascular disease, according to U-curve regression studies comparing mortality and total cholesterol levels in different countries.

We do not know for sure that the participants in this study were consuming a lot of refined carbohydrates and/or sugars at baseline. But it is a safe bet that they were, since they were consuming 214 g of carbohydrates per day. It is difficult, although not impossible, to eat that many carbohydrates per day by eating only vegetables and fruits, which are mostly water. Consumption of starches makes it easier to reach that level.

This is why when one goes on a paleo diet, he or she reduces significantly the amount of dietary carbohydrates; even more so on a targeted low carbohydrate diet, such as the Atkins diet. Richard K. Bernstein, who is a type 1 diabetic and has been adopting a strict low carbohydrate diet during most of his adult life, had the following lipid profile at 72 years of age: HDL = 118, LDL = 53, trigs. = 45. His fasting blood sugar was reportedly 83 mg/dl. Click here to listen to an interview with Dr. Bernstein on the The Livin' La Vida Low-Carb Show.

The lipid profile improvement observed (e.g., a 14 percent increase in HDL from baseline for men, and about half that for women, in only 3 weeks) was very likely due to an increase in dietary saturated fat and cholesterol combined with a decrease in refined carbohydrates and sugars. The improvement would probably have been even more impressive with a higher increase in saturated fat, as long as it was accompanied by the elimination of refined carbohydrates and sugars from the participants’ diets.

Reference:

Clifton, P. M., M. Noakes, and P. J. Nestel (1998). LDL particle size and LDL and HDL cholesterol changes with dietary fat and cholesterol in healthy subjects. J. Lipid. Res. 39: 1799–1804.

12 comments:

P. Hentermine said...

take healthy diet daily and avoid fatty food,which help us to control our cholesterol level.

Ned Kock said...

Yeah, right!

Avoid fatty food and you're back to refined carbs and sugars - a great recipe for disaster!

Unless you intend to feed exclusively on protein powders, protein-rich foods are usually fatty.

But what am I doing responding to a spam post!?

Anonymous said...
This comment has been removed by a blog administrator.
generic viagra said...
This comment has been removed by a blog administrator.
Ned Kock said...

Two spam comments deleted.

Eddie Marthin said...

Hello Ned,

Great information, thanks for sharing your research.

Dr. Ron Rosedale MD seems to be one of the most knowledgeable in the application of leptin. If you have not yet read his work, you may want to Google (Rosedale leptin insulin) to see some of his awesome articles. His info on the problems with too much protein has motivated me reduce protein to about 120 gm/day. ( add protein to the Google to read his article)

His book, "The Rosedale Diet" has great info about how to 1) lose weight in a very easy way through high fat, adequate protein, low carbs, while achieving lower total cholesterol, triglycerides, LDL increasing HDL. 2) obtain benefits of a caloric restriction diet, while eating lots of calories. I've had great success with this diet.

I have read that main factor in production of dense LDL is high insulin and leptin levels. I intend to get a VAP test soon, and hopefully I will be mostly the fluffy LDL.

Your reference to the 1998 study on fats & cholesterol is one that will greatly help me in selling my case to my father that he needs to decrease his sugars/carbs, and increase his saturated fat, and monounsaturated fat intake while eliminating the oxidized commercial polyunsaturated vegetable oils (corn, soy, canola etc). Much of my info from Dr. Mary Enig.

Also, you may want to consider looking at Inflammaging (combination of inflammation and aging) , I believe it is a main factor in the diseases of aging, such as cardiovascular disease, osteoporosis, Alzheimer's etc.

First medical use of Inflammaging http://www.ncbi.nlm.nih.gov/pubmed/17116321

Theory that it may be an autoimmune disease http://www.immunityageing.com/content/3/1/12

Very glad I found your blog. I intend to read some more of your posts.

Thanks for your help. Keep up the good work.

Have a Blessed Day, in Christ,

Eddie Marthin

Ned Kock said...

Hi Eddie.

Yes, Dr. Rosedale has some very interesting ideas. I am not sure all of them are right, but they are certainly interesting.

For example, he argues that billions of years ago plants poisoned the environment with oxygen. Then animals had to develop metabolic processes that relied on oxygen, because it was so plentiful.

The problem with this hypothesis is that the main constituent of air is not oxygen. The main constituent of air is, by far, nitrogen.

As for the idea that high insulin levels are the problem, which Dr. Rosedale strongly espouses, it is not consistent with the study reviewed in this post:

http://healthcorrelator.blogspot.com/2010/05/postprandial-glucose-levels-hba1c-and.html

The problem seems to be glucose levels, particularly post-prandial glucose. I say this because protein also leads to an insulin response. And I don't think that is a problem.

Btw, your intake of protein seems reasonable to me.

But the above is mostly an academic issue, because insulin levels tend to rise to unnaturally high levels in response to the ingestion of refined carbs and sugars. So the two, insulin and glucose levels, are going to be highly correlated in most westernized populations.

acai buy said...
This comment has been removed by a blog administrator.
Ned Kock said...

Spam comment above deleted.

viagra online said...

This is something hard because I love eating junk food, I know I have to avoid it because I've had serious problems, by the way this is perfect to avoid my behaviors.m10m

generic cialis said...

I always try to avoid fats and sugars because they made me fat and I have some kind of fobia to fat, anyway I always try to eat healthy stuff, and use special oil for food and vegetables, specially vegetables and meats, thanks for the advice.

low cholesterol diet said...

rstHi administrator, I’ve just a little request. I had been just googleing for some information on the subject you printed and found this post. Some very nice materials you posted proper here. Can I if possible discuss this submit on my new website I am creating? This might be terrific. I will verify again but once more afterwards to find out how you replied. Many thanks