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LDL, HDL, VLDL, and What's a Good Blood Lipid Profile?


#1

I wanted to start a thread to learn more about more recent understanding of what constitutes a good or bad blood lipid profile.

Used to be cholesterol was the go to number.

Then it was total/HDL ratio, good to be under 5, great to be in the 3s
(this still seems to be valid)

Then a look at triglycerides, and their relationship to sugar intake.

Then LDL and now VLDL (which seems to be predicted by triglyceride level very well)

What is the structural difference between LDL and VLDL? What about harms?

Are there lipids in the blood panel that are easier to get oxidized? My understanding is that the worst is triglycerides build with omega-6 fatty acids as a high percentage of the overall fatty acid makeup.


#2

I found this "Coffee by the Tank Car Does Not Increase Risk of Coronary Heart Disease" http://www.medpagetoday.com/Cardiology/Dyslipidemia/3154

Interesting because I used a press for a few years and felt bad, and switched back to a drip coffee maker.


#3

Bad link.


#4

Fixed.

I've also read recently that LDL gets used up fighting infections, expecially viruses, so low LDL can be a sign of infection and can even get higher if you haven't had an infection in a long time.


#5

It also looks now like I had a misunderstanding about one point. It looks like VLDL particles are LARGER than LDL particles, and VLDL lose something (triglycerides?) to produce LDL so they are higher "density" but smaller particles with more cholesterol and less triglyceride.


#6

There's a huge difference in situations between being, for example, an insurance actuary with access to blood data of tens of thousands of the insured and needing to predict the company's future health costs, versus being an individual trying to understand how his numbers affect him.

All kinds of papers and research exist which would be useful for the first. Low ratio of total to HDL cholesterol? For populations, good predictor of cardiovascular risk! For an individual wanting to understand what's happening in his body or what to do or when he's likely to die of heart disease, this measure is merely correlative, not causative and doesn't directly speak to mechanism though it's suggestive.

We do know mechanistically that oxidized LDL (at least past being mildly oxidized) is harmful, and high levels definitely correlate with direct risk and are probably causative. It's also at least correlative with increased risk of metabolic syndrome, and quite plausibly actions that reduce high oxidized LDL also reduce risk of developing metabolic syndrome. Glycated LDL also appears mechanistically to be a problem. I don't know of a test for it.

The great majority of studies cannot be used too conclusively because there are so many possible correlations rather than causative factors, and too many differences in subjects that may not be accounted for, and could never realistically be accounted for. The subjects of study that for example had lower LDL may have also had different dietary intake that wasn't accounted for and if thought of would have been thought unimportant or even having opposite than actual effect, to give one example. For example, "Oh, high corn and soybean oil intake, very good, that certainly can't be part of the observed increase in death rate so it must be this other correlated thing instead."

What we do know is that when per capita sucrose intake and linoleic acid as percentage of fat intake wasn't anything like now, and people were more active, there wasn't all this heart disease or metabolic disorder and we do have mechanistic reasons as to why these are highly plausible main factors and for expecting that improving them will be of help.


#7

Is oxidized LDL typically formed from triglycerides with a lot of PUFA fatty acids on them?

I am trying to understand and it seems from my reading that Saturated and MUFA's don't oxidize much, if at all.

Do we know what leads to glycation of LDL? Is it connected to high blood sugar or carbs in general or specifically fructose?

It would seem to me that the three keys are:

1) minimize fatty acids that are easily oxidized especially linoleic
2) maintain stable blood sugar which over lifetime involves maintaining insulin sensitivity
3) avoiding excessive oxidative stress (seems to show up in the aerobic research that runners have increase in CHD when they average more than about 25 miles a week, some studies are saying 15).

Where does fructose fit in? Does it mostly damage the liver? Could it make the liver insulin resistant leading to blood sugar problems? I know that when rats hit 4% fructose or 4% PUFA in their diet their lifespan drops and falls fast as those percentages increase.

Also how good are antioxidants at limiting oxidative stress? So they reduce oxidized triglyceride levels? Are they LESS important if you are not a) eating too much omega 6s or b) not running 25 miles a week?


#8

The oxidized fatty acid in oxidized LDL is usually linoleic acid.

Saturated fatty acids definitely don't oxidize at all, and MUFA as you say not much.

Glycation generally is promoted by high blood glucose, oxidative stress, and dietary AGE consumption.

While fructose often gets blame for being, reportedly, 8-10x more potent (effective per amount of concentration) in glycation than glucose, in the non-diabetic individual even when consming it fructose levels are on the order of 100 times lower than glucose, so glucose is still the main contributor of the two.

In individuals with diabetes, excess glucose causes much more metabolism by the polyol pathway which yields high cellular levels of fructose and therefore high glycation by this fructose.

Excess carbs in general can generate higher than desirable blood glucose levels if insulin sensitivity isn't as good as it might be, but don't necessarily have to generate high blood sugar, particularly if matching activity.

Dietary antioxidants can be of health benefit but I think usually not so much simply from being anti-oxidants per se. Loading up on beta carotene, Vitamin E (even mixed tocopherols) and Vitamin C for example won't do much for improving measurable parameters. Some phytochemicals which act to improve expression of metabolically important genes and/or to reduce production of inflammatory cytokines are also antioxidants but not all antioxidants will do the same. It's really a matter of specific properties rather than pure antioxidant ability.

Agreed with your keys!


#9

So are all AGES harmful, and given the concentrations in different foods: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704564/table/T1/ How do we minimize the harm?

Butter looks to be high in AGES. Does Ghee eliminate those problems? Also milk and milkfat has almost none. What's up with that?

If AGES are bad, why do we humans like seared meats, and carmelized/browned foods?

Also the highest AGE food is fried bacon. Aside from cooking less harshly is there a key to controlling AGE intake?


#10

Also, can saturated fat be glycated? (is is the same as glycosylated?).

Anyway, wondering if sat fat can be glycated because perhaps saturated fat becomes bad in people who have high blood sugar? It probably doesn't matter because the options are more glucose polymers, or more unsaturated fats which are not going to be any better.


#11

The conclusions here seem a bit stretched. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704564/

Heavy cream is far better than vegetable oils. Whole milk is better than soy milk. There is nothing that shows "full fat" dairy to be worse than reduced fat and yet the discussion specifically mentions low fat dairy.

Thinking about the butter 23,000 looks high, but 100 grams of butter is a lot of cals.

Quoting: The current dAGE database demonstrates that a significantly reduced intake of dAGEs can be achieved by increasing the consumption of fish, legumes, low-fat milk products, vegetables, fruits, and whole grains and by reducing intake of solid fats, fatty meats, full-fat dairy products, and highly processed foods. These guidelines are consistent with recommendations by organizations such as the American Heart Association (42), the American Institute for Cancer Research (43), and the American Diabetes Association (44). It should, therefore, be possible to integrate this new evidence into established guidelines for disease prevention as well as medical nutrition therapy for a wide variety of conditions.


#12

Though technically accurate in terms of the literature saying so, I wrote too quickly in saying "Glycation generally is promoted by... dietary AGE consumption."

That's probably an oversimplification. Many AGE's are poorly absorbed, and at least one study I particularly remember stated that circulating AGE's are mostly from production in the body rather than absorption from diet. (That said, addition to a rat's diet does have adverse effect, but how much does that apply to humans? Not directly known.)

Inasmuch as with even various all-raw diets that might be imagined, dietary AGE intake can easily be 10,000 AGE kU per day, so I suppose that sort of total level represents something pretty natural that is no problem.

Some of the extreme increases in foods that are seen with frying in particular but also other higher temperature forms of cooking could I suppose represent an issue, but it seems inadequately studied and I really can't say. I suppose a cautious person would substitute boiling, steaming etc and they might be right to do so, or they might miss flavor to no benefit, again can't say. As opinion I suppose the more at risk one sees oneself, the more the potential payoff of a bet to change cooking methods on the theory.


#13

And how do you reduce AGE production in the body? The only thing I've read is that galactose can produce it somehow.


#14

For moderating formation of AGE's in the body, these are plausible I think but not directly proven to be true in practice for humans:

healthy level of oxidative stress,
good antioxidant intake in general,
good glutathione stores,
healthful intake of gamma-tocopherol (as opposed to the alpha-tocopherol used in inexpensive vitamins),
reduction of inflammatory state if present, carb intake in moderate range neither very low nor very high,
probably moderation of linoleic acid intake if high (as a category of reduction of inflammatory state),
and possibly moderation of fructose intake, if high.


#15

Thanks for your informative post!


#16

Enjoying the thread so let me ask this, what do you want to see. You come out of the doctor's office with your cholesterol test in hand and what results would you love to see for

Total Cholesterol
LDL
HDL
Triglycerides
Any other you might think of

Conversely, what would you not want to see.

As was pointed out at the start, the shift has switched around so much on what are warning/bad signs that many doctors are going to be behind and giving out of date advice. Just curious about your answer and if you two(Mert and Bill) will be in agreement.


#17

This is tough because none of the numbers can be taken in a vacuum. Also total Cholesterol does not matter if LDL is good, and LDL does not matter if oxidized and glycated LDL (especially VLDL) is bad.

If you don't get more than 10 grams a day of PUFA's and your blood sugar is good and you don't get more than 25 grams a day of net fructose and you don't run more than about 15 miles a week or do other comparable high oxidative exercise then you probably don't have a lot of glycated and oxidized VLDL even if your cholesterol and LDL and triglycerides are high.

You could have a 300 cholesterol and 170 LDL and have zero problem if you

avoid the PUFAs
Fructose
high blood sugar
aerobic exercise above optimal health benefits (even elite runners who had adapted to aerobic stress started to have increase in heart disease when they averaged over 25 miles a week).

So you definitely want to see a HbA1C that is under 5.7, ideally under 5.3, and probably getting better down to 4.9 and maybe improving down to 4.6 though if the PUFAs and other problems are minimized I'd say that under 5.3 would be great.

If your HbA1C is under 5.3 you reduce your glycated VLDL already even if you have a lot of VLDL particles. IF you don't eat high omega-6 sources you are unlikely to have a lot of oxidized VLDLs and so honestly the externals are more important to me than the blood test results.

Less than 10 grams PUFA
Less than 25 net fructose
Less than 30% of maintenance calories from carbs plus some to meet post workoutout needs.
Less than 15-25 miles of running, or about 1 days worth of calories burned a week in aerobic activity above a few METS.

3) I would definitely want to see an A1C under 5.6, really under 5.3

I would want to see a cholesterol that is not too low and I think 185 is too low. We bring it down to 185 because for most people this will reduce the glycated and oxidized VLDL, but you can virtually eliminate those with diet with a 250 cholesterol.

2) So maybe a 200-240 total cholesterol, perfect maybe 220. higher could mean that you have microvascular damage and that the cholesterol is raised to HEAL it, but it is not the cause. I'd rather have a 265 than a 165.

LDL? You need LDL to fight infections if they arise. A very low LDL can mean a chronic infection or autoimmune problem but a high LDL can mean thyroid deficiency.
I would definitely want a total to HDL of 5 or less, and at least 40 HDL, so 200 and 40 or 250 and 50. I'd prefer more like 225 and 65 for about a 3.5 to 1 ratio.

They probably should not even be testing total cholesterol any more except that it might tell you that you have inflammation, but lowering it with a statin is defeating the purpose of cholesterol unless you have blockages already.

So it depends on whether you already have ischemia or not. Without ischemia and with diet in order and stress managed there is nothing wrong with a 250+ cholesterol.

I hope others will chime in. I would say that if your cholesterol or LDL is high the worst thing you can do is try to lower it with cholesterol lowering high omega 6 plant oils because it will just mean that now your LDL particles are high, and also easily oxidized, or to take a statin or even try to lower your cholesterol if you have no ischemia.


#18

Regarding blood sugar and HbA1c, I can't link, but here is an excerpt of a comparison of "good" HbA1C and "too low". Some believe that the lower the better down to 4.0, but large studies show lowest mortality with an HbA1C of 5.0-5.4, and higher mortality both above and below those marks.

"The U-shaped mortality curve is very clear. In raw data and all models, the lowest mortality is with HbA1c between 5.0 and 5.4. Mortality increases with every step down in HbA1c: in Model 1, mortality is 8% higher with HbA1c between 4.5 and 4.9, 31% higher between 4.0 and 4.4, and 273% higher below 4.0."


#19

I suspect that HbA1C correlates well to the percentage glycation of VLDL. It doesn't mean that moderate glycation is better than low, but that there are advantages in having an average blood sugar above 90 (stroke survival, etc.).


#20

Anyone know much about LPA? Supposed to be largely genetic, doesn't respond to stains, diet, or lifestyle. And substantially increases cardiovascular risk (by like 300%). Only niacin is supposed to help.

I'm still unclear if LPA is actually counted as LDL in a standard cholesterol test. I know you can get tested for LPA as a separate test.