The many faces of LDL

29. January 2008 William Davis (0)
Pam has an LDL cholesterol of 144 mg/dl.

To most people, this means that she has a mildly elevated LDL value. Many people would respond by cutting the saturated fat in their diet. Most physicians would concur and talk about prescribing a statin drug.

Let me tell you what an LDL cholesterol of 144 mg/dl means to me:

1) It could mean an LDL of all large particles (which is good) or an LDL of all small particles (which is very bad). Or, perhaps it's some combination of big and small. I can't tell which just by knowing that LDL is 144.

Small LDL responds to a diet reduced in processed carbohydrates and wheat flour; large LDL does not. Small LDL responds in an exagerrated way to niacin; large LDL does not. It makes a difference.

2) It could mean that, hidden within LDL, is lipoprotein(a), or Lp(a). Recall that Lp(a) is a high-risk genetic pattern that can provide the false appearance of high LDL cholesterol. If Pam were prescribed a statin drug, it would have little effect and little benefit. (See Red flags for Lipoprotein(a).)

Knowing that Pam has Lp(a) can point us in an entirely different direction than just LDL cholesterol. It might mean high-dose fish oil, a more serious approach to niacin, hormonal treatments like DHEA or testosterone. It might mean more attention to warning your children about the possibility that they, too, might share this genetic trait.

3) It could mean both small LDL and Lp(a) are present simultaneously, an especially dangerous combined pattern that is among the highest risks for heart disease known.

4) Because Pam's LDL of 144 mg/dl was not measured, but calculated, it means that it is subject to tremendous inaccuracy.

In my office, calculated LDL cholesterols can be inaccurate by 50 or 100 mg/dl--commonly. So Pam's LDL of 144 mg/dl could really be 70 mg/dl, or it could be 244 mg/dl. Once again, it's a big difference.


Just like The Three Faces of Eve, the 1957 film in which Joanne Woodward played the three wildly different sides of Eve's personality--the daytime Eve White, the fun-loving and daring Eve Black, and Jane--so can LDL assume several different faces, all with different personalities, different implications.

Accepting LDL cholesterol as LDL cholesterol is a fool's game. It is only a starting point, nothing more. Accepting a statin drug based on LDL is, likewise, a trap fraught with uncertainty, the potential for limited or ineffective results, the price being your heart and health.
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Lipoprotein(a) treatment alternatives

Lipoprotein(a) treatment alternatives

1. November 2006 William Davis (2)
A question from a reader:


Two years ago, my doctor recommended a comprehensive lipid screening because both of my parents had heart disease. My only blood component way out of line was LP (a) [lipoprotein(a)]. It was 130. According to the lab that conducted the screening, Berkeley Heart Lab, a level above 30 should be cause for concern. I was stunned that mine was more than quadruple the danger level.

I began taking two grams [2000 mg] of niacin a day in addition to the Lipitor I was already taking. The next reading, a few months later, was 87. Over a period of about 18 months, I had a total of four readings from Berkley Heart Lab. My LP (a) fluctuated in the 80-130 range – still way above normal. My doctor said there was little else I could do to control it.

That doctor has since retired. I now see another doctor who uses a different lab. My first LP (a) reading with him a few months ago was 17, which is normal. I am still taking the same amount of niacin and Lipitor and I can’t think of anything that would account for the huge discrepancy. I’m going to have another test again soon.

Is one of the labs giving erroneous readings? If so, how can I tell which? If Berkeley Heart Lab is correct, is there anything I can do about my increased coronary risk due to high LP (a)?
Tom D.

Tom's frustration on the variation of Lp(a) is due to the fact that laboratories run the Lp(a) test by several different techniques and will generate tremendous variation in values. The key is to stick to the same measure over and over from the same lab, else you'll be terribly confused and frustrated. Tom essentially should ignore the value obtained that was unexpectedly low.

Another issue: Lp(a) is a turtle. It responds very slowly. In fact, we rarely check it more than once or twice a year. Check it too soon after a treatment change and it won't fully reflect the effect. You've got to wait at least several months before re-checking.

How about treatment alternatives? They are:

--More niacin. Not my favorite choice, since niacin >2000 mg per day begins to generate more side-effects, but it is a choice. You can go to 4000-5000 per day, but only with your doctor's supervision due to liver effects.

--Testosterone for males. We use topical testosterone from Women's International Pharmacy in Madison, Wisconson. Prescription patches like Testim are also effective.

--Estrogen for females. This is less "clean" than testosterone, introducing questions about endometrial and breast cancer risk, but it is a choice.

--DHEA--A small effect but every little bit can help. We use 25-50 mg per day, depending on blood levels and only if you're 45 years old or older.

--l-carnitine--In my experience, a small effect. It requires 2000 mg per day, which is expensive. Sometimes, an expected large effect develops, so it's worth a try if it fits in your budget.

--Fibrates--These are the drugs Tricor and Lopid. I don't like these agents very much because I think they're weak, including the effect on Lp(a) reduction. But they are choices for you and your doctor.

Lastly, you can simply be guided by your heart scan score. For example, if Tom's initial heart scan score is 200, and he continues his current program and one year later his score is 300, then alternative treatments are worth considering. But what if Tom's score is 189--he's regressed his coronary plaque. Then, who cares what his Lp(a) is?

Another issue to keep in mind is that, in the presence of Lp(a), keeping LDL to very low numbers (e.g., 60 mg/dl) may added value in preventing coronary plaque growth.
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Comments (2) -

  • Anonymous

    3/13/2010 10:53:24 PM |

    I also have super high little (a) and my other cholesterols are fine.  No heart disease I know of yet, but have had bilateral carotid endarterectomies and now one has re-stenosed in less than a year. (likely scar-tissue, as the older endarterectomy site remains perfectly clear).  I'll get a stent soon.  I take niacin, fish oil, etc.  I, too, was told there's no other treatment, but that is not entirely true.  I have been receiving LDL apheresis every two weeks for a year and it brings my Lp(a) down to mid-twenties from about 120 (rebound?). When diagnosed it was 253.  Apheresis is extreme and is only used in people who have had an "episode" like a stroke, heart attack or related surgery, but I'm pretty sure it's what's keeping me alive and able-bodied.  I hope doctors will become more aware of this option for their patients who really need it.  BTW--it gets my LDL as low as 6 (!) What you said about keeping LDL low is critical; the liver needs LDL to make all that nasty little (a).  Thanks for bringing up the subject!

    Karen P

  • buy jeans

    11/2/2010 7:53:17 PM |

    Another issue: Lp(a) is a turtle. It responds very slowly. In fact, we rarely check it more than once or twice a year. Check it too soon after a treatment change and it won't fully reflect the effect. You've got to wait at least several months before re-checking.

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Aspirin, Lipitor, and a low-fat diet

Aspirin, Lipitor, and a low-fat diet

17. April 2009 William Davis (0)
Despite all the hoopla heart disease receives in the media, I continue to marvel at how many people I meet who still think that aspirin, Lipitor, and a low-fat diet constitute an effective heart attack prevention program.

It doesn't. No more than washing your hands prevents all human infections. It helps, but it is a sad substitute for a real prevention program.

Of course, aspirin, Lipitor, and a low-fat diet is the same recipe followed by the unfortunate Tim Russert and his doctors. You know how that turned out. Mr. Russert's experience is far from unique.

What is so magical about aspirin, Lipitor and a low-fat diet?

There is a simple rationale behind this approach. Aspirin doesn't reduce atherosclerotic plaque growth, but it inhibits the propagation of a blood clot on top of a coronary plaque that has "ruptured," thereby reducing likelihood of heart attack (which occurs when the clot fills the artery). So aspirin only provides benefit if and when a plaque ruptures.

Lipitor and other statin drugs reduce LDL cholesterol, promote a modest relaxation of constricted plaque-filled arteries (normalization of endothelial dysfunction), and exerts other effects, such as inflammation suppression.

A low-fat diet is intended to reduce saturated fat that triggers LDL cholesterol formation and to encourage intake of whole grains that reduce cardiovascular events and LDL cholesterol.

If that is the extent of your heart disease prevention program, you will have a heart attack, bypass surgery, or stent--period. It may not be tomorrow or next Friday, or even next month. Aspirin, Lipitor, and a low-fat diet may delay your heart attack or procedure for a few years, but it will not stop it.

Some flaws in the aspirin, Lipitor, low-fat program:

--Aspirin can only exert so much blood clot-blocking effect. It can be overwhelmed by many other factors, such as increased blood viscosity, increased fibrinogen (a blood clotting protein that also triggers plaque), and plaque inflammation.
--Lipitor reduces LDL, but does not discriminate between the relatively harmless large LDL and the truly plaque-triggering small LDL--it reduces all LDL, but small LDL can still persist, even at extravagant levels since neither aspirin nor Lipitor specifically reduces small LDL, while a low-fat diet increases small LDL.
--Low-fat diet--A diet reduced in fat and loaded with plenty of "healthy whole grains" will trigger increased small LDL (an enormous effect), c-reactive protein, high blood sugar, resistance to insulin, high blood pressure, and an expanding abdomen ("wheat belly").


Aspirin, Lipitor and a low-fat diet do not address:

--Vitamin D deficiency
--Omega-3 fatty acid deficiency and the eicosanoid path to inflammation
--High triglycerides
--Small LDL particles
--Distortions of HDL "architecture"
--Lipoprotein(a)--the worst coronary risk factor nobody's heard of
--Thyroid status

In other words, the simple-minded, though hugely financially successful, conventional model of heart disease prevention is woefully inadequate.

Don't fall for it.

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The Omega-3 Index: The higher, the better?

The Omega-3 Index: The higher, the better?

6. October 2009 William Davis (26)
So you take a few fish oil capsules every day and eat fish once or twice a week. What is the blood and tissue level of omega-3 fatty acids generated by your habits?

A number of variables enter into the equation. For instance, if you take fish oil capsules, what is the concentration of omega-3 fatty acids? How well are they absorbed? After absorption, how effectively are omega-3 fatty acids incorporated into cell membranes?

Even if you take fish oil supplements, it is hard to know just how much you’ve increased blood levels. It is now possible to measure the amount of omega-3 fatty acids in your bloodstream, a value called the omega-3 index. Too little and you might still be at high risk for cardiovascular events.


The Omega-3 index and sudden cardiac death

Two large studies have demonstrated that higher omega-3 blood (the level in red blood cells, or RBCs) levels were associated with reduced likelihood of sudden cardiac death. The risk for sudden cardiac death was 10-fold higher for the lowest omega-3 RBC levels compared to the highest.



Harris WS 2008; adapted from Siscovick DS et al 1995 and Albert CM et al 2002
(The omega-3 Index was derived from whole blood omega-3 levels, which correlate with RBC omega-3 levels, and are thus “estimated.”)


What’s the average omega-3 RBC level for Americans? Most Americans have omega-3 RBC levels in the 2.5-4.0% range, consistent with the tallest bars at the left and associated with greatest risk for sudden cardiac death. People with heart disease can have levels less than 1%. Some authorities propose that this new measure be called the omega-3 index.

Subsequent studies have shown that the omega-3 index has greater power to discriminate who will have a heart attack or die from sudden cardiac death better than any other common laboratory measure of coronary risk, including LDL cholesterol, HDL cholesterol, triglycerides, total cholesterol to HDL ratio, homocysteine, and c-reactive protein.

Just as hemoglobin A1c offers a 3-month look into blood glucose levels, the omega-3 index reflects your long-term omega-3 intake. The quantity of RBC omega-3s also closely parallels the quantity of omega-3s in heart tissues.


What is an ideal omega-3 index?

The above studies relating RBC omega-3 levels and sudden cardiac death suggest that a level of 6.3-7.3% is associated with far fewer fatal events?but events are not eliminated at this level. Is there even greater benefit with levels higher than 6.3-7.3%?

A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks. This suggests that even higher levels are necessary to prevent non-fatal events.

Should we target 10%? 12%? Maybe higher? Any higher and we are toeing the level achieved by the Inuits, the “Eskimoes” of Greenland, northern Canada and Alaska who have been observed to have a low rate of heart disease.


What’s your omega-3 index?

The appreciation of the importance of omega-3 fatty acids marks one of the greatest health revelations of the last 50 years. We can now measure it.

The ability to measure the proportion of omega-3 fatty acids in red blood cells may provide yet another means for all of us to further reduce risk for cardiovascular events.

If you are interested in knowing your omega-3 index, we are now making the fingerstick test kits available by going here.
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Comments (26) -

  • Red Sphynx

    10/6/2009 5:05:01 AM |

    Cool.

    But reading your ad page, it isn't clear to me.  Does this kit measure the abundance of all the ω-3 and ω-6 (including the n-18 linoleic / linolenic acids)?  Or is it specific to the long chain (EPA+DHA / AA)?

  • antidrugrep

    10/6/2009 9:05:37 AM |

    One thing that seems to be left out of this analysis: omega-3 to omega-6 RATIO. There is some evidence that the ratio is what is important, and biochemically it makes some sense. The PUFAs compete for the enzymes in the eicosanoid pathways, determining relative strength of the inflammatory response. Nowadays, the typical developed-world diet contains far more vegetable oil (rich in omega-6) than people are adapted to. To keep the ratio favorable would require far more omega-3 than a traditional Inuit would need to achieve the same effect on chronic inflammation. To my patients, I stress the importance of limiting use/consumption of vegetable oils as much as seeking extra fish oil.

    And by-the-by, there may be a trade-off for the Inuits' lower risk of heart disease - I can't cite a source at the moment, but do you recall hearing that their risk of hemorrhagic stroke is/was higher? The speculation being that the less-active omega-3-based thromboxanes permitted more bleeding to occur. Don't misunderstand me, I'm a big proponent of omega-3 supplementation (I take 6+ grams of fish oil daily myself). But I'm thinking that there must be an optimal ratio/dose, leading to a "trough" in mortality.

  • Dr. William Davis

    10/6/2009 10:48:49 AM |

    Red-

    The omega-3s measured are EPA and DHA.


    Antidrugrep--

    Interesting name!

    To my knowledge, the question has been raised but not confirmed. However, there is prolongation of a measure called "bleeding time" in some Inuit groups, though not all.

  • Health Man

    10/6/2009 1:35:48 PM |

    I've had this test done using the home kit. My test measured RBC levels of EPA, DHA, ALA, 4 monounsaturates, 7 omega-6s, 4 saturated fats and 3 trans fats.  It also shows Omega-6/Omega-3 ratio and AA/EPA ratio.

    For what it's worth, I was taking 1,600 mg of total EPA/DHA and my Omega-3 index was only 7.3%.  I've upped my intake to 2,000 mg EPA/DHA daily to try and get it over 8%.

  • Dr. B G

    10/6/2009 3:20:32 PM |

    Awesome post Dr. Davis!!!


    antidrugrep -- I concur! that wins for  name of the year! *haa*

    For 24 mos I took high dose omega-3 4-8 grams daily (SUPER EPA by Now -- I have no finanacial afflilation with them). For my ENTIRE life I consumed a LOT of omega-6
    --cooked with gallons of canola oil (dep on the brand may be 20-30% omega-6 LA)
    --ate fast food
    --ate margarine in the 1970-1990s
    --ate restaurant food and still do (it's ALL n-6 PUFAs and worse trans-fat unless you are in NYC)


    Omega-6 stays in our cell membranes for up to 18-24 mos (or longer). On the hand omega-3s (flaxseed, EPA DHA) are used up and depleted very quickly for cellular processes, cemm membrane structure/ compositon, nerve conduction, heart rate regulation, and in the control of cardiac and mitochondrial energetics.

    A few years ago, the ratio of n-6:n-3 in the U.S. was estimated to be 30:1 however I believe it is somehow far worse. The AHA recommendations will push it even further up (subequently raising cancer and CAD rates).

    You bring up an excellent point -- I believe the Inuit experience hemorrhagic strokes if the ratio is below 1.0 (n-6:n-3). This low ratio would be  VERY hard to establish consuming modern foods. All industrial lot cheese, milk, dairy, eggs,  beef, pork, chicken of CHOCK FULL of n-6.  

    This low ratio is difficult as well to achieve when inflammation is present
    --heart disease (post-cabg, PTCA, MI, revasc)
    --subclinical heart disease
    --food allergies (gluten, A1 casein, dairy,e tc)
    --hypertension, diabetes, Metabolic Syndrome, hyperinsulinemia, obesity, asthma, chronic kidney disease (Cr > 1.0-1.2), low HDL/high sdLDL, etc
    --chronic pain syndromes, fibromyalgia, LBP, migraines, etc
    --mental illness (SAD, depression, schizo, bipolar which occurs freq in inflammed or CAD patients)

    -G

  • Kismet

    10/6/2009 9:30:17 PM |

    I'm just not sure, if high N-3 doses are necessary for otherwise healthy people.
    The JELIS study suggests that there is no significant benefit in primary prevention from 1800mg EPA in a Japanese population (high background consumption of fish), while there were significantly more side-effects.
    The study looked somewhat stronger when it comes to secondary prevention, but, again, only soft endpoints were affected (if I recall correctly).

    Due to the small rate of eventes, the study apparently lacked power to detect changes in some of the sub-groups, but it really did not look that impressive for primary prevention...

  • Dr. William Davis

    10/6/2009 10:45:38 PM |

    Hi, Kis--

    I believe that JELIS showed a 19% (relative reduction) in cardiovascular events in a primary prevention population when 1800 mg EPA was added to the already substantial omega-3 intake of the nearly 19,000 Japanese participants.

  • Neonomide

    10/7/2009 12:15:21 PM |

    I might add that in JELIS study the japanese used EPA ethyl ester, which has a bit different pharmacological profile thaan common EPA.

    For example, EPA ethyl ester (E-EPA) may cross blood-brain barrier more easily than common EPA.

    http://www.ncbi.nlm.nih.gov/pubmed/19442696

  • Boris

    10/7/2009 1:54:13 PM |

    The test looks kind of pricey. If I take the test once as a baseline then when should I take it again after making a change in my omega-3 intake? 6 months? 6 weeks? A year?

  • Boris

    10/7/2009 6:45:31 PM |

    I don't mean to hijack the topic but can someone tell me what the difference is between omega-3 and ethyl ester based omega-3?

  • Nameless

    10/7/2009 8:23:47 PM |

    Hey Kismet,

    One thing about the Jelis study that shouldn't be overlooked is the fact they used EPA only.

    If I remember my Pubmed studies correctly, DHA tends to be the Omega 3 that increases HDL, and decreases trigs more than EPA does.

    And fish (real fish) usually have a higher DHA/EPA ratio than fish oil capsules do. I sometimes wonder if a higher DHA ratio or DHA alone may be a better therapy for heart people.

    As for forms, I'm not sure if ethyl ester matters... maybe? Perhaps it absorbs less than the trigylercide form does, but most studies tend to use ethyl esters anyway. Populations studies excluded, of course, as they just eat fish.

  • homertobias

    10/7/2009 11:42:36 PM |

    I just don't understand the utility of taking a test.  Why?  Just to look at a number?  Similiar tests have been available for a number of years, are not reimbersible by insurance, and may be of questionable accuracy.  
    To me, both limiting omega 6's and increasing DHA/EPA is a slam dunk.  Of course it should be done and there is no way that any of us will get anywhere near the Intuit's 1:1 ratio.  Anyway, hemorrhaggic strokes, even if you were to double your risk, would still be a rare event especially compared to an MI or thrombotic stroke.  
    Too much fish oil?  Your pocketbook may limit you, your rosacea may limit you, diarrhea/ GI side effects may limit you, but not a blood test.
    Too little Omega 6?  I guess Borage Oil is ok for a transfat but I wouldn't pay money for it. And the food industry's Omega 6 PUFA's,.....well you know.

  • Roger

    10/8/2009 12:16:02 AM |

    It's all a bit confusing.  We're told that nuts are associated with improved heart health, yet nuts are chalk full of Omega-6.  (Even walnuts, the nut with the most Omega-3, is still 4 to 1 Omega 6.)

  • susan allport

    10/8/2009 2:00:56 PM |

    I thought you would be interested in my article on omega-3s in Prevention Magazine: http://health.msn.com/nutrition/articlepage.aspx?cp-documentid=100245164

  • Robb Wolf

    10/8/2009 5:55:13 PM |

    doc-
    Outstanding piece and blog. I've been a fan of your work for a long time, keep it up!!

  • Dr. William Davis

    10/8/2009 10:07:41 PM |

    Hi, Robb--

    Good to see you here!

    You are doing absolutely fabulous work on your blog.

    Anyone interested in an exceptionally insightful discussion of the role of diet, exercise, and supplements would benefit from reading Robb's wonderful blog: Robb Wolf: Intermittent Fasting, Fitness, Paleo & CrossFit Nutrition
    at http://robbwolf.com.

  • Dr. William Davis

    10/9/2009 2:28:11 AM |

    Hi, Boris--

    My understanding is that the ethyl ester form is simply a modification to allow more omega-3s to be contained within a smaller volume. While prescription Lovaza uses the ethyl ester form, so do some quality retail brands, such as Costco's enteric-coated ethyl ester fish oil.

  • Nameless

    10/9/2009 4:57:28 AM |

    Costco's Kirkland enteric-coated ethyl ester failed a Consumer Labs test, just in case people didn't know. The enteric coating didn't work right and released the oil too soon. The actual fish oil in the capsule is fine, or should be  (Meg-3, which it uses, is considered pretty good). But if anyone is taking it solely because of the enteric coating, and are getting fishy burps, perhaps it isn't working correctly.

    http://www.healthnews.com/natural-health/vitamins-supplements/consumerlab-finds-fifty-fish-oil-supplements-free-contaminants-1553.html

    You can find the same Meg-3 from Jarrow pretty cheap, although it's not enteric coated and capsules are somewhat large.

  • Boris

    10/10/2009 1:28:40 PM |

    Speaking of Enteric coating, Nordic Naturals posted that the coating is a cover-up for cheap quality.

    http://www.nordicnaturals.com/en/General_Public/FAQs/264/#19

    What do you think?

  • Anonymous

    10/13/2009 1:46:31 PM |

    Nordic Naturals has a history of lying to consumers to promote their own product.  For example, right now they promote their fish oil concentrates as being in a "natural triglyceride form".  The truth is that their concentrates are reconstituted triglycerides that were once ethyl esters.  ALthough still healthy to consume, they are anything but natural form.  Furthermore, there will always be a small fraction of residual ethyl esters left in a triglyceride concentrate because the transesterification process is never 100%.

  • Boris

    10/14/2009 8:02:13 PM |

    It's interesting to hear that Nordic Naturals may not be the most honest business out there. Do you have any proof of that? It's not that I don't believe you. I just want to read more about it. All I can find are articles like this:

    http://www.reuters.com/article/pressRelease/idUS123643+11-Feb-2009+PRN20090211

    That one says Nordic Naturals became the official omega-3 supplement of the American Pregnancy Association.

  • Arne Orgiba

    10/16/2009 5:22:57 PM |

    Nice post! Base from the previous posts, it's not only how high the Omega-3 but the ratio between Omega-3 and Omega-6. I'm not the expert here but I found a FOOD that has the perfect ratio of Omega-3 and Omega-6. You check it out here http://tinyurl.com/ykvj3uw

  • Rick

    10/25/2009 11:21:09 PM |

    Dr B.G. (or anyone),
    Why are restaurant foods full of Omega-6? And how is NYC different?

  • l

    10/30/2009 3:03:31 AM |

    Rick,

    Back in 2006 NYC banned transfats from restaurants:
    http://www.nytimes.com/2006/09/27/nyregion/27fat.html?ex=1317009600&en=e20e688e95d428bd&ei=5090&partner=rssuserland&emc=rss

    The article cites Americans consume 5800 mg of transfats daily. OMG. Transfats are worse than omega-6, they are artificially hydrogenated omega-6 which biologically stay in our lipid bilayers (the coating of EVERY CELL OF YOUR BODY), visceral fat depots (eg, our meno-pots and beer bellies), subcutaneous fat stores (under our skin), and in our brains -- where fat comprises 60% of this very important master controller... Trans fats wreak havoc b/c our bodies don't know how to dispose, metabolize or eliminate these synthetically derived oils. That is why there is a HIGH HIGH incidence of heart disease and transfats. All progressive cities and states should follow suit with New York City. Otherwise the food expenses for a transfat ban are being shifted to disability, mortality, and health care dollars!

    -G

  • Keenan

    7/8/2010 5:15:25 PM |

    Doc,

    I'd love to know your thoughts on the ratios of DHA to EPA. I notice that NOW brands now makes a DHA-weighted supplement that is enteric coated and free of additives.

    What ratio of DHA to EPA do you recommend, and what sort of literature/studies have you found discussing the differences between them?

  • buy jeans

    11/3/2010 7:00:34 PM |

    Even if you take fish oil supplements, it is hard to know just how much you’ve increased blood levels. It is now possible to measure the amount of omega-3 fatty acids in your bloodstream, a value called the omega-3 index. Too little and you might still be at high risk for cardiovascular events.

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