"But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL."

So what?

Wolf, Sears, and Poliquin recommend a high fish oil dose of 0.5g-1.9g EPA/DHA per 10lbs BW; this generally equates to 9-10g range.  All three have had amazing success with sedentary, chronically ill individuals and elite level athletes.

I believe you yourself have stated in the past that fish oil causes a shift from VLDL and IDL to large particle LDL---a benign, if not beneficial action.

So is the raising of LDL in high dose fish oil even a concern?  Some clarification on this would be appreciated.

Gosh... what an ODD response to fish oil! *wink* Do you actually believe it?  The reports would be contrary to the literature.  At least fish oil would have a strong role in stabilizing plaque and prevents soft ruptures in growing plaque (just like the Tokelau and Masai, high carb H-G societies)!

Nowhere in the literature that I can find reports omega-3 increases dense LDL. Perhaps there is a TYP program-omega3 interaction? Or perhaps this only occurs in those who take high-dose statins and fail to convert to Pattern A (due to the overstatination phenomenon, as reported by researchers where TG <  150)) and complain annually about their EBCT plaque progression 10-25%??  I have tried to admonish the statin overuse but apparently that doen't go over well with this individuals as you are aware. Oh well.

I have noticed that in the summers people's HDLs drift down.  Have you Dr. Davis in your practice?  I suspect a strong fruit-effect on splaying out dense LDL. Thoughts?

IMHO many on the TYP members consume WAY way way too much grains, orange juice, oat bran, oatmeal, FRUITY SHAKES (e.g. JJ) and consume several servings of fruit all day (e.g Jeg). Do you think this may play any part of complaints related to higher dense LDL?  My first thoughts are ALWAYS... diet.  

Your observastions are always UNIQUE!!  Thank you putting the highlights on the omega-3 index and the role of n-6 to n-3 on inflammation, the root cause of CAD!  You are certainly the biggest quantum EVOLVER.

http://drbganimalpharm.blogspot.com/search/label/Evolver

Gosh... what an ODD response to fish oil! *wink* Do you actually believe it?  The reports would be contrary to the literature.  At least fish oil would have a strong role in stabilizing plaque and prevents soft ruptures in growing plaque (just like the Tokelau and Masai, high carb H-G societies)!

Nowhere in the literature that I can find reports omega-3 increases dense LDL. Perhaps there is a TYP program-omega3 interaction? Or perhaps this only occurs in those who take high-dose statins and fail to convert to Pattern A (due to the overstatination phenomenon, as reported by researchers where TG <  150)) and complain annually about their EBCT plaque progression 10-25%??  I have tried to admonish the statin overuse but apparently that doen't go over well with this individuals as you are aware. Oh well.

I have noticed that in the summers people's HDLs drift down.  Have you Dr. Davis in your practice?  I suspect a strong fruit-effect on splaying out dense LDL. Thoughts?

IMHO many on the TYP members consume WAY way way too much grains, orange juice, oat bran, oatmeal, FRUITY SHAKES (e.g. JJ) and consume several servings of fruit all day (e.g Jeg). Do you think this may play any part of complaints related to higher dense LDL?  My first thoughts are ALWAYS... diet.  

Your observastions are always UNIQUE!!  Thank you putting the highlights on the omega-3 index and the role of n-6 to n-3 on inflammation, the root cause of CAD!  You are certainly the biggest quantum EVOLVER.

http://drbganimalpharm.blogspot.com/search/label/Evolver

My EFA results showed an Omega3 index of 11.7% and a Omega 6:3 ratio of 2.3/1. I supplement with 1600mg EPA and 800mg DHA daily. I follow a low carb (high fat) I can't afford to eat "grass fed", but I do avoid processed foods whenever possible and my dietary fats are from coconut oil, lard, beef tallow, butter, olive oil and small amounts sesame oil. The Omega 3 Index test was a bit pricey, but...it did give me some comfort that I am on the right track.

For those who witnessed an increase in LDL, what was the profile of small, dense VLDL vs large, fluffy VLDL reflected in the increase?

Also, first-time commenter. Thank you for a great, informative blog.

"But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL."

I'm hoping (and wondering if...) that while those diligent enough to take that high a dose of omega-3's may have higher measured LDL levels, they indeed have much larger, fluffier particles now than when they began the megadosing.  That would be something marvelous to hear.
Good stuff here, as usual!
-Adam

If one's LDL's raise dramatically on omega-3's, without the corresponding increase in hdl, or decrease in trigs, is it better to lower the omega 3's?

Ex:

pre-omega
tc 240
hdl 45
ldl 165
tg 70

during 2000mg omega-3's
tc 320
hdl 58
ldl 240
tg 90

Also, the pattern size of the ldl's are type a with a low carb, no grain diet.

I'd very much like to know what subfraction of LDL was elevated in the TYP followers on 9,000 plus omega 3's a day.  My experience is that large fluffy LDL increases but not small dense.

What about lipid peroxidation on high dose of fish oil?

The form of LDL that increases depends.

It seems to depend on the genetic basis for small LDL. In other words, if the triggers of small LDL have been removed along with other efforts aimed at reducing small LDL like niacin, and there is no genetic basis for small LDL, then large LDL increases.

If small LDL is genetically programmed (a lot more common than many think), then small LDL can increase explosively.  

Having performed many thousands of lipoprotein panels, the latter situation in which small LDL increases is worrisome.

I am unsure of the implications of the first situation. Sure, we can extrapolate and speculate that it might not be related to increased risk. But I am not willing to gamble someone's health and life on pure speculation with no human data.

The only references to an increase in LDLC with fish oil supplementation is from WS Harris who authors 95% of the omega 3 index studies including a 2008 review which concludes that the omega 3 index is superior to omega 3/omega 6 ratio.  When 95% of literature comes from one man who promotes a pricey lab test I can't help but wonder if he gets part of the profits. I have no data to say he does though.

He has two 1997 publications,one showing that Omnacor given at 4 g epa/dha a day raised ldlc by 10%. 1997 was the predawn era of advanced lipids.  In his second publication individuals with severe hypertriglyceridemia (baseline fasting levels on statins of 500 to 2000) did have a 32% rise in LDLC.  
Harris has ties to Big Pharma (the maker of Lovasa/Omnacor) and to Monsanto.
Data that I can easily access ascide from Harris shows effecacy of fish oil supplementation up to 4 grams of epa/dha a day.  5 grams a day for plaque stabilization/ antiinflammatory effect.  9 or 10 grams a day only in obese heart failure patients.  
My bottom line:  if your baseline tg's are 500-2000, watch out for your ldlp on high dose fish oil.  If you are an obese heart failure patient, lose weight.

I believe that when people use theraputic levels of fish oil (more than 3gm EPA=DHA)  they should follow their omega profile and lipoprotein analysis closely.  It is possible to push the eicosanoid synthesis pathways toward the arachadonic acid side depending on your diet.   Once you know your optimal dose, then you can adjust it up in certain circumstances.  I attended a football tailgate and found some of the mixed nuts were cooked in soy oil, so I took an extra dose of fishoil when I got home to compensate.

Thanks for your thoughts on this.  Regarding LDL particle size, how dependable would TG/HDL ratio be?  Sears indicates a ratio less than 2 indicates large benign LDL.  In my own experience over the past few years, as I've increased my fish oil intake (along with a Paleo diet) my HDL has gone up, my LDL has gone up, and my TGs have decreased.

I have increased my intake of omega-3 since I answered the poll. My problem was that I couldn't take it all at once. Too much fish oil gave me a super upset stomach. Granted, it was the impure Nature Made brand sold at Walmart (34% pure). Now that I am using Omapure, I take one capsule with every meal and then one before bed time. It 6x more expensive than the Nature Made junk but I'm not getting sick from it.

Does it matter that I break up my intake over the course of the day rather than swallow four capsules all at once?

great information here, thanks all.

To follow on Dr.BG's note on statin overuse :  there is an interesting presentation of baylor college's lipidsonline.org with discussion of guidelines for statin dosage.  The presenter notes how very little value is obtained from subsequent doubling of a statin dose and the risks for side effects.

http://www.lipidsonline.org/slides/slide01.cfm?tk=82

Dr. D.  Thank you for the caution on fish oil. I take 1650mgs EPA/DHA twice per day.  Might be a good idea to cut out a dose if I eat salmon or other oily fish.

Would love to see more info on MK4/Mk7 K2 and MCFAs like coconut oil.

Hi, Mike--

While the Triglyceride/HDL ratio can serve as a useful measure of small LDL in a population, it performs poorly when applied to specific individuals. This is because small LDl, while influenced by the situation creating low HDL and high triglycerides, can also behave independently.

Small LDL is, in my view, best measured specifically.

It's pretty straightforward to end up in the middle of the pack on that poll.  But don't take gels or you'll be there all day.  One tablespoon of Carlson's Finest has 4800mg O-3's with 2400mg EPA and 1500mg DHA.  One swallow just as I'm sitting down to breakfast makes for a great start to every day.

I was told than an ApoE 4 Patient should not be on therapeutic doses of fish oil (for reasons which you have stated- raising LDL).

Dr Davis:

I would like to know which WS Harris 2008 you referenced and the reference for the females in the Harvard School of Public Health please.
I also would like to know if there was a correlation between baseline tg levels and those who experienced a more marked elevation of sd LDL on fish oil.

I guess that this is my day to ask you questions.
When you read a MDCT, do you also measure pericardial fat?
What do you think of Dr. Ding's new MESA findings re pericardial fat.  Thanks in advance.

I take 6000 units daily or more, but I also consume a few tablespoons of ground flax seed daily as well.
AND still eat fish a few times a week, especially oil rich sardines.

Homertobias:

Lots of interesting work being done on pericardial adipose tissue (PAT) and using CT imaging done in conjunction with CAC scoring to more precisely determine the relationship between PAT and the development of CAD and calcified plaques, i.e., in order to more precisely "score" the level of PAT and to determine association and/or causality with calcific lesions.

Dr. Lerber at University Hospital in Munich, Germany has observed that PAT accumulation precedes the development of calcified plaques, that increased volume of PAT are associated with reduced levels of  adiponectin and higher CRP.   So the idea is that with more precise measurements and concomittant imaging of both PAT and CAC, we might be able to better detect the presence of disease in an earlier stage.   There is also some push among those doing such research to link PAT thickness assessment with administering routine echo stress testing but this hasn't gained much traction yet other than in a small circle of folks.   The hope though is that PAT can also be used as another surrogate marker for diagnosing preclinical atherosclerosis.

But as of now, I don't think anyone who does a routine CAC scan, whether with MDCT or EBT is doing any form of assessment of PAT, at least not until there is more data on the reliability of using this as a clinical marker of disease.

Personally, I think there's a lot of interesting info that can come from this, and the idea of deposition of fat into muscle tissue and necrosis of that tissue, inflammation and the relation to levels of saturated fats consumed from dietary sources is an area that is just begging to be better researched.

Oh, and by the way, don't believe everything you read here from BG about what foods I consume, how much statin I take, or much else when it comes to me.  In fact, I'd prefer that she simply not make references to me in her writings wherever they appear.  This will obviate the need for me to continue to correct her misstatements about me, my lipids, and drug and supplement usage, as well as the fact that she continues to misrepresent that I have not achieved plaque stability and/or demonstrated regression through serial MDCT CAC scoring over a period of three years despite very low dose use of rosuvastatin.

A correction....  My serial scan scores show that I have achieved stability and optimally regression of coronary calcium.   My point is that Dr. BG continues to claim that those taking rosuvastatin at doses of ~10mg daily cannot possibly achieve regression on EBT/MCDT scanning, and that just isn't so.

I happen to be one of those whom I believe Dr. Davis was referring to with "too much of a good thing" with reference to EPA/DHA dosing.  My dose was upped from ~1-2 grams per day (of EPA/DHA) to ~10 grams based on recommendations from Dr. BG.  This occurred in or around December 2008 and continued until very recently. Based on five consecutive, quarterly NMR's and VAP's, my sdLDL-P remained at >85% of LDL-P, and my trigs went from ~40 to ~75, and, more significantly, my overall LDL-P rose from ~1000 to ~1300.   No other significant impacts were noted, other than CRP dropping to 0.7, which I attribute not to the n-3's, but instead to continued use of rosuvastatin together with combined high dosing of both boswellia and 5-Loxin and large doses of aspirin (taken specifically as an anti-inflammatory due to nerve and muscle pain from a herniated cervical disc in the month immediately prior to the last VAP testing).

The point though is that in some, excess fish oil can convert to higher trigs and higher LDL, and will not improve the concentration or ratios of sdLDL-P/LDL-P.

Yes, n=1, but I'm the n, so that's really most important to me, not what Wolf, Sears or anyone else has to say about this.  After all, what we're after is personalized medicine, not epidemiological observations that may be valid in large population studies but which may have no relevance to a particular individual.

Hi JEG,
Thanks for the references.  I am truly upset that you andBG seem to be having a cybertiff.  She has a big heart, alot of enthusiasm, alot of intelligence and makes me laugh. You are a sincere intellectual, very bright, searching for truth in medicine and are doing a good job of it.  I can learn from both of you and want to continue to do so.
As to omega 3 and dosage.  I can't seem to find any solid benefit to doses over 4g to maybe 5g per day. This seems to max out tg lowering, ldl improvement in particle size, minimal increase in hdl, bp lowering, improvement in tnf alpha, interleukin 6.  Reports on irs effect on HSCRP are conflicting.  One interesting report, Thies F, in Lancet 2003 took 188 patients scheduled for carotid endarterectomy and treated them with either DHA/EPA, sunflower oil, or placebo for an average duration of 42 days prior to surgery.  There was a significant difference in thickness of the fibrous cap over the plaque,the degree of monocyte  infiltration of the fibrous cap, percent DHA etc.  This directly addresses plaque stability.  I love it.

Homertobias,

That is a great plaque stablization article -- will have to ck out!



Jeq,

I must be correct again as indicated by the length and duration of the post!

Let me get this straight -- the lipoproteins were less than desirable for both you and JJ/Jim for the past 2008 to 2009 (you reported increased sdLDL?), yet both of you posted regression recently on BOTH of your EBCT/MDCT results....  

Gosh... I wonder if the high dose fish oil had anything to do with it?

EPA DHA get infiltrated directly locally into calcified plaque and has immense immeasurable benefits for regression BEYOND lipoproteins.  I think you have seen some them, personally IMHO.

-G

Homertobias,

That is a great plaque stablization article -- will have to ck out!



Jeq,

I must be correct again as indicated by the length and duration of the post!

Let me get this straight -- the lipoproteins were less than desirable for both you and JJ/Jim for the past 2008 to 2009 (you reported increased sdLDL?), yet both of you posted regression recently on BOTH of your EBCT/MDCT results....  

Gosh... I wonder if the high dose fish oil had anything to do with it?

EPA DHA get infiltrated directly locally into calcified plaque and has immense immeasurable benefits for regression BEYOND lipoproteins.  I think you have seen some them, personally IMHO.

-G

By the way, congratulations to you two gentleman, JJ and Jeg, for achieving regression with Pattern B! I have looked for regression in Pattern B forum posters, but turned up none. You two are the FIRST at TYP that I can find...

Do you think omega-3 had any role in your success since that appears to be the common link as well as major supplement change you guys identified?

I wonder what the omega-6:3 ratio is now off the fish oil?

By the way, congratulations to you two gentleman, JJ and Jeg, for achieving regression with Pattern B! I have looked for regression in Pattern B forum posters, but turned up none. You two are the FIRST at TYP that I can find...

Do you think omega-3 had any role in your success since that appears to be the common link as well as major supplement change you guys identified?

I wonder what the omega-6:3 ratio is now off the fish oil?

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)?

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.

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.

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%.

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

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...

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.

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

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?

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?

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.

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.

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.)

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

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

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.

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.

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.

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?

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%.

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.

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

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

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

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?

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.