How old are you?

George walks into my office. I ask him his age.

"I'm 21 years old," he declares.

Yet I look at George. He's got gray thinning hair, his posture is slumped forward rather than erect, the flesh on his upper arms hangs loosely, he's got wrinkles on his hands and face, brown spots on the back of his hands and arms. He looks more like 70 years old to me. "I don't think you're 21 years old. I think you're 70."

"Prove it," he says.

Okay. What now? Minus any formal identification like a driver's license, how do I prove that George is really 70-something and not 20-something? Not an easy thing, when you think about it. If George were a tree, I'd cut him down and count his rings. Is there such a phenomenon in humans?

This is actually a fascinating area of research, looking for reliable biomarkers of aging.

Among the most quantitative markers of aging is telomere length. Telomeres were once dismissed as nonsense sequences in DNA. However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.

What can slow or stall the shortening of telomere length? There are two I'm aware of:

1) Caloric deprivation--i.e., taking in fewer calories. This was among the theories explored by Dr. Roy Walford during his Biosphere2 experience, based on his work in mice that showed that caloric deprivation nearly doubled lifespan.

2) Vitamin D--Richards et al (2007) found that, the higher the vitamin D, the longer the telomere length. The highest vitamin D levels conferred a 5-year effective difference in telomere length.

So, if I could look inside George's cells and count his telomeres, I could judge with confidence whether he was 21 or 70. Or, he could take vitamin D sufficient to increase blood levels to a healthy range and be more like 65.

No high blood pressure

Primitive cultures that were, until recently, unexposed to the modern world, reveal some important insights into blood pressure.

The Yanomamo of South American, the Xingu Indians of Brazil, rural Kenyans, and the natives of Papua, New Guinea have average blood pressures of 103/63 mmHg. Even more incredibly, while 90% of modern Americans will develop high blood pressure as they age, the members of these primitive cultures do not develop age-related hypertension.

What's the secret? Perhaps the full "secret" of their remarkably low blood pressure has not been fully unraveled, but several observations have emerged:

--They are not exposed to modern processed foods like pretzels, crackers, and breakfast cereals.
--Low-carbohydrate foods. Carbohydrates are largely the product of the food industry, convenience foods bought in stores. No such thing in the jungle.
--Living outdoors, having to forage and hunt, walk to your destination, not drive or wait in line for food.
--Outdoor lives, wearing little more than a few strands of clothing, exposes you to plentiful vitamin D activation from sunlight exposure.
--Consuming wild game, rich in omega-3 fatty acids, enhances endothelial health and reduces blood pressure.
--Wild plants, roots, and berries, as well as wild game, along the coast, are richer in iodine.

The studies examining the habits of the Yanomamo and other primitive cultures focused principally on sodium intake. Indeed, the very low sodium intake of primitive cultures was associated with lower blood pressure--up to 6 mmHg reduction. But there's clearly more to learn than "cut your salt."

Name that food

What common food can:

• Cause destructive intestinal damage that, if unrecognized, can lead to disability and death?
• Increase blood sugar higher and faster than table sugar?
• Trigger an autoimmune inflammatory condition in the thyroid (Hashimoto’s thyroiditis)?
• Create intestinal bloating, cramps, and alternating diarrhea and constipation, often labeled irritable bowel syndrome?
• Trigger schizophrenia in susceptible individuals?
• Cause behavioral outbursts in children with autism?
• Cause various inflammatory diseases such as rheumatoid arthritis, ulcerative colitis, dermatitis herpetiformis, systemic lupus, pancreatic destruction, and increase measures of inflammation like c-reactive protein?
• Cause unexplained anemia, mood swings, fatigue, fibromyalgia, eczema, and osteoporosis?


The food is wheat. Yes, the ubiquitous grain we are urged to eat more and more of by the USDA (8-11 servings per day, according to the USDA food pyramid), American Heart Association, American Dietetic Association, and the American Diabetes Association. Wheat is among the most destructive ingredients in the modern diet, worse than sugar, worse than high-fructose corn syrup, worse than any fat.

What other common food can result in such an extensive list of diseases, even death?

Celiac disease alone, a severe intestinal inflammatory condition from wheat gluten, affects an estimated 3 million Americans (Celiac Disease Foundation). The medical literature is filled with case reports of deaths from this disease, often after many years of struggle with incapacitating intestinal dysfunction and the sufferer's last days plagued by encephalopathy (brain inflammation).

What happens when you remove wheat from the diet?

The majority of people quickly shed 20-30 lbs in the first few weeks, selectively lost from the abdomen (what I call “wheat belly”); blood sugar plummets; triglycerides drop up to several hundred milligrams, HDL increases, LDL drops (yes, wheat elimination is a means of achieving marked reduction in LDL cholesterol, especially the small, heart disease-causing variety); c-reactive protein plummets. In addition to this, intestinal complaints improve or disappear, rashes improve, inflammatory conditions like rheumatoid arthritis improve, diabetes can improve or be cured, and behavioral disorders and mood improve.

Along with the ill-fated low-fat dietary advice of the last 40 years, the advice to eat plenty of "healthy whole grains" is responsible for untold disease and suffering. Yes, if you start with a fast food and junk diet and replace some of the calories with whole grains, you will be better off. (That was the logic--the Nutritional Syllogism--of the studies that established the benefits of whole grains over processed, "white" grains.)

But eliminate wheat grains and health takes a huge leap forward. And, no, there is no such thing as wheat deficiency--B vitamins, insoluble fiber, some protein--can easily be replaced by other foods.

Heart Defects Simplified



For as long as I've known him, echocardiography technologist, Ken Heiden, has had a deep fascination with congenital heart disease. Ken has just written a wonderful book on congenital heart disease called Heart Defects Simplified.

While this is a bit off-topic for the Heart Scan Blog, I know that there is a serious lack of helpful information for people with congenital heart disease and parents of children with congenital heart defects. So I asked Ken to tell us something about his book.



WD: I've reviewed your book and have been thoroughly impressed with the clarity and detail with which you handle a complicated topic. You somehow manage to make it easy to grasp, far more than any other resource I've used in past. Do you feel that your book serves a previously unmet need?

KH: This book serves an unmet need in that it presents the complex subject of congenital heart defects in a simplified manner. Most books on this subject are anywhere from 300-1700 pages in length and tend to be written for doctors. Further, most of these books have very few diagrams, and they rely upon their explanations to describe these defects.

Heart Defects Simplified is 104 pages in length, describes the most common defects, including surgical repairs, in a two-page format with full-color diagrams on the left and complete descriptions on the right of each chapter. The book is particularly written for sonographers, nurses and parents, but it is valuable for anyone interested in this subject. It is particularly useful in clinical situations because it is convenient to lay out at your side with a coil-bound format and durable pages. Further, there are appendixes which include "Surgical Procedures in Alphabetical Order," "Prevalence of Congenital Heart Disease," "Scanning Protocols for Echocardiographers," "Imaging Tips," a glossary and a worksheet for echocardiographers.


WD: I know that many people with loved ones who have congenital heart defects, particularly parents of children with such conditions, are often kept in the dark about the details of the condition. Is your book suitable for the non-technical reader, such as parents?

KH: This book is an excellent resource for parents. It is written in language that is understandable by parents as well as technologists and nurses. The full-color diagrams provide invaluable insight into this very complex world. Most importantly, this book attempts to make the subject of congenital heart defects accessible to anyone who wishes to comprehend this subject.


WD: I understand that people with congenital heart defects and parents are active participants in online discussion groups. Will your book serve as a resource for people who participate in these groups?

KH: This book is not only a resource for sonographers and parents, but the book is accompanied by a blog (HeartDefectsforEveryone.blogspot.com) that attempts to address many of the concerns commonly encountered with congenital heart defects. This blog is a work in progress, but I hope to provide a forum for parents, healthcare personnel, and others to share their questions and concerns about congenital heart disease.

My experience with the omega-3 index

I just got back my own results from the Gene Smart laboratory reporting my omega-3 index and omega-6:omega-3 ratio.

My results:

Omega-3 index: 8.2%

Omega-6:omega-3 index: 3.2 to 1

Not too bad, but not as good as I'd expected. Hmmm.

Although the omega-3 index of 8.2% puts me in the lower risk category for sudden cardiac death, I was hoping for a level of 10% or slightly greater, the level that I believe is more likely to be related to plaque inactivation or reversal. I obtained this level of omega-3 averaging an intake of EPA and DHA of about 2500 mg per day.

I was somewhat disappointed by the omega-6:omega-3 index. Although it's clearly better than the American average range of 20:1, it is short of the ideal of 2:1 or even 1:1. Since I purposely avoid omega-6-rich sources like corn oil, vegetable oils, sunflower or safflower oils, I wonder if I've overdone the nuts. The two ways to improve the omega-6:omega-3 ratio are to 1) decrease omega-6, or 2) increase omega-3. I'm going to do both.

So I thought I was doing pretty well. But there's clearly room for improvement.

Remember: If just reduction of cardiovascular risk is your interest, then a lackadaisical attitude towards these issues might work. But if your interest is elimination of risk and reversal of atherosclerotic plaque, then it pays to go the extra mile. In this case, knowing your omega-3 index and omega-6:omega-3 ratio might tighten up your program.

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

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.

Vitamin D increased my cholesterol

A friend told me this story.

Her friend, Linda, had added vitamin D to her daily supplements. Because she'd had a vitamin D blood level of 22 ng/ml, she was taking 6000 units per day.

However, Linda also had a high cholesterol value with a total cholesterol of 231 mg/dl. After several months on the vitamin D, she had another cholesterol panel. Total cholesterol: 256 mg/dl.

"It must have been the vitamin D! So I stopped it right away."

Is this true? Does vitamin D raise the level of blood cholesterol? Yes, it does. But it's a good thing. Let me explain.

Followers of The Heart Scan Blog know that total cholesterol is really a mix of 3 other factors:

Total cholesterol = LDL cholesterol + HDL cholesterol + triglycerides/5

This is the Friedewald equation, still used today in over 95% of cholesterol panels. So, by the Friedewald equation, anything that increases LDL, HDL, or triglycerides will increase total cholesterol.

One of the spectacular changes that develops over a year of taking vitamin D is that HDL cholesterol skyrockets. While sensitivity to this effect varies (probably on a genetic basis), HDL increases of 10, 20, even 30 mg/dl are common. A starting HDL, for instance, of 45 mg/dl can jump up to 65 or 70 mg/dl, though the effect requires up to a year, sometimes longer.

Vitamin D can also reduce triglycerides, though the effect is relatively small, usually no more than 20 mg/dl or so. Likewise, the effect on LDL is minor, with a modest reduction in the small type of LDL.

So the dominant effect of vitamin D from a cholesterol standpoint is a substantial increase in HDL. Looking at the equation, you can see that an increase in HDL is accompanied by a commensurate increase in total cholesterol. If HDL goes up 25 mg/dl, total cholesterol goes up 25 mg/dl.

So Linda is absolutely correct: Vitamin D increases cholesterol--but it's a good thing that reduces risk for heart disease and is an important part of a coronary plaque-reversal program.

This is yet another reason why I advocate elimination of total cholesterol on lipid panels. There is no useful information in the total cholersterol value, only the potential for misinformation.

Nutrtional ignorance is not unique to the U.S.

Heart Scan Blog reader from Australia, Michaela, also a mother of a son with a complex congenital heart defect, wrote this series of e-mails to me. (Published with Michaela's permission.)


I've been reading the article, Valve disease and Vitamin D from April '07, by Dr William Davis. I'm hoping you may have some information on the topic. I'm hoping someone will have time to help me.

I have been supplementing my 15 year old son with Vit D for 4 months but only 1000 (U) per day. I would like to increase the dosage but am not sure if I would do him more harm than good.

I have been researching vitamins and supplements on the net for a few months and have been amazed at what I have found. I only wish I had done it years ago. My son has been let down by the Australian Medical Profession and it's a race against time now to keep him well and avoid a heart transplant.

My son was born with aortic stenosis and had a valvotomy at 4 weeks of age. This damaged the aortic valve and he had a Ross Repair procedure at aged 3. This left him with a damaged heart muscle and leaking aortic & pulmonary valves. In May '08, his heart grew more enlarged, causing the mitral & tricuspid valves to also leak.

I took him to Bangkok in Feb this year where he had 70 million of his own Adult Stem Cells directly injected into his heart muscle with the hope of strengthening the muscle and eventually valve replacement.

My son has recovered from the surgery and is once again symptom-free, thanks to the wonderful advice followed by the Author & Cardiologist, Stephen T. Sinatra. I have followed his supplement regime and what a difference! Of course, this won't last while my son's valves continue to leak.

My son has also developed secondary hyperparathyroidism, bone thinning and hypothyrodism. Vit D & Calcium have something to do with this I believe.

My Australian Doctors have never made mention of any vitamins or supplements .... EVER! Transplant is all they will consider and we are not having it.

If you have any info or links to any sites which may be useful to me, could you email them to me? I would be grateful for any help I could get.

Sincerely
Michaela



I responded to Michaela's e-mail:

Hi, Michaela--

Vitamin D is extremely important. Sometimes, hyperparathyroidism and calcium derangements are caused by vitamin D deficiency. You might be able to get help with this from an endocrinologist, since they are the ones who deal with hyperparathyroidism. An endocrinologist might even be familiar with several recent studies that document this phenomenon:

Vitamin D therapy in patients with primary hyperparathyroidism and hypovitaminosis D

Vitamin D deficiency and primary hyperparathyroidism

Also, see the discussions at www.vitamindcouncil.org from Dr. John Cannell.

Because of the complexity of your son's health, it might be hazardous to stray too far away from conventional care though you and I know that there are limitations to that perspective. For that reason, I would urge you to press for answers from a knowledgeable endocrinologist.

I hope you find the answers you need.

William Davis, MD



Several months later, Michaela provided this update:

Hi Dr Davis,

I wrote to you back in July regarding my 15 year old son's need for a Heart Transplant through a failed Ross Repair and the possible Vitamin D connection. You sent me some valuable links and I thank you again for that.

I just wanted to let you know, I think you have given me the answers. I increased Lee's Vitamin D supplement to 6000U a day and, along with the recommended nutritional supplements of US Cardiologist Dr Stephen T Sinatra, there have been remarkable improvements! Lee also had 70 million of his own Adult Stem Cells injected into his heart in February. As we know, Stem Cell Therapy takes time and Lee was looking like time was quickly running out.

I have removed him from the transplant list. He is now reading normal Kidney function, the BNP (Brain Natriuretic Peptide, a measure of heart failure] has dropped by 7000 and his liver size has reduced to where it no longer causes him discomfort. The liver tests show it's still affected but it's function is improving each month. His last Echo was in early July and there had been a reduction in the size of his heart, which is so important.

To the Doc's, Lee can't get better, there is only transplant or death so you can imagine the surprise on their faces to see him looking and feeling so well with their tests to back it up. Still, even though it's staring them in the face, they don't want to know about it. They have no interest in what supplements he is on or Stem Cell therapy. God help their other patients. I view them in the waiting room and think of them as lambs to the slaughter.

We are not spoiled for choice with Doc's here in Western Australia. I have to take what I can get and there is not many who would take on Lee's case. He was number 1 on the transplant list and a most urgent case. Not many were willing to even look at him with his cardiac history and all I had to help was the arrogant Doc's at the Advanced Heart Failure Unit. They were not at all interested in his secondary hyperparathyroidism. I suppose it didn't matter what else he had compared to his heart problems.

Anyway, I'm writing to thank you. Lee would be transplanted or dead now if it wasn't for Dr's like you sharing their knowledge online. I wish I had researched things years ago, Lee might not have sunk so low if I had. I don't know if the transplant can be held off indefinitely, but like I tell Lee, "Stay well. There are amazing people out there doing amazing things, if you can just hang on. The miracle is around the corner." He's so well, you'd have to see him to believe it. But I have 7 kids and Lee is as physically active and as well as the other 6! For how long he can stay like this, I don't know but if his ejection fraction [a measure of left ventricular strength] can keep climbing and his body gets stronger, I have hope for another attempt at valve replacement.

I'm still shocked and angry that nutritional supplements have never been mentioned in the 15 years I've been dealing with cardiologists. Surely they know about them. I have read through dozens of reports online of the benefits of them--Why haven't they?! Thank God for the online Doc's such as yourself, the valuable info would never make it out of a Doctor's office in Western Australia! I've had to leave my country for Stem Cell therapy and then implore overseas Doc's for advice and information. What does that say for the Australian Medical Profession? Not a lot! They put him in the position he is in yet don't want to help get him out.

I'm so very grateful to you, thank you and God bless.

Michaela



Note: The above is not meant to be an implicit endorsement of stem cell therapy. This was just part of Michaela's story about her son.

Eat cranberries

Most people already know that cranberries are useful for preventing urinary tract infections. Cranberries can also be useful for preventing other sorts of infections, such as dental cavities and stomach ulcers because of cranberry's ability to block bacterial adhesion.

Cranberries can also be a useful component of a heart healthy program.

Several unique properties of cranberries contribute to various aspects of heart health:

• Cranberries are a rich source of pectin--Pectin is a soluble fiber, the sort that binds bile acids in the intestinal tract and naturally reduces LDL cholesterol.
• Cranberries are a rich source of polyphenols and flavonoids--Including the wonderfully fascinating anthocyanins, the flavonoids that confer the beautiful red color. Surprisingly, cranberries are richer in polyphenols and flavonoids than blueberries, strawberries, and grapes. Cranberry juice is also rich in these compounds. However, beware of cranberry juice "cocktail," which is diluted with other liquids such as high-fructose corn syrup. Like grapes, cranberries are a source of resveratrol, the polyphenol also found in red wines that some believe is responsible for reduced risk for heart disease and extending life.
• Cranberries have high antioxidant activity--Cranberries are among the highest in antioxidant capacity against superoxide radicals, hydrogen peroxide, and hydroxyl radicals, oxidizing factors believed to underlie heart disease, cancer, and aging. Cranberries also reduce the oxidation of LDL cholesterol particles.
• Cranberries block uric acid production--Cranberries have the unique ability to block the activity of an enzyme, xanthine oxidase, that converts xanthine to uric acid. Uric acid is believed to add to heart disease risk and is the factor responsible for gout.
• Cranberries increase HDL cholesterol--Cranberry juice increases HDL by 3-4 mg/dl.

Cranberries are only modest sources of sugars, with 7.19 grams “net” carbohydrates (total carbohydrates minus fiber content) per cup of whole raw cranberries.

The best way to eat cranberries is to consume the real thing: eat the whole berry, as in sugar-free cranberry sauce or added to baked dishes like chicken. Second best are dried cranberries. However, be careful of the overly-sweetened dried cranberries that contain added sugar (for a total of 78 grams sugar per cup--far too much). Unsweetened dried cranberries can be purchased, or you can dry them yourself.

Cranberry juice is another way to obtain the health benefits of cranberries; the unsweetened juice, while quite tart, is the best with 30.5 grams sugar per 8 oz--so don't drink more than 4 oz at a time. The more common cranberry juice “cocktails” are generally too sugary and/or too dilute for full health benefit.

The cranberry harvest season in Wisconsin, Michigan, Oregon, Massachusetts, and New Jersey is just getting underway, so we should be seeing fresh cranberries on store shelves or farmers' markets any day now.

Procedures 'R Us

Kay came to the office for an opinion.

Over the past 8 months, she'd received a stent to the left anterior descending coronary artery and, during a separate procedure, a stent to the left subclavian artery.

"My cardiologist was very capable doing procedures. But when I asked, 'What do I do now?' he barely said a word and handed me a presciption for Crestor."

This kind of incredible neglect is the norm: Write a prescription for statin drug, delegate dietary advice to the hospital dietitian who advocates a heart disease-causing low-fat diet, followed by hospital discharge. You are expected to report any recurrent symptoms (which are inevitable), at which point you might "qualify" for another procedure.

It would be malpractice if it were not the prevailing standard in the community. Yes, the prevailing standard is neglect--neglect to identify, quantify, and correct all the identifiable causes of heart disease; neglect to discuss the nutritional methods that actually correct the abnormal patterns that cause heart disease; neglect to discuss nutritional supplements or medications beyond statins that further reduce heart disease risk and "need" for more procedures. In other words, the prevailing community standard is to stent, bypass, prescribe statin. It is not to understand why the disease occurred in the first place, correct the causes and minimize or eliminate any future danger or need for procedures.

I see consultation after consultation involving stories just like Kay's. People are frightened and they sense intuitively that nobody raised the question of why they have a potentially fatal disease.

Don't allow yourself to fall victim to this incredibly neglectful mode of practice, the one that has enriched hospitals, the drug industry, many cardiologists, but does little to address the actual disease.
Heart Scan Blog readers take impressive doses of omega-3s

Heart Scan Blog readers take impressive doses of omega-3s

Here are the results from the latest Heart Scan Blog poll:

What is your dose of omega-3 fatty acids, EPA + DHA, from fish oil? (Add up the total content of EPA + DHA per capsules; multiply times number of capsules.)

The 479 respondents answered:

Less than 1000 mg per day
65 (13%)

1000-1999 mg per day
145 (30%)

2000-2999 mg per day
98 (20%)

3000-3999 mg per day
79 (16%)

4000-4999 mg per day
33 (6%)

5000-5999 mg per day
14 (2%)

6000 mg per day or more
45 (9%)


The poll did not discriminate between who has heart disease, who does not; who is taking omega-3 fatty acids for high triglycerides or for reduction of lipoprotein(a) (which requires high doses), or other indications. So variation is to be expected.

We can say that nearly all respondents are likely receiving sufficient omega-3s to impact cardiovascular risk, since the benefits begin just by consuming fish twice per month. I am especially impressed at the proportion of respondents (53%) who take at least 2000 mg per day of EPA + DHA. It's clear that people are really embracing the notion that omega-3 fatty acids pack a real wallop of health benefits.

Because different people in different situations and lipid/lipoprotein patterns have different omega-3 needs, there is really no "right" or "wrong" dose of omega-3 fatty acids.

However, there are several factors that enter into knowing your ideal omega-3 intake:

--Higher triglycerides require higher doses
--Lipoprotein(a) can respond to higher doses
--Having coronary or carotid plaque means you desire a "therapeutic" dose of omega-3s, not just a "preventive" dose

Time is a factor, also: The longer you take omega-3s, the higher your blood levels go. You can accelerate the replacement of non-omega-3s with higher doses of omega-3s.

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.

Much of the uncertainty about dosing will also be cleared up as we get more experience with the Omega-3 RBC Index, i.e, the proportion of fatty acids in red blood cells that are omega-3s. We are currently aiming for an Omega-3 Index of 10%, given the heart attack reductions observed at this level.

Comments (28) -

  • Mike

    10/24/2009 3:52:01 PM |

    "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.

  • Dr. B G

    10/24/2009 4:44:35 PM |

    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

  • Dr. B G

    10/24/2009 4:44:35 PM |

    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

  • TrueDharma

    10/24/2009 5:50:45 PM |

    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.

  • Jae

    10/24/2009 5:53:26 PM |

    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.

  • Adam Wilk

    10/24/2009 8:59:52 PM |

    "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

  • Steven Horvitz, D.O.

    10/24/2009 9:35:20 PM |

    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.

  • homertobias

    10/24/2009 11:29:56 PM |

    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.

  • Kevin

    10/25/2009 8:36:26 AM |

    What about lipid peroxidation on high dose of fish oil?

  • Dr. William Davis

    10/25/2009 2:52:27 PM |

    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.

  • homertobias

    10/25/2009 5:07:57 PM |

    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.

  • William Trumbower

    10/25/2009 5:31:50 PM |

    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.

  • Mike

    10/25/2009 5:40:54 PM |

    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.

  • Boris

    10/26/2009 1:30:58 AM |

    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?

  • Anonymous

    10/26/2009 1:49:07 AM |

    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.

  • Dr. William Davis

    10/26/2009 1:58:12 AM |

    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.

  • Ross

    10/26/2009 5:52:24 AM |

    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.

  • Anonymous

    10/26/2009 1:54:50 PM |

    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).

  • homertobias

    10/26/2009 2:46:23 PM |

    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.

  • homertobias

    10/26/2009 4:14:20 PM |

    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.

  • Alan S David

    10/26/2009 6:16:55 PM |

    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.

  • jegesq

    10/26/2009 9:28:03 PM |

    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.

  • jegesq

    10/27/2009 12:16:24 AM |

    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.

  • homertobias

    10/27/2009 4:05:13 PM |

    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.

  • Dr. B G

    10/30/2009 5:06:04 AM |

    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

  • Dr. B G

    10/30/2009 5:06:04 AM |

    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

  • Dr. B G

    10/30/2009 5:14:21 AM |

    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?

  • Dr. B G

    10/30/2009 5:14:21 AM |

    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?

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