ERA JUMP: Omega-3 fatty acids and plaque


The results of the uniquely-constructed ERA JUMP Study were just released, a fascinating study of the relationship of omega-3 fatty acids to coronary and carotid plaque.

The study adds insight into why the Japanese experience only one third of the heart attacks of Americans, and why Japan occupies the bottom of the list for least heart attacks among all developed countries.

The Electron-Beam Tomography, Risk Factor Assessment Among Japanese and U.S. Men in the Post-World War II Birth Cohort Study (ERA JUMP), a collaborative U.S.-Japanese effort, compared three groups of men:

-- 281 Japanese men living in Japan
-- 306 non-Japanese men living in the U.S. (Pittsburgh, Pennsylvania)
-- 303 Japanese Americans (having both parents Japanese without “ethnic admixture”) living in Hawaii.

The last group represents a group that is genetically similar to the group in Japan, but exposed to an American diet and lifestyle.

Three main measures were compared:

-- Blood levels of omega-3 fatty acids, EPA and DHA)
-- Carotid intimal-medial thickness (CIMT, the thickness of the carotid artery lining that can serve as an index of body-wide atherosclerosis)
-- Coronary calcium (heart scan) scores.

Interestingly, at the start of the study, the Japanese men possessed an overall cardiovascular risk profile worse than the Americans: Though more slender (BMI 23.6), Japanese men were more likely to be smokers, alcohol drinkers, had more high blood pressure, and were less likely to take cholesterol medications. The Americans, conversely, although heavier (BMI 27.9), were less likely to be smokers and drinkers, and had a four-fold greater use of cholesterol medications.

The Japanese Americans were the most likely to be hypertensive, diabetic, with a similar proportion of overweight as the non-Japanese Americans.

Despite the overall greater heart disease risk for profile for Japanese men, compared to non-Japanese Americans they had 10% less CIMT. In addition, only 9.3% of Japanese men had abnormal coronary calcium scores vs. 26.1% of non-Japanese Americans. Japanese-Americans were the worst, however, with nearly 10% more CIMT than non-Japanese Americans and 31.4% with abnormal calcium scores.

The most intriguing finding of all was the fact that, of all the various groups and degrees of atherosclerosis, whether gauged via CIMT or coronary calcium scores, the blood level of omega-3 fatty acids was inversely related, i.e., the greater the omega-3 blood level, the less plaque by either measure was detected.

Japanese men had the highest omega-3 blood levels: twice that of the non-Japanese Americans. The Japanese-Americans had levels only slightly greater than non-Japanese Americans.

While other studies, like the GISSI Prevenzione study, have persuasively demonstrated that omega-3 fatty acids substantially reduce heart attack, a weak link in the omega-3 argument has been a study that links greater omega-3 intake with less atherosclerosis. The unique construction of the ERA JUMP Study, employing two groups with sharply different omega-3 intakes, very powerfully argues for the plaque-inhibiting effects of this fraction of fats.

How much omega-3 fatty acids do Japanese people eat? Estimates vary, depending on part of the country, coastal vs. inland, age, etc., but Japanese tend to ingest anywhere from 5 to 15-times more omega-3 fatty acids than Americans. The actual intake of omega-3 fatty acids (EPA +DHA) in Japanese ranges from 850 to 3100 mg per day.

Comments (5) -

  • Jenny

    8/1/2008 12:41:00 AM |

    Thanks for pointing this out.

    But I cannot help but wonder about what these Japanese men got if they did NOT get heart disease.

    It was my impression that the rate of stomach cancer was higher in Japan than anywhere else in the world.

    I also know that the Honolulu study found a much higher rate of dementia in men who ate traditional diets high in tofu.

    Finally, and most concerning, I personally know two people who ate "healthy" diets high in fish only to came down with mercury poisoning bad enough that they had to undergo chelation therapy. (These were people whose mainstream doctors sent them for the therapy, not adherents of alternative medicine.)

    Having observed what happens to people who do not get heart disease but do live long enough to develop both cancer and dementia, and having concluded that heart disease is much to be preferred, I'm not entirely sure that we should rush to eat the Japanese diet.

    We are all going to die of something. I would much prefer a swift heart attack to a decade of cancer and dementia.

  • TedHutchinson

    8/1/2008 8:45:00 AM |

    Dr Cannell says at http://www.vitamindcouncil.org/health/autism/vit-D-and-brain.shtml#hd4 "activated vitamin D lessens heavy metal induced oxidative injuries in rat brain. The primary route for brain toxicity of most heavy metals is through depletion of glutathione. Besides its function as a master antioxidant, glutathione acts as a chelating (binding) agent to remove heavy metals, like mercury."

    It may be that, as well as keeping your vitamin D3 status optimal, using molecullarly distilled fish oil or krill avoids the pollution problems?

  • Peter

    8/1/2008 2:52:00 PM |

    I wonder how eating fish compares to drinking fish oil.

  • carolina1954

    8/2/2008 4:57:00 AM |

    I must demur from some of Jenny's comments.

    First,  I do not believe that the overall effect of the Japanese diet is to trade heart disease for cancer, as she seems to imply.   E.g., the Japanese, despite smoking multiples more than Americans, have a rate of lung cancer less than half ours.

    Second, although it is true that eating a lot of certain species of fish, such as shark, swordfish, and large tuna, creates a risk of mercury poisoning, other species, such as salmon, have very low levels of mercury and may be eaten virtually ad libitum.

    Third, dying from heart attack, or its evil twin stroke, is not necessarily "swift".  If a heart attack interrupts blood flow for a few minutes, it causes massive brain damage but not necessarily death.  It can also cause terminal congestive heart failure, which is also not my idea of going "gentle into that good night."

  • Rich Lee

    8/14/2008 6:39:00 PM |

    Which fish oil brand is recommended?

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Carbohydrate sins of the past

Carbohydrate sins of the past

Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Comments (15) -

  • Matt Stone

    2/18/2010 3:13:57 AM |

    The government advice to "eat more healthy whole grains" is not off-base.  But that's not what Americans did.  Instead they ate more fructose and replaced saturated fats with more polyunsaturated fats.  This is totally fundamentally different than eating a low-fat, high-carbohydrate diet like that of the rural Zulu tribe studied by T.L. Cleave or the Africans studied by Denis Burkitt and Hugh Trowell that were diabetes and obesity-free.  

    Americans are still not even coming close to the grain consumption of a century ago, when such diseases were exceedingly rare.

  • Mat

    2/18/2010 5:38:50 AM |

    This video is very good:

    "Vitamin D and Diabetes-Can We Prevent it?"

    http://www.youtube.com/watch?v=wTtmvMvgfl0

  • TedHutchinson

    2/18/2010 9:54:56 AM |

    At this link you'll find the slides of a short presentation on
    The Influence of high vs. low sugar cereal on children's breakfast consumption.
    There are some surprising findings.

    I found it at Cerealfacts.org website

    The situation in the UK is much the same. The breakfast cereals most likely to find at discounted prices are those with the most sugar.

    It's  often the case the choice of cereal going into the trolley is made by the child rather than the parent. There should be more restrictions on the promotion of pre-sweetened cereals to kids.

  • Anonymous

    2/18/2010 12:36:43 PM |

    In my early 60s I notice that I don't get much "kick" out of sugary foods as I might have earlier.  I've gotten to the point where I can't believe the amount of sugar in say cookies or ice cream...which I no longer buy.  

    I do now take several phyto-extracts...pomegranate...blueberry...cocoa...resveratrol...green tea...grape seed...etc.

    Pomegranate at least has been shown to moderate insulin response and maybe reverse atherosclerosis.

    http://www.lef.org/LEFCMS/aspx/PrintVersionMagic.aspx?CmsID=114814

  • Dr.A

    2/18/2010 2:04:35 PM |

    Great post!
    I've just blogged about my eating history too...  years of low-fat, high starch, high fruit eating led me to the brink of diabetes. I'm amazed I survived childhood!

  • SuzyCoQ

    2/18/2010 5:34:51 PM |

    Interesting, but this leaves out neogenesis within the pancreas. Assuming that glucose intake is reduced, wouldn't new beta cells be undamaged and have full functionality? [Unless progenitor cells are also damaged...]

  • Nancy

    2/18/2010 8:15:00 PM |

    Wouldn't this be more along the lines of adult onset type 1 diabetes (insulin dependent)?  It seems like that is growing too but the real swell seems to be in Type 2 diabetes where you produce copious amounts of insulin but your tissues are resistant to it.

  • whatsonthemenu

    2/18/2010 10:28:00 PM |

    "Interesting, but this leaves out neogenesis within the pancreas. Assuming that glucose intake is reduced, wouldn't new beta cells be undamaged and have full functionality? "

    That explains why my obese elderly mom has normal blood sugars even though she has always eaten diet high in simple carbs.

  • DrStrange

    2/19/2010 5:46:28 PM |

    Dr. A, your previous diet was indeed low fat and starch based but there was not much actual, real food in it!  I am missing the connection both here on this thread and in your blog, between people eating manufactured, food like substances that don't have much fat in them and are loaded w/ refined/highly processed starch carbs w/ almost zero fiber or nutrients in them, and the eating of actual whole grains, either fully intact or minimally processed.

  • whatsonthemenu

    2/19/2010 9:43:28 PM |

    "Wouldn't this be more along the lines of adult onset type 1 diabetes (insulin dependent)? It seems like that is growing too but the real swell seems to be in Type 2 diabetes where you produce copious amounts of insulin but your tissues are resistant to it."

    If you haven't already, check out Jenny Ruhr's blog, Diabetes Update, and her related website, Diabetes 101.  Type II is being subdivided according to short and long-term beta cell function and insulin resistance.  Different genes cause different impairments.  Emerging is MODY (mature onset diabetes of the young), or type 1.5.  A defining characteristic is that the ability of the pancreas to secrete insulin declines slowly over time, rather than suddenly as in type I, but it declines no matter what the treatment.

  • Michael Barker

    2/20/2010 5:40:01 AM |

    I am a Ketosis Prone Type 2 diabetic and it isn't necessarily true that glucose toxicity leads to permanent loss of pancreas functioning.

    Typically, we will lose all pancreas secretion and will go DKA, at that point we are essentially type 1's. We need insulin to survive but after 2 to twelve weeks of normal blood sugars we can be taken off insulin and we will have near normal blood sugars.

    Weird, yes, but there are thousands of us out there so this isn't uncommon.

    Narrative Review: Ketosis-Prone Type 2 Diabetes Mellitus
    http://www.annals.org/content/144/5/350.abstract

    My blog has more information, if you are interested.

    We seem to be severely intolerant of carbs so I too wonder what would have been the case, if years ago the carbs were taken out of my diet.

  • Anonymous

    2/22/2010 5:20:40 AM |

    Michael Barker - your blog is fascinating. Thanks for the pointer. Will you be allowing comments?

  • Anonymous

    2/26/2010 9:30:44 PM |

    What a great resource!

  • Nigel Kinbrum

    2/27/2010 3:35:57 PM |

    Matt Stone said...
    "The government advice to "eat more healthy whole grains" is not off-base. But that's not what Americans did." The public were conned. Manufacturers turned whole grains into dust and formed the dust into junk. Because everything that was in the grain was in the junk, they called the junk "whole grain".

  • Anonymous

    10/20/2010 3:35:26 AM |

    Sadly, this is what happened to me. I had glucose problems by age 15, but they told me for years I was fine. There was less information available in those days. I stopped all soda and junk, but it was too late, my fate was sealed. My pancreas and teeth were damaged. Somehow I managed to eat fruit without getting headaches years later, so I thought fruit in moderation was healthy. I though my fatigue was from my mercury fillings, but now I realize some of my fatigue was from fruit sugar. I blame society and my parents, although I forgive my parents. I was fed tons of soda and every type of high glycemic junk food you can imagine.

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