Eggs: Good, bad, or indifferent?

Eggs have been in the center of the cholesterol controversy almost from the very start.

The traditional argument against eggs went that eggs, high in cholesterol (210-275 mg per egg)and with some saturated fat (1.5-2.5 grams per egg), raised blood cholesterol (and LDL). Out went the daily fried, scrambled, poached eggs that many Americans indulged in most mornings. (We replaced it with more breakfast cereals and other carbohydrate conveniences, then got enormously overweight.)





A large Harvard epidemiologic study in 1999 called this observation into question. They tracked the fate of 117,000 thousand people and then compared the rate of heart attack, death, and other cardiovascular events among various people correlated to the "dose" of eggs they ate. Egg intake varied from none to 7 or more per week. Lo and behold, people who ate more eggs appeared to not suffer more events.

This study, large and well-conducted by an internationally respected group of investigators, seem to reopen the gates for more egg consumption, though most Americans still consume eggs cautiously.

Deeper down in this study, however, was another observation: People with diabetes who ate 1 egg per day had double the risk of heart attack. Because this study was observational, no specific conclusion as to why could be drawn.

A new study conducted by a Brazilian group may shed some light. Healthy (non-diabetic) men were fed an emulsion of several eggs. Inclusion of plentiful yolks caused a dramatic slowing of fat clearance from the blood. Specifically, "chylomicron remnants" were abnormally persistent in the blood. Chylomicron remnants are potent causes of coronary plaque. (Chylomicron remnants can be measured fairly well by intermediate-density lipoprotein and VLDL by NMR, or IDL by VAP.)

Diabetics are know to have substantial disorders of after-meal fat clearance, including an excess of chylomicron remnants. Could the Brazilian observation be the explanation for the increased event rate in diabetics in the Harvard study? Interesting to speculate.

We continue to tell our patients that eating eggs in moderation is probably safe. After all, there are good things in eggs: the high protein in the egg white, lecithin in the yolk. It is the yolk's contents that are in question, not the white. Thus, you and I can eat all the egg whites (e.g., Egg Beaters) we want. It's the safety of yolks that are uncertain.

The abnormal after-eating effect suggested by the Brazilians opens up some very interesting questions and confirms that we should still be cautious in our intake of egg yolks. One yolk per day is clearly too much. What is safe? The exisitng information would suggest that, if you have diabetes, pre-diabetes, or a postprandial disorder (IDL, VLDL), you should minimize your egg yolk use, perhaps no more than 3 or so per week, preferably not all at one but spaced out to avoid the after-eating effect.

Others without postprandial disorders may safely eat more, perhaps 5 per week, but also not all at one but spaced out.

Track Your Plaque Members: Be sure to read our upcoming Special Report on Postprandial Disorders. It contains lots of info on what this important pattern is all about. Postprandial disorders are largely unexplored territory that hold great promise for tools to inhibit coronary plaque growth and drop your heart scan score. The Brazilian study is just one of many future studies that are likely to be released in future about this very fascinating area.




Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC.A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999 Apr 21;281(15):1387-94.

Cesar TB, Oliveira MR, Mesquita CH, Maranhao RC. High cholesterol intake modifies chylomicron metabolism in normolipidemic young men. J Nutr. 2006 Apr;136(4):971-6.

Comments (3) -

  • Dani Aldred

    5/22/2009 7:56:58 PM |

    G'Day

    I stumbled upon your article when I google searched "Egg yolk Robb Wolf" ... First off, I eat two omega 3 eggs every morning and take 6g of fish oil per day (0.5g per 10lbs body weight). I like that you are open to both sides of the great egg debate. Personally, I think Egg Beaters are crap:

    http://lifespotlight.com/health/2009/03/16/selling-ill-health-real-foods-fake-foods/

    How do you feel about omega 3 eggs? Are they safer? Can we eat more of them if we are cutting out those damn dirty grains and supplementing with fish oil?

  • Anonymous

    10/24/2010 9:07:47 PM |

    Seems to have changed his mind - http://heartscanblog.blogspot.com/2010/08/whats-for-breakfast.html

  • buy jeans

    11/3/2010 6:45:59 PM |

    Diabetics are know to have substantial disorders of after-meal fat clearance, including an excess of chylomicron remnants. Could the Brazilian observation be the explanation for the increased event rate in diabetics in the Harvard study? Interesting to speculate.

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Don't wet yourself

Don't wet yourself

While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.



Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.

Comments (13) -

  • Anonymous

    4/3/2011 6:52:08 PM |

    Doc Davis,

    Thank you for all of your generosity and energy.  You've 50 posts on fish oil and 84 or vit D.

    I'm sending people to your site, but sometimes they're overwhelmed.

    Since these seem very important topics to you, would it be possible to summarize them in a definitive, proscriptive pair of posts.

    Thank you,

    DG

  • Might-o'chondri-AL

    4/3/2011 10:03:28 PM |

    Spino-cerebellar Ataxia (SCA) researchers claim to be associated with 28 (29?) variations of gene positions (loci) on human chromosomes; with gene mutations in 17 of those loci. Hereditary neuro-degeneration becomes clinicaly symptomatic in due time, not neccessarily when young.

    Gluten/gliadin responders who make anti-bodies to tissue trans-glutamin-ase (enzyme) have this anti-body implicated in ataxia syndrome. Spino-cerebellar ataxia is a category encompassing more than stumbling (SCA clinically includes psychiatric symptoms, etc.).

    Serum from humans with ataxia and the tissue trans-glutaminase anti-bodies was injected into normal mice, and the mice temporarily got ataxia. And then serum from humans who did not have ataxia, but did have tissue trans-glutaminase anti-bodies (ie: gluten sensitive)injected into normal mice also gave the mice temporary ataxia. In other words the gluten anti-bodies, irregardless of person having pre-existing ataxia or not, were enough to trigger ataxia in the mice.

    Doc cites study with average age of 48 as development of ataxia; this is explainable as fitting classic pattern of genetic neuro-degeneration. What I do like about Doc's linkage is the  concept that the gluten/gliadin anti-bodies may be a trigger of some sort.

    As for people "without positive celiac anti-bodies" who get spino-cerebellar ataxia (including any SCA associated symptoms)at the study's average age of 48 I am  skeptical. "Idiopathic" anything is a fancy way of saying something just so happens to be; as in patient Q has idiopathic XYZ and nobody knows for sure why, it just is XYZ.

    Doc has me thinking that if SCA genetic tendencies occur in an individual along with sensitive gluten genetics then cutting out the one risk factor controllable makes sense. Since genetic tests for SCA isn't readily done the no gluten tactic had to be tried out, and Doc seemingly noticed a % of encouraging results.

  • Dr. William Davis

    4/4/2011 1:23:28 AM |

    Hi, DG--

    Point taken.

    Perhaps a "Best of the Heart Scan Blog" would be in order.

    Thanks for the excellent suggestion.

  • Dr. William Davis

    4/4/2011 1:24:40 AM |

    Hi, Mighto-o,

    You've got some wonderfully unique insights.

    I'd like to see more of your ideas chronicled. Are you blogging or writing in some form?

  • dextery

    4/4/2011 2:10:33 AM |

    Recently there have cases of four people in the TV entertainment/news on air business that for some reason start speaking in gibberish...the latest being Judge Judy.
    http://vigilantcitizen.com/latestnews/judge-judy-the-4th-to-talk-gibberish-on-air/

    Do you suspect we may be seeing some brain atrophy from consumption of wheat?  I wonder how many times this may happen to ordinary people and they don't seek medical help because it passes.

  • Might-o'chondri-AL

    4/4/2011 3:42:08 AM |

    Hi Dr. Davis,
    I am not qualified to practise medicine, nor claim to be a true
    expert on things I discuss. Most of my work has been in developing countrys, which challenged my perspective and what pick-up on.

    The only other blog I read (and comment)is Whole Health Source.
    No personal blog or publication until another 1/4 century proves my advice worthwhile.

  • majkinetor

    4/4/2011 11:41:51 AM |

    How can it prove, if there is absence of digital forms Smile ?
    You should express your thought, definitely, in whatever form.
    Bring open source to medicine !

    Cheers.

  • Dr. William Davis

    4/4/2011 12:14:29 PM |

    Hi, Dextery--

    Interesting thought.

    Making the connection between wheat/gluten consumption and a neurological syndrome can be tricky. The most confident means to establish probable cause-effect is brain biopsy or autopsy. Most people would not submit to such things, so we rely on indirect measures like HLA DQ genetic markers and the reversal of the syndrome with elimination of wheat and gluten.


    Might-o--

    Well then, keep your wonderful insights coming!

  • Geoffrey Levens

    4/4/2011 4:12:33 PM |

    "Recently there have cases of four people in the TV entertainment/news on air business that for some reason start speaking in gibberish...the latest being Judge Judy.
    http://vigilantcitizen.com/latestnews/judge-judy-the-4th-to-talk-gibberish-on-air/"

    Some of my more paranoid friends think this is from "EMF mind control experiments" being performed by our govt, NSA, CIA, etc.

  • Anonymous

    4/5/2011 7:00:11 AM |

    Geoffrey

    well that certainly proves brain atrophy, if not in those 4 tv anchors but somewhat in your friends!!

    Wink

    PS

  • Medicomp INC.

    4/12/2011 4:11:14 PM |

    While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

    Disheartening, but facts are facts.  It's somewhat mind-boggling to fathom how much wheat is consumer everyday, and the amount of adverse effects that can inflicted among the population.  The best thing is to stay informed-It should be a priority for everyone to understand at least fairly well what we are ingesting daily.

  • Daniel A. Clinton, RN, BSN

    4/17/2011 2:57:59 AM |

    It saddens me that a gluten-free diet for six weeks isn't recommend for a whole host gastrointestingal, neurological, and automimmune diseases. Celiac markers are just numbers. Exclude gluten from the diet and see if there is improvement. That's the best way to assess wheat's role.

  • Todd

    1/25/2012 12:03:22 PM |

    Hi Mitochonri'Al!

    I love your commentaries!  Anyway, just wondering, a hypothesis of mine, given your citation about the human blood serum and mice experiment above, can trans-glutiminase anti-bodies be present in grain-fed meat and dairy products (pasteurized)?  Would that be another argument in favor of grass-fed beef and dairy (and the raw dairy of that group, if wanted)?

    Just a hypothesis, as i notice a lot of people that eat very low carbs to zero carb paleo eating start to have issues that are arthritic and ataxiatic (sic) and conditions that seem neurologic (incontinence, lower back pains, and other inflammatory issues) even from heavy whipping cream consumption.  And anecdotal journals, they tell of self-experimentation with and without dairy, and the pains depart, return and then depart again almost to a tee...

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Power in Numbers

Power in Numbers



In his book, The Wisdom of Crowds, author James Surowiecki begins with the story of an ox judging competition in which 800 people—not ox experts nor breeders, just ordinary people attending a county fair—were asked to guess the weight of the ox. The competition was conducted by a scientist, Francis Galton, who held a low opinion of the intelligence of the average person, remarking that “the stupidity and wrong-headedness of many men and women being so great as to be scarcely credible.” He hoped to prove, by examining the various guesses, that the average person had no idea of how to judge the real answer. After all participants casted their written votes, Galton tallied up the total and averaged the result: 1,197 pounds—just one pound off from the real weight of 1,198 pounds. Few individuals actually guessed the correct weight themselves but, when the opinions of many were combined, the result was near-perfect.

Crowds can also be a source of irrational behavior, panic, and stampede. Witness any modern football or soccer game, for instance, in which fights break out over an issue as minor as a disputed call or a heckle. Or go back through history to the countless events when mass hysteria ruled, such as the Salem Witch Trials or Orson Welles’ War of the Worlds radio broadcast.

Let’s put aside examples of mass emotional chaos of the sort that causes crowds to stampede store doors on Black Friday. Let’s focus instead on conscious, considered, thoughtful opinions. We all accept that there are as many opinions on issues as there are people, not uncommonly with widely divergent views. But can we, as Galton’s famous experiment did, combine the opinions of many and come away with some fruitful insight—the correct answer? Just as the people participating in Galton’s experiment were not experts, so Cureality participants—a crowd-sourced collection of opinions—are not experts. If we were to poll everyone to identify their area of expertise or experience, it would likely include finance, the retail industry, raising children, or teaching—but not health. Yes, we have experts curating the direction of content, but we also crowd-source collective opinion.

Right now, Cureality is based on existing science, the philosophy of self-directed health, combined with guidance and community to help the participant along in the sometimes complex world of health questions. But as our processes and procedures improve, can we—like Galton’s ox weight guessers—come away with coalescent wisdom, answers to our health questions, near-perfect solutions to health conditions that have eluded the “experts” for centuries?

I think that we can. No, I know that we can. We enter a new age in information and harness the power of the crowd-sourcing of solutions, even when no single individual has the complete answer herself.

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Prototypical Lipoprotein(a)

Prototypical Lipoprotein(a)

Here's the prototypical male with lipoprotein(a):



Several features stand out in the majority of men with lipoprotein(a), Lp(a):

Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight.

Intelligent--Above average to way above average intelligence is the rule.

Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a).

Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

Are rabid fans of Star Trek.


Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a).

Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise.

Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.

Comments (23) -

  • Anonymous

    2/24/2010 8:24:18 PM |

    arthur ashe and steve larsen (the cyclist who recently died at age 39) seem to fit the profile...

  • Jolly

    2/24/2010 8:57:16 PM |

    Great, I fit most of this risk profile.  (BMI is 17), although I prefer rock climbing to aerobic work.  

    Maybe I should get my Lp(a) levels tested.

  • Bob

    2/24/2010 9:41:58 PM |

    Dr. Davis,

    Thanks for sharing this, very interesting. Are these your personal observations or do you know of any studies indicating any of the above?

  • Anonymous

    2/24/2010 11:44:25 PM |

    Doctor Davis,

    While many people are sensitive to profiling, I think you are on to something and it should be investigated. The rate of how a person ages definitely seems to be indicative of how healthy their heart. I look at pictures of John Ritter in his younger years and compare them to just before he died. Yikes, he looks like a mess! How our chins droop and stomachs grow shows something. Being pruney is one thing. Looking old is another.

    -- Boris

  • Onschedule

    2/24/2010 11:56:56 PM |

    The profile you outline for your typical lp(a) patient describes me perfectly. I'll even admit to liking Star Trek...

    My lp(a) = 88 mg/dl (prior to treatment). I've lowered it significantly, in part, by following the advice on your blog.

    Many thanks for all of the time you spend sharing your wisdom and experience with the world!

  • Dr. William Davis

    2/25/2010 12:16:44 AM |

    Hi, Bob--

    Pure, unadulterated anecdote. No data whatsoever.

    Nonetheless, I marvel at how often it holds true. I see several people a week who fit the description.

  • ramon25

    2/25/2010 1:03:09 AM |

    Hello doctor, I know this is a little off topic and for that I apologize. I ask because I am a little desperate for an answer. I hope it would not be an inconvenience to answer. I take a vitamin k supplement from the LEF brand, this one-http://www.lef.org/Vitamins-Supplements/Item01224/Super-K-with-Advanced-K2-Complex.html
    It has a lot of K. I wanted to know If that high amount of k would require me to take HIGHER levels of vitamin D? Or would the regular 6000- 8000 iu would suffice, I ask that knowing that Vitamin D status is an individual thing ( I am an avid reader of your blog) But as a general rule for how they interact, I cant find any info on this. Thank you very much for your time, and keep up the good work!

  • Stan (Heretic)

    2/25/2010 3:00:32 AM |

    Dr. Davis,

    Thank you for very thought-provoking posts, but I have to say I have a slightly different slant on this:  the type of people you show have so little body fat that our (yes, I am one too) metabolism runs exclusively on what we put on our plate rather than using our body fat (intermittently) for ketogenic cycling in between meals. We lack ketone bodies.

       If we consume a high carbohydrate diet then our body has to use glucose for energy 100% of the time.   Our abnormal (on high carb) lipid profile may be (probably) a consequence of that rather than of some genetical differences.  This is the simplest explanation and may be sufficient to explain the entire plethora of observations.

    That is why I used to have hypoglycemia (and beginning of angina) at the age of 42 on a  low fat vegetarian diet, 11 years ago.  That's probably why you were developing diabetes on Ornish diet.  That's why many if not most low fat vegetarians are not doing particularly well especially after a couple of years once they loose their body fat.

    Regards,
    Stan (Heretic)

    Refs:

    Carbohydrates and Diabetes

    Snacking and glucose/ketogenic cycling

    Very-Low-Fat Diets: What Are the Benefits?

    Diabetes, liver, fructose and omega-3

    It's the glucose, stupid!

    Food Choices and Coronary Heart Disease

  • Dr. William Davis

    2/25/2010 3:13:28 AM |

    Hi, Ramon--

    To my knowledge, there is no interaction. Many of my patients are on the combination and I've not noticed any shift in dose requirements. I DO believe, however, that there is an important synergy between the two in both prevention/reversal of coronary disease and bone health.

  • Dr. William Davis

    2/25/2010 3:15:52 AM |

    Hi, Stan--

    Not so fast.

    Recall that Lp(a) is "activated" by the presence of small LDL. Small LDL particles are spectacularly created by  . . . carbohydrates!

    So I wouldn't be so eager to live on carbohydrates if you are a super skinny Lp(a) person.

    With small LDL and Lp(a), the basic theme is fat, fat, and more fat.

  • ramon25

    2/25/2010 4:12:36 AM |

    Dr. Davis, thank you so much for your response! But even with such a high level of K? the dosage I am taking is over 2500% of the DV. Do you think that amount has health benefits?
    thanks Dr. Davis I really appreciate you help.

  • Anonymous

    2/25/2010 4:29:36 AM |

    Dr. Davis,

    What of someone who initially fit the profile but then managed to add a fair amount of muscle tissue through hard training and enough calories and nutrients? Does this change anything?

    I'm not advocating going hog wild, but do you feel that a formerly golden fit for this profile who now has more muscle mass and is quite active has a bit more of a buffer zone in terms of carbohydrate consumption?

    I ask because in my work in gyms, I have known many men who would initially be carbon copies of the profile you proposed, but after 6 months to 2 years or somewhere in that range, people who just met them would never guess they had fit the profile at some point in the past.

    -Steve Janzek

  • Mat

    2/25/2010 5:25:03 AM |

    I am not sure of HeartHawk's BMI but he sure looks like has this problem.  From his blog:

    "I have high Lp(a) with an otherwise world-class lipid panel."

    "I am proactively fighting my extraordinarily high Lp(a)"

  • Dr. William Davis

    2/25/2010 3:46:54 PM |

    Hi, Mat--

    Yes, indeed. Our beloved Track Your Plaque Heart Hawk does indeed have Lp(a). He also fits the physical/mental pattern, including the Star Trek part.

    Anonymous--

    Lp(a) is genetically-determined. Muscle mass has no effect, unfortunately.

  • Kent

    2/25/2010 4:26:16 PM |

    Dr Davis,

    I've received mixed messages concerning LP(a) and LDL. Many have said that lowering one's LDL will not lower LP(a), yet I'm a little curious as to what happened with my LP(a).

    LP(a) started at 198 nmol/l, with LDL at 105 or so. I started 2000mg Niaspan, 4800mg fish oil, Pauling therapy, no wheat and a few other things you reccomended in your book for LP(a). In 3 months LP(a) was down to 109 nmol/l. In 9 months my LP(a) was down to 45 nmol/l! But my LDL was down to 26! My liver enzymes had gone from 20 to 60, my Testosterone had dropped sigmicantly and my energy was zapped.  

    Therefore, I went from 2000mg Niaspan to 2000mg Niacin IR because I was told it was easier on the liver and wouldn't shoot the LDL so low while keeping HDL high. Well next test LDL was back up to 89, and felt better, but LP(a) had jumped back up to 150 nmol/l. That would lead me to believe it is tied to LDL. Would you agree?

    Thanks,
    Kent

  • StephenB

    2/25/2010 7:01:44 PM |

    It's quite funny how well I fit the criteria: 46, electrical engineer, BMI of 22, and a marathon runner. I have eliminated wheat, have 62 mg/dl 25-H levels, and enjoy extra saturated fat with my saturated fat. I may have to spring for LpInnocent testing next time around.

  • jd

    2/25/2010 7:49:54 PM |

    I am getting mine tested shortly, once LEF puts their blood tests on sale.   I fit that profile very closely although I can gain weight if I pig out over a period of days.  I do stay away from all empty carbs but do get carbs from fruit and veggies like butternut squash & sweet potatoes.  I always eat my carbs with a protein and/or fat source to slow the assimilation into the bloodstream.

  • Drs. Cynthia and David

    2/25/2010 9:25:18 PM |

    Very interesting observations!  It might explain why some healthy-looking people have heart attacks anyway.  I am curious whether the observation will hold up as you gather more info, and what other insights it might bring.

    @ramon25, take a look at Chris Masterjohn's post about D, A, K1 and K2. Apparently D increases the use of and need for K, but is somewhat modulated by A. It's really interesting stuff. http://blog.cholesterol-and-health.com/2009/04/tufts-university-confirms-that-vitamin.html

    Cynthia

  • zach

    2/26/2010 3:34:21 PM |

    Wow. I just realized that all of myteachers of higher math and physics were all really, really skinny guys. You're right!

    @Stan

    That makes a lot of sense.

  • shelley

    5/21/2010 8:04:17 PM |

    Interesting stuff.  I am a 46 year old woman, runner, fit, low weight/body fat, good cholesterol levels, but have Lp(a) levels of 62mg/dl.  Huge family history of early death from sudden cardiac arrest.  I'd say add women to the profile. Smile

  • Viagra Online

    8/23/2010 10:41:10 PM |

    I had a friend like this men he was so intelligent but when we were talking about something he said that he always was right and everybody was wrong it was a really bad problem I wouldn't like to be intelligent if I were like him.

  • papermoz

    9/20/2010 12:24:38 PM |

    Thanks for this great post it was very informative and helped me with my own project I am attempting to complete.
    Dissertation | Thesis | book report

  • buy jeans

    11/2/2010 7:35:48 PM |

    Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

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