In search of wheat: Emmer

While einkorn is a 14-chromosome ancient wheat (containing the so-called "A" genome), emmer is a 28-chromosome wheat (containing the "A" and "B" genomes, the "B" likely contributed by goat grass 9000 years ago).

Both einkorn and emmer originally grew wild in the Fertile Crescent, allowing Neolithic Natufians to harvest the wild grasses with stone sickles and grind the seeds into porridge.

Having tested einkorn with only a modest rise in blood sugar but without the gastrointestinal or neurological effects I experienced with conventional whole wheat bread, I next tested bread made with emmer grain.

The emmer grain was ground just like the other two grains, cardiac dietitian Margaret Pfeiffer doing all the work of grinding and baking. Margaret added nothing but water, yeast, and a little salt. The emmer rose a little more than einkorn, but not to the degree of conventional whole wheat.

I tested my blood sugar beforehand: 89 mg/dl. I then ate 4 oz of the emmer bread. It tasted very similar to conventional whole wheat, but not as nutty as einkorn. Also not as heavy as einkorn, only slightly heavier than conventional whole wheat.

One hour later, blood sugar: 147 mg/dl. I felt slightly queasy for about 2-3 hours, but that was the end of it. No abdominal cramps, no sleep disturbance or crazy dreams, no nausea, no change in ability to concentrate.

I asked four other wheat-sensitive people to try the emmer bread. Likewise, nobody reacted negatively (though nobody tested blood sugar).

So it seems to me, based on this small, unscientific experience, that ancient einkorn (A) and emmer (AB) wheat seem to act like carbohydrates, similar to, say, rice or quinoa, but lack many of the other adverse effects induced by conventional wheat.

Modern wheat , Triticum aestivum, contains variations on the "A," "B," and "D" genomes, the "D" contributed by hybridization with Triticum tauschii at about the same time that emmer wheat hybridization occurred. It is likely that proteins coded by the "D" genome are the source of most of the problems with wheat products: immune, neurologic, gastrointestinal destruction, airway inflammation (asthma), increase in appetite, etc. This is consistent with observations made in studies that attempt to pinpoint the gliadin proteins that trigger celiac, the area in which much of this research originates.

If I ever would like an indulgence of cookies or cupcakes, I think that I will order some more einkorn grain from Eli Rogosa.

Comments (13) -

  • Stephan

    6/23/2010 5:24:11 PM |

    Thanks for subjecting yourself to these experiments!  Very interesting.  I have a friend who reacts poorly to wheat but tolerates spelt.

  • Anonymous

    6/23/2010 5:35:44 PM |

    Wheat is eaten everywhere in the world. I'd hope GM crop scientists design a variety which can solve this problem.

  • k

    6/24/2010 2:40:27 AM |

    If I am not mistaken, corn is also the result of the domestication of wild grasses existing some 8,000 years ago. Fooling with mother nature put us on a collision course with consequences.

  • Anne

    6/25/2010 2:25:31 AM |

    My concern is that the body could be reacting without symptoms. Could  these ancient grains cause inflammation even though there is no obvious reaction? I have lived 7 years without gluten and have no desire to add it back to my diet. Before I eliminated gluten I was very ill. It is not worth the risk to me.

  • Anonymous

    6/25/2010 4:11:10 AM |

    Dr. Davis,

    In your experience, in terms of small LDL and the like, what's better: a high peak of 150 that's brought down relatively quickly or a lower peak, but extended over a longer duration?

    Thanks,
    David

  • Dr. William Davis

    6/25/2010 3:25:38 PM |

    Anne--

    Please don't interpret these casual observations to mean that we should eat einkorn.

    My goal with this little experience is to gain an understanding of where along the way of wheat's 10,000+ year human consumption history did things go wrong.

    It seems to me that humans could have gotten away with eating einkorn much more freely, with fewer health problems than with modern wheat. I still would like to know where the extreme adverse effects were acquired, however. I suspect this occured in the 1960s and 1970s with the hybridization experiments conducted in Mexico. more on that later.

  • Dr. William Davis

    6/25/2010 3:26:15 PM |

    Anon--

    No data. I suspect that the high peak is worse, but that is based on no formal data.

  • Anonymous

    6/26/2010 9:48:57 AM |

    FODMAPs comprise a monosaccharide (fructose), a disaccharide (lactose), oligosaccharides (fructans and galactans), and polyols.

    In one study, as obese people lose weight, the balance between the Firmicutes and the Bacteroidetes changes - the latter increasing in abundance as an overweight person gets slimmer.

    Fructans, found in wheat, are fermented by bacteria in the large intestine into short chain fatty acids.


    Besides human metabolism, the digestion of wheat is also affected by how it is metabolized by the particular intestinal flora inhabiting a person.


    Sources:

    Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach

    An obesity-associated gut microbiome with increased capacity for energy harvest


    Food tables: fructose




    Fructose in the diet appears to be even more dangerous in the presence of trans-fats.


    Source:

    High Levels of Fructose, Trans Fats Lead to Significant Liver Disease, Says Study

    "The investigators found that mice fed the normal calorie chow diet remained lean and did not have fatty liver disease. Mice fed high calorie diets (trans-fat alone or a combination of trans-fat and high fructose) became obese and had fatty liver disease.

    "Interestingly, it was only the group fed the combination of trans-fat and high fructose which developed the advanced fatty liver disease which had fibrosis," says Dr. Kohli. "This same group also had increased oxidative stress in the liver, increased inflammatory cells, and increased levels of plasma oxidative stress markers.""

  • Tom Moertel

    6/26/2010 7:47:08 PM |

    Your experience with einkorn and emmer is interesting. They do not seem to cause you the problems that wheat does, and that evidence supports the theory that they are less harmful than wheat.  But the same evidence makes another theory equally plausible: that foods such as wheat harm you through pathways that form only through repeated exposure.  Under this theory, einkorn and emmer could be just as harmful as wheat but, being novel to your diet, haven't had enough time for their pathways to form.

    It would be interesting, then, to learn what happens if you were to incorporate einkorn or emmer into your diet more regularly.

  • carrmh37

    6/27/2010 1:48:06 AM |

    This abstract would seem to support your view that it may be a modern phenomenon.

    Journal of Medicinal Food
    Effects of Short-Term Consumption of Bread Obtained by an Old Italian Grain Variety on Lipid, Inflammatory, and Hemorheological Variables: An Intervention Study

    http://www.liebertonline.com/doi/abs/10.1089/jmf.2009.0092

    Michael

  • Anya

    9/9/2010 11:45:05 AM |

    Naturopath David Getoff recently did a podcast on this subject, it is worth listening to: http://naturopath4you.com/mp3s/Gluten%202010%20Final.MP3

  • lindaharper

    9/11/2010 8:47:02 PM |

    Just wondering if you have experimented with fermenting the wheat or sprouting wheat and then drying it to make bread. I've read  that making bread through this method helps celiac problems and wondered if there is a connection  since soaking and/or sprouting neutralizes the phytic acid and supposedly aids in digestion and keeps blood sugars from rising as much.

  • Janet Creamer

    11/30/2012 3:07:09 AM |

    Wondering if there is a difference in European wheat types verses American. I have illness, vomiting and nausea when I consume wheat here in the US. But when I tried it in France, Germany and Switzerland, I did not have any problems. I thought it might be the way US wheat is processed, but it might be the wheat type, as well.

    Thank you,
    Janet Creamer

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If you take niacin, you must exercise

If you take niacin, you must exercise

We use a lot of niacin in the Track Your Plaque program.

Niacin:

--Increases HDL and shifts HDL towards the large, protective fraction

--Reduces small LDL--In fact, niacin is the best treatment we have to reduce small LDL after wheat elimination and carbohydrate reduction.

--Reduces fasting and postprandial (after-eating) triglycerides

--Reduces heart attack risk by 20-28%--even as a sole agent.


But . . . niacin also triggers higher blood sugar because it partially blocks the effects of insulin (insulin "resistance").

While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

Yes, through exercise. Here's one interesting observation in obese (BMI 34.0), sedentary men given placebo, exercise, niacin (1500 mg Niaspan, once per day), or niacin + exercise:





From Plaisance et al 2008.

Blood was drawn following a high-fat meal challenge. (Yes, a high-fat challenge, not a carbohydrate challenge. In this study, there were only 17 grams carbohydrates in the test meal, but 100 grams fat. More on this in future.) Exercise consisted of walking for 50 minutes at a moderate pace one hour prior to the meal challenge.

You can see from the graph that exercise partially corrected the increased insulin level provoked by niacin.

Judging from this and other studies, exercise can help minimize the insulin-blocking effects of niacin. It doesn't take much, just moderate exercise for at least 30 minutes.

Adequate sleep can also help, since sleep deprivation is a potent trigger for insulin resistance, only worsened in the presence of niacin. Vitamin D supplementation to achieve desirable blood levels (which I define as 60-70 ng/ml) is also an effective means to minimize this effect.

Comments (23) -

  • karl

    12/29/2009 11:16:55 PM |

    What about adding P-5-P to the Niacin?

    I've heard things about cinnamon lowering Blood sugar, but I'm not convinced.

  • Grandma S.

    12/30/2009 1:59:12 PM |

    Thank you for posting this.  I am exercising everyday sometimes twice a day to equal 45-60 minutes and see some help with the glucose level.  My LDLs continue to be around 100 and my Dr. wants to increase the Niacin.  Will that help?  It's a fine line, keep the sugars down and get the LDLs down. I appreciate your blog!

  • Renrew

    12/30/2009 2:42:42 PM |

    Cinnamon does reduce blood sugar but the effect is minimal, even at higher doses.

  • Adolfo David

    12/30/2009 3:06:07 PM |

    About Karl comment, you can add many supplements to niacin to counteract this effect. Chromium, resveratrol, standarized cinnamon, green tea extract... Life Extension has launched a niacin with quercetin for example (but now out of stock).

  • Nigel Kinbrum BSc(Hons)Eng

    12/30/2009 3:19:47 PM |

    Would reducing sugary/starchy carbohydrate intake be an effective way to reduce hyperglycaemia?

  • Anonymous

    12/30/2009 10:00:47 PM |

    Thanks for posting Dr. Davis.

    Is splitting 1500 mg of Niacin to two 750mg doses,one in morning, one in evening ok?
    Or should  the 1500 be taken all at once?

  • Anonymous

    12/31/2009 1:13:38 AM |

    Both times I started Niacin, I developed Gout.
    The second time I cut the tablets in half hoping to avoid another bout but still, Gout in a different joint.

  • Mark

    12/31/2009 4:56:24 AM |

    It has been my experience that over time (2-3 Months)the Slo-Niacin I use has less effects on raising blood glucose levels like it does at the onset. It is well advised that everyone should get in the exercise regardless of niacin intake.

  • Boris

    1/1/2010 3:48:15 PM |

    I took 500mg of Niacin every day to get my HDL up. Plus, there was niacin in my multivitamin. My HDL didn't go up at all. I exercise plenty too. All I got out of it were a few itchy flushes that made my ears feel clogged. I'm going to finish my bottle of Slo-Niacin and try a red yeast rice that was tested by Consumerlab.com.

  • Anonymous

    1/1/2010 8:29:23 PM |

    Regarding splitting the dose of Niacin.  I am pretty sure I have seen a post from Dr.D saying to take all at once.  

    I used to split my dose. I thought I was being smart by distributing the Niacin over the day.  My local pharmacist told me not to split the dose because of impacts to Liver function.

  • Anonymous

    1/2/2010 2:10:06 PM |

    I avoid sustained release niacin.

    I get around 80 mg niacin per day in a multivitamin and don't want to add extra.

    http://www.lef.org/LEFCMS/aspx/PrintVersionMagic.aspx?CmsID=114620

    pomegranate...

    Despite the patients’ advanced atherosclerosis, ingesting pomegranate juice produced statistically significant reductions in the thickness of their carotid artery walls, which is correlated with decreased risk for heart attack and stroke. After only three months, the average thickness declined by 13%, and after 12 months, the thickness dropped 35% compared to baseline. During this same 12-month period, the average carotid artery thickness of the placebo group increased by 9%.

  • Anonymous

    1/2/2010 2:39:54 PM |

    Thank you so much for posting this!  I have bee na niacin devotee for about 15 years, and wanted to get my LDL back up after a dx of T2D (with Antibodies) ... and having my niacin "taken away" by my internist.  MY Endo put me back on a lower dose of slo-niacin ... exercise is helping but I may need to up my anti-IR meds.

  • Anonymous

    1/4/2010 4:14:05 AM |

    When is the best time to take niacin?

    morning or night?

    before or after exercise or meals?

  • Dr. William Davis

    1/4/2010 11:27:02 PM |

    We've had best results dosing niacin with dinner or the largest meal of the day.

  • Anonymous

    1/12/2010 2:37:54 PM |

    Dr.Davis

    Just asking this again, could you could please help me out.

    Is splitting 1500 mg of Niacin to two 750mg doses,one in morning, one in evening ok?
    Or should the 1500 be taken all at once?

  • Anonymous

    3/19/2010 4:24:19 PM |

    I had a terrible time with Niacin and insulin resistance.

    I tried exercising but to keep my BG down, I would have to exercise 3 or 4 times a DAY, which is simply not feasible.  Oh, and I am a low-caber, too.

    I would exercise extreme caution in starting to use this, with any Diabetes. (I am a T1.5).

  • lnoonan

    5/19/2010 4:14:15 PM |

    Dr Davis,

    What kind of exercise would you recommend for a Senior lady who is handicapped?  It is difficult for her to do any exercise, so do you know of something she would be able to do while she is taking niacin?  Or, would it be better for her to stop the niacin since exercise is difficult and try other supplements?  Thanks for your help.

  • Anonymous

    5/27/2010 5:00:58 AM |

    Assuming your recommended Slo-niacin...is it better to split your doses up (500 mg morning and 500 mg at night) or take all 1000mg at once? If its better to take all at once is night or morning better?

  • kimberly

    8/11/2010 5:57:09 PM |

    I love to practice exercise, i think this activity is the best option to keep our total welfare and it is very fun. When we exercise frequently we can notice a change not only in our shape but in our mood too. Actually we can improve our sexual performance. When some cases when the erectil dysfunction present like a problem  to buy viagra is a great alternative, how ever you must to combine it with exercises and a good feed.

  • buy jeans

    11/4/2010 5:11:30 PM |

    While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

  • Anonymous

    12/15/2010 1:49:29 PM |

    Taking niacin before vigorous exercise has one benefit for me.  The flusing is minimized or even eliminated.

    I've seen different recommendations for dosing frequency.  Three times a day is the "standard" dosing regimen.  However, when I haved switched to three times a day dosing, I have experienced elevated liver enzymes.  I've never had a problem with twice a day dosing.

  • bob

    2/7/2011 4:55:57 AM |

    I am not aware of any data to support 24% risk reduction for MI with the use of Niacin, can you provide citations?

    Primary or secondary prevention?

    Bob Hansen MD

  • John

    6/2/2011 5:01:34 PM |

    Cinnamon doesn't lower blood sugar per se.  The apparent mechanism occurring here is a slowing down of carbohydrate absorption in the gut.  The mechanism is believed to involve a class of molecules known as flavonoids, which either reversibly compete for the glucose receptor or have their own receptor on the GLUT 2 (glucose transport 2) protein.  This action only slows down the absorption of carbohydrates, but all (that's 100%) sugar is absorbed into the body.  It is the only thing you intake that is absorbed 100% and it doesn't matter if it's glucose, sucrose, fructose, or a complex carb.  Anywho, not that I want to debate the finer points of carbohydrate biochemistry.  For more on flavonoids and GLUT2 you can look up this paper (Kwon O., Eck P., Chen S., Corpe C., Lee J-h., Kruhlak M., Levine M. (2007) Inhibition of the intestinal glucose transporter GLUT 2 by flavonoids. FASEB Journal 21, 366-77.).

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Alternatives to fish oil capsules

Alternatives to fish oil capsules

Occasionally, someone will be unable to take fish oil due to the large capsule size, excessive fishy belching, or stomach upset. The easiest solution is usually just to try a different brand, e.g., Sam's Club (Makers' Mark brand) enteric-coated.

However, sometimes liquid fish oil preparations may be preferred. Here'a list of products we've used successfully. All cost more than plain old fish oil capsules, but fish oil is so crucial to your heart scan/coronary plaque control efforts, that it really pays to search out alternatives.



Liquid fish oil alternatives to capsules:

Liquid fish oil--e.g., Carlson's liquid fish oil. Most liquid fish oil comes flavored either lemon or orange.



Frutol--A very clever re-formulation of fish oil that makes it water-soluble and non-oily. The Pharmax company has put their fish oil into a fruit flavored base that tastes pretty good and is not too expensive.
Go to www.pharmaxllx.com for more information. Unfortunately, I do not believe it's available in stores.





Coromega--another non-oily preparation, though available in some health food stores. Coromega comes in little single-serving foil dispensers. It tastes kind of fruity (though I personally like the Frutol better for taste and consistency). It's kind of pricey ($1.40 per day for two packets).



Regardless of what preparation you choose, you can determine the dose needed by adding up the EPA+DHA content. For the basic prevention effect, the starting dose for the Track Your Plaque program, you need a total of 1200 mg per day of EPA+DHA. Higher doses, e.g., 1800-2400 mg per day, may be required for correction of high triglyceres or postprandial (after-eating) abnormalities.

Comments (2) -

  • buy jeans

    11/3/2010 7:01:54 PM |

    Regardless of what preparation you choose, you can determine the dose needed by adding up the EPA+DHA content. For the basic prevention effect, the starting dose for the Track Your Plaque program, you need a total of 1200 mg per day of EPA+DHA. Higher doses, e.g., 1800-2400 mg per day, may be required for correction of high triglyceres or postprandial (after-eating) abnormalities.

  • cheap viagra

    4/25/2011 2:38:16 PM |

    I think you're right that'll be the easiest solution and it'd be nice if you can add more about the same topic with different solutions and versions to understand all the alternatives.
    23jj

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Are there still unexplored causes of heart disease?

Are there still unexplored causes of heart disease?

I met a woman today. She had her first heart attack at age 37. She just had her 2nd heart attack this morning, at age 40.

Several issues are surprising about her story. First, she's pre-menopausal. Heart attacks before menopause are unusual. We'll occasionally see women have a heart attack before or during menopausal years only if they're heavy smokers and/or they have had diabetes (either type I or type II) for many years. But this young woman had neither. She is slender and has never smoked.

Even more surprising are her basic lipid values: LDL cholesterol 35 mg/dl, HDL 150 mg/dl, triglycerides 317 mg/dl. This is a very unusual pattern.

Unfortunately, this is all developing acutely in the hospital. (I've just met her today--she's not a Track Your Plaquer!) Lipoprotein analysis would be extremely interesting. In particular, I'd like to see whether she has any other markers besides elevated triglycerides of a "post-prandial" abnormality, i.e., persistence of abnormal particles after eating. The high triglycerides make this quite likely.

If this proves true, the omega-3 fatty acids from fish oil will be a lifesaving treatment for her, since they dramatically reduce both triglycerides as well as persistent postprandial particles like intermediate-density lipoprotein (IDL). (Track Your Plaque Members: See the Special Report on Postprandial Abnormalities on the present home page at www.cureality.com for a more in-depth discussion of this fascinating collection of patterns that is just started to be explored.)

In the real world, especially acute care medicine, there's always a kicker: she speaks no English. Unfortunately, communicating the intricacies of a powerful program like ours that aims to identify all causes of heart disease, then corrects then and aims for coronary plaque regression, is difficult if not impossible.

I also do occasionally worry that, given this woman's extraordinary risk at a young age, and overall very unusual lipid patterns (HDL 150?!), if there are causes presently beyond our reach. We have to make use of the tools available to us for now.
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How many ways can you disguise sugar?

How many ways can you disguise sugar?

I came across this shockingly silly report on AOL, who obtained their info courtesy Health Magazine:

The Best New Healthy Foods for Busy People
from Health


The foods on their list:

Kettle Brand Bakes Hickory Honey BBQ--the healthy claim is based on the lack of trans-fatty acids and low-fat.










Post Healthy Classics Raisin Bran Cereal Bars, Cranberry--Likewise, low-fat, sweet, and addictive means healthy to these people.




Amy’s Mediterranean Pizza With Cornmeal Crust --Please!!



Horizon Organic Colby Cheese Sticks --Because it's made by cattle without use of growth hormone or antibiotics, they declare this healthy. I guess we can ignore the saturated fat content and high total fat content.

100% Whole Grain Chips Ahoy! Cookies --You mean we can add the bran back to wheat products and make it healthy?!


This kind of mass-market marketing trickery leaves me incredulous. Don't believe it for a moment. This is typical of the food industry: Take one aspect of nutrition that is truly healthy, such as high-fiber, or low-fat, or organic. Then add undesirable, unhealthy ingredients. The current fad is to add lots of sugar and or sugar-equivalents (usually flour and other wheat products). Because there's one healthy ingredient, they'll call the end-product healthy, too.

If you want to see what health looks like if you indulge in "healthy" products like this, just look up and down the grocery aisles at your neighborhood grocery store. You're likely to see the results: Gross obesity, diabetes, and arthritis.

You won't, of course, see the huge acceleration of growth in coronary plaque, but it's there, ticking away.
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Why haven't you heard about lipoprotein(a)?

Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

Comments (26) -

  • Matt Stone

    7/1/2010 4:18:14 PM |

    Ah, thyroid normalization. My favorite. Of course, this has a trickle-down effect on DHEA, estrogen, and testosterone as well. Perhaps Lp(a) is one mechanism by which Broda Barnes was able to prevent heart attacks in his patients?  

    http://180degreehealth.com

  • Anonymous

    7/1/2010 4:39:21 PM |

    Aw darn it. Again health info to be confused about. From Taubes' GCBC I read it was apoB supposed to be the one associated with smaller and denser LDL, "the bad LDL", and I thought apoA was the "large and fluffy" or more benign LDL. I'm pretty sure Dr. Lustig says pretty much the same in his "Sugar, the bitter truth" video. There goes my newly acquired "understanding" out the window again.

  • Anonymous

    7/1/2010 4:42:40 PM |

    The last of the 4 treatments doesnt' seem very specific...

    is "T3" a supplement.. if not, how does one go about normalizing the Thyroid?

  • Mike

    7/1/2010 8:12:19 PM |

    That's a lot of fish oil. I take about 1/5 that amount and would find it irritating to have to increase my intake by a factor of 5.

  • Drs. Cynthia and David

    7/1/2010 9:52:19 PM |

    If the pharma industry could actually come up with drugs that work and don't just chase surrogate markers, I'm sure that would be helpful.  I'm all for nutritional and lifestyle fixes, but this won't work perfectly for everyone all the time, so useful drug therapies would be nice too.

    Anonymous, I think you're confusing LDL pattern A and B ("fluffy" vs dense) with apoA and ApoB (HDL associated vs LDL associated proteins).

    Cynthia

  • Anthony

    7/1/2010 10:20:10 PM |

    Dr. Davis,
    How low do you like to see Lp(a)? I've seen recommendations of below 30mg/dl, below 20, and below 10. Mine is 19. Thanks,

    Anthony

  • Dr. William Davis

    7/2/2010 1:12:23 AM |

    Anthony-

    Excellent question . . . for which there's no solid answer.

    Despite all we know about Lp(a), no endpoint data have been generated. However, I can tell you that using particle count measurements in nmol/L a level of 60 nmol/L works very well. In mg/dl, a measure of weight per volume, it depends on the method of measurement used. If the "normal" range is 30 mg/dl or less, then aiming for around 20 mg/dl has worked well.

  • Anonymous

    7/2/2010 1:32:33 AM |

    I asked my cardiologist about it (heads up preventive cardiology at a major research institution in Texas) and he said:

    "Well, there's not anything we can do about it, so why test it?"

  • Anonymous

    7/2/2010 1:55:40 AM |

    My cardiologist and PCP have never ever discussed this with me even though I brought it up for discussion. I think my PCP didn't know much and ignored it. I desperately need a new cardiologist (I live in the SF bay area). Anybody here love their cardiologist and like to share some details? I will be forever thankful Smile

    TIA

  • Paul

    7/2/2010 6:09:32 AM |

    I found this to be a very interesting post over at the Animal Pharm blog concerning this very subject:
    Auto-Tuning Lp(a): Value of Low Carb, High Sat Fat


    They basically come to a very simple conclusion in controlling Lp(a); eat some damn saturated fat! And stay away from the damn carbs!

    Now, let me get back to making my LDL the plain and fluffy kind... someone pass me the ghee please...

  • Harry

    7/2/2010 2:41:24 PM |

    Anonymous and Drs. Cynthia and David, there are several "A" designated particles that frequently get confused. Dr. Davis is talking about lipoprotein(a), with a lower case "a", which consists of an LDL particle with a particle of apolipoprotein(a) attached to it. This apolipoprotein is also designated by a lower case "a". Lp(a) is very atherogenic, and should be minimized.

    Apolipoprotein A, with an upper case "A", on the other hand, is an atheroprotective particle that is a component of HDL. It comes in several varieties. The most plentiful one is designated Apolipoprotein A-I, or Apo A-I, which is the main particle that participates in reverse cholesterol transport, which is the principal way that HDL protects against atherosclerosis, by removing cholesterol from plaque and transporting it back to the liver for disposal. There are also particles designated Apo A-II and Apo A-IV that are also associated with HDL, but their function is not well understood. All the HDL-associated apo A particles are described with the upper case "A".

    Finally, there is the LDL pattern A, which indicates that the LDL particles are mostly large, whereas LDL pattern B indicates that LDL particles are mostly small. These are usually designated with an upper case "A" and "B", and the A pattern is thought to be less atherogenic than the B pattern.

    It is easy to confuse these "A" types, especially Apo A and Apo a, which are two very different particles, the large A apo is good and the small a apo is bad.

  • Kent

    7/2/2010 3:21:25 PM |

    My LP(a) started a year and a half ago at 198 nmol/L, it is now down to 35 nmol/L. Thanks to Dr, Davis's advice that I followed in the Track Your Plaque book, including 4800mg combined EPA, DHA fish oil and 2000mg Niaspan, etc.

    I also want ot mention though that I have been following the Linus Pauling protocol as well, which I believe has a synergistic effect with the other principles applied.

    An interesting thing happened that is worth mentioning, my LP(a) had been gradually dropping over that period of a year and a half from 198 to 45 nmol/L, then I switched to immediate release niacin and my LP(a) jumped back up to 150 nmol/L. That was the only change I made, so I switched back to Niaspan and that is when it went back down to 35 nmol/L.

    Kent

  • Alfredo E.

    7/2/2010 3:35:40 PM |

    Hi All.The following paragraphs were taken from http://www.drlam.com/opinion/Lp(a).asp

    Lipoprotein A, commonly called Lp(a), is a major independent risk factor for cardiovascular disease. The optimum laboratory level should be under 20 mg/dl and preferably under 14 mg/dl.

    Currently, there is no medicine or drugs that to effectively lower your Lp(a). A high Lp(a) is genetically linked. Fortunately, Mother Nature has provided us a much better non-toxic alternative. It consists of large doses of vitamin C, L-lysine, and L-proline.

    Many conventionally trained physician uses niacin to reduce Lp(a). This does work to a limited extend. Niacin reduces the production of lipoprotein A in the liver, and helps to bring down the lipoprotein A in the blood. This is what most conventional doctors use. However, this approach has its limitations because until the endothelial wall is optimized and cleared, the lipoprotein A level will not be able to reduce significantly. The effects of niacin usually hit a plateau after 6-9 months of therapy. If you are on niacin, make sure the liver enzyme levels are taken periodically to make sure the liver is able to handle the high dose of the niacin.

    This last flower:
    Replacing carbohydrates with proteins ignores the fact that protein, once in the intestinal tract, converts to amino acid. Amino acids increase insulin secretion. It is unclear, however, whether proteins are as potent as carbohydrates in stimulating insulin secretion.

    My comment: Is it possible that protein can produce high insulin secretion? So, what is left for simple humans? No carbs, no protein?

  • Anonymous

    7/2/2010 3:52:13 PM |

    Is the LDL carried in the blood by a protein or has it already been oxidized. I'm trying to understand what form chlorestral is in the blood.

  • David

    7/2/2010 6:17:02 PM |

    Alfredo,

    It's true that protein stimulates insulin, but the key is that it doesn't only stimulate insulin. Glucagon, insulin's counter-regulatory hormone, is also stimulated. Insulin secretion  is undesirable in the context of low glucagon (which is what we have with high carbohydrate intake), but it's not such a big deal when the ratio of the two are more balanced (which is what we have with low-carb protein intake).

    David

  • Jack C

    7/3/2010 12:03:08 AM |

    The VAP cholesterol profile, which gives the distribution of LDL and HDL particle sizes a other information, shows an upper limit of 10 mg/dl for Lp(a)cholesterol.

    In recent tests, my wife had an Lp(a) of 6 while mine was 8. Through no fault of our own I might ad.

  • Dr. William Davis

    7/3/2010 12:13:49 AM |

    HI, Kent--

    Great results!

    You are living proof that Lp(a) can indeed be tamed. It sometimes requires some unusual strategies, but huge reductions are possible . . . and Lipitor is not part of the equation.

    Long-term commitment to the effort is the key.

  • Anonymous

    7/3/2010 1:29:29 AM |

    what kind of doctor shoudl i see to get the right tests done.  I know I have high Lipo(a) from a previous test at Mayo.  They recommended that I take drugs and I declined.  Now I'm realizing I don't have the complete story.  I need to know more than just my lipo(a) is high.

    thanks!
    Linda

  • Anonymous

    7/3/2010 6:04:15 AM |

    Hi
    Are there stats on people with lp(a) that don't develop any plaque?
    Also does the same happen with lp(a) as with ldl? that is that is better to have a higher mg/dl with big paricles than a lower mg/dl with small particles?
    Santiago

  • Hans Keer

    7/3/2010 7:28:36 AM |

    I would say apoprotein(a) is normal phenomenon. What is not normal is the abundance of small dense LDL which apoprotein(a) binds to. So the best way to avoid LP(a), is to avoid the abundance of sugars and starch in the diet. All the other (still costing) treatments for Lp(a) won't be necessary then.

  • jd

    7/3/2010 5:39:38 PM |

    Hi,   I recently had a VAP test done via LEF -- I seem to have some very good numbers and some bad LDL ones.  Any comments would be appreciated.

    all values in mg/dl
    LDL 105
    HDL 71
    VLDL 14
    Total Cholesterol 190
    Triglycerides 51
    LP(a) 4.0
    IDL 3
    HDL2 18
    HDL3  53
    VLDL3 8
    LDL1 PatternA 5.4
    LDL2 PatterA 7.5
    LDL3 PatternB 61.6
    LDL4 PatternB 22.4


    LDL Density pattern = B, flagged abnormal

    Vit D  65.4 ng/ml
    Homocysteine 6.2
    C-Reactive Protein 0.2

    I am 55 yr of age, 6'0", 165 lbs, exercise regularly.

    Heart disease in family, mother's father died of heart attack at 66, other 3 grandparents lived into 90s.  father died leukemia cancer 53, mother living at 80 in good health.  Thanks,   Jim

  • Anonymous

    7/7/2010 4:40:46 PM |

    I use Lugols solution 2% and I have absolutely no idea what dosage I should be using.  I have been using one drop about twice a week, but I would like to have a better idea of proper dosage.  Can you help?

  • James L.

    7/13/2010 9:52:15 PM |

    My cardiologist is treating my high Lp(a) with Niaspan, but even with high doses, it has not had much effect. What do you mean by items 3 and 4 on DHEA and T3? Please be more specific. Thanks.

  • Anonymous

    7/29/2010 9:06:55 PM |

    Could you give some dose for T3 and DHEA that you are recommending?

    Thanks!

  • Anonymous

    8/10/2010 8:38:43 AM |

    "If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. "

    Does that mean that high levels of Lp(a) is not inherited from the father?

    Thanks

  • LisaMichelle

    8/24/2011 11:46:03 PM |

    Dear Dr. Davis,

    I'm a 44 yr old female.   I recently had a consultation w/ a cardiologist here in Canada.   I was sent for the consultation because of some strange left jaw and low chest tightness I'd experienced at work the week prior (had been seen then in the ER, normal ECG x 2, normal CXR, normal bloodwork).  Prior to the appt I was told I needed to have fasting bloodwork (so that results were available for the cardiologist to review at my appt).  

    HDL good, LDL good (though at the higher end of the normal range).  Lipoprotein A was 0.55 g/L (which i guess works out to 55 mg/dl which is what the usual unit of measurement is for this one in the U.S.).  The cardiologist told me that all of my bloodwork was normal and that I was very low risk for a heart attack but I requested a copy of my results just to have on file.   I am surprised she didn't mention the elevated Lipoprotein A (normal range for this lab is: 0.00 to 0.33 g/L).   So that got my on my search for info on what exactly Lipoprotein A is, and what it indicates.

    My question is:   I was only told to fast for 12 hours prior to my bloodwork, nothing was said about ensuring I didn't smoke.   Well I did smoke over the 12 hours up until the blood was drawn (even about 30 minutes prior to).   Now I'm reading online that one should not smoke prior to blood being drawn for Lipoprotein A, HDL and LDL, etc.    So could my smoking right up to the time bloodwork done have negatively impacted the results?   Could smoking have made my LDL and Lipoprotein A higher?    Should I have these redone but ensure I don't smoke for 12 hrs prior to blood draw?  (I have a 'quit date' set for next Saturday, so don't worry, I will be quitting).

    Thanks so much,
    Lisa

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The epidemic of small LDL

The epidemic of small LDL

Of the patients I saw in my office yesterday, virtually EVERYONE had small LDL.

Small LDL is emerging as an extraordinarily prevalent lipoprotein pattern that drives coronary plaque growth. Previous estimates have put small LDL as affecting only 20-30% of people with coronary disease. However, in my experience in the last few years, I would estimate that greater than 80% of people with measurable coronary plaque have small LDL.

If you have a heart scan score >zero, chances are you have it, too.

I call small LDL a "modern" disease because it has skyrocketed in prevalence recently because of the great surge in inactivity in Americans.

When's the last time you walked to the grocery store and back, lugging two bags of groceries? How many years has it been since you've push-mowed your lawn? All the small conveniences of life have permeated further and further into our activities. Most of us spend the great majority of our day right where you are now--on your duff.

On the bright side, small LDL in most people is reducable by simply getting up and going. But the old teaching of 30 minutes of activity per day is now outdated. This was true when the other hours of your life included physical activities, like housework or a moderately active job. However, if the other 23 1/2 hours of your day are sedentary, then 30 minutes a day won't do it. An hour or more of activity, whether exercise or physical labor of some variety will get you better small LDL-suppressing results.

For most people with small LDL, fish oil and niacin are also necessary to fully suppress small LDL to the Track Your Plaque goal of <10 mg/dl.
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