What are "normal" triglycerides?

12. April 2011 William Davis (67)
Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.
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Comments (67) -

  • Stephan Guyenet

    4/11/2011 6:58:50 PM |

    Hi Dr. Davis,

    I searched for that reference but I wasn't able to find it.  I found two papers from Austin et al. in 2000 but neither contained that graph.  Would you mind giving a more detailed reference for it?  I'd like to have that paper as a reference.  Thanks!

  • Anonymous

    4/11/2011 7:14:14 PM |

    HI Dr. Davis--

    Since I have been having my cholesterol levels checked, my triglyceride level has always been on the very low side...ave. around mid 30's.  My hdl  and ldl are generally around low to mid 80's.

    Could you say something about the people who have low triglycerides...is this healthy or a concern?

    My doctors usually think this is great , but I wonder.
    Thank you.

  • Dr. William Davis

    4/11/2011 9:40:20 PM |

    Hi, Stephan--

    Here's the URL for the abstract on Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/2372896

    I also see that I got the year wrong: It was 1990. (Now corrected.)


    Anon--

    Low triglycerides are wonderful. Your values are at the biologically perfect range.

  • Anonymous

    4/11/2011 10:07:10 PM |

    This is from Anon , who wrote you about my very low triglycerides-in the 30's.  Thank you so much for responding--I had been concerned there was something wrong with me!  
      
    I do not think my levels are due to genetics as my siblings have cholesterol issues. I think it is my diet and ex.

    Do you see many people with tri's in the 30's?  
    Thanks again!

  • Frank Hagan

    4/11/2011 10:13:07 PM |

    I must be doomed; even with vlc diet (less than 30g per day), fish oil and niacin, my triglycerides have never been under 103. They started at 440, so that's progress, but I suspect I have familial hypertriglyceridemia, as I can't get them to budge lower after two years.

    I tried going off niacin at one point, and they rose to 140 again. So I continue with the fish oil (1200mg of EPA and 900mg of DHA), niacin (1500mg 1x day) and vlc diet.

  • Might-o'chondri-AL

    4/11/2011 10:36:00 PM |

    Triglyceride (Trig.)clearing relys on the enzyme lipo-protein lipase being able to function at the capillary endothelium. If a Trig can get into a cell it is not taken out of circulation.

    Trigs move around in the circulation bound to lipo-proteins, and one natural component (among several components) of the lipo-protein molecules that carry Trigs is identified as Appoliprotein (Apo) C III. When there is an un-naturally high proportion  of Apo C III involved  this inhibits the working of the enzyme lipo-protein lipase, which is an essential enzyme for clearing Trigs from the blood stream (note: this is not discussing how Trigs get formed).

    Apo C III blocks the lipo-protein lipase enzyme from functioning at the capillary endothelium; Apo C III doesn't actually bind to the lipo-protein lipase enzyme.  It (the enzyme) can't get to work at that capillary inter-face when Apo C III over-abundant; so, there is less lypo-lysis (ie: Trig cleaving off) done to the Trig carrying lipid molecules (ie: VLDL, IDL and chylomicron lipids burdened with Trigs).

    So, what complicates the natural process when there is no underlying genetic cause obstructing Trig clearing from the blood stream ? If you said "insulin" you are correct; insulin signaling has a distinct regulatory affect on the APOC3 gene expression, which encodes for Apo C III.

    Docs interventions keep Trigs down in the obvious manner of setting up less substrate for Trig formation. What contiues to intrigue me is how insulin is involved in metabolic signalling beyond text book role of "driving" glucose into cells.

  • Might-o'chondri-AL

    4/11/2011 10:39:55 PM |

    edit last comment (mine) 1st paragraph, 2nd sentence to read:
    " If a Trig can NOT get into ...."

  • Anonymous

    4/11/2011 11:05:37 PM |

    When I had my last lipid analysis, I had been fasting for about 36 hours.  I frequently do intermittant fasting. My numbers were very contradictory and I wonder if my LDL levels were artificially increased due to the extended fast. My triglycerides were 69, VLDL were too few to be measured, but the number of small LDL particles was very high.  Thank you for addressing this issue.

  • Harry

    4/11/2011 11:21:54 PM |

    might, as I understand it, as VLDL loses trigs, it becomes IDL, and after further loss of trigs and all apolipoproteins except ApoB, it becomes LDL. I have been wondering if receptors in the LDL family are part of the process whereby VLDL and IDL and LDL lose trigs to cells throughout the body. Is this the way it works, or are receptors of the LDL family all or  mostly in the liver?

  • Adam Michael

    4/11/2011 11:35:42 PM |

    Anonymous, would you mind sharing your typical diet and lifestyle practices, including exercise?  I'm sure all curious minds could benefit!  Thank you.

  • Anonymous

    4/12/2011 1:11:53 AM |

    Adam M--In response to your question about my regimen. There really is nothing extreme about it so I have been baffled for years with my cholesterol results esp. the tri's in the 30's.

    For the past 20 yrs. I have almost totally avoided processed foods.Basically no junk food at all. Most of that time I ate no red meat. I have probably not eaten enough food...I  have always been a light eater and on the thin side. Lowish bmi but def. not anorexic or any eating disorder . I haven't eaten butter, though I do drink no-fat, or low fat milk and eat yogurt  daily as well. I use olive oil as much as I care to have, and eat walnuts and almond butter.I don't drink alcohol except on the very rare occassion--maybe a few times a yr.

    No special supplements...but fish oil over the past 8yrs. and a good level vit d. for the past few years. I was probably vit d deficient most of my life before supplementing vit d.


    For the past 10 years, I have walked briskly at least 6 days a week 4-6mi. I lift weights  (dumbbells #15-3-4 days a week. Do some tai chi.

    So you can see ...nothing too special but I do think vastly different than most Americans.

    My guess is that I am reaping the benefits of some good habits from the past 20 plus years. As I said my siblings take bp meds and statins....I don't take either. I think they have bad eating habits, don't exercise consistently and drink alcohol . Though 2 siblings have fairly decent diets, don't drink much and still need a statin and bp meds.

    I am female in my late 50's and siblings a bit older and a bit younger, male and female.

    Hope this helps. Anon.

  • Might-o'chondri-AL

    4/12/2011 1:12:10 AM |

    Hi Harry,
    The liver exports most Trigs bound to VLDL; when measuring fasting Trigs these are mostly complexed to VLDL. IDL (intermediate density lipo-protein) is really a spin off phase of a VLDL remnant, and is itself short lived (ie: IDL degrades quickly).

    When measuring fed (post-prandial) Trigs these are some appearing in VLDL (ie: liver exported) and some Trigs the chylo-microns carry (ie: from the intestine, a different source of Trigs); a relatively minor amount would be Trigs carried by IDL. When fasting (ex: overnight) there are very sparse amounts of Trigs associating with chylo-microns and IDL would be neglibible.

    HDL also has to carry Trigs; it (HDL) brings them back to the liver, which hydrolizes (cleaves) those Trigs for the liver to "play" with again. The HDL Trigs are not scavenged from the long enduring VLDL lipo-protein; but are Trigs HDL had picked up (ie: from the peripheraly circulating short lived IDL & chylo-microns).

    My understanding is that it is not the LDL receptors that are key to how & when Trigs physically get "off" of any molecule that is carrying a Trig. The Apo C III (detailed previously) is one of several proteins ( Apo C molecules exist in different iso-forms, do so simultaneously and sometimes as mutations); a lot of sub-groups get "bundled" to the Apo B complex.

    Apo C III component having excessive expression is what interfers with the enzyme  (lipoprotein lipase) involved in cleaving off Trigs. LDL receptor dynamics only add mitigating circumstances to how/where/when a circulating Trig is coming to be (or not be) presented for cleaving off.

  • Paul

    4/12/2011 3:00:41 AM |

    At least 50% of my caloric intake consists of fat, mostly saturated and monounsaturated from grass-fed tallow, ghee, butter, cheese, coconut, olive oil, almonds, avocados, and one tsp. fish oil... I get plenty from organ meats, wild salmon, free-range eggs, chicken, and beef too.  Not to mention I avoid grains, starch, and sugar as though they are poison.

    I'm a 50 y.o. male, and try to perform at least three apposing compound weight resistant exercises every day (bench-presses, pull-ups, squats, military-presses, rows, lunges, dead-lifts, power-cleans, or clean-&-jerks.)

    I've been doing this for a couple years.

    Along with very (visibly) favorable body comp muscle/fat ratios, my last 12 hr. triglyceride measurement came in at 52 mg/dl.  I think I'll stick with what I'm doing.

  • Rick

    4/12/2011 3:15:34 AM |

    Dr Davis,

    I'm a bit confused about number 4. You suggest that a postprandial value of greater than 88 is dangerous, but accept levels of up to 90 in your program. Are you sure the figures are correct?

    Also, are the 4 points in the order you intended?: you move from fasting triglycerides being too high (1), to being low (2), then to being too high again (3), then you move to non-fasting triglycerides in 4, starting with quite a very low figure (88), and suddenly jumping to 400+. How about more typical non-fasting figures in the 100+ or 200+ ranges?

  • Anonymous

    4/12/2011 5:35:26 AM |

    I must really be screwed. Even on six fish oil caps a day and a gram of niacin, I'm at 292.. my all time low was 157. I'm on even more fish oil and cut out breakfast cereal and other sources of high fructose corn syrup. What I need is a whole new genotype....

  • Alex

    4/12/2011 6:00:44 AM |

    Dr. Davis,

    While I understand that your target audience are probably Americans, as a European, I would be very grateful if you would also post values of the tests you speak of in the measurements used on the other side of the Atlantic. Here we speak of triglycerides in mmol/L, not in mg/dl, so whenever I read your posts I have to sit here with a conversion sheet and calculator, and considering that I can't make notes on other people's websites, I have to do so EVERY time I read your posts, even for the second or third time. It would be very helpful (and probably not too much work for you) if you could post values in both measurement systems, so I can put down the calculator and conversion sheet in the future and put all my attention to the contents.

    Thanks for listening.

  • LifeCoachAndy

    4/12/2011 7:38:17 AM |

    To ' I must be screwed up, VLC diet may be working for , so you  may want to try a different approach, eg. low fat plant based diet, do some fasting, also may need some attention to your liver.

  • Anonymous

    4/12/2011 8:44:10 AM |

    @Alex: +1

    Australia uses mmol/L also as it's the SI standard.

    Perhaps a converter on your site or quick reference table?

  • majkinetor

    4/12/2011 11:20:59 AM |

    "I must really be screwed. Even on six fish oil caps a day and a gram of niacin, I'm at 292.. "
    If you didn't do this, you may try exercising, sesame butter and soy lecithin.

    @Alex:
      +1
    We need M measure too. I have to convert each read, too.

  • Medicomp INC.

    4/12/2011 3:58:11 PM |

    Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

    Interesting point. Many people think that fat is the most important part of a diet to assess, other factors definitely play a role in heart complications.

  • Might-o'chondri-AL

    4/12/2011 4:43:59 PM |

    Exertion (ex: manual work, breathing harder exercising, endurance training, etc.) improves insulin resistance; the
    sedentary, overweight, obese and Type II diabetics are told to actively exercise. Less insulin lingering in circulation means less insulin signals to ratchet up the Apo C III level; Trigs can clear out of circulation (as detailed above).

    Lipo-protein lipase enzyme can then robustly cleave of circulating Trigs for then getting into cells. In the cell the Trig must be processed into a "droplet" molecule for storing inside the cell; up to 1% of our genome is suspected to be involved in the biochemistry of achieving fat "droplet", which reflects it's importance.

    Fat Storage-Inducing Transmembrane Protein (FITM) in the cell's endoplamic reticulum make this conversion of Trigs into droplets (again note: this is not how Trigs are initially assembled). FITM uses the enzyme di-acyl-glycerol O-transfer-ase
    to do the job; then the droplet is rendered into the storage form called di-acyl-glycerol.

    FITM 1 is what exists in skeletal muscle endoplasmic reticulum to make muscle stores of di-acy-glycerol. When we exert ourselves and run out of glucose to burn the muscle takes back off the acyl-CoA fractions
    from stored di-acyl-glycerol; then it cobbles back together tri-acyl-glycerol molecules (note: this is the same molecule as a tri-glyceride, the more commonly used term just skips mentioning the acyl group) to burn and meet the demand for energy.

    Quite conveniently, for those who exert themselves, sustained activity also induces more di-acyl-glycerol transferase enzyme production; it is positive feed back augmenting the rate at which muscles can access their stored "fat" to burn (ie: training increases endurance).

    With muscle fitness burning up the on site reserves of di-acyl-glyceride the muscle can then take up more Trigs from the blood stream. Thus Trigs readings are lower for most geno-type individuals who regularly exert themselves (there are a few instances, mostly disease related, where low circulating Trigs are due to the liver holding on to too many Trigs).

    Our fat (adipose) cells' endoplasmic reticulum are the other site of a lot of lipid droplet processing for storage; there the adipose cells use FITM 2. When there is no exertion (ie: muscle cells have made no room for more stored di-acyl-glycerides) the Trigs slowly  get into the adipose cells(and some other tissues); so for the sedentary individual burning off that fat "reserve" is extremely difficult.

  • Harry

    4/12/2011 5:40:24 PM |

    Might, have you seen Mendivil's paper "Metabolism of VLDL and LDL containing apolipoprotein C-III and not other small apolipoproteins" It's at

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818784/

    It seems to me that there must be some docking involved when a VLDL or LDL particle sheds trigs either in the liver or elsewhere in the body. Maybe it's not receptors of the LDL family that do the docking, but as I understand it, lipoprotein lipase isn't carried by the ApoB containing lipoprotein, but rather, is a component of the receiving cell that facilitates transporting the trigs through the receiving cell wall. The process may not involve full endocytosis, where the whole ApoB-containing particle is engulfed by the cell, but it seems to me that there must be some sort of adhesive or attractive region on the cell to trap the VLDL or LDL at least for a while so that the trig can be unloaded. Any idea how this works?

    From what I've read, it appears that the longer half-life of LDL in the circulation, vs that of VLDL and IDL, is due to ApoE being contained in VLDL and IDL, but not LDL. Since ApoE can attach to LDL receptors as well as or better than ApoB can, this results in more rapid clearance of VLDL and IDL than LDL.  

    As a result of this discussion and some references like Mendivil's paper, it appears that ApoC is involved also. Since LDL carries only ApoB, maybe that also contributes to the longer half-life of LDL.

    Might, have you considered joining Dr. Davis' Track Your Plaque (TYP) forum? I'm a member, and we have many interesting discussions of CHD issues. There is a small fee involved, but we discuss many things before they make it into the Heart Scan Blog. For example, we discussed the subject of this blog thread about a year ago, and as a result, I purchased a cardiochek meter and did a postprandial trig test. My fasting trig level was 57, and I then drank 6 oz of heavy cream. My trigs peaked 4 hours later at 69, which showed that my low-carb diet (30 g/day) had acclimated me to rapid removal of trigs. We learn a lot from each other's experiences.

    Anyway, your knowledge of cellular and molecular processes would make a great addition to the TYP forum. There are a number of ApoE3/4, E2/4, and E4/4 people there as well as E3/3's, and We sometimes discuss posts you have made in other fora. I hope you will consider joining us. And by the way, I'm not connected in any way with the TYP forum other than being a member who likes to get into the nitty gritty of CHD issues.

  • Renfrew

    4/12/2011 6:40:45 PM |

    Might o'chondria:

    I am enjoying your posts, though they are quite technical and mostly go over my head. It seems you are a very knowledgeable contributor here.
    I have one request: You'd be of service for many, if you could add some "behavioral" recommendations or at least sensible things to do/to avoid after you analyze/report/explain physiological parameters and biochemical findings.

    A simple sentence, like: Because of this, it would make sense to do this... or that.... or avoid this...would be much appreciated.
    Thanks.

    Renfrew

  • Might-o'chondri-AL

    4/12/2011 7:47:20 PM |

    Hi Renfrew,
    This is Dr. Davis' blog so it is my feeling that specific health
    recommendations be his; and he does make them (some here & apparently more specifics  elsewhere). I am not a medical doctor, and do not follow
    all his recommendations (as I know them)for that matter.

    The fancy words I use are there because contemporary science has coined them to describe the complex details researchers keep finding. A lot of the hyphens (ex: "...-...-...") in words are inserted by me; this breaks up technical words into their component parts. I chose to do this so readers might identify some of the key parts  researchers coined that word from and not just tune out because of the jargon.

  • Brent

    4/12/2011 8:26:47 PM |

    To Frank Hagan (I Must Be Doomed) and Anon (I Must Be Screwed) - It does not seem like either of you take enough fish oil.  I visited Doc a month ago and he moved me from 2,400 mg DHA & EPA per day up to 3,000 mg per day - and I my Trigs were in the upper 70's.  Have not tested since.

    My understanding of TYP dosages is that you start around 3000 mg per day (DHA & EPA) and you go up from there, as high as 6,000 mg per day until your triglycerides are under 60.

  • Renfrew

    4/12/2011 8:53:45 PM |

    Whatever happened to KRILL OIL ? Has it been forgotten?

    I have read that KRILL oil is far more bioavailable than fishoil and chemically more stable, thus less prone to go rancid. Also because we are talking about phospholipids here which are absorbed much btter than ordinary fishoil, I would assume KRILL is the better choice.
    Unfortunately there does not seem to be much science on this. Probably because big pharma cannot make a buck out of this.
    I'vew been taking Krill oil for a year now and my trigs went from 250 to 56 in about 1 month. Stable since then. Unfortunately it does not seem to reduce LDL or raise HDL.
    Any experience, comments or details on KRILL?
    Renfrew

  • Ensues

    4/12/2011 9:58:35 PM |

    Hi Frank-

    I am exactly the same way.  Mine started over 1000 then to 769.  On fish oil, VLC, and Tricor (200mg) the lowest I have been able to achieve is 229.  My HDL is very low <25.  Neither of my parents have issues.  Very frustrating.  I am hoping my body/metabolism is healing and it my tri's will come down with time.

  • Ellen

    4/12/2011 10:06:13 PM |

    Hey Anon-- you ain't the only one! my triglycerides are always around 31. I always thought they were too low as well because they flag low for the lab range.

  • Paul Mcgrath

    4/12/2011 10:14:34 PM |

    @Renfrew

    No offense, but Might-o's valuable contributions here are clear to me on what specific behavior would be a healthy one.

    It can be summed up in one word... move. Well, maybe two more words would be clearer... lift something.  You would literally have to be blind and deaf not to notice all the effective programs  to help reach your goals. I particularly love Erwin Le Corre's Movnat - http://movnat.com/

    Our distant ancestors didn't have cars, automated climate controlled houses, refrigerators, cooking stoves, grocery stores, TV's, computers, game consoles, or various other modern conveniences that relieved or distracted them from having to go do physical work... just to survive.

    Combine that with today's widely available, tasty, cheap high carb food sources, you have a perfect synergistic formula for diseases of western civilization.

  • Anonymous

    4/12/2011 10:55:41 PM |

    MCA:

    You are my bochemistry reference guide and I really appreciate your posts. Please keep posting because you have the ability to answer why.
    Moving ones body has got to be one of the best investments in physical and mental health. I would rather do that then obsess or stress-out about numbers on a lab test. Get out in the woods and mountains and cover a lot of miles. I am fortunate because I live in Montana and have the wilderness in my backyard.

  • Might-o'chondri-AL

    4/12/2011 11:33:19 PM |

    10 mg/dl  =    0.555 mmol/L
    10 mmol/L =  180.0   mg/dl

    Maybe this scale of 10s will help those who need to do quick conversions.

  • Anonymous

    4/13/2011 2:08:11 AM |

    Put me in the genetically hopeless camp.  Tri's are 150 despite vegetables being my only source of carbs and intense activity 3 x's per week (about 1.5 hrs total), body fat and natural musculature that could have me as a paleo-bod model.  I feel hopeless on the blood lipid front.

  • michael goroncy

    4/13/2011 5:43:17 AM |

    Easy to confuse....
    Chol.LDL&HDL are on a different scale than TRIGS.
    To convert mmol/l to mg/dl multiply by 39 for cholesterol.
    For TRIGS multiply by 89.

  • Anonymous

    4/13/2011 12:34:20 PM |

    @Might-o'chondri-AL said...
    " 10 mg/dl = 0.555 mmol/L
    10 mmol/L = 180.0 mg/dl"

    When you are doing molar conversions there is a different factor for every chemical. Glucose, triglycerides, ...whatever. All have VERY different figues.

  • Anonymous

    4/13/2011 12:46:46 PM |

    Since removing bread and starch from my life my values have never been so good.  I do *very* occasionally have some rice or soaked beans or lentils...but my fasting triglycerides were 33, my total cholesterol 221, my HDL was 94 and LDL 121.  Just posting in case you are collecting data Smile

  • Anonymous

    4/13/2011 1:15:52 PM |

    My fasting triglyceride level fell from 81 to 46 over a 9 month period.  During this time, I doubled my exercise from 30 mins a day to 60 mins a day (every day of the week).  I believe that this is the cause.  For those trying to cut out animal fat, I have to report that I eat chicken skin and pork fat and this does not affect my cholesterol levels.

  • Stargazey

    4/13/2011 2:07:01 PM |

    I think Might-o'chondri-AL was giving us the conversion factors for glucose.

    My triglycerides went from 118 pre-Atkins to 43 after a few years on it. No change in exercise; I just cut out the carbs.

  • Might-o'chondri-AL

    4/13/2011 3:10:33 PM |

    Thanks M. Goroncy & Stargazey,
    for correcting my mistake; I do make them, so anytime welcome errors being pointed out.

  • Geoffrey Levens

    4/13/2011 4:13:21 PM |

    "Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role."

    I exercise moderately daily, HIIT and resistance. Eat Fuhrman's ETL diet so I get about 30% calories from fat (raw nuts and seeds)and get about 250-300 grams carbs per day (zero refined carbs though).  My fasting trigs just read at 56.  High dose fish oil can elevate trigs, refined carbs also. Not so much apparently for whole foods, unrefined carbs.

  • Eric

    4/13/2011 4:38:58 PM |

    Well stated Paul Mcgrath!

  • Travis

    4/13/2011 9:43:17 PM |

    Dr. Davis,

    2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

    I have lower fasting triglycerides since going on a low carb, higher protein and fat diet similar to what you suggest (they dropped from about 100-120 to 60-90). Yet, when I've had an NMR Lipoprofile done, it shows that I have high amounts of small LDL particles (in particular 850 nmol/L of small LDL-P and 1720 nmol/L LDL-P). I'm disappointed both that my triglyercides don't seem to be consistently low and that my small LDL-P is high. I'm otherwise healthy, not obese, no signs of insulin resistance, and eat primarily meat, eggs, dairy, and leafy green vegetables (with some starchy vegetables and fruit).
    I recognize you suggest this may be partly genetic, but what does this mean for me and is there anything I can do about it? Have you written about this elsewhere that I can't find? Thanks!

  • Eric

    4/13/2011 10:25:49 PM |

    Travis- This might help ApoE.

    ApoE 4/4 have to be more selective in their fat selections and amounts than an Apo 3/3.

    This may be just 1 genetic marker that can account for your numbers.

  • Adam

    4/14/2011 1:07:53 PM |

    2 years ago, when I had a case of the flu, and it didn't go away for 3 months, my doc ordered me a blood panel. My fasting triglycerides were 240mg/dL.

    Of course, i also suffered from the typical symptoms of metabolic syndrome: high BP, high cholesterol, obesity (40" waist), diabetic level of fasting blood glucose, low HDL... He told me to eat more "healthy whole grains" and cut out all fat and eat no red meat, to which I answered "that is exactly how I have been eating for decades!"

    Google then revealed to me Marks Daily Apple, I cut out all forms of sugar, grains, legumes, partially hydrogenated oils, and most dairy. Added in more grassfed beef, wild fish, coconut. Exercise sessions are short but as intense as physically possible.

    2 years later, I'm 40kg (88lbs) lighter, my waist is now 29" (smaller than my mom and I'm a man!), no more high BP, no more high cholesterol, HDL is 90+mg/dL.

    Triglycerides? 38mg/dL.

    Good thing I didn't listen to my doctor and take a heap of pills which he said I have to take for the rest of my life.

  • Steve

    4/14/2011 1:59:16 PM |

    Fascinating NYTimes article (4/13): "Is Sugar Toxic" by Gary Taubes. LINK

  • Frank Hagan

    4/14/2011 2:00:02 PM |

    Brent, thanks for the comment re: fish oil dosage. I am at 3,900mg of EPA&DHA combined (specifically 2400mg of EPA and 1500mg of DHA).

    I have a blood test coming up in June; I may increase to 5,200 mg to see if that has more effect.

  • Frank Hagan

    4/14/2011 2:07:07 PM |

    Ensues, you might check with your doctor about using niacin (not sure if there's an issue taking it with Tricor so I would check with him; I couldn't continue on Tricor due to an allergic reaction to it).

    My lowest triglyceride reading was when I was combining VLC, fish oil at 3,900mg EPA & DHA daily and 1,500mg of niacin.

    Dr. Davis has a lot of info here on niacin, including recommendations for using SloNiacin (over the counter) instead of the prescription version (Niaspan, I think) to save money. And he has some tips to avoid the flusing most of us get (what works for me is a regular aspirin 30 minutes before taking the niacin, and drinking plenty of water.)

  • Anonymous

    4/14/2011 7:35:37 PM |

    I notice some comments about large doses of fish oil (3+ grams daily) in order to reduce triglycerides.

    Any concerns over immune suppression at these doses? Or even 1-2g doses?

    I recall one pubmed study showing close to a 50% reduction in NK activity at a rather paltry EPA dose of 720mg/daily.

    http://www.ncbi.nlm.nih.gov/pubmed/11237929

    3+gm of fish oil might scare me a bit, longterm, if that study is correct.

  • Tim Tom

    4/14/2011 8:44:56 PM |

    I agree with your last statement that carbohydrates are a much bigger culprit to high triglyceride levels than fat intake. Looking forward to that post.

  • Dash

    4/15/2011 5:32:32 AM |

    Thank you for all of this information, it was really helpful for one of my classes.

  • Might-o'chondri-AL

    4/15/2011 5:53:06 AM |

    Hi Annon,
    NK, a type of lymphocyte cell, is mostly effective against circulating and metastasizing tumors; solid tumors are much less vulnerable to NK action against them. I failed pursuing your link so couldn't read the study, yet the premise that EPA inhibits NK is sound; EPA works  partly because it does keep lymphocytes from getting into tissue cells. Other very common factors that inhibit NK are fats, alcohol and steroids.

    EPA is showing itself to be useful against cancer; I seem to recall several types of neoplastic growths are less with EPA  supplementation. The EPA incorporated into a tissue cell's lipid membrane come into play through a series of steps; benefit is not as the EPA  molecule is being carried through the circulatory system.

  • woly

    4/15/2011 8:05:52 AM |

    Might-o'chondri-AL: can you please do us all a favour and start your own blog? I have started reading the comments section of many blog posts simply to see what you have written. All your posts are incredibly interesting, please keep up the good work!

  • Ensues

    4/15/2011 3:20:29 PM |

    Thanks for the info Frank.  I had indeed read up on niacin.  I started taking 500mg a couple months ago and then bumped to 1000mg after about a month.  I have not had a blood test yet to check the results.  I am hopeful though.  As for flush.  I have tolerated extremely well with really no problems except for one night.  After 2-3 months of no issues I experienced what I would call a crazy severe flush.  My skin was burning so bad I wanted to get it off.  Head to toe, hot and painful.  Not the "mild annoyance" I have read about.  It was nuts.  Lasted maybe an hour and a half.  Drank as much water as I could and a couple of aspirin.  Resumed 1000mg the very next day and have not had an issue since.  Very strange.  Thanks again for the comment.

  • Anonymous

    4/15/2011 4:44:01 PM |

    Be very careful when taking Niacin.  I can not tolerate even the small amount in a B-complex. My blood sugar increases, but even worse I become irrationally angry at the slightest provocation.

  • Anonymous

    4/15/2011 4:57:49 PM |

    Question regarding the reduction in NK cell activity ... could it pose a problem longterm?

    Would it possibly lead to a greater chance of infections (as some rodent studies have shown)?

    If someone had a metastasizing tumor, wouldn't fish oil then be contraindicated? I seem to recall DHA having some immune suppression activity too (not via NK however), but perhaps Vit E would counteract that.

    And then there is also that fish oil/rodent/colon cancer study:
    http://www.emaxhealth.com/1275/fish-oil-increases-risk-colitis-colon-cancer-mice

    Which seems to indicate DHA may be implicated negatively with colon cancer (in mice).

    And finally... I also recall the study testing oxidation values in people, using increasing doses of DHA (which is a bit of a messy way to test, but... whatever).

    http://www.futurepundit.com/archives/006499.html

    Somewhere between the 800mg and 1600mg levels of DHA, urinary isoprostane increased, which probably isn't such a good thing.

    I'm not anti-fish oil, as I take it myself. I am just wondering if too much (2-3+ g), may have some negative consequences longterm.

  • Might-o'chondri-AL

    4/15/2011 7:47:19 PM |

    Hi Anon,
    I have no suggestion on how to dose fish oil; I'd like to hear
    Doc's limitation on use for high
    trigs. This is for orientation on what you are discussing, as I understand things.

    Rodent and human models for chronic disease (inc. cancer) involve immune systems that are dissimilar; thus no cancer treatment has (to my knowledge) come from rodent results. That Michigan Univ. (2010) study fed mice that were geneticly pre-disposed to inflammatory bowels, in addition to fish oil, corn and safflower oils; those other oils can be converted into Arachidonic Acid, which is itself pro-inflammatory in some instances.

    Isprostanes in the urine are a bio-marker of oxidative activity; their existance is not automaticly evidence of damage to healthy cells. Some isoprostanes are also carried in an esterified form by our good old HDL.

    Isoprostanes come in several forms; they are mostly (but not exclusively) by-products of our natural anti-oxidants glutathione and glutathione peroxidase activity.  In other words when see isoprostanes in the urine it shows not only that the body had/has oxidative "stress", but that the body did something about it (ie: glutathione was busy doing it's job).

    DHA apparently works to increase the apoptosis (cell suicide/programmed death) of cancer cells, including bladder cancer. One of the theories explaining this effect is that fish oil integrates into the cancer cell lipid membrane; then it becomes part of a cascade of events that along the way produces levels of endo-peroxides
    (made inside the cell hydrogen peroxide).

    A threshold (ie: high enough
    dose)of fish oil must be reached to sustain a level of hydrogen peroxide that the cancer cell will take as a signal (ROS are internal cell signal molecules)
    to go into apoptosis. While all that hydrogen peroxide is being spun off, again and again, the cancer cell's innate anti-oxidant glutathione is trying to
    keep apace and neutralize it; so an endproduct (but not the endgame of the apoptosis dynamic that can "kill"
    developing cancer) is more isprostanes showing up in urine.

  • Renfrew

    4/16/2011 1:08:20 PM |

    When talking about dosage for fishoil what are we actually talking about?
    Milligrams per pill or mg for DHA/EPA.
    I am reading here 2-3 grams of DHA/EPA. So are we talking about the pure DHA/EPA content?
    1000 mg of fishoil is surely different from 1000 mg of DHA/EPA.

    Renfrew

  • Anonymous

    4/16/2011 5:30:28 PM |

    Renfrew: amounts of EPA/DHA.

    Total content of a fish oil capsule, which is typically 1g, is meaningless without concentration numbers.

    So when 3g is mentioned, it's 3g of EPA/DHA, not simply 3, one gram capsules. 3g of EPA/DHA could be up to ten capsules.

  • Renfrew

    4/17/2011 11:35:46 AM |

    Thanks for the clarification.
    How about minimizing the number of capsules in taking KRILL oil?
    Krill oil is a lot more bioavailable (phospholipids), compared to ordinary fish oil capsules. Less capsules for the same bioavailable amount of EPA/DHA.
    It also contains Astaxanthin which is good for brain, eye and prostate health.
    The ORAC test results in much higher anti-oxidant capacity.
    Why aren't we all taking krill oil??

  • Anonymous

    4/17/2011 5:40:37 PM |

    The reasons against krill oil:

    It's not cost-effective nor is it less capsules for an equivalent amount of EPA/DHA (in fact, it's many more).

    I know of one comparison study which did show krill oil being about 50% or so more bioavailable that fish oil. But krill oil is like 5-10x the price of fish oil (based on EPA/DHA dosing). So one can do the math there.

    And there is also the fact that krill oil has been much less studied than fish oil has.

    Astaxanthin is interesting and one day I'd love to see Dr. Davis touch upon it on this blog, state if any of his patients use it, etc. But if you want astaxanthin, I'd think it'd make more sense and be a lot cheaper just to buy astaxanthin (from algae). I've seen it going for as low as $8 for 120, 4mg caps and even non-sale prices are like $10/60 caps. Much cheaper than krill oil.

  • reikime

    4/18/2011 4:27:51 AM |

    I have considered krill oil as i am very intolerant of anchovies and most fish oil caps contain it.

    Tried the Salmon oil, but ewww...nasty!

    Need the benefits of fish oil, but not the side effects.

    Thoughts? Time to take the Krill?

  • Anonymous

    4/18/2011 9:35:23 AM |

    Hey Dr Davis

    Have a look at Gary Taubes' latest post with blood lipid test results:

    http://www.garytaubes.com/2011/04/before-sugar-were-talking-about-cholesterol/

    Nina

  • Caveman

    4/30/2011 1:12:18 AM |

    Any reason to be concerned with very low trigs? Below are my latest blood test results and the trigs seem to be very low. Does this indicate anything?


    Glucose = 68.4 mg/dl
    HDL = 59 mg/dl
    LDL = 98 mg/dl
    Triglycerides = 17 mg/dl

  • James

    5/23/2011 4:24:46 PM |

    A little confused
    Before I had my latest blood test I thought having low trigs and a good TC/H ratio was the best indicators of CVD. Thanks to Dr. Davis I discovered the NMR LipoProfile and Vitamin D tests and  added them to my panel.

    The good part:
    Trigs: 50
    Total Chol: 198
    HDL-C: 70
    LDL-C: 118 (slightly elevated)

    That gives me a TC/H of 2.8, which I assume is excellent.

    But now, the surprising not so good news:
    LDL-P: 1410 (High)
    Small LDL-P: 613  (High)
    Vit D: 31.4 (Low)

    So, how can I have trigs below 60 and have a high LDL particle number and 43% of them small LDL-P?

    Can anyone help me interpret these results? BTW, I am  a 50 yo man in good shape and weight.

    Thanks in advance

  • Alfredo

    6/2/2011 3:57:56 PM |

    Hi, Dr. , please check your email system, I have not been recieving my emails since you moved to this new site.

    THanks

  • Bill

    6/10/2011 8:48:01 PM |

    The text
    "1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

    2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

    3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

    4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack."
    does not appear to be sourced from the sole referenced article in this blog post. The referenced article (Austin et al, 1990) is examining a specific human genetic phenotype in regards to triglyceride, HDL and LDL levels. Is there another source of this information, or are there specific page(s) I can read of the article to derive the same information?

  • Paul Lee

    7/6/2011 12:47:01 PM |

    Just got back from the docs and have mixed feelings as she prescribed a daily statin! However reading up on the low carb sites and on this blog it might not be all bad news! Fasting Triglycerides were 1.1 (96) and TC was 7.1 (6.22) I'm in the UK and hope I hope I've converted properly. I eat low carb, avoid cereals and am reasonably active, in addition to intermittently fasting. I think I've lost weight, that was one of the reasons I went to see the doctor as I thought my weight loss had stalled, but my BMI was down to 23 from 25/6. Its slow but getting there but I did read on some of LC forums that Triglycerides might be elevated whilst actively loosing weight. Clearly there is more work to do and I'm tempted to get a second test. I won't be taken a statin even though its free (provided on the NHS).

  • Rickey

    10/20/2011 5:47:51 AM |

    I know very little about Krill Oil. There had been a bunch of posts regarding Krill oil Brand on the various forums and blogs. After doing all research on internet, i came across with Krill oil Professional, this brand product is awesome. I ordered it online from there website at very competitive pricing. And now iam feeling very much relaxed from my Arthritis joint pain/stiffness relief.

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Super size me in little bits and pieces

17. October 2006 William Davis (1)


Alvin came into the office for consultation on his cholesterol values: LDL 198 mg/dl, HDL, 43 mg/dl, triglycerides 143 mg/dl. He says that he doesn't really try to choose healthy foods but he restricts his overall calorie intake by following the Weight Watcher's exchange approach.

Every morning, 7 days a week, Alvin eats a Sausage McMuffin for breakfast. He justified this by skipping lunch to make up for the 450 calories in the Sausage McMuffin, and not eating anything until dinner.

Can this work? Can you eat foods with unhealthy ingredients but make up the excessive calories by cutting back elsewhere?

The nutritional composition of McDonald's Sausage McMuffin includes 27 grams of total fat (10 gm saturated); 255 mg cholesterol; 950 mg sodium; 31 gm carbohydrate; 2 grams fiber. In other words, it's essentially the same as butter with sugar on it--pure fat, processed wheat, with little fiber or nutritive value.

For Alvin, this is an extremely unhealthy way to eat. His lipid patterns are just the tip of the iceberg: multiple hidden factors are also at work to create heart disease, atherosclerosis in other territories outside the heart, diabetes, high blood pressure, and cancer.

I think the effects are not much different than what Morgan Spurlock achieved in his Super Size Me documentary, but in little bits and pieces. Eating at McDonald's "restaurants" three times a day yielded frightening changes in his lipids, liver function, kidney function, not to mention his appearance and the way he felt. Alvin is doing the same thing, though in less dramatic fashion.

I see this very frequently: people mimicking the experience of Spurlock, just a little at a time, with overindulgence in processed fats and starches.

When you seen a set of Mcdonald's golden arches (or any fast food restaurant, for that matter), run as fast as you can in the other direction. Such indulgences, even in small bits and pieces, still creates a mess of your health.

View from the precipice

15. October 2006 William Davis (0)

Many people, upon first learning of their CT heart scan score, feel like they're on the edge of a sharp drop. It can feel like you're facing a vast, unknown abyss. At the bottom, all those dreaded things that can happen to you: heart attack, heart failure, hospitals, even dying.

I've encountered this "deer in the headlights" look many times. It truly can be frightening to hear that your heart scan score is 300, or 500, or whatever.

What I find truly frightening, however, is when your score prompts the usual array of misinformation commonly dispensed by physicians: "That's so bad you need a heart catheterization", "Nobody knows why people get calcified plaque", or "Reversal is impossible". All absolute bunk.

Let your fear motivate you to do something about your risk for heart disease. Aim for reversal of your coronary plaque and seek out the tools to achieve this. It is possible and, in fact, we do it all the time. I can't claim 100% success, but the majority of people who engage in an effort like the Track Your Plaque program to reverse coronary plaque succeed. Even a substantial slowing of plaque growth from the expected 30% per year is better than submitting to the conventional approach.

At the very least, get both LDL and HDL cholesterol around 60 mg/dl. This alone is a major plus in reducing the risks associated with your heart scan score. It doesn't guaranteee reversal, but it sure tips the odds in your favor.

Organic Rice Krispies?

13. October 2006 William Davis (0)


Breakfast cereal manufacturing giant, Kelloggs, is launching a line of three cereals that will carry the "organic" designation: Organic Rice Krispies, Organic Raisin Bran, and Organic Frosted Mini-Wheats.

This reminds me of the advertisements I've seen for "fresh fried chicken", or "fresh from the can", or "contains only pure cane sugar". How about organic tobacco? Would that make cigarettes healthier?

The TV ad ends with the slogan "Childood is calling!" Oh, those marketers are a shrewd, clever bunch. I worry that they're so clever that most people will fall for these ludicrous tricks.

Don't fall for these thinly-shrouded marketing shenanigans. Organic? Who cares. These foods remain unhealthy whether or not they contain pesticide residues. Take a look at the nutritional composition: Rice Krispies, organic or not, is sugar to your body. It is the sort of food that creates pre-diabetes, diabetes, makes us fat, and fans the flames of lipoprotein patterns like small LDL, VLDL, and postprandial particles, all of which is like throwing cow manure on the weed patch of your coronary plaque.

Nuts as functional foods

13. October 2006 William Davis (0)
Food manufacturers gave nuts a bad name when they started adding evil ingredients to them. "Party mix", "honey-roasted", mixed nuts, etc., are made with added hydrogenated oils, salt, sugar, excessive quantities of raisins, or other added ingredients that turned a healthy food--nuts--into something that made us fat and hypertensive, raised LDL, dropped HDL, and raised blood pressure.

But nuts themselves are, for the most part, very healthy foods. The very best are nuts with a brown fiber coating like almonds, walnuts, and pecans. Nearly all nuts also come rich in monounsaturated oils similar to that in olive oil. Although calorie-dense, nuts tend to be very filling and slash your appetite for other foods. I have never seen anyone gain weight by adding raw nuts to their diet. In fact, I find adding raw nuts cuts craving for sweets.

Nuts are also among the most concentrated sources of magnesium, containing around 150 mg per 1/2 cup serving. As most Americans are at least marginally if not severely deficient in magnesium, this really helps. Magnesium deficiency is a prominent aspect of "metabolic syndrome" and resistance to insulin.




Some nuts have added benefits like the l-arginine content of almonds or the linolenic acid content of walnuts. However, I think the real health "punch" comes from the fiber and monounsaturate content.

Add 1/4-1/2 cup of raw almonds, walnuts, or pecans per day to your diet and what can you expect? The effects that I see every day that are relevant to plaque control/heart scan score-reducing efforts include:

--Reduction in LDL--usually a 20 mg/dl drop, sometimes more.

--Reduction in triglycerides, especially if nuts replace processed carbohydrate calories. This may be because the fiber and monounsaturate content of nuts reduces blood sugar and the effective glycemic index of any accompanying foods.

--Modest blood pressure reduction.

--Though somewhat inconsistent, partial suppression of the dreaded small LDL particle pattern. We struggle with turning off the small LDL pattern in some people, and raw nuts can provide a real advantage.

If that isn't enough, the fiber content also makes your bowels regular.

Unless there's some reason to avoid nuts (e.g., allergy), nuts should be a part of your heart scan score reducing program. Shop around, as prices can vary wildly. I've been paying $12.99 for a 3 lb bag of raw almonds from Sam's Club, though I've seen almonds elsewhere for up to $12.99 per pound.

For additional commentary, go to one of my favorite Blogs, http://fanaticcook.blogspot.com. The Fanatic Cook's recent post, The Season for Walnuts , provides additional discussion on walnuts and the recent study showing how they improve "endothelial function". The nutritionist behind this Blog has fabulous insights into food, including the concept of "functional foods", i.e., using foods as a treatment tool. She is also unfailingly entertaining.

Can you tell the difference?

12. October 2006 William Davis (0)
Stan is 55 years old. He feels fine, is in moderately good physical condition. His LDL cholesterol is 135 mg/dl, HDL 43 mg/dl, triglycerides 167 mg/dl, total cholesterol 211 mg/dl.

Can you tell me whether Stan has heart disease or not?

How about Charles? Charles has an LDL cholesterol of 127 mg/dl, HDL of 44 mg/dl, triglycerides of 98 mg/dl, and total cholesterol of 191 mg/dl. He is also reasonably fit and feels fine. Can you tell whether Charles has heart disease?

If you can't, don't feel bad. Neither can your doctor. But this is the folly of using cholesterol for risk prediction.

Stan's heart scan score: 0

Charles' heart scan score: 978

Look even more closely at Stan's and Charles' cholesterol numbers. Is there some fine distinction we overlooked? What if we calculated total cholesterol to HDL ratio? Or LDL/HDL ratio?

No matter how you squeeze it, shake it, beat it with a stick, you simply cannot use cholesterol numbers to predict heart disease in specific individuals. Yes, the higher your LDL cholesterol and lower your HDL, the higehr your total cholesterol to HDL ratio, the greater the likelihood of heart disease. But you can simply cannot tell in a specific individual at a specific point in time. If you've seen your doctor puzzle over the numbers, understand that he/she is trying to make sense out of something that doesn't make sense, no matter how hard he/she tries.

You simply need to measure the disease itself: get a CT heart scan, the only measure of atherosclerotic coronary plaque that you have access to.

By the way, if you haven't seen it yet, go to the Track Your Plaque website (www.cureality.com) to see the news piece reporting the American Heart Association's much overdue position statement on CT heart scanning. The AHA has finally released a statement which, in effect, provides their "official" endorsement. Blocked by political shenanigans behind the scenes for several years, the guidelines finally made it to press. The only real difference it makes to me is that my patients may finally get their heart scans paid for by insurance, once the insurance companies realize that it's getting tougher and tougher to dodge their responsibility.

Statin agents and muscle aches

11. October 2006 William Davis (2)
How common are muscle aches with the statin drugs?

It depends on who you ask. If you ask the drug manufacturers, they will tell you no more than 2% of people who take them. They back this up with the experience in tens of thousands of people in published clinical trials.

What if we ask people who take them outside of clinical trials. How many then? I estimate, from my large experience, over 80%! In other words, muscle aches are inevitable in nearly everyone who takes them. The longer you take them, the higher your dose, the more likely muscle aches are going to be.

Why the disconnect between published data and real-world experience? I really don't know. In some instances, the differences are dramatic. The ASTEROID trial, for instance, in which Crestor, 40 mg, was given for two years, only resulted in 8% of people dropping out because of side-effects. My experience: everybody--nobody can tolerate this dose for any length of time.

Let me qualify what "muscle aches" mean. It means achiness and/or weakness, usually mild, occasionally moderate to severe, worse upon awakening and less with use. It can affect many muscles or it can involve only one. Rarely is it incapacitating but it is commonly annoying and frightening. It commonly shows up as gradually diminishing strength with exercise. Strength usually returns promptly upon stopping the offending drug.

"Rhabdomyolysis", or true muscle destruction is, fortunately, very unusual in otherwise well people. People with abnormal kidney function, diabetes, and other concurrent illnesses are somewhat more prone. But in reality, rhabdomyolysis is unusual. I've personally seen it twice, both in people sick for other reasons.

Coenzyme Q10 (CoQ10) supplementation has been a godsend for us. At least 4 out of 5 people who require statins and develop muscle aches respond favorably, but it requires 100 mg per day. The preparation must be oil-based to work, not powder in a capsule which exerts no effect. Some people get by with less; some require as much as 300 mg per day. I've had favorable experiences with the CoQ10 from Sam's Club, GNC, Vitamin Shoppe, and Life Extension (www.LEF.org).

The Track Your Plaque target for LDL cholesterol is 60 mg/dl. Many people do indeed use statins to achieve this level, the level of LDL that amplifies your chances of heart disease reversal, i.e., reduction of heart scan score. The only drawback that I'm aware of with CoQ10 replacement is cost. Beyond this, it's a benign supplement that even supplies higher energy for some people who take it.

More catheterizations would make me happy!

11. October 2006 William Davis (0)
I received this fax today from a cardiologist seeking a position:

"I would prefer to perform as many interventions [stents, angioplasties, etc.] as possible..."

That about sums it up, doesn't it? The goal of this young man, trained in major universities including Columbia University, Harvard, and Emory, is not to pursue an avenue of investigation or healthcare that yields real answers. His goal is to perform as many procedures as possible.

This attitude is deeply ingrained in cardiologists. It's also shared by all procedural medical specialties: the drive to do more and more procedures. It's not because it does more good for the public, but it fulfills a primitive impulse to spread your influence, enlarge your territory, and--of course--make more money.

Personally, I find this impulse repulsive. The fact that this young cardiologist looking for a position is willing to make this statement out in the open demonstrates how widely accepted this attitude is. Imagine your cancer surgeon, looking for a new job, said, "I'm looking to remove as many tumors as I can."

My colleagues have lost sight of the fact that we're trying to reduce or eliminate disease, not enrich our pockets or service some primitive impulse to beat others at our game.

"I hate fish oil!"

9. October 2006 William Davis (1)
I get this comment occasionally, usually from the fishy belching that can occur, rarely because of other crazy effects like rash, fishy body odor, etc.

In the vast majority, fish oil is a benign but wonderfully effective agent. Track Your Plaque followers know that fish oil, starting at 4000 mg per day of a standard 1000 mg capsule preparation, dramatically reduces triglycerides and thereby raises HDL, partially suppresses small LDL, and is the best agent available for reducing postprandial (after eating) abnormalities like IDL and certain VLDL fractions.

However, an occasional person (about 1 in 20) just doesn't like the effects. Are there alternatives? Fish oil packs such a wallop of beneficial effects that can not be replaced by any other single agent or lifestyle practice. For this reason, we have a number of easy strategies to enhance your tolerance for fish oil. (Of course, if your and/or you doctor determine that you're allergic to fish oil, then you should indeed avoid it; thankfully, this is rare.)

Helpful strategies include:

--Refrigerate fish oil capsules--this cuts back on fish belching.
--Take only with meals. This also may increase fish oil's benefits on suppressing after-eating lipoprotein abnormalities.
--Take an enteric-coated preparation--this delays breakdown of the tablet/capsule, making fishy belching less of an issue. Sam's Club has an inexpensive preparation.
--Take liquid fish oil. Usually orange or lemon flavored, liquid fish oil may be a faint fishy taste and odor, but usually not as prominent as the capsules. There's also less stomach upset.
--Coromega--a paste form of fish oil available at health food stores or through http://www.coromega.com. Coromega tastes fruity and comes in little squeeze envelopes.
--Frutol--Pharmax, a British company, makes another fruity fish oil that is non-oily and tastes like apricot. It's actually fairly reasonably priced, too. However, it is hard to find. The only way I know to get is to go online at www.pharmaxllc.com. You may have to actually order through a health care provider.

When using any preparation of fish oil, the best way to determine your dose is to add up the EPA and DHA content. For instance, if you use a fish oil liquid that contains 320 mg EPA and 240 mg DHA per teaspoon, you will need two teaspoons a day to achieve the equivalent of our starting dose of 1200 mg of EPA+DHA, usually provided by 4000 mg total in 4 capsules. Note that some lipid and lipoprotein disorders will require higher doses, e.g., 1800 mg EPA+DHA for high triglycerides (>200 mg/dl) or high IDL.

Sudden death in athletes

6. October 2006 William Davis (0)
A recent report in the Journal of the American Medical Association details how a group in the Veneto region of Italy cut back on the incidence of sudden cardiac death in athletes by a simple screening program.



You can read the abstract of the article at http://jama.ama-assn.org/cgi/content/full/296/13/1593.

Although sudden death in athletes is still a rare event, it is especially tragic when it happens. In this population, the incidence was 3.6 deaths per 100,000 athletes aged 12 to 35 years. By implementing a simple screening program that involved only a physical examination and an EKG, an astounding 89% reduction in sudden death was documented.

What lessons does this hold for those of us interested in coronary plaque reversal? Beyond the obvious lesson of pointing out the great benefit of simple screening of athletes, I believe that it tells us the value of simple screening tools for heart disease in general. It is my strong belief that, if we were to implement CT heart scans among the broad population of men 40 years and over, women 50 years and over--without regard to cholesterol or other relatively lame risk identifiers--we could slash the risk for heart attack and death 90% or more. Putting CT heart scans into the hands of the public makes your coronary risk obvious. It takes the guesswork out of risk predictors like cholesterol and high blood pressure.

But heart scans are already available, you say! Yes, of course they are. But the lack of insurance reimbursement continues to be a restricting factor for many people, despite the number of lives that could be potentially saved and the money that would be saved in the long run by reducing need for major heart procedures. The continuing resistance to prevention by my cardiology colleagues and the persistent ignorance of primary care physicians also remain major impediments.

But it's getting better. You don't have to be chained by ignorance. Put your CT heart scan to good use.

My heart scan was wrong!

6. October 2006 William Davis (0)


Tom came into the office ready for a confrontation.

Tom's wife insisted that he see me to discuss the implications of his CT heart scan score of 459. At age 50, this was clearly bad news that placed Tom in the 99th percentile (worst 1% of men in his age group).

But Tom had already undergone a stress test. There had apparently been a small abnormality, and a heart catheterization had been performed by another cardiologist. "They told me they didn't need to do anything. No stent, no ballon, no bypass, nothing!"

I asked, "Did they tell you that there was any plaque or blockages seen?"

"Yeah, but he said it was nothing. So the heart scan was wrong!"

I've been here many times before. I explained to Tom that, no, his heart scan was not wrong. All the tests he'd undergone siimply provided a different perspective on the same disease. You could say:

--The stress test, being a test of blood flow, may have been abnormal because of the abnormal constrictive behavior of arteries containing plaque, known as "endothelial dysfunction", because the inner lining of arteries (the endothelium) control the tone of the artery. Abnormal constriction in arteries with plaque is quite common.

--The catheterization simply showed that no plaque had collected in a configuration to block flow, thus no stent, etc., since flow was normal. But there was indeed plaque.

All three tests were right; none were wrong. They all provided a little different perspective on the same process. Of course, I favor the heart scan as the means to identify, precisely measure, and track the atherosclerotic plaque in your arteries. The stress test is too crude and only measures flow, the catheterization is not something you'd want to undergo year after year. Catheterization also is too crude a measure to precisely track plaque growth or reversal.

So I explained to Tom that, even though a stent or similar procedure was unnecessary, he remained at substantial risk for heart attack due to plaque "rupture". In fact, Tom's heart attack risk was 5% per year, or approximately 50% over the next decade. That is, indeed, substantial. In fact, you might say that, of the three tests Tom underwent, only the heart scan revealed his true risk.

Why do the Japanese have less heart disease?

24. April 2011 William Davis (49)
We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

20. April 2011 William Davis (52)
Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0

18. April 2011 William Davis (0)

Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

12. April 2011 William Davis (67)
Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

9. April 2011 William Davis (30)
In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

7. April 2011 William Davis (37)
Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."

When MIGHT statins be helpful?

7. April 2011 William Davis (17)
I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

5. April 2011 William Davis (0)
Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

4. April 2011 William Davis (5)
The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.


The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

3. April 2011 William Davis (13)
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.
All posts by william-davis

What to eat: Part I

6. April 2010 William Davis (0)
I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

4. April 2010 William Davis (16)
There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

4. April 2010 William Davis (0)
Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

3. April 2010 William Davis (1)
It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.



The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.



One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

2. April 2010 William Davis (12)
Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

1. April 2010 William Davis (11)
The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

28. March 2010 William Davis (16)
Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

26. March 2010 William Davis (20)
Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

23. March 2010 William Davis (24)
Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

21. March 2010 William Davis (19)
No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.