Blast triglycerides

15. May 2009 William Davis (0)
The conventional answers to high triglycerides levels are generally: low-fat diet, a fibrate drug (Tricor, Lopid), a statin drug, and--most recently--prescription fish oil.

This is the regimen to take if you want the drug industry to get even richer and more powerful than they already are. After all, what CEO of a pharmaceutical company can stand to have his salary and benefits slashed to below $200 million this year? It's outrageous!

If you really want to blast the heck out of your triglycerides and achieve numbers like 50 mg/dl, then the regimen to consider consists of:

--Elimination of sugars, wheat, and cornstarch
--Fish oil--Sam's Club would do fine at $8 for 350 capsules, or the high-potency at $14.99 for 180 capsules (at 680 mg EPA +DHA, nearly the same potency as prescription Lovaza at 842 mg)
--Vitamin D supplementation sufficient to achieve normal blood levels (60-70 ng/ml)

Those three strategies alone can reduce triglycerides far more than any drug combination. In fact, it is rare for someone with triglycerides as high as 900 mg/dl to not reduce them to the <100 mg/dl range.

Cheerios: Prescription required?

13. May 2009 William Davis (15)
Followers of The Heart Scan Blog know my feelings about Cheerios:


Can you say "sugar"?

Cheerios and heart health


There's an interesting tussle going on between the makers of Cheerios, General Mills, and the FDA.

The FDA says that the Cheerios' package claims of:

• "you can Lower Your Cholesterol 4% in 6 weeks"
• "Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is ... clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol."

constitute a medical claim, i.e., trying to promote Cheerios as a drug.

I'm glad that the FDA has come down on General Mills. But I find this entire episode laughable: The debate is over the purported health benefits of what I would regard as pure junk food, no better in my view than claiming that a cupcake has health benefits, or a carton of ice cream.

In my experience, Cheerios does not 1) reduce risk for heart disease, nor 2) reduce cholesterol.

It does, however, cause blood sugar to skyrocket and increase the small type of LDL--you know, the type that causes heart disease.

"Placebos are frequently of value"

12. May 2009 William Davis (1)
The treatment of angina pectoris, generally speaking, is unsatisfactory.

Any procedure that relieves mental tension is valuable. Since patients suffer particularly during the winter, I encourage winter vacations in a southern climate.

I insist that obese patients lose weight, and have found small doses of benzedrine, 10 to 20 mg. daily, helpful in curbing the appetite.

I generally forbid smoking. This is a particularly disturbing task for many patients to carry out. In such cases, I suggest that 3 or 4 cigarettes be smoked daily, knowing full well that regardless of what I say or recommend, the patients is going to continue to smoke.

Innumerable drugs, most of which are of questionable value, have been used to prevent attacks of angina pectoris. In fact, placebos are frequently of value.

Testosterone--The male sex hormone has been effective in my experience. Whether it acts as a vasodilator or merely by promoting a sense of well-being is not known.

Alcohol--Alcohol (whiskey, brandy, rum) has been used for many years in the treatment of angina pectoris. I have prescribed it in moderate quantity--an ounce several times a day--and while I have not made alcoholics of any of my patients, I also have not cured any of them with it. Preparations, such as creme de menthe, are of value in relieving "gas" of which so many patients complain.


From Heart Disease Diagnosis and Treatment
Emanuel Goldberger, MD
1951

Iodine is not salt

12. May 2009 William Davis (3)
I've noticed a point of confusion recently, something I hadn't noticed in my patients before: Because of the public health advice from the FDA, American Heart Association, and Surgeon General's office to reduce sodium/salt intake, people have thought this meant reducing iodine, too.

I believe that people have drawn an equation in their minds:


Sodium = iodine


Of course, they are two entirely unrelated things.

Recall that the only reason iodine is added to many (not all) salt products is because it was a public health solution to solve the substantial nationwide iodine deficiency prevalent during the 20th century. But it was a solution conceived in 1924, when the FDA thought this was the best way to get iodine into Americans. And it worked.

Unfortunately, sodium does indeed present adverse effects in some people. As a result, "get your iodine from salt" has evolved into "reduce your sodium intake." Everyone forgot about the iodine: They forgot about the large disfiguring goiters, the poor school performance in iodine-deficient schoolchildren, the mentally-impaired offspring of iodine-deficient mothers.

So don't confuse sodium with iodine. You may need less of the former, but more of the latter.

For more on this, see "Help keep your family goiter free."

"You can't reduce coronary plaque"

10. May 2009 William Davis (9)
"I told my cardiologst that I stumbled on a program called 'Track Your Plaque' that claims to be able to help reduce your coronary calcium score.

"My cardiologist said, 'That's impossible. You cannot reduce coronary plaque. I've never seen anyone reduce a heart scan score."

Who's right here?

The commenter is right; the cardiologist is wrong.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Quantify and work to reduce the atherosclerotic plaque? No way! That's work, requires thinking, some sophisticated testing (like lipoprotein testing), even some new ideas like vitamin D. "They didn't teach that to me in medical school (back in 1980)!"

Welcome to the new age.

Atherosclerotic plaque is 1) measurable, 2) trackable, and 3) can be reduced.

We do it all the time. (Amy still holds our record: 63% reduction in plaque/heart scan score.)

Though I pooh-pooh the value of statin drug studies, there's even data from the conventional statin world documenting coronary plaque reversal. The ASTEROID Trial of rosuvastatin (Crestor), 40 mg per day for one year, demonstrated 7% reduction of atherosclerotic plaque using intracoronary ultrasound.

I have NEVER seen a heart attack or appearance of heart symptoms (angina, unstable angina) in a person who has reversed coronary plaque (unless, of course, they pitched the whole effort and returned to bad habits--that has happened). Stick to the program and coronary risk, for all practical purposes, been eliminated.

A heart scan score is not a death sentence. It is simply a tool to empower your prevention program, a measuring stick to gauge plaque progression, stabilization, or regression. Don't accept anything less.

Lethal lipids

8. May 2009 William Davis (15)
There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself


This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).


If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.

"Get regressive"

6. May 2009 William Davis (0)
This caught my eye:



Niaspan, prescription niacin, now sold by Abbott Laboratories, is now promoting its advantages in regressing coronary plaque:



In patients with a history of coronary artery disease (CAD) and hypercholesetgerolemia, Niaspan (niacin), in combination with a bile acid-binding resin, is indicated to slow progression or promote regression of atherosclerotic disease.



And the new slogan: "Get regressive."



Interestingly, the new marketing campaign is based on relatively old data. They base this new claim on 3 studies:



1) Cholesterol-Lowering Atherosclerosis Study (CLAS)--a 1987

CRP House of Cards

4. May 2009 William Davis (15)
Lew has coronary plaque with a heart scan score of 393. At age 53, that's in the 90th percentile (higher score than 90% of men in his age group).

On our search for causes of his coronary plaque, we identify low HDL of 41 mg/dl, high triglycerides of 202 mg/dl, small LDL (83% of total), calculated LDL of 133 mg/dl, and severe vitamin D deficiency with a starting blood level of 25-hydroxy vitamin D of 19 ng/ml.

His c-reactive protein: 4.1 mg/dl--above the cut-off of 2.0 mg/dl that the pharmaceutical industry is targeting as a mandate for statin therapy, particularly given the JUPITER data.

Lew instead eliminates wheat and other small LDL-provoking foods and, as a result, loses 28 lbs in 3 months; adds omega-3 fatty acids from fish oil; supplements vitamin D sufficient to increase his blood level to 70 ng/ml.

Along with dramatic correction of his starting abnormalities, his c-reactive protein: 0.4 mg/dl--no statin drug.

In my view, increased CRP is nothing more than a surrogate for the inflammatory phenomena that arise from high-carbohydrate diets, overweight, and small LDL. Correct those and CRP drops off a cliff. In fact, it is exceptionally rare for CRP to not drop to very low levels following this formula.

I believe that CRP is one more item on the list of reasons--the house of cards--the pharmaceutical industry is building to persuade us to take more and more statin drugs. LDL not low enough? Take more statin. Diabetic with low cholesterol? Take a statin. Inflammation? Take a statin.

Enough already.

At-home blood tests

2. May 2009 William Davis (6)
Our at-home blood tests are proving a hit.

So far, vitamin D is the number one most popular test, no surprise.

Second--to my surprise--is DHEA. I would have predicted it would have been thyroid testing.

Our male and female hormone panels are also proving popular.

I've personally been using the thyroid and vitamin D testing to monitor my levels. I increased my Armour thyroid based on a low free T3 value, while my vitamin D was perfect at 77 ng/ml on 8000 units vitamin D3 (cholecalciferol) per day.

The process of performing the blood spots is straightforward. The finger pricks are virtually painless using the automatic spring-loaded finger stick devices:





The number of blots to make depends on how many tests you'd like. Just a vitamin D test requires 2 blots. If 6 or more tests are ordered at a time, then all 12 blots should be made. (Two spring-loaded lancets are provided in each kit.)





If you are interested in any of our at-home blood tests, go here.

Our own Heart Hawk has posted an editorial on about blood spot testing on Health Central:

Simple, affordable home blood testing is a real game-changer in the arena of informed, self-directed healthcare. For the first time broad access to home blood testing, on a scale similar to that enjoyed by persons who routinely test their blood sugar, is available to virtually everyone and it removes doctors as the gatekeepers of these tests. Even private insurance companies and Medicare are beginning to understand the potential for improving healthcare and decreasing costs and are slowly beginning to expand coverage of home blood testing much as they do for diabetics or persons taking anti-coagulants.

"Help keep your family goiter free"

1. May 2009 William Davis (10)
People ask, "If I need iodine, should I go back to iodized salt?"

First of all, how did this notion of iodized salt originate?

In 1924, J. Edgar Hoover was appointed head of the FBI, Marlon Brando and Doris Day were born, and Calvin Coolidge was elected President of the United States. Half of American households had a car, while 1 in 4 Americans were illiterate.



In the 1920s, cities were a fraction of their current size and a third of the U.S. population, or 36 million people, lived in small rural communities.

Goiters were also wildly prevalent in 1924. Up to a third of the population in some areas of the country, particularly the Midwest, suffered from goiters, thyroid glands that enlarged due to lack of iodine.

Goiters were not only unsightly, but sometimes grotesque, causing a visible bulge in the front of the neck. Occasionally, they would grow so big that it compressed adjacent structures, like the trachea, and would have to be surgically removed. Goiters were commonly associated with thyroid dysfunction, especially low thyoid or hypothyroidism, that resulted in low IQ's in schoolchildren, debilitation in adults. Women of childbearing age delivered retarded children.

So iodine deficiency in early 20th century America was a big problem. How to solve this enormous public health problem in a large nation without television, few radios, no internet, with a largely rural and often illiterate population?

Thus was iodized salt born, a simple, technologically available solution that could be implemented on a large scale nationwide at low cost. The FDA chose this route in 1924, figuring that it was the best way to ensure that most Americans could obtain sufficient iodine through liberal use of iodized salt. Public health officials urged Americans to use salt. Morton's salt label proudly bore the slogan "Help keep your family goiter free!"

It worked. Goiters largely became a thing of the past.

How about today? The American Heart Association recommends limiting salt, recently announcing that they would like to limit intake to 1500 mg per day. The American Medical Association has been lobbying the FDA to set lower salt limit guidelines. The FDA has been clamping down on food manufacturers to reduce the quantity of salt in processed foods.

Why limit salt? The concern is that there are segments of the population (not all) that are salt sensitive, particularly African Americans, people with certain genetic forms of high blood pressure, conditions that cause water retention, and any degree of heart or kidney failure. Salt in these peoplem, in fact, can be disastrous.
So adding iodine to salt was the solution to epidemic goiter. And it worked.

But salt is not a perfect solution, just one that served its purpose back in 1924. What we need is a 21st century solution.
You will find that in the various iodine supplements at your health food store. My favorite is kelp--inexpensive, available, and a form that mimics the way Japanese people obtain iodine (though by eating seaweed, rather than with tablets).


Image of kelp courtesy Wikipedia
Handy dandy carb index

Handy dandy carb index

25. March 2011 William Davis (21)
There are a number of ways to gauge your dietary carbohydrate exposure and its physiologic consequences.

One of my favorite ways is to do fingerstick blood sugars for a one-hour postprandial glucose. I like this because it provides real-time feedback on the glucose consequences of your last meal. This can pinpoint problem areas in your diet.

Another way is to measure small LDL particles. Because small LDL particles are created through a cascade that begins with carbohydrate consumption, measuring them provides an index of both carbohydrate exposure and sensitivity. Drawback: Getting access to the test.

For many people, the most practical and widely available gauge of carbohydrate intake and sensitivity is your hemoglobin A1c, or HbA1c.

HbA1c reflects the previous 60 to 90 days blood sugar fluctuations, since hemoglobin is irreversibly glycated by blood glucose. (Glycation is also the phenomenon responsible for formation of cataracts from glycation of lens proteins, kidney disease, arthritis from glycation of cartilage proteins, atherosclerosis from LDL glycation and components of the arterial wall, and many other conditions.)

HbA1c of a primitive hunter-gatherer foraging for leaves, roots, berries, and hunting for elk, ibex, wild boar, reptiles, and fish: 4.5% or less.

HbA1c of an average American: 5.2% (In the population I see, however, it is typically 5.6%, with many 6.0% and higher.)

HbA1c of diabetics: 6.5% or greater.

Don't be falsely reassured by not having a HbA1c that meets "official" criteria for diabetes. A HbA1c of 5.8%, for example, means that many of the complications suffered by diabetics--kidney disease, heightened risk for atherosclerosis, osteoarthritis, cataracts--are experienced at nearly the same rate as diabetics.

With our wheat-free, cornstarch-free, sugar-free diet, we have been aiming to reduce HbA1c to 4.8% or less, much as if you spent your days tracking wild boar.
Tags :

Comments (21) -

  • Anonymous

    3/25/2011 3:19:26 AM |

    Dr. Davis,

    Can someone have a good HbA1c but still have an undesirable amount of small particle LDL? ..Like perhaps someone with FHC that has their LDL particles floating around longer in the bloodstream and hence exposed longer to oxidants.

    Thank you.

    John M.

  • Tyler

    3/25/2011 3:51:56 AM |

    I love your blog but I have to clarify on this point. Check out the post by chris kresser: http://chriskresser.com/blog/why-hemoglobin-a1c-is-not-a-reliable-marker/

    a1c is not reliable for many people because of the variation in RBC life length. healthy people's red blood cells may live as over 4 months whereas diabetic's live only as 60 days. This results in vast discrepancies.

    For example my fasting BG averages 77 and postprandial peak is 85-90, but my hemoglobin A1c is 5.7

    This doesn't make sense unless you account for differences in RBC lifetime.

  • Kris @ Health Blog

    3/25/2011 11:45:32 AM |

    I'm wondering what your opinion is of glycation and aging.

    I've been reading that a major part of the aging process might be caused by glycation of proteins in the body, mostly caused by elevated blood sugar.

    Do you believe that practically, one could expect a longer life expectancy to correlate with lower blood sugar levels?

  • Larry

    3/25/2011 12:09:46 PM |

    The other day on the tv show, "The Doctors", they profiled a young woman concerned about her FBG.
    She said that Diabetes ran in her family.
    They did a bloodtest and announced that her FBG was 111.
    The scary part was when they told her that reading was okay.
    With that FBG, one can assume that everytime she eats, her post-prandial FBG is heading into dangerous territory.
    But they told her not to worry.
    She was right about her concern...as Diabetes will continue to run in her family.
    Especially with that advice.

  • Jonathan

    3/25/2011 2:44:03 PM |

    I found Walmart carries a Bayer at home A1c test kit that gives results in 5 minutes.  It came with two test cartridges so I was able to take one when I started lowcarb and another one 4 months later to see how much it came down.  (I came down from 8.3 to 5.2 in 4 months)

  • revelo

    3/25/2011 4:45:55 PM |

    What is HbA1c for those long-lived okinawans with their rice-based diet, or those long-lived cretans with their wheat-based diet?

    Wouldn't a lean healthy body (especially if there is occasional fasting) eventually clean up glycated and otherwise damaged proteins?

  • Might-o'chondri-AL

    3/25/2011 6:22:18 PM |

    Glycation picks on the amino acid valine "wing" on the molecule of haemoglobin's B-chain portion. Aldehydes, both glucose aldehydes and non-glucose ones can become bound to that valine.

    This can occur several ways. Glucose oxidation yields a byproduct, called gly-oxal; this is what most people monitor. In the glyco-lytic pathway called Embden-Meyerhof triose-phosphate drives gly-oxal into the molecule methyl-glyoxal (MG).

    Type 1 diabetics have circulating methyl-glyoxal (MG) levels that are +/- 6 times greater normal. MG is a glycation end product.

    Tyler's comment links to a discussion of fructosamine monitoring. This is from a non-enzyme driven reaction, called Amadori, where fructo-selysine and the fructos-amine 3 kinase cascade generates 3 De-oxy-glucos-ane (3DG); another glycation end product.

    Enzymatic glycation occurs in pathological states. Macrophage activity spins off  the enzyme myelo-peroxidase; this generates hypo-chlorite. Hypo-chlorite pulls in the amino acid serine and then together they cause the formation of certain advanced glycation end-products; namely glyco-aldehyde and glycer-aldehyde.

    Yet another non-enzyme chain of events can generate advanced glycation end products. This is when the molecule per-oxy-nitrite (ONOO-)gets stalled inside the cell and it induces the formation of gly-oxal/gluco-sone/aldehyde molecules that can contribute to glycation.

    ONOO- normally is part of healthy cell signaling. When a metabolic processes is under sustained "stress" it (ONOO-) can't shift the cell function over to what it (the cell) needs to do (in order to adapt and cope). Instead of briefly signalling, signing off and going away ONOO-
    lingers in the cell; a situation that may also be related to ageing.

  • Anonymous

    3/25/2011 7:10:22 PM |

    I wonder if Dr. Davis can comment on situations where carb intake is reasonable and the patient has a decent HBA1c, yet still has higher than normal triglycerides and small LDL?

    My own HBA1c has been in the 4.5-4.6 range, yet my trigs hover around 140-150, and I still have more small LDL than I'd like.

    If restricting carbs doesn't work, D levels normalized, etc. what else could be the cause of higher than optimal triglycerides?

    I know people with HBA1cs in the 5.4+ range, eat many more carbs than I do, yet still have lower trig numbers.

  • Might-o'chondri-AL

    3/25/2011 8:58:10 PM |

    Hi Revelo,
    Vitis vinifera leaf inhibits advanced glycation end product (AGE) formation. That is what many cultures, like Crete, eat wrapped around their cereal grain; we call it Grape Leaves in English (ex: stuffed grape leaves, a.k.a. Dolma in Greek).

    Japan researchers (2009?) took 1 kilogram of dried grape leaves in 20 liters of water and stirred it for 3 hours at 80*Celcius. They administered the decoction in various dosages and found it can reduce the AGE of 3DG (3 de-oxy-gluco-sone) and also a marker of AGE in kidney disease, pentosidine, down to 1/5th the level from that study's AGE control levels.

    The same study experimented with Anthemis nobilis using the same extraction technique detailed above. They propose the active ingredient responsible for the AGE inhibition is the compound called chamaemoliside.

    Chamomile is the name of this plant in English; I suspect it is drunk as a tea in Crete. In the range of AGE inhibitors that they tested Chamomile was better acting than any other; grape leaves efficacy came in second.

    Plants studied that inhibit AGE forming, in no particular order of effectiveness may interest you. These are: Crataegus oxyacantha (English = Hawthorn berry), Houttuynia cordata (English = Chameleon plant) and Astragalus membranaceous (English = Astragalus). Chameleon plant is a regular condiment used in Vietnamese and some south-east asian food; it smells kind of "fishy".

  • revelo

    3/25/2011 9:02:19 PM |

    According to Steven Gundry MD, it is MEAT which is the primary cause of AGE's. (He doesn't cite any references for this in his "Diet Evolution" book.) He recommends Atkin's style low-carb/high-protein to lose weight, then low-fat (15% of calories from fat) as the maintenance diet. He is not too keen on grains, tubers or fruit, but rather emphasizes green vegetables.

  • Tyler

    3/25/2011 9:50:41 PM |

    Thanks for the nice explanations Might-o'chondri-AL

  • Might-o'chondri-AL

    3/25/2011 10:46:23 PM |

    Diabetic nephro-pathy (ie: kidney complication), and kidney disease have elevated AGE. These are monitored as pento-sidine, gly-oxal, methyl-gly-oxal and 3 de-oxy-gluco-sane; which the body tries to excrete as carbonyly compounds.

    Carbonyl compounds are hard to get through the kidney filters and cause an increase in uric uremia, which can be toxic. Too many carbonyls can cause, the so called, "carbonyl stress" of diabetic nephro-pathy.

    Diabetic patients' kidneys eventually can't excrete enough sodium (Na); and that contributes to the high blood pressure (hyper-tension) diabetics tend to suffer from.

    Ketones merit mentioning too. One of the markers for AGE in the kidneys is N-carb-oxy-ethl-lysine; which may (or may not) be a side effect of ketones. Type 1 diabetics do show elevated ketone levels incidently.

    I am not able to offer any perspective on ketogenic diets and AGE however. However, vitamin C is known to decrease ketone bodies. (In the previous post, "Battery acid ...", more
    diabetic responses to vitamin C appears among the comments.)

  • Anonymous

    3/26/2011 4:46:17 AM |

    I've been eating low-carb (basically paleo) for the last 4-5 mo and just got my lipid panel results.  They sky-rocketed.

    Cholesterol 300
      
    Triglyceride 150  
        
    HDL          33
        
    LDL             237


    Every number got worse.  The part that really sucks, is that the diet makes me feel great and nearly all my body fat is gone.  I'm 37, 5'11, 180 lbs and probably about 9% body fat.  Now I'm wondering what kind of trade-off I'm making.  Any thoughts, doc?

  • Peter

    3/26/2011 12:55:22 PM |

    Testing different foods one hour after meals, it seems like a good rule of thumb for me is that each ounce of carbs raises my blood sugar about 10 mg,and that the kind of carb doesn't matter nearly as much as the quantity.

  • Might-o'chondri-AL

    3/26/2011 6:31:09 PM |

    Paradoxical low carb yet relatively high HbA1c & higher carb but relatively lower HbA1c is reported by Annon. Doc assuredly deals with cases like these and has to resolve their enigma one by one.  

    The gene HFE (human hemochromatosis protein, nicknamed High Fe  where iron = Fe)can have a variation (reference code = HFE rs1800562). This variation is seen in +/- 5% of Caucasians, but is not found in East Asian nor African genes.

    More hemoglobin is in circulation for those having this HFE genetic variation. In this case, the same amount of blood sugar that can contribute to glycation of hemoglobin has more hemoglobin surfaces to glycate. Think of it as the glycation has to spread itself thin; the dilution of it's effect makes the % of Hb1Ac less (ie: lower Hb1Ac % measured in the blood sample).

    On the other hand, genetic variation rs855791 of the gene TMPRSS6 (trans-membrane protease, serine 6)is implicated in anemia. In these individuals Hb1Ac readings range higher; there is less hemoglobin relative to the glycation potential in their blood stream. Think of it as the relatively low proportion of hemoglobin which has to bear all the glycation burden
    (ie: Hb1Ac % is higher in their blood sample).

    Anemic (hemolytic) tendency is also driven by variation of gene HK1 (hexo-kinase 1). This enzyme modulates how glucose inside the cell goes through  it's processing pathways.

    This gene (HK1) codes for the unique iso-form of erythrocytes; erythrocyte configuration can figure in to low hemoglobin. In other words it is also a factor in high Hb1Ac readings; glycation potential in the blood over burdens the limited amount of hemoglobin around.

  • Dr. William Davis

    3/26/2011 6:34:23 PM |

    In response to several questions about the potential disconnect between small LDL/triglycerides and HbA1c: Yes, there are people in which one measure is more resistant. It varies based on the mix of underlying genetic predispositions, so it's hard to generalize.


    Might-o'-chondri-AL--

    Great discussion. Thanks, as always. You bring an incredibly sophisticated perspective!

  • Dr. William Davis

    3/26/2011 6:35:48 PM |

    Jonathan--

    Spectacular! And within an unusually brief timeline for HbA1c.


    Revelo--

    Might-o'chondri-AL is referring to endogenous glycation. You are citing a discussion about exogenous glycation, two separate phenomena.

  • Might-o'chondri-AL

    3/27/2011 1:31:59 AM |

    Might Jenny's observation and Nigel's study reference be reconciled somewhat ? I'll tag on my disclaimer of being unqualified to judge low carb or specific diets; since I've never struggled with weight or diabetes, and am not a doctor.

    The study Nigel linked was done with all Kuwaiti subjects. In that country co-sanguinity in marriage is practised by +/- 54.3 % of Kuwaitis. And 1 in 5 are reported to be diabetic.

    The data is very admirable; my suggestion is that the data trend may not exactly transfer to a modern Caucasian population; which is essentially interbred from migration and war (rape). This may be why Jenny sees a +/- 6 month plateau among her respondents and the co-sanguine Kuwaitis saw changes continue for a year +.

    Genetic poly-morphisms influence fasting glucose (GCK, G6PC2 and MTNR1B), are implicated in Hb1Ac, triglyceride levels, HDL levels & so on. That said, I personally would try the low carb approach if I was diabetic.

  • Might-o'chondri-AL

    3/27/2011 1:32:47 AM |

    oops posted this in wrong thread

  • Anonymous

    3/27/2011 3:12:44 AM |

    Re: Anonymous with Cholesterol 300,  Triglycerides 150,  HDL 33 ...

    Suggest you try a technique many dieabetics find helpful to understand food consumption influence on their blood sugar profile,"eating to your meter".
    For a few days, record your blood sugar level immediately before eating a "normal" meal, and then after the meal get 1-hour and 2-hour post-meal blood sugar readings. Separate meals by at least 4 hours. Concentrate on monitoring your main meals and ignore snacking for the first go around. Better however, if you can actually avoid all snaking during period of the testing. Also you will want to add to your journal the foods, ammount consumed, and time it was consumed. If post-meal blood sugar values are high, then to determine a pattern folllowing a meal do a series of hourly post-meal readings until you reach 85 mg/dL or so. As a graph, these results should be helpful to you. Expect that the results will be revealing to you with unexpected high blood sugar values even after following a paleo diet. And if so, it does mean that paleo is not for you, only that you need to more discriminating in what and how much you actually consume.

    I would be interested in hearing about your findings. By the way, you did not mention the blood glucose or HbA1c results of your recent lab tests.

    My regards and good luck ... spo

    BTW: practice good technique with the finger sticks. Do a quick but good hand wash using soap and a warm water rinse prior to a stick. Dry hands well. Dont squeeze hard at the site to encourage blood flow. The original stick should be sufficent to raise a drop of blood for the test strip. Using alcohol swabs and changing out lancets is not necessry when only working on youtself. Keep the test strip vial tightly closed other then when removing the current test strip. If you encounter an "extreme" value, retest for confirmation but clean hands again prior to the retest. My experiences regarding unexpected readings seems to usually invovle hand and finger contamination of some form.

    Finally, on Amazon.com I am able to purchase unexpired test strips in 50 strip lots for my old AcuCheK Confort Curve meter for less than $0.16 or so a strip and often with free shipping. You just have to broswe around a bit.

  • Jonathan

    3/30/2011 2:47:32 PM |

    @ Anonymous with 300 TC
    I would say it could possibly be your liver cleaning itself out (it could have been getting fatty).  The higher Trig might be a sign you are getting too many carbs from somewhere (at least till your sugar stores empty some and insulin sensitivity goes back up) but it could be the liver cleaning out as well.  I think HyperLipid posted something about this once.

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