Do you eat wheat? I thought so.

I'm itching to say that face-to-face to anyone from the wheat industry--agribusiness, baking, retail distribution . . . anybody. Because it's obvious; it's written on the face . . . and belly, and brain, and knees, and hips. And I believe I will soon have the opportunity.

Taking such a controversial stand in my new book, Wheat Belly, i.e., that wheat products, whole or refined, have NO ROLE IN THE HUMAN DIET whatsoever, was bound to provoke criticism and counterattacks. The wheat world has already taken a blow to the chin with the growing popularity of the (misguided) gluten-free movement and they're going to have to get into the business of media damage control.

Take a look at this press release from the Grain Foods Foundation:

RIDGWAY, COLO. — The Grain Foods Foundation has unveiled plans to counter media publicity attracted by “Wheat Belly.”

“Mullen, working with key members of the Grain Foods Foundation’s scientific advisory board, is addressing ‘Wheat Belly’ through proactive media outreach and its ongoing rapid response program,” said Ashley Reynolds, a Mullen account executive. “In particular, the public relations team will be contacting health and nutrition reporters at print and on-line media outlets, as well as editors at major women’s magazines to influence any diet-related stories that may be published in the coming months.”

. . . Ms. Reynolds, a registered dietitian, noted the author relies on anecdotal observations rather than scientific studies; wheat elimination “means missing out on a wealth of essential nutrients;” six servings of grain-based foods are recommended daily in the Dietary Guidelines for Americans; healthy weight loss depends on energy balance rather than elimination of specific foods; and elimination of wheat products makes sense only for those with medical diagnoses such as celiac disease or gluten sensitivity.

She said the group will lean on its scientific advisory board members to “discredit the book and ensure our messages are backed by sound science. “


Here's some of their starting salvos on their Six Servings Blog.

This reminds me of the fight with Big Tobacco in the '70s: "No, sir, we in the tobacco industry know of no research demonstrating that smoking is bad for health," complete with shots of tobacco executives puffing away on cigarettes.

So brace yourself for a fight. These people are protecting a multi-billion dollar franchise, not to mention their livelihoods and incomes. It could get ugly.

Wheat Belly explodes on the scene!



Wheat Belly is finally available in Barnes and Noble and all major bookstores nationwide! Also available at Amazon. Electronic versions for Nook and Kindle, as well as an audio CD, will also be available.

The notion of Wheat Belly got its start right here on The Heart Scan Blog and the diet developed for the Track Your Plaque program to conquer heart disease and plaque.



Chapters in the book include:

Not Your Grandma's Muffins: The Creation of Modern Wheat
Whence and where did this familiar grain, 4 1/2-foot tall "amber waves of grain," become transformed into a 2-foot tall, high-yield genetically unique plant unfamiliar to humans? And why is this such a bad thing?

Cataracts, Wrinkles, and Dowager's Humps: Wheat and the Aging Process
If you thought that bagels and crackers are just about carbs, think again. Wheat consumption makes you age faster: cataracts, crow's feet, arthritis . . . you name it, wheat's been there, done that and brings you one step closer to the big nursing home in the sky with every bite.

My Particles are Bigger than Your Particles
Why consuming plenty of "healthy whole grains" is the path to heart disease and heart attack and why saying goodbye to them is among the most powerful strategies around for reduction or elimination of risk.

Hello, Intestine: It's Me, Wheat
No discussion of wheat is complete without talking about how celiac disease and other common intestinal ailments, like acid reflux and irritable bowel syndrome, fit into the broader concept of wheat elimination.

Here's a YouTube video introduction to the book and concept posted on the YouTube Wheat Belly Channel. Also, join the discussions on The Wheat Belly Blog and Facebook. Have that last bite of blueberry muffin, because I predict you won't be turning back!

Good fat, bad fat

No, this is not a discussion of monounsaturated versus hydroxgenated fat. This is about the relatively benign fat that accumulates on your hips, rear end, or arms--the "good"--versus the deep visceral fat that encircles your intestines, kidneys, liver, pancreas, and heart--the "bad."

And I'm not talking about what looks good or bad. We've all seen the unsightly flabby upper arms of an overweight woman or the cellulite on her bulging thighs. It might look awful but, metabolically speaking, it is benign.

It's that muffin top, love handle, or wheat belly that encircles the waist, a marker for underlying deep visceral fat, that:

--Increases release of inflammatory mediators/markers like tumor necrosis factor, leptin, interleukins, and c-reactive protein
--Is itself inflamed. When examined under a microscope, visceral fat is riddled with inflammatory white blood cells.
--Stops producing the protective hormone, adiponectin.
--Traffics in fatty acids that enter the bloodstream, resulting in greater resistance to insulin, fat deposition in the liver (fatty liver), and increases blood levels of triglycerides
--Predicts greater cardiovascular risk. A flood of recent studies (here's one) has demonstrated that larger quantities of pericardial fat (i.e., visceral fat encircling the heart, visible on a CT scan or echocardiogram) are associated with increased likelihood of coronary disease and cardiovascular risk.

You can even have excessive quantities of bad visceral fat without much in the way of fat elsewhere. You know the body shape: skinny face, skinny arms, skinny legs . . . protuberant, flaccid belly, the so-called "skinny obese" person.

Nobody knows why fat in visceral stores is so much more evil and disease-related than, say, wheat on your backside. While you may struggle to pull your spreading backside into your jeans, it's waist girth that is the problem. You need to lose it.

You could take vitamin D or . . .

You could take vitamin D and achieve a desirable blood level of 25-hydroxy vitamin D (I aim for 60-70 ng/ml), or you could:

--Take Actos to mimic the enhanced insulin sensitivity generated by vitamin D
--Take lisinopril to mimic the angiotensin-converting enzyme blocking, antihypertensive effect of vitamin D
--Take Fosamax or Boniva to mimic the bone density-increasing effect of vitamin D
--Take Celexa or other SSRI antidepressants to mimic the mood-elevating and winter "blues"-relieving effect of vitamin D
---Take Niaspan to mimic the HDL-increasing, small LDL-reducing effect of vitamin D
--Take naproxen to mimic the pain-relieving effect of vitamin D

So, given a choice, what do most doctors choose? Of course, they choose from the menu as presented by the sexy sales representative sitting in the office waiting room. These medications, of course, are among the top sellers in the drug world, taken by millions of Americans and not just one at a time, but several per person.

The Food and Nutrition Board of the Institute of Medicine, the panel of volunteers charged with drafting a Recommended Daily Allowance for vitamin D, says that you are already getting enough vitamin D, so don't bother taking any supplements and continue to wear your sunscreen. Wonder whose side they're on?

I continue to be impressed that many of the conditions that plague modern people are little more than deficiencies peculiar to modern life, such as vitamin D deficiency, or the result of the excesses of modern life, such as consumption of sucrose, fructose, corn, and "healthy whole grains."

I take 8000 units of gelcap vitamin D and haven't felt better.

More lipoproteins zero!

A few posts back, I talked about how more people are showing us zero lipoprotein(a) and zero small LDL. That was about 4 weeks ago. By then, I had seen 3 people with zero values on both.

Well, it's now up to 9 people: 9 people who have achieved zero lipoprotein(a) and zero small LDL. These are people who started with typical lipoprotein(a) values of 150-300 nmol/L and small LDL values of 1000-2000 nmol/L, both substantial.

I still don't know how many people or what percentage can expect to show such extravagant results. But the sharp increase over a relatively brief period of time is extremely encouraging!


Diet: One size does NOT fit all

Heart Scan Blog reader, Frustrated, posted this comment:

Dr. Davis,
I have spent the last 5 months eating a diet that completely eliminated all wheat products. It was very low carb, and consisted of relatively high protein (eggs, grass fed beef, grass fed raw cheese, oily fish, chicken), good level of olive oil, walnuts, fish oil (3 mg per day), raw vegetables, little bit of fruit. So I had good amount of monounsaturated fat as well as saturated fat from eggs and grass fed products.

My recent NMR showed:
LDL-p. 2,800
Small LDL particle 1700
Small HDL particle 20
HDL-C 40
LDL-C 114
Trigs. 224
Total chol 208

So I was disappointed. Where have I gone wrong? No wheat and sky-high LDL-p and 1700 small LDL particles.


This is indeed unusual. I see this perhaps 5 or 6 times over a year's time, while thousands of other people show the usual expected respone. I don't have Frustrated's lipoprotein panel prior to starting the diet, but I'll bet the starting panel was similar to this "after" panel.

The overwhelming majority of people who follow a diet like the one described--no wheat, limited carbohydrate, grass fed beef, fish, chicken, vegetables, limited fruit--obtain extravagant reductions in small LDL, increased HDL, and reduced triglycerides. So why did Frustrated end up with such disappointing results, values that potentially provide for high risk for heart disease?

There are several possibilities:

1) He/she is in the midst of substantial weight loss. When labs are drawn in the midst of weight loss, stored energy is being mobilized into the blood stream. This energy is mobilized as fatty acids and triglycerides which, upon entering the blood stream, cause increased triglycerides, reduced HDL, chaotic or unpredictable small LDL patterns, and increased blood sugar sufficient to be in the diabetic or pre-diabetic range. This all subsides and settles down to better values around 2 months after weight loss has plateaued.

2) Apo E4--If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the "rescue."

3) Apo E2 + Apo E4--It's possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.

4) Other variants--There are probably a dozen or more other genetic variants, thankfully rare, such as apo B and apo C2 variants, that are not generally available for us to measure that could influence Frustrated's response.

5) The low-carb diet is not truly low-carb--Frustrated sounds like a pretty sharp cookie. But it's not uncommon for someone to overlook a substantial source of carbohydrate exposure that triggers these patterns. Fruit is a very common tripping point, since people generally regard unlimited fruit as a healthy thing. This does not seem to be Frustrated's problem. Others indulge in quinoa, sweet potatoes, millet or other carbohydrate sources that look and sound healthy but, in sufficient quantities, can still trigger this pattern.

6) Other--Hypothyroidism, kidney disease, nephrotic syndrome, hypercortisolism and some other relatively rare conditions are worth considering if none of the above apply.

Anyway, that's the list I use when this peculiar situation arises. If obvious weight loss is not the culprit, the next step is apo E testing. However, the wrong response is to reject the low-carbohydrate notion altogether and just limit fat, since this typically leads to uncontrolled small LDL, high triglycerides, and diabetes. It can often mean limiting carbohydrates while also limiting fats. Just as with the combination of apo E4 with Lipoprotein(a), I lump many of these patterns into the emerging world of genetic incompatibilities, genetic traits that code for incompatible metabolic phenomena.


Why ATP-3 is B--- S---

A Heart Scan Blog reader posted the link to this very excellent presentation by Dr. David Diamond, a neuroscientist at the University of South Florida.

ATP-3, or Adult Treatment Panel-3, is the set of cholesterol treatment guidelines as established by the National Cholesterol Education Panel, the guidelines used by practicing physicians nationwide. They are also the metric by which the "quality" of care is being judged by agencies like Medicare, health insurers, and other parties interested in policing healthcare. Dr. Diamond ably recounts how we ended up in this mess, the conflagration of "cut your fat, reduce cholesterol, and take a statin drug."

I was very impressed that, in his closing comments, he briefly discusses the pivotal role of glycation in heart disease causation. You will see in coming conversations how important an understanding of glycation is to create a healthy diet and lifestyle.

How far wrong can cholesterol be?

Conventional thinking is that high LDL cholesterol causes heart disease. In this line of thinking, reducing cholesterol by cutting fat and taking statin drugs thereby reduces or eliminates risk for heart disease.

Here's an (extreme) example of just how far wrong this simpleminded way of thinking can take you. At age 63, Michael had been told for the last 20 years that he was in great health, including "perfect" cholesterol values of LDL 73 mg/dl, HDL 61 mg/dl, triglycerides 102 mg/dl, total cholesterol 144 mg/dl. "Your [total] cholesterol is way below 200. You're in great shape!" his doctor told him.

Being skeptical because of the heart disease in his family, had a CT heart scan. His coronary calcium score: 4390. Needless to say, this is high . . . extremely high.

Extremely high coronary calcium scores like this carry high likelihood of death and heart attack, as high as 15-20% per year. So Michael was on borrowed time. It was damn lucky he hadn't yet experienced any cardiovascular events.

That's when Michael found our Track Your Plaque program that showed him how to 1) identify the causes of the extensive coronary atherosclerosis signified by his high calcium score, then 2) correct the causes.

The solutions, Michael learned, are relatively simple:

--Omega-3 fatty acid supplementation at a dose sufficient to yield substantial reductions in heart attack.
--"Normalization" of vitamin D blood levels (We aim for a 25-hydroxy vitamin D level of 60-70 ng/ml)
--Iodine supplementation and thyroid normalization
--A diet in which all wheat products are eliminated--whole wheat, white, it makes no difference--followed by carbohydrate restriction.
--Identification and correction of all hidden causes of coronary plaque such as small LDL particles and lipoprotein(a)

Yes, indeed: The information and online tools for health can handily exceed the limited "wisdom" dispensed by John Q. Primary Care doctor.

The best artificial sweeteners

Our new recipes, such as New York Style Cheesecake and Chocolate Coconut Bread, are wheat-free and low- or no-carbohydrate. They fit perfectly into the New Track Your Plaque Diet for gaining control over coronary atherosclerotic plaque, not to mention diabetes, pre-diabetes, hypertension, small LDL particles, high triglycerides, high inflammation (c-reactive protein) and other distortions of metabolism.

However, there's one compromise: We include use of non-nutritive sweeteners. It's therefore important to know that artificial sweeteners are not all created equal.

One common tripping point: maltodextrin.

Maltodextrin is composed of polymers (repeating subunits) of glucose, as few as 3 or as many as 20 or more glucose subunits. So maltodextrin is glucose sugar. While it lacks the especially destructive pentose sugar, fructose, maltodextrin is metabolized to glucose and thereby increases blood sugar substantially.

Many artificial sweeteners are bulked up with maltodextrin. For instance, granulated Splenda and Stevia in the Raw, two sweeteners billed as low-calorie and sugar-free that is used on a cup-for-cup basis like sugar, are primarily maltodextrin--with only a teensy bit of Splenda or stevia.

The best artificial sweeteners, i.e., the most benign without a load of maltodextrin, are:

Liquid stevia--Just the extract from stevia leaves and water. It can be a bit pricey, e.g., $10 for a 2 oz bottle, but a little goes a long way.

Truvia--While I'm not too fond of the manufacturer (Cargill), I believe that Truvia is among the better sweeteners around. It is a mixture of the natural sugar, erythritol, that generates little to no blood sugar effects and rebiana (rebaudioside), an isolate of stevia. Some people aren't too fond of the mild menthol-like cooling effect of the erythritol nor the slight aftertaste. I find it works pretty well in most recipes.

Be aware that, no matter which artificial sweetener you use, it has the potential to stimulate appetite. I therefore like to not eat foods sweetened with liquid stevia or Truvia in isolation but as part of a meal. That way, any appetite stimulation that results is substantially quelled by the proteins and fats ingested.

Sugar Nation



Former Men's Health editor, Jeff O'Connell, has just released his new book, Sugar Nation.

Back in 2009, Jeff contacted me to obtain some background insights into diabetes and its relationship with diet. He recently sent me a copy of his new book that contains some brief quotes from me.

Jeff is a writer, not a physician nor scientist. But I think that you will find his grasp of diabetes and the nutritional and lifestyle events that led him there far exceed the insights held by most practicing physicians. Like many of us, Jeff discovered how to find his way back from pre-diabetes through lessons he had to learn on his own, but not from his doctor.

Jeff tells this story as reporter, son of an estranged diabetic father with whom he reconnects as he approaches the end of his life, and as fellow sufferer of the pre-diabetic/diabetic mess that modern habits and "official" dietary advice have given us. Jeff's book is worth a read to see yet another dimension of the human stories that are emerging from this incredible nutritional tangle we find ourselves in.

Here's a unique YouTube video about Jeff's story.
Diet: One size does NOT fit all

Diet: One size does NOT fit all

Heart Scan Blog reader, Frustrated, posted this comment:

Dr. Davis,
I have spent the last 5 months eating a diet that completely eliminated all wheat products. It was very low carb, and consisted of relatively high protein (eggs, grass fed beef, grass fed raw cheese, oily fish, chicken), good level of olive oil, walnuts, fish oil (3 mg per day), raw vegetables, little bit of fruit. So I had good amount of monounsaturated fat as well as saturated fat from eggs and grass fed products.

My recent NMR showed:
LDL-p. 2,800
Small LDL particle 1700
Small HDL particle 20
HDL-C 40
LDL-C 114
Trigs. 224
Total chol 208

So I was disappointed. Where have I gone wrong? No wheat and sky-high LDL-p and 1700 small LDL particles.


This is indeed unusual. I see this perhaps 5 or 6 times over a year's time, while thousands of other people show the usual expected respone. I don't have Frustrated's lipoprotein panel prior to starting the diet, but I'll bet the starting panel was similar to this "after" panel.

The overwhelming majority of people who follow a diet like the one described--no wheat, limited carbohydrate, grass fed beef, fish, chicken, vegetables, limited fruit--obtain extravagant reductions in small LDL, increased HDL, and reduced triglycerides. So why did Frustrated end up with such disappointing results, values that potentially provide for high risk for heart disease?

There are several possibilities:

1) He/she is in the midst of substantial weight loss. When labs are drawn in the midst of weight loss, stored energy is being mobilized into the blood stream. This energy is mobilized as fatty acids and triglycerides which, upon entering the blood stream, cause increased triglycerides, reduced HDL, chaotic or unpredictable small LDL patterns, and increased blood sugar sufficient to be in the diabetic or pre-diabetic range. This all subsides and settles down to better values around 2 months after weight loss has plateaued.

2) Apo E4--If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the "rescue."

3) Apo E2 + Apo E4--It's possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.

4) Other variants--There are probably a dozen or more other genetic variants, thankfully rare, such as apo B and apo C2 variants, that are not generally available for us to measure that could influence Frustrated's response.

5) The low-carb diet is not truly low-carb--Frustrated sounds like a pretty sharp cookie. But it's not uncommon for someone to overlook a substantial source of carbohydrate exposure that triggers these patterns. Fruit is a very common tripping point, since people generally regard unlimited fruit as a healthy thing. This does not seem to be Frustrated's problem. Others indulge in quinoa, sweet potatoes, millet or other carbohydrate sources that look and sound healthy but, in sufficient quantities, can still trigger this pattern.

6) Other--Hypothyroidism, kidney disease, nephrotic syndrome, hypercortisolism and some other relatively rare conditions are worth considering if none of the above apply.

Anyway, that's the list I use when this peculiar situation arises. If obvious weight loss is not the culprit, the next step is apo E testing. However, the wrong response is to reject the low-carbohydrate notion altogether and just limit fat, since this typically leads to uncontrolled small LDL, high triglycerides, and diabetes. It can often mean limiting carbohydrates while also limiting fats. Just as with the combination of apo E4 with Lipoprotein(a), I lump many of these patterns into the emerging world of genetic incompatibilities, genetic traits that code for incompatible metabolic phenomena.


Comments (33) -

  • David Horry

    8/24/2011 6:03:44 AM |

    Hi Dr Davis,
    I am an apoe4 carrier. My trig=62, HDL=69; LDL-C=175 after 16 months on a carbohydrate restricted, gluten free diet. Wondering whether I need to also reduce my fat intake. But then what is left to eat? Making up the calorie difference with protein does not sound too healthy.

    David

  • Dr. William Davis

    8/24/2011 12:24:19 PM |

    Hi, David--

    I would urge you to NOT rely on the calculated LDL value, since on a low-carb diet with potential conversion of small to large LDL particles calculated LDL can substantially overestimate true LDL.

    The best: LDL particle number through NMR lipoprotein analysis. The next best: apoprotein B, widely available from nearly all labs.

    When you're armed with this information, then you can make an intelligent decision about diet changes.

  • Paul

    8/24/2011 1:43:34 PM |

    Regarding Item 6

    There was some traffic between Chris Kresser and Jimmy Moore on Twitter yesterday regarding whether low carb caused low T3 in susceptible individuals. Clearly bad news for heart health.

    I am a treated hypothyroid and this was my recent experience - I had gone low carb and ended up with an abscess in the roof of my mouth that needed antibiotics.  When tested, my T3 had fallen from 5.5 to 3.8 (RR 4 - 6.8) - however, my TSH was 0.672 (RR 0.35-4.5).  In the UK, this low T3 would normally would have been missed as there is a TSH only testing policy here unless the TSH is found to be outside the reference range - I elected to pay privately for the T3 test.

    I remain on low-carb (and wheat free of course) as it is the only approach which allows me to lose weight, and have increased my meds from 75T4+20T3 to 100T4+40T3.

    I would query whether you consider hypothyroidism to be rare. I suspect it is very common.

  • steve

    8/24/2011 6:52:16 PM |

    Hi Dr. Davis:
    What if the patient  followed the above diet, had a particle count of 2,100, but only 200 were small and HDL 69 and Trgs 66.  Would this be acceptable, and better than a particle count of 640, less than 90 small, HDL 64, Trgs 45, but on statin and Zetia?  Assume thyroid and D all normal, and Apo E3/3
    Thanks for all the input

  • Chris

    8/24/2011 7:26:24 PM |

    Hi Dr Davis,
    This post really hit home with me (and ironically this is my first visit to your site).  I had a heart attack 2 years ago (34 years old, ate well or so I thought, in great physical condition at 5'9" 150 lbs).  My cardiologist advised the usual low fat diet and pravastatin, and while my lipids are better than they were, I'm still very concerned they are not near where they should be.

    About 5 weeks ago I found the primal diet and began eating that diet.  Last week I had another lipid test and my numbers actually got worse (not by much).  Would you mind reviewing my numbers and if you have any suggestions I would appreciate it.

    8/31/2009 heart attack
    total chol 115
    LDL 74
    HDL 16
    Triglycerides 126
    VLDL 25

    07/19/2010 checkup
    total chol 138
    LDL 64
    HDL 33
    Triglycerides 203
    VLDL 41

    03/21/2011 Healthfair
    total chol 122
    LDL 69
    HDL 31
    Triglycerides 111
    VLDL 22

    8/19/2011 walk in lab:
    total chol 159
    LDL 98
    HDL 34
    Triglycerides 135
    VLDL 27

    Glucose 97
    hsCRP 1.2
    A1c 5.5

    Do you suggest giving the "primal" diet more time or do you suspect I may have another condition causing this?

  • Chris

    8/24/2011 7:36:33 PM |

    Also in May of this year I had the following tests done at the cardiologists:
    Date of service: May 13, 2011
    CAT Scan MRI & NMR
    Diagnostic Radiology X-Ray
    Cardiovascular Stress Test

    I was told everything was fine.

  • Might-o'chondri-AL

    8/25/2011 2:28:51 AM |

    Track Your Plaque once gave a desirable level of ApoB  as under 70 mg.dl as surrogate marker for the desirable LDL particle number (which is less than 700 nm/l) if one only has ApoB testing.  Maybe some one else can recall the conversion ratio of ApoB into LDL particle numbers.

    A cholesterol fractions normal transfer from HDL to ApoB is governed by  the cholesterol ester transfer protein (CETP). Genetic variants of CETP can cause differences in the numbers of  small LDL and sparse CETP can cause cholesterol to stay stuck in HDL  ( CETP has little impact on numerical % of HDL). So genetic variants of ApoB can influence the levels of cholesterol shunting around.

    In  the liver ApoB normally gets it's lipids when ApoB goes into a cell's endoplasmic reticulum. And if the ApoB doesn't improperly degrade ( ApoB needs "enough" microsomal triglyceride transfer protein SREBP-1c, the sterol regulatory element binding protein, to avoid degrading) then ApoB can pick up triglycerides to form VLDL molecules. So, if there is not enough liver SREBP-1c  then lipids can't be transferred over to make triglyceride rich VLDL; conversely lots of liver SREBP-1c provokes extra VLDL.

    Doc says carbohydrate related  post-prandial high glucose not only induces  more VLDL output  from the liver but that this is part of the mechanism whereby carbs can boost body fat. High carbohydrate intake causes extra lipo-genesis in the liver because a significant  reflex of high post -prandial liver insulin is a signal that upregulates SREBP-1c. Then SREBP-1c expression rises and that in turn activates genes for the lipogenic enzymes (ex: fatty acid synthesase & acetyl CoA carboxylase),

    Rogue readings of VLDL may be due to viral hepatitis proteins, flavivirus and pestivirus, which can decrease VLDL formation and secretion while dropping levels of ApoB. Viral proteins "smear" onto lipids and this blocks SREBP-1c action and viral proteins can also "stick" on to the HDL protein fraction ApoA1 inside of the  liver cells' Golgi Apparatus. Thus in chronic liver disease and hepatitis circulating VLDL associated triglycerides eventually decreases so there are more non-VLDL  triglycerides in play.

  • Jack Daniels

    8/25/2011 11:49:38 AM |

    Hi Dr. Davis,

    I was just wondering, due to many healthy cultures including the kitava, okinawan's...etc, who indulge in rather high carb intakes and retain rather pristine health, is it possible that high trigs, low hdl..etc may just be a lipid profile reflecting high carb* intake rather than suggesting atherogenic buildup ?

    *when based on safe starchy type carbs

  • Dr. William Davis

    8/25/2011 3:42:09 PM |

    Hi, Paul--
    In the population I see, hypothyroidism is exceptionally common, both in people on low-carb but also in people prior to initiating their low-carb efforts. So, without a formal analysis, I'm skeptical that low-carb in and of itself causes free T3 to drop.
    There are also numerous inhibitors of the 5'-deiodinase enzyme that converts T4 to T3, including perchlorate residues from fertilizers in vegetables and polyfluorooctanoic acid, the residue of non-stick cookware, just to name a couple.

  • Dr. William Davis

    8/25/2011 3:43:29 PM |

    This is the BIG unanswered question. Sadly, there are next to no data that speaks to this question.
    My day to day answer has been to 1) eliminate small LDL, then 2) maintain LDL particle number 1500 nmol/L or less. But that is pure speculation on my part.

  • Dr. William Davis

    8/25/2011 3:45:22 PM |

    Hi, Chris--
    Something doesn't compute: Every panel you list is the pattern of excessive carbohydrate consumption and/or sensitivity. So something is sneaking through. There is no question that a "primal" or low-carbohydrate approach works for this pattern.  

    You might also have an Apo E2 gene that amplifies carbohydrate sensitivity.

  • Dr. William Davis

    8/25/2011 3:47:01 PM |

    Hi, Might--
    As always, you are an incredible fountain of unique insights!

  • Dr. William Davis

    8/25/2011 3:47:44 PM |

    Sorry, Jack, I didn't understand your question. Could you rephrase?

  • Chris

    8/25/2011 4:28:55 PM |

    Thanks.  I've only been eating primal/paleo for about five weeks, so only the last panel would reflect this (if thats enough time to be reflected in my lipid panel).  I will re-test after another few months.

  • Jack Kronk

    8/25/2011 4:53:55 PM |

    Dr Davis. Jeez. This sounds similar to my story (Frustrated's #s). I have eaten Paleo for over a year now, I have done exceedingly well with body composition in that time. See my "Share You Paleo Before and After" here ---> http://paleohacks.com/questions/7058/share-your-paleo-before-and-after/28493#28493. But this only adds to the confusion for me (and others).

    For some reason, my labs came back on July 8, 2011 with small dense LDL and pathetic HDL at 40, despite a diet rich in GF beef, pastured eggs, bacon, pasture butter, coconut oil, ghee, veggies, starch and fruits only for carb sources, etc etc. I spend mega money to eat well. We don't mess around. I posted my VAP panel results on PaleoHacks last month and it has resulted in a lot of attention on this very subject. Chris Masterjohn weighed in with his thoughts. Dr Kruse wrote a blog all about it.

    http://paleohacks.com/questions/50347/hack-jack-kronks-vap-test-results

    I will be retesting again in about a month, as I have made some changes, like eliminating bananas, less heavy cream and pasture butter, etc.

    My lab said it's $390 just to do the ApoE test. Is this a normal price? If not, where do you recommend people get the testing done?

    I'm genuinely confused. It's like my body is saying... "Yes Jack. Good job. I am very happy with what you are eating. I will continue to keep fat off and pack on muscle." But then my heart is saying "Nooooo. Stop!!"

    How can this be?

  • Jack Daniels

    8/25/2011 5:29:06 PM |

    I was questioning if your pathological interpretation of a blood lipid profile that exhibits low hdl and high triglycerides, could instead just be a reflection of a high carb diet rather than suggesting an increased risk for CVD. I was referencing a couple high carb cultures, such as the Okinawa and the kitava, who exhibit a similar lipid profile but have very small incidence of CVD. Compared to other cultures with similar lipid profiles, such as the Swedes and Americans, who have much higher rates of CVD would suggest it's more about quality of blood lipids rather than their certain partitioning. Hopefully that's a better re-phrasal?

  • steve

    8/25/2011 5:57:08 PM |

    This is the BIG unanswered question. Sadly, there are next to no data that speaks to this question.
    My day to day answer has been to 1) eliminate small LDL, then 2) maintain LDL particle number 1500 nmol/L or less. But that is pure speculation on my part.

    My understanding related to your above comment is that large LDL is nearly as athrogenic as small LDL and that you want the particle number low with mix between largle and small LDL taking secondary importance.  Of course, that is based on a diet that the avg american consumes,  and not on the low carb with wheat sugar and cornstarch elimination you advocate.
    Am i under a correct understanding regarding large LDL being dangerous as well and therefore the need to minimize this even with your dietary recommendations?  Also, i thought you advocated a total LDL particle number to approach 600?  Is your 1500 number a revised viewpoint based on newer diet or clinical observations?
    Thank you again.

  • Might-o'chondri-AL

    8/25/2011 7:53:36 PM |

    Server error blocking me again ... testing after hour passed.

  • Might-o'chondri-AL

    8/25/2011 8:49:34 PM |

    ApoE is crucial to VLDL & chylomicron formation. Variant ApoE 2 less efficient at transfering lipids to liver and is binding lipids up an extra +/- 2%; result is that lipids take longer to clear from circulation and more can go wrong. From my notes, here is the rate some ancestral populations have at least 1 copy of ApoE2: 2-4% of Mexican-american & American Indian, also  3-4% of Japanese & West African. There is 0% of South American Indians with ApoE2 and one wonders which variation of  ApoE  might be in Kitava melanesians. .
    ApoE4 degrades easiest of all ApoE forms, leaving protein fragments in cell's cytosol which then can affect a mitochondria's lipid binding region impairing the performing of  tasks. In addition ApoE4 fragments diminish gene PPAR gamma expression; and this depresses the desirable bio-genesis of mitochondria. The affects on mitochondria may be why high levels of dietary fat is problematic for ApoE4 individuals; there may be too sparse output of viable mitochondria and mitochondria membranes are involved in how efficiently we burn fat or glucose.  .
    In light of these ApoE4 nuances it is interesting to know that fasting raises free fatty acid levels (from fats in the body and not loose fats from recent food); and then those free fatty acids upregulate  gene for PPAR gamma in the liver. Fasting makes one put out ketones  because of the extra PPAR gamma programing and this ketogenesis is also one way that activating more PPAR gamma improves insulin sensitivity. This suggests to me that individuals with ApoE4 may (?) find some benefit from modified fasting; possibly something like decidedly fewer meals in a day and also simply not grazing on snacks (ie: in addition to just trying to select what foods to eat) between meals that are regularly spaced apart (ie: very early breakfast to let meal times spread put more evenly) .

    Finally again from my notes, here is the rate some ancestral population have at least 1 copy of ApoE4: .14-19% Germans & Finns, also 7-12%  French & Italians. Of course America is one of the world's melting pots so an individual's propensity for ApoE 4 & ApoE 2 is hard to pin point.

  • Jack Kronk

    8/25/2011 9:02:36 PM |

    This is fascintaing Might. I have been guilty of snacking too much. All healthy snacks, but still the concept of grabbing bites of delicious foods between meals might be messing with my liver. For my VAP test, I did not fast. Chris Masterjohn believes this was the reason (or at least the reason for dismissal) of my increase in triglycerides in the blood. I am most concerned about my low HDL, because if I raise my HDL, I believe my LDL will become more dominantly pattern A.

  • Paul

    8/25/2011 11:04:33 PM |

    Thank you for the reply.  I would like to share a speculation.  Strict low carb means gluconeogenesis means an increased cortisol demand? OK in young fit Paleo men, but what about long-term un(der)treated hypothyroid individuals?

    In "Safe Uses of Cortisol", Dr William Mck Jefferies (p. 183/4) observes that low dose (20mg/day) of hydrocortisone taken by a patient with hypothyroidism increases T3,  lowers T4 and improves patient energy levels suggesting such low dose cortisol enhances T4 to T3 conversion.

    Could VLC, by putting demands on potentially weakened adrenals, have the opposite effect?

  • Might-o'chondri-AL

    8/26/2011 12:10:58 AM |

    HDL molecules hold triglycerides (there are 45 different variations of triglycerides in circulation, which are based on what their esterified fatty acid component is), cholesterol esters (about 13 - 27% of the HDL surface particles), shingomyelins and glycerophospholipids. HDL's principle proteins are +/- 70% ApoA1 and +/- 20% ApoA2;  yet any changes in the ratio of ApoA2 from genetics (Kitavans?, I propose so) or drugs (ex:fibrates) can have effects.  

    Usually people with low levels of  HDL have more trigs on their HDL surface (compared to those with high levels of HDL) and low HDL is associated with the passing of more cholesterol esters to VLDL & chylomicrons. Also, when HDL trig levels go up that makes it easier for the liver enzyme hepatic lipase to cleave off more ApoA1 for the kidneys to clear away; and that further tends to keep HDL levels low.  

    In comparison people with high levels of HDL have more cholesterol esters on their HDL; which may be due in part to cholesterol esters affinity for ApoA1 in HDL. And statisticly high levels of HDL are usually associated with bigger ("large") HDL molecule size. Both large HDL and ApoA1 are considered to be more protective factors against atherosclerosis.

    I suspect that Kitavan melanesians' low HDL fortuitously correlates with a geneticly higher than normal % of ApoA2; and ApoA2 configures more deeply nestled into the HDL complex than ApoA1. It (ApoA2) influences molecular  interactions all the way to the HDL surface and limits certain lipid dynamics.

    ApoA2 holds ApoA1 off of mature HDL molecules and this results in a shunting of ApoA1 into forming up the pre-Beta HDL; these lipid poor ApoA1 configurations are great at doing reverse cholesterol transport that brings back cholesterol  to the liver for excreting as bile acids. Those pre-Beta HDL are small, yet notably excellent at taking cholesterol away from nefarious macrophage foam cells (the large HDL  molecule also picks cholesterol nicely from foam cells).

    Experiments see that preceeding type of change with fibrate drug doses, which only minimally raise HDL & ApoA1 yet increase the ApoA2 amount in HDL by over 25%. Since fibrates are agonists activating the peroxisome proliferator activiated receptor PPAR alpha it might be instructive to see if anything in the Kitavan diet is a similar agonist, such as heirloom tuber roots derived from wild yam with high diosgenin content (diosgenin is well known to affect PPAR gamma).

  • Dr. William Davis

    8/26/2011 5:15:14 PM |

    Hi, Steve--
    There really is no final word on what the desired endpoint is when small LDl has been eliminated and you have pure large LDL. In a perfect world, I'd wish for a particle number of 600 nmol/L with pure large LDL. But I'm no longer entirely sure this is necessary. But this remains anecdotal. There are no formal data, nor do I have any formal analysis of our own data on this question.

  • Dr. William Davis

    8/26/2011 5:17:32 PM |

    Hi, Jack--
    Don't know, since I've never seen any genuine lipoprotein data on these populations. Most of the data I've seen has been total cholesterol, which is far too crude to draw any conclusions from.

    Have you seen lipoprotein data on these populations?

  • Jack Kronk

    8/26/2011 5:33:12 PM |

    Might. Do you suspect that I have low HDL and highish Trigs/VLDL in the blood for this reason? I do take in a fair amount of protein (including a whey isolate daily). Also, plenty of eggs. Does dietary protein consumption have any actual affect on HDL's principle protein and/or surface cholesterol esters?

  • The Surgical Blog

    8/27/2011 3:52:44 AM |

    Yes Jack Kronk, it seems that you have low HDL and highish Trigs, I do also think.

  • Nancy Milligan

    8/28/2011 7:51:57 PM |

    Just wanted to comment. I've been a long time low carb person, gluten-free too. I also had my thyroid ablated with RAI many years ago. I have found, as have many low carbers, that my reverse T3 is very high and Free T3 is scraping the bottom or below the range.

    Unfortunately this does seem to be a common side-effect of low carb eating. It's even documented in studies on the topic.

    We had a low carb eater recently watching his LDL climb to very high levels after he began eating low carb. He started taking cytomel and his LDL is coming down very nicely.

    Did he get a sudden onset of hypothyroidism that just coincided with low carb eating? I suppose that's possible, but I do think there's something more going on.

    I'm taking Armour thyroid myself, but I still have the tendency to turn T4 into reverse T3 and I suppose that means the Free T3 can't get to the receptors. I'm going to experiment with raising my carbs a little higher and sticking to things like yams and squash for my carbs.

  • Espen Rostrup

    8/31/2011 12:33:45 PM |

    Dear dr. Davis,
    I just attended the annual cardiology congress of the European Society of Cardiology. Amongst others, the new guidelines on dyslipidemia were presented and I had the opportunity to ask the working group the question you mention above in your first of opportunities : What about measuring lipids during an ongoing substantial weight loss? The were not able to give me a proper answer.
    Do you have any scientific references saying that weight loss induce a temporary dyslipidemia or is it based on your experience?
    I would be most thankful for your comment on this.
    Best regards
    Espen Rostrup, MD, PhD-fellow
    Bergen, Norway

  • Dr. William Davis

    9/2/2011 2:56:29 AM |

    Dr. Rostrup--

    Unfortunately, I know of no published data documenting this effect. However, I have seen it hundreds of times. It is, in fact, quite predictable: drop in HDL, rise in triglycerides, variable small LDL effects, increased blood glucose. It all subsides and improves over time.

    It would indeed be an interesting study to chronicle the changes serially in a small number of people.

  • Dana

    9/8/2011 8:28:14 PM |

    I am also seeing a heck of a lot of omega-6 intake there.  Also, the healthfulness of monounsaturated fats is a bit overstated.  I've heard of studies where they had 3 groups of people.  One got their normal saturated fat, one group replaced the saturated fat with olive oil and the third group replaced the sat-fat with corn oil.  The corn oil eaters did the worst in health outcomes, but the olive oil group wasn't great either--both groups that replaced the sat-fat did more poorly.  I've heard of other studies where lard was compared with olive oil and the lard-eaters turned out better.  Bottom line, the human body seems to like saturated fat best.  (Lard is not as saturated as butter, but it is more saturated than olive oil.)  If I were in a position to make medical recommendations (I'm not), I'd tell someone like this to ixnay on the plant oils for a while and see what happens.

    It should be noted that one of the more dubious selling points of grass-finished meat is that it is lower in saturated fat.  To me, this is not a selling point.  If this person were only getting PUFAs from their grass-finished meat it would be one thing--at least then it'd be closer to a 1:1 omega-6/omega-3 ratio.  But that's not what's going on here.  If they were just eating the fish they might still be OK (depends on the fish--cold-water is better).  But they're adding in walnut oil and chicken consumption and those are going to add more omega-6, even if the chicken's pastured.

    I'm curious what this person's inflammation markers are.  If they're off the map the LDL may still be high because the body's trying to repair the inflammation.  That would explain the low HDL too; LDL takes cholesterol out to the body from the liver, and HDL returns it to the liver.  If the cholesterol is *needed* elsewhere in the body then of course it won't be returned to the liver.

    Even if inflammation markers are normal, this person's diet may not be meeting their needs for saturated fats in the cell membranes, which may mean they need more cholesterol in their cell membranes to try to make up the deficit.  Not an ideal situation.

    Get the PUFA reduced, get the inflammation down if any, see what the lipids do and then we can talk about weird genes.  Absent the necessary DNA profile we really don't know, anyway.

  • Dana

    9/8/2011 8:31:06 PM |

    "just eating the fish" = in addition to the pastured beef.  I would not drop beef in favor of fish, there's too much good nutrition a person would be giving up, but fish in addition to beef's not bad.  Chicken used to be a luxury food, you had it on Sundays if then.  Best that it's relegated to that role again.  The white meat is too dry and the dark meat's rife with PUFAs.  Other fowl are not much better.  A foray into the USDA's nutritional database is an eye-opener.

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