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This one's down to me! Please accept my apologies for this - I'll see to it that the developer responsible for this happening is given 20 lashes (but only after he or she has fixed this problem).

Homocysteine and coronary plaque

8. April 2007 William Davis (4)
If you’ve watched the news over the past year, you know that doubt has been cast over the idea that reducing homocysteine blood levels with high doses of B vitamins (B6, B12, and folic acid, or B9) results in reduced risk for heart attack.

Is the homocysteine concept dead? Shall we empty our bottles of costly B vitamins into the trash and move on?

I don’t think so. As detailed in one of our Track Your Plaque Special Reports from a few months ago, I think the homocysteine issue still deserves lots of respect and further investigation. After all, hundreds of clinical studies have connected higher homocysteine levels with greater risk for heart disease, stroke, and aneurysm. Numerous studies, for example, have repeatedly and consistently demonstrated a tripling of heart attack risk when homocysteine levels exceed 14 ?mol/l. Can we dismiss this association because several more recent studies—NORVIT, HOPE, and VISP—suggested that, when starting homocysteine levels are 12.5, that B vitamin supplementation does not reduce heart attack risk?

I think there’s lots more to know about the homocysteine connection. That said, I have never seen a patient who I thought had heart disease strictly because homocysteine was increased.

I believe that we can at least use homocysteine as an index of lifestyle: the higher the homocysteine, the poorer the diet, or the less effective the absorption of B vitamins (especially vitamins B12 and folic acid). Homocysteine levels of <9 micromol/l suggest both adequate intake and absorption of these B vitamins.

If homocysteine is tightly connected with risk for heart disease, yet supplementation of B vitamins fails to reduce risk, might there be another means of connection? Or, could both homocysteine and heart disease be connected in some way that has nothing to do with B vitamins?

Don’t close the book on homocysteine. Just because conventional experience fails to draw connection does not necessarily mean that none exists. If it’s any consolation, taking B vitamins has been correlated with better memory, concentration, and other health benefits, even if no reduction in heart disease develops.

Big heart scan scores drop

6. April 2007 William Davis (0)
High heart scan scores of, say, greater than 1000 are more difficult to reduce than lower scores.

I learned this lesson early in the experience of trying to drop scores. In the first few years of trying to drop scores, I saw relatively modest scores of 20, 50, or 100 drop readily, even when the usual targets were not fully achieved, and even before the incorporation of some of the more exciting recent additions to the Track Your Plaque program, like vitamin D.

But big scores of 1000, 2000, or 3000 are a tougher nut to crack. In the first few years, what I usually saw was a slowing , or "deceleration," of growth from the expected rate of annual score increase of 30% that would continue for a year or two, followed by zero change. In the first year of effort, for example, a score increase of 18% was common. 10% was common in year two, then finally zero change in year three. Somehow, the more plaque you begin with, the more "momentum" in growth is present and the longer it takes to stop it. Kind of like stopping a compact car versus stopping a freight train.

But more recently, I'm seeing faster drops. Today, Charlie came to the office to discuss his second heart scan. 18 months earlier, Charlie's first scan showed a score of 3,112, high by anybody's standard.

His repeat score: 3,048. While the drop is relatively small on a percentage basis and may even fall within the expected rate of error for heart scans (which tends to be <2% at this high a score), I told Charlie that it still represented a huge success. Not only did he not increase his score by the expected 30% per year, he also brought a charging locomotive to a rapid stop.

Next year, Charlie is targeting a big drop. Given the tools he now has available, I'm optimistic that he will succeed.

Watch for the Track Your Plaque May, 2007 Newsletter in which we will detail Charlie's story further.

Does the American Heart Association diet reduce heart disease?

5. April 2007 William Davis (0)
If you have a heart attack and land in the hospital where, invariably, you will have a heart procedure. Or, if you get a stent or coronary bypass operation, sometime before your discharge from the hospital, a well-meaning hospital staff dietitian will provide instruction in the American Heart Association (AHA) diet.

Does this diet reduce the risk of heart disease?

The answer depends on where you start. If you begin with a conventional American diet that is enormously influenced by convenience, food manufacturers like Nabisco, General Mills, Quaker Oats, ADM, and Cargill, or food distributors like McDonald’s, Pizza Hut, and Taco Bell, then the American Heart Association diet is indeed an improvement. But just a small one. If LDL cholesterol is the yardstick, the average reduction in LDL is between 10 and 15 mg/dl. This is the same amount of change you’d experience by adding 1 tablespoon of oat bran to your diet. Hardly worth boasting about. HDL, triglycerides, blood glucose, and body weight do not change.

The diet could be substantially better. After all, it’s become common knowledge that other diets, such as the so-called Mediterranean diet, the South Beach Diet, and similar broad projects result in far greater changes than the AHA diet dispensed by your hospital and cardiologist. These diets more effectively reduce LDL, raise HDL, reduce triglycerides, reduce C-reactive protein, reduce blood pressure. Diets like South Beach also yield substantial weight loss and reversal of diabetic tendencies, with the magnitude of benefit dependent on the amount of weight lost.

Why this stubborn adherence to the outdated concepts articulated in the AHA diet? Cardiologists would argue that insufficient data has been generated to permit widespread application of these diets. They also differ on whether they really work. Of course, the majority remain ignorant and dismiss them as fad diets.

A little digging into the financial disclosures of the AHA suggests another, more malignant influence: who is paying the bills? Until recently, drug manufacturers were major contributors to the AHA. However, more recently AHA administrators have become sensitive to the public perception that they might be nothing more than a voice box for the drug industry. They have since limited contributions from the drug companies to 8% of annual charitable revenues.

The drug manufacturers have been replaced by the food industry. In addition to food manufacturers that make the cereals on your grocery shelf, it includes the multi-national conglomerates that produce unimaginable revenues and carry enormous political clout, like ADM and Cargill. Ever wonder how it is that Honey Nut Cheerios received a “Heart Healthy” endorsement from the AHA?

The AHA diet does not provide the answers we’re looking for, not even close. It is a perversion from an organization that has its strings pulled by industry. The answers to health will not come from the AHA, AMA, the American College of Cardiology, the American Hospital Association, and it won’t come from your doctor. It won’t come from a titillating report on the evening news or Good Morning America. It will come from collective and expanding wisdom placed directly into the hands of the public. It will be untainted by the temptation of drug industry dollars. It will not be dirtied by million dollar contributions, or the multi-million dollar behind-closed-doors lobbying of the food manufacturers. It will come from the truth relayed to the healthcare-consuming public. I hope you recognize it when you see it.

If you want a healthy diet for your heart, throw away the pamphlets from the AHA unless you are partial to bread, breakfast cereals, corn, and the supporters of their misguided nutritional advice.

Vitamin K2 and coronary plaque

4. April 2007 William Davis (1)
The vitamin K2 story, though still preliminary, is becoming increasingly interesting from the perspective of CT heart score reduction.

The origin of this concept came from some unexpected observations. One, the observation that osteoporosis (lack of bone calcium that leads to fractures) arises from deficiency of vitamin K2. Two, deficiency of K2 leads to unrestrained calcium deposition in animal models, leading to heart attack in just weeks.

Vitamin K2 has been largely ignored for years, since the more widely understood K1 is rarely deficient. K1 deficiency can occur from prolonged antibiotic use, or from severe malnutrition. But deficiency in otherwise well people is very uncommon. Vitamin K2, however, may be a different story. Deficiency may be common.

The Rotterdam Heart Study of cheese-eating Dutch showed that greater K2 intakes resulted in a halving of heart attacks. Cheese (traditional varieties, not Velveeta or other make-believe cheese products) is a modest source of K2, as is the Japanese native food, natto. (If you've ever seen natto, I dare you to eat it. I have a pretty strong stomach and curiousity for food, but natto is the one thing I could not eat--it is truly horrible.)

The weight of evidence suggests that vitamin K2 supplementation may prove to be a useful addition to your coronary plaque control program. Clearly, more data are needed, particulary therapeutic obserations, i.e., observing people who take dose X of a K2 prepartion and tracking some feedback measure, e.g., bone density, CT heart scan score, "events" like heart attack, etc.

Nonetheless, the K2 story is clearly worth reading about, perhaps even considering supplementation. Please watch for the Special Report on the www.cureality.com website in the coming days.

Exercise and blood pressure

4. April 2007 William Davis (5)
The media has gotten a hold of a case report from the University of Maryland describing a 51-year old physician who, despite being a long distance runner, had a high heart scan score.

An example of the report can be found at

Heart Disease In A Marathon Runner: Is Too Much Exercise A Bad Thing?

http://www.sciencedaily.com/releases/2007/03/070315091100.htm in Science Daily.



"The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range."


When this man was put on a treadmill for a stress test, his blood pressure skyrocketed from a normal 118/78 to 230/78--extremely high, even for exercise. The physicians reporting the case raised the question of whether long-distance running represents a risk for heart disease and if the high blood pressure with exercise is a contributor or cause of the high heart scan score.

These are phenomena we are very familiar with. We have stressed the importance of exercise blood pressure as a trigger for coronary plaque for years. While 230/78 is clearly too high, we find that any blood pressure over 170/80 with exercise adds to the fire and can trigger plaque growth.

However, I think it is absurd to suggest that marathon running itself is a trigger of coronary plaque. I think it is far more likely that the person described in the report had lipoprotein(a), a potent trigger for both exercise-induced hypertension and high CT heart scan scores in seemingly well people. He likely also suffered from a deficiency of vitamin D deficiency, another contributor. There's no need to indict exercise.

If you are in the Track Your Plaque program, you know that stress tests are of questionable helpfulness for the detection of hidden heart disease. But they are useful for assessment of blood pressure responses during exercise. If BP exceeds 170/80 at 10 mets (a measure of exercise effort achieved by walking 3.4 mph at a 14% grade for 3 minutes), then blood pressure may be a contributor to your heart scan score.

"Fish oil is stupid"

3. April 2007 William Davis (13)
"Fish oil is a waste of time and money. It's stupid. Just stop it."

So a patient of mine was advised by another physician when he complained that he occasionally experienced a fishy aftertaste.

This attitude perplexes me. After all the confirmatory data that support the enormous health benefits of omega-3 fatty acid supplementation, including the 11,000 participant GISSI-Prevenzione Trial, you'd think this attitude would be history. What's a little fish aftertaste when heart attack risk is slashed 28%?

Perhaps the tendency to pooh-pooh fish oil is because it's available as a nutritional supplement. This shouldn't make fish oil appear inconsequential. Far from it.

If you witness the extraordinary power for fish oil to reduce triglycerides, you will be immediately convinced of its effectiveness. The ability of omega-3 fatty acids from fish to eliminate intermediate-density lipoprotein (IDL), the persistent abnormal lipoprotein which signals an inability to clear dietary fats from the blood, can also convince you. More than 90% of people with excessive IDL have it completely eliminated by 4000-6000 mg of fish oil (providing 1200-1800 mg EPA + DHA) per day.

The fact that fish oil is available as a prescription "medication," as well as an over-the-counter supplement, causes some physicians to dismiss the power of the supplemental form. This is nonsense. The over-the-counter form is every bit as effective as the prescription form.

The makers of prescription Omacor also make the claim that their preparation is safer and purer. That may be true, but I'd like to see independent verification from the FDA, USDA, or an unbiased organization like Consumer Reports before I accept their marketing as fact--particularly at $120 to $240 per month! If Omacor proves to contain substantially less mercury and pesticide residues, then that will need to be factored in. (Please note that both Consumer Reports and Consumer Labs measured no substantial mercury or pesticide residues in their analyses of 16 and 41 brands, respectively.)

I try to persuade my colleagues that the idea of taking supplements is a wonderful trend that allows people to express ownership of their own health. What people need is guidance, not salesmanship for a more expensive version, nor dismissal of nutritional preparations that actually possess considerable benefits.

More Vitamin D and HDL

2. April 2007 William Davis (8)
I’m seeing more and more of it and I am convinced that there is a relationship: significant boosts in HDL cholesterol from vitamin D supplementation.

To my knowledge this remains an undescribed and uncharacterized phenomenon. There have been several observers over the last two decades who have noticed that total cholesterol shows a seasonal fluctuation: cholesterol goes up in fall and winter, down in spring and summer; year in, year out. This phenomenon was unexplained but makes perfect sense if you factor in vitamin D fluctuations from sun exposure.

I have come across no other substantiating evidence about fluctuations of HDL. But I am convinced that I am seeing it. Replace vitamin D to a blood level of 50 ng/ml, and HDL goes up if it is low to begin with. If HDL is high to begin with, say, 63 mg/dl, it doesn’t seem to change.

But, say, starting HDL is 36 mg/dl. You take niacin, 1000 mg; reduce high-glycemic index foods like breakfast cereals, breads, cookies, bagels, and other processed carbohydrate foods; exercise four days a week; add a glass of red wine a day; even add 2 oz of dark chocolate. You shed 15 lbs towards your ideal weight. After 6 months, HDL: 46 mg/dl. Better but hardly great.

Add vitamin D at a dose of, say, 4000-6000 units per day (oil-based gelcap, of course!), and re-check HDL two or three months later: 65 mg/dl.

I’ve seen it happen over and over. It doens't occur in everybody but occurs with such frequency that it’s hard to ignore or attribute to something else. What I’m not clear about is whether this effect only occurs in the presence of the other strategies we use to raise HDL, a “facilitating” effect, or whether this is an independent benefit of HDL that would occur regardless of whatever else you do. Time will help clarify.

We are tracking our experience to see if it holds up, how, and to what degree on a more formal basis. Until then, a rising HDL is yet another reason—-among many!-—to be absolutely certain your 25-OH-vitamin D3 level is at 50 ng/ml or greater.

How high is an ideal vitamin D blood level? If 50 ng is good, is 60 or 70 ng even better? Probably not, but there are no data. We have to wait and see. Unlike a drug that enjoys plentiful “dose-response” data, there are no such observations for vitamin D into this higher, though still “physiologic,” range.

Thin ice

2. April 2007 William Davis (0)
How long can an industry built on ignorance and deception continue its practices in the new Information Age?

I don’t think it can for long. I talk to hospital administrators who believe that their source of competition is the hospital across town, battling for the same patients. I speak to my colleagues, the cardiologists, who believe that the current model is sustainable—take every willing body to the catheterization laboratory or operating room for heart procedures, the revenue-generating engine of income and expanding heart programs.

I speak to primary care physicians, who are dumbfounded and perplexed and have no idea which way things are going. They are trapped in a peculiar position: most have signed contracts and are employees of the hospital. They are legally bound to support the cardiologists who take anybody possible to the catheterization laboratory or direct patients to other profit-making procedures.

Much of this system depends on the willingness of the participant, meaning you and the health care seeking public. What happens when the truth comes out and disseminates widely through the thinking populace? What happens to hospitals and physicians and the vast structures they’ve built when the bottom drops out for 50% of their “market?

The proverbial cow manure will hit the fan. Upheavals in the medical industry will rival the changes that the automobile or telephone brought early in the last century. Cardiologists, immense hospital heart programs, and the vast economic infrastructure they spawned will go the way of stage coach manufacturers and the telegraph.

What form will the broad exposure of detailed information in health take? I’m not sure, but it will certainly come. The collaborative efforts that created the Linux operating system and have challenged the monopoly of Microsoft Windows, or the emergence of the extraordinary Wikipedia as a repository of human knowledge that dwarfs the venerated Encylopedia Brittanica, will eventually overtake the American medical system, the heart disease industry in particular.

If you base your future on the welfare of your local hospital or the manufacturers of stents, operating room equipment for heart bypass, or similar industries, watch out. The ice is thin. And as the spring warms the air around you, it gets thinner.

The Track Your Plaque program is our first step in broadcasting the message of self-empowerment in heart health care and an attempt to wrestle control away from the profit-seeking forces that dominate. As we grow, we not only hope to broadcast the message more widely, but expand the message to other areas of health. I predict that the collaborative, let’s-all-pitch-in-and-help spirit of the Information Age, “version 2.0,” will spark the change.

Vitamin D and cancer

30. March 2007 William Davis (0)
Although this is a Blog about heart scans and heart disease, I came across a helpful video from Dr. Joseph Mercola about vitamin D and cancer that's worth viewing. Though I do not agree with many of Dr. Mercola's on-the-edge views, he does come up with some good thoughts and, in this instance, a useful educational tool about vitamin D.

You can view his video (which he claims crashed his server, due to the excessive demand for downloads) by cutting and pasting the address into your URL bar (above):

http://v.mercola.com/blogs/public_blog/How-to-Reduce-Your-Risk-of-Cancer-By-50--8790.aspx

Also, for my many patients who I've directed to look in my Blog for Dr. Reinhold Vieth's webcast presentation on vitamin D, here's the address:

http://tinyurl.com/f93vl

Perhaps I carry on too much about vitamin D. But I've come to respect this "nutrient" as among the most powerful strategies I've seen for dramatically improving control over coronary plaque growth as well as other aspects of health, as Drs. Mercola and Vieth eloquently detail.

Lipoprotein(a), menopause, and andropause

30. March 2007 William Davis (0)
Lipoprotein(a) is a curious lipoprotein. Not only is it a genetic pattern with numerous variations, it is also one that shows a predictable age-dependent rise.

Women in particular are prone to this effect, men to a lesser degree. As we age, many hormones recede, particularly growth hormone, testosterone, the estrogens (estradiol, estriol, estrone), progesterone, and DHEA, among others. This is not a disease but the process of senescence, or aging.

When we're young, estrogens, testosterone, and DHEA all exert suppressive effects to keep lipoprotein(a), Lp(a), at bay. But as a woman proceeds through her pre-menopausal and menopausal years, and as a male passes through his fourth decade, there is an accelerated decline of these hormones. As a result, Lp(a) crawls out of its cave and starts to sniff around.

Typically, a woman might have a Lp(a) of 75 nmol/l (approximately 30 mg/dl) at age 38. Ten years later, at age 48, her Lp(a) might be 125 nmol/l (app. 50 mg/dl), all due to the decline of estrogens and DHEA. A parallel situation develops in males due to the drop in testosterone. For this reason, it may be necessary to re-check Lp(a) once after the fourth decade of life if you've had a level checked in your younger years.

This opens up some interesting therapeutic possibilities. If receding hormones are responsible for unleashing Lp(a), hormones can be replenished to reduce it. In males, this is relatively straightforward: supplement human testosterone and Lp(a) drops about 25%.

In women, however, it's a bit murkier, thanks to the negative experince reported using horse estrogens (AKA Premarin) in the HERS Trial and Women's Health Initiative. You'll recall that women who take horse estrogens and progestins (synthetic progesterone) do not experience less heart attack and develop a slightly increased risk of endometrial and breast cancer. There was, however, a poorly-publicized sub-study that showed that women with Lp(a) experience up to 50% fewer heart attacks on the horse/synthetic combination.

Wouldn't it be nice to have a large trial examining the safety/advisability of human estrogens and progesterone? To my knowledge, no such confident study in a significant number of women exists, since there's so little money to be made with human hormonal preparations.

For these reasons, we use lots of DHEA, generally at doses of 25 to 50 mg per day. It makes most people feel good, boosts energy modestly, increases muscle, and reduces Lp(a) up to 18% in women, a lesser quantity in men.
The exception to low-carb

The exception to low-carb

31. July 2011 William Davis (60)
I witness spectacular results restricting carbohydrates, both in the office as well as in my online experiences, such as those in Track Your Plaque. Of course, the diet I advocate is not just low-carb; it starts with elimination of wheat (for a long list of reasons). So the diet is wheat-free in the setting of low-carbohydrate.

What does this accomplish? Here's a partial list:

--Weight loss-Specifically, loss of visceral fat, the kind hinted at on the surface as "love handles" or what I call "wheat belly."
--Reduced blood sugar and HbA1c (reflecting prior 60-90 days glucose)
--Marked reduction in small LDL and triglycerides, increased HDL
--Reduced inflammatory measures like c-reactive protein
--Reduced leptin and leptin resistance, increased adiponectin
--Reduced estrogen and prolactin in men, accompanied by shrinkage or loss of enlarged breasts ("man boobs"); reduced estrogen in females accompanied by reduced risk for breast cancer

Pretty impressive. But there's one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.

Everybody has two genes for apo E; the most common type is apo E 3/3. Around 1 in 4 people have 1, less commonly 2, genes for apo E4.

I hate apo E4. I hate apo E4 because it means I've got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that's what apo E4 people have to do. But it doesn't end there.

Apo E4 people also typically have plenty of small LDL particles triggered by carbohydrates. Put fats and carbohydrates together and you get an explosion of small LDL particles. Remove fats, small LDL goes down a little bit, if at all. Remove carbohydrates, small LDL goes down but total LDL (mostly large) goes up. The large LDL in apo E4 does seem to be atherogenic (plaque-causing), though the data are fairly skimpy.

So apo E4 creates a nutritional rock and a hard place: To extract full advantage from diet, people with apo E4 have to 1) go wheat-free, low-carb, then 2) not overdo fats, especially saturated fat.

It still gives me the creeps to tell an apo E4 person that they've got to watch their fats, worse than watching Starsky and Hutch reruns.
Tags :

Comments (60) -

  • Simon

    7/30/2011 10:45:35 PM |

    What does one eat if they are wheat free, low carb, and low saturated fat? Can anyone give a sample day for this plan?

  • Paul

    7/30/2011 11:44:42 PM |

    Have you tried T4/T3 adjustments with apo E4?

  • PeggyC

    7/30/2011 11:48:10 PM |

    How can one find out if one has Apo E4?

  • steve

    7/31/2011 12:38:22 AM |

    Is it possible to have the same reactions to fats such as large increase in LDL, mostly large with little small LDL?  At one point i was 100% small LDL; restrcting carbs and increasing fats of all kind(good ones only) my NMR was 2098 LDL of which 200 were small were small.  HDL was 69 and TRGs 62.  Only way to get these numbers down is to be on statin and zetia.  Thought i was an ApoE 4, but test showed i am ApoE 3/3.
    Perhaps i am a hyper-absorber of fats- maybe as bad as ApoE4?   With statin and zetia i can reduce the numbers to LDL total of 640 and <90 small.    So maybe the high fat diet is not so great even for those who are not ApoE4.
    Thanks for your thoughts.

  • Buckaroo Banzai

    7/31/2011 5:19:21 AM |

    I'm getting my ApoE status tested soon.  I've been quite liberal with the healthy fats (olive, avocado, pastured eggs) and include saturated coconut oil and dark chocolate.  I also have high LDL particles - about 1500, but only 139 are small without statins.  I would love to find out I am 3/3 because I've already restricted grains and a variety of foods that I tested as allergic too including nuts.  I asked Dr. D on the forum if having <10% small particles was good news, but he was still worried about the total LDL.  I guess we will see how worried I should really be shortly.  BTW, I've got high Lp(a) at 26mg/dl, so I really don't need another strike against me in my plaque battle.

  • Might-o'chondri-AL

    7/31/2011 6:35:43 AM |

    Lost a nice technical ApoE explanation  I spent a lot of my time on to "server error" .
    I'll just lurk from now on.

  • Renfrew

    7/31/2011 12:46:17 PM |

    Mighto:
    Please stay here and enlighten us with your comments. Glitches can happen. I made it a habit a long time ago to just copy my text (Ctrl.A, Ctrl. C, on WINDOWS) before sending it. It is easy and takes no time. Text is preserved and you can try again.
    I for one am enjoying your musings tremendously.
    Cheers, Renfrew

  • Beth@WeightMaven

    7/31/2011 2:17:43 PM |

    What Renfrew said. I've run into this problem on blogger regularly where it decides to log me off while posting a comment. Now I always save any longish comment before posting. Better safe?

  • Jolly

    7/31/2011 2:26:04 PM |

    Digging into my 23andMe data, it reports back on APOE e4 status Smile

    You can find this as part of the https://www.23andme.com/you/journal/alzheimers/overview , or just check the rs7412 & rs429358 SNP's directly.

  • Gene K

    7/31/2011 3:39:12 PM |

    I am an APOE 3,4, and here’s what I eat on week days.
    Breakfast.
    Steamed raw vegetables (eggplant, zucchini, bell peppers, mushrooms, Mexican or yellow squash). Add yellow mustard and dry spices.
    Natto twice a week (1 box Mito natto, throw away their soy sauce and mustard packages).
    Frozen blueberries (1/8 cup), 3 tbsp flaxseed meal, 1 cup unsweetened almond milk - all microwaved for 2 min. Add ground cinnamon.
    Half-ounce piece of part skim milk mozzarella cheese.
    Coffee.
    Lunch.
    Frozen vegetables (California blend – cauliflower, broccoli, carrots) microwaved (reheat). Add a boiled egg, 1/4 avocado, yellow mustard.
    Dinner.
    Cooked or baked vegetables (cauliflower, bok choy, green cabbage, rapini).  
    Sautéed or baked fish (tilapia, salmon, perch, trout), chicken breast, or ground turkey meat balls. Add yellow mustard, horseradish, and dry spices.
    Generous amount of raw vegetables (green lettuce, pickles, tomatoes, bell peppers) with hummus.
    Decaf tea with a 1/10 serving piece of 90% dark chocolate, half-ounce mozzarella cheese, and some almonds or sunflower seeds.

  • Gene K

    7/31/2011 3:43:03 PM |

    My daily fruit serving includes a cup of frozen dark berries (blueberries, raspberries, blackberries) from the Costco Three Berry bag.

  • mallory

    7/31/2011 4:18:37 PM |

    back incollege i did a report on cancer and ottowarburg and i remember this gene being incredibly linked to cancer risk....any truth to that?

  • Dr. William Davis

    7/31/2011 4:48:42 PM |

    Hi, Steve--
    There are indeed genetic predispositions outside of apo E4 that can provide for this response, e.g., apo B receptor variants. What is not known is when you've crossed a threshold of mostly or purely large LDL that is undesirable. Despite $2 billion spent on statin drug-related research, we still have no answer on this question.

  • Dr. William Davis

    7/31/2011 4:50:18 PM |

    Hi, Buck--
    Similar issue as the question posed above by Steve: We just don't know what an "allowable" quantity of mostly or purely large LDL particles are. For a working value, I've been trying to keep NMR-derived LDL particle number 1500 nmol/L or less when LDL is purely large, but I have no endpoint data to justify this.

  • Dr. William Davis

    7/31/2011 4:51:22 PM |

    Great program, Gene, given your pattern. And I am impressed at your courage to eat natto!

  • Dr. William Davis

    7/31/2011 5:06:39 PM |

    Hi, Mallary--

    Hardly my area, but I believe that the relationship between apo E4 and cancer in various sites is complex and modulated somewhat differently than in other apo E genotypes. Some discussion:
    http://aje.oxfordjournals.org/content/170/11/1415.long

  • Dr. William Davis

    7/31/2011 5:08:35 PM |

    Hi, Simon--

    The full diet is articulated in detail, including scientific rationale, in several reports on the Track Your Plaque website; link above. Chapter 9 of the New Track Your Plaque Guide is also devoted to this.

    As you see, I will be putting out recipes here and on the Track Your Plaque website in coming months.

  • Might-o'chondri-AL

    7/31/2011 7:28:48 PM |

    even 1 reconstructed paragraph just  lost to "server error"

  • Might-o'chondri-AL

    7/31/2011 7:33:54 PM |

    ApoE joins with ApoB and is carried in VLDL and chylomicrons; it is ApoE that binds to tissue cell LDL receptors to start normal uptake. Inside the ApoB with lipids breaks off and heads into tissue cell lysosome.
    Meanwhile ApoE and the LDL receptor head back to that cell's membrane, with ApoE carrying some cholesterol out of that cell to build into an HDL molecule for recycling.

  • Tim Dietz

    7/31/2011 8:32:10 PM |

    I have the worst of both worlds, I think, as I am E2/E4.  Dr. Davis, do you have a specific program for patients with this genotype?

  • Tim Dietz

    7/31/2011 8:49:56 PM |

    So, Gene, I'm curious.  It looks like you have an extremely low intake of protein.  How are your labs and what kind of activity do you do during the day?

  • Gene K

    8/1/2011 4:13:05 AM |

    Eggs, natto, fish, poultry, and nuts are all rich in proteins, correct? I increase my portions of fish and poultry when I go to gym. I also add canned fish on these days like tuna in water or sardines in mustard sauce. I used to consume large amounts of tofu, but stopped recently based on some negative information I learned from a TYP member forum.
    Every weekday I typically walk to and from the train station, 25 min each way. I work out two or three days a week following the slow burn routine; I do cardiovascular, too. I also ride my bike for 2 hrs every weekend.
    I am a software engineer, so I spend most of my business hours in front of a computer.
    Before I learned about my APOE 4, I used lots of olive and canola oil and was a vegetarian, but had already reduced carbs. My labs were pretty bad and actually much worse than when I ate lots of bread and oatmeal every day. In mid-December 2010, I started eating as described above plus taking niacin (500 mg) and Crestor (10mg). I was already taking the standard TYP supplements – vitamin D3, fish oil, iodine. At the end of March 2011, my NMR was the best I had ever had: LDL-P 568, LDL-C 70, HDL-C 55, Trig 24, HDL-P 29.5, Small LDL-P 293, LDL size 20.4, HDL size 9.7, Large VLDL-P 0.7, insulin resistance 16. I don’t have genetic lp(a). I know the results can be better, so I am looking forward to my next NMR due in the fall.

  • TimK

    8/1/2011 7:34:36 AM |

    I'm confused. When you say 1 in 4 have this gene are you saying it's a *problem* in 25% of everyone? As in one-quarter of us should be eating like Gene K (above)? Or is a case where the gene isn't always active or something?

  • Dr. Jack Kruse

    8/1/2011 12:21:31 PM |

    I recently wrote about Alzheimer's on my blog and this question came up in the comment section.  I think about APoE4 completely differently than you do and here is why.  APoE4 confered humans the ability to migrate out of the sahara and north and south to live in climates with less solar radiation.  It allowed us to live with lower vitamin D levels.  Moreover, its presence alone means nothing unless it is accompanied with the epigenetic triggers that make it dangerous.  Dr Davis you and I both know the disease you treat (heart disease) and the one I treat (Cerebrovascular disease) are the same disease just found in different organs.  SO i think we have a lot in common in what we do but how we think about thi sissue is different.  Here is my take.  I posted this answer on another forum and I think it needs to be discussed here.

    I think the ApoE4 story is an interesting one and one I briefly touched upon in my AD blog.......I will revisit it.......but ultimately I dont think it is that important if you live an optimal life from 20-60. ApoE4 means much if you make poor epigenetic choices. I think people who come here do do what the rest of America does.

    The other reason I think it means little is the epidemiology of ApoE4 in those over 80 yrs old. It does not have any major impact on healthy aging once you get to old age. That tells me that the epigenetic signals need also be present for it to matter.

    ApoE4 is like dynamite.......and high insulin and high PUFA consumption and lowered total brain cholesterol (due to altered lipid uptake) are the major lit matches. If they exist by themselves they are harmless......but if they are brought together you are going to get heart disease and AD early and get taken out.

    Dr Kruse

  • Peter Silverman

    8/1/2011 6:24:50 PM |

    So everyone who is eating or planning to eat a high fat diet should get tested for E4, or are there some things that indicate it's probably unnecessary?

  • Jack Kronk

    8/1/2011 8:12:52 PM |

    Dr Kruse -

    It's pretty scary for me to think that maybe I am not supposed to be eating very much saturated fat. If it's true that is unbelievably lame. This is why I'm thinking I need to check to see if I am ApoE4. (How do I test for that?) If I am, then it may explain why, even on a Paleo diet, my LDL is mostly small dense. Are you suggesting that if I keep PUFA very low, like cut out my only remaining source (almonds/pecans), that this could be a key to producing more pattern A LDL? (By the way... I have chosen to eliminate all nuts and nut butters, regardless).

    -Jack Kronk

  • Patri Friedman

    8/1/2011 8:58:31 PM |

    Thanks so much for the thoughts - I am an E4/E4 eating a Paleo 2.0 diet.  As I understand it, high-protein is not a healthy diet, so low-fat & low-carb is not a good idea.  Fat is the healthiest macronutrient, so I'd love your opinion on which types of fat are best for E4s.

    It sounds like you have concerns about saturated fat, and of course I avoid n-6 PUFAs and get lots of n-3s from grass-fed animals & fish oil.  What about coconut oil?  Olive oil?

    What sort of HDL/LDL/etc  numbers would you look for in an E4/E4 as warning signs?  As health signs?

    BTW, I blog occasionally on APOE4 at primale4.wordpress.com, am going to quote your post there.

  • Tim Dietz

    8/2/2011 1:42:49 AM |

    Thanks for that, Gene.  I may need to go your route with my profile.  I'm following TYP pretty religiously and am having my 6-mo labs this month, so hopefully they will be improved from last time.

  • Dr. Jack Kruse

    8/2/2011 3:51:19 AM |

    Jack as I mentioned to you on my blog I think you clearly need context.  I think your epigentics are telling you something.  But here is what I cant tell you and neither can anyone else.......without testing!  You need to be tested to get that context.  I think your diet you posted gave many clues......but even I did not jump to the easy conclusion.  I think your real underlying issue is multifactorial but your VAP strongly points to a leaky gut as a source of the sdLDL.  I think the bananas and cream are problems too.  Your O6/O3 ratio maybe bad and yes......you may have a bad set of allele's for ApoE4......but guess what!  Your HS CRP was very very low.  This tells me that your match is not lit.  So you may only be carrying a stick of dynamite.  Again......carrying dynamite is not going to blow you up.  This is why you need testing to get more context.

  • Dr. Jack Kruse

    8/2/2011 4:05:59 AM |

    We send our ApoE4 patients to an nearby academic lab for testing.  One is likely available in your community because cardiologist and neurologist are ordering this test quite often now.  I think your PUFA content of your diet and of your tissues is critical.  In fact for AD the PUFA content is a major factor.  I believe it is a huge factor for CAD disease as well.  Wheat, Carbs, and PUFA's all drive sdLDL production.  Its not just one part of the diet that does it.  Moreover, the more leaky the gut the more sdLDL one will have as I laid out in my VAP blog that I dedicated to yourself.  I think your case is quite representative to many thousands of people and I am glad we are talking about it here because Dr Davis is a cardiologist and is coming at this issue from a different angle than I am.  I think however when the story plays out.......we will be in the same neighborhood because human biochemistry pathways are constant.  The fuels and hormone status and the situations in our guts are the covariables that make this issue more confusing.  I think people need to know why Apoe4 is important.  It conferred an adaptive advantage to move away from the equator to lower solar radiation and lower vitamin D levels.  This adaptation is seen in many american african americans.  The other interesting finding is that the liver of these patients makes more cholesterol to try to raise the D level and pregnenolone level to offset the deficit.  It never does.  But when this set of circumstance is mixed with a high carb low fat SAD (PUFA rich) it destroys the heart, vessels and brain.  This is what we see today in many parts of the world.  Their diet is now completely mismatched for the original adaptation.  I think if you tweek the diet when you know the epigenetic variables you can easily over come an Apoe4 positive test if youre willing to change.   But you need to test!

  • Dr. William Davis

    8/2/2011 11:01:58 AM |

    Hi, Tim--
    Very rare, as you likely know.
    I believe that you simply deal with this on a practical level, i.e., deal with the small LDL and insulin resistance issues and postprandial abnormalities from apo E2 as you ordinarily would. Then deal with the LDL-accumulating aftermath from the apo E4 component.

  • Dr. William Davis

    8/2/2011 11:07:23 AM |

    Thanks for the insightful thoughts, Dr. Kruse.
    I'm not sure how your approach folds into mine, though fascinating. I do agree that apo E4 is made much worse by the means you cite, i.e., polyunsaturates, carbohydrates that trigger small LDL. This is why, despite the LDL-accumulating effect of apo E4, I focus first on reducing the small LDL component, in effect an anti-inflammatory, glycation-reducing, oxidating-reducing approach, followed only then by dealing with any large LDL-increasing aftermath.
    What is not clear to  me is how atherogenic the large LDL is at higher levels in the setting of apo E4. As you know, one of the greatest concerns in apo E4 is that its effects may not be confined to lipid effects, but may extend into non-lipid effects. But that is such poorly charted territory.

  • Dr. William Davis

    8/2/2011 11:12:52 AM |

    Hi, Patri--
    The formal data on the various fat fractions and apo E4 are, unfortunately, very skimpy.
    Saturated fat clearly increases whatever LDL dominant form there is. However, other forms of fat, even omega-3 fatty acids, also increase apo E4. This become a problem, for instance, when we try to use high-dose omega-3 fatty acids to reduce Lp(a) in the presence of apo E4.
    As I commented above in response to Dr. Kruse's comments, as a practical matter I believe it is best to address the worst fraction of LDL particles first, i.e., take dietary steps to reduce small LDL particles, meaning reduce carbohydrate triggers of small LDL. Then deal with the large LDL that emerge by varying fat intake and gauging effect.
    Odd thing: Even among apo E4 people, fat intake yields variable LDL-increasing effects, quite variable sometimes.
    Also, recall that health extends beyond LDL. So there may be benefits to monounsaturates or omega-3 polyunsaturates, say, that extend to issues like brain and liver health.

  • Melinda

    8/2/2011 2:57:02 PM |

    Hi Melinda,
    Please copy and post this in previous thread for ApoE4 … .
    Continuation about ApoE4:
    % of ApoE4 messes dynamic inside tissue cell so that ApoB turns to use Scavenger Receptors to try to start cascade which gets signal transducer (Specificity Protein 1) to up-regulate the cell membrane transporter protein ( ABCA1, ATP binding cassette transporter A1) that puts excess cholesterol out from that cell. I believe this is where Doc Davis’ stated ApoB irregularities add to the problem with ApoE4 (since normal human ApoE3 works all by itself to get that signal transducer to bind to ABCA1 to work shucking cholesterol) . When cholesterol gets to build up inside the cell the large LDL can acetylate and form excessive “droplets” in that cell’s cytoplasm; while the small LDL can oxidize from CuSO4- and load up inside that cell’s lysosome.

    Meanwhile % of ApoE4 doesn’t just dock with tissue cell LDL receptors and so the macrophage scavenger receptors pick up too much cholesterol laden ApoB/ApoE lipo-protein carrier molecules. Once in the macrophage the same problem of oxidized LDL piling up in lysosome and acetylated LDL burdening cytoplasm occurs; and for that matter, in macrophages, it is down to ApoB to get the signal transducer going if any cholesterol is to be put out by cell membrane transporter protein ABCA1. This is the recipe for risky pro-atherogenic “foam cell” formation; while the individual genetics of ApoE, ApoB, assorted receptor types, signal transducer and transport protein all make it hard to predict how ApoE4 plays out.

    Dr. Kruse broaches ApoE4 in alzheimers and this is in large part because ApoE4 causes the brain neurons to get less than optimal cholesterol from the brain’s astrocytes. It is ApoA1 working in HDL complex that controls the astrocyte cholesterol balance and when there is inflammation there is a risk of ApoA1 mis-folding to foster amyloid aggregations. Low intact ApoA1 and ApoE4 together increase the risk factor for cognitive problems and dementia several fold.

    Diabetics with ApoE4 have that % of ApoE4 as an additional limitation; however, irregardless of the ApoE iso-form diabetic dementia risk arises from their glucose loads impairing kidney tubules, and thus fostering the uremic environment that stymies ApoA1 bio-synthesis. The normal role of ApoA1 is to bind to the transport protein which secures cholesterol into a safe bond with HDL; so low ApoA1 from any factor will challenge the brain neuron over time. I suggest there are individuals whose age impaired kidneys contribute to senile dementia from impairing ApoA1 levels being made and also possibly speeding up the normal 4-6 days kidney elimination of ApoA1 ; and so Patri’s comment on limitation of high protein intake is relevant due to it’s demand on aging kidneys.

    Reply

  • Melinda

    8/2/2011 3:01:05 PM |

    The above comment was written by Might-o'chondri-Al.  He asked me to post it in this thread as he is having trouble posting here.

  • Jack Kronk

    8/2/2011 4:52:20 PM |

    Ok I will test! But I have been asking around how to test and still don't know how? Is this something that I would just ask my doctor about? Maybe I go to the same lab that did my VAP? Since I got my results 3 weeks ago, I have made the following changes: zero bananas, reduced my cream intake by about 70% or so, lowered my overall fruit intake signigicantly, added 2 teaspoons of red palm oil daily, decreased caffeine intake (and now I am doing no coffee in August). I have also decided to eliminate all nuts and nut butters as of 2 days ago. Now my only real source of PUFA left in my diet is bacon, occassional chicken, and avocado. It's weird too, because on SAD, I was probably getting 10 times the PUFA, at least. I cooked in canola, ate loads of grain bread and corn products like tortillas. Maybe adding the saturated fats makes everything more amplified. The only thing now that I am VERY reluctant to give up is starches like potatoes and white rice. If I do, I will surely be VLC again, as I don't eat breads and very little fruit now, and rarely ever indulge in sweets. This means, by default, that most of my calories would then be sat and mono fats. Isn't that not good if I am ApoE4? What a mess! Dr Davis is right about being between a rock and a hard place. Jeez!

  • Jack Kronk

    8/2/2011 5:01:51 PM |

    "high protein is not a healthy diet". you mean specifically for ApoE4 folks? I haven't been tested for it yet, but I suspect I may be ApoE4. I take whey protein daily and eat lots of eggs and beef. I do this on purpose because I do weight training 5x per week and am building muscle. Could it be true that people who are ApoE4 are not supposed to build much muscle? (logically speaking, due to the restriction on protein)

  • Might-o'chondri-AL

    8/2/2011 5:20:02 PM |

    Is server cooperating now ?

    ApoE4 degrades more readily than ApoE 3 or ApoE2; ApoE4 protein fragments that get into a tissue cell's cytosol can have bad effect on that cell's mitochondrial membrane lipid binding . This decreases the mitochondrial efficiency  when they try to perform glycolysis for generating energy.

    ApoE4 degradation in a cell cytosol can  decrease the level at which that cell advances it's bio-genesis of  robust mitochondria; this is due to how ApoE4 fragments depresses PPAR gamma expression & PPAR gamma is what promotes making good mitochondria. (Specificly in the case of human fat tissue PPAR gamma is what regulates transcription of pre-adipocytes differentiation into true adipocytes. Hence Avandia & glitazone drugs that target the receptor of PPAR gamma do short out adipocyte differentiation;  and yet risk the side effect of increasing heart disease due to mitochondrial impairment.)

    In Alzheimers the form of ApoE makes a difference; and the brain amyloids react to insulin differently with different ApoE iso-forms. The ratio of insulin in cerebro-spinal fluid as compared to insulin in plasma changes with different genotypes of ApoE.   Alzheimer patients tend to have lowered glucose utilization in their brains with  less insulin and insulin-like growth factor receptors, despite the Alzheimer brain harboring fewer insulin degrading enzymes. Which engenders a paradox whereby diabetic brain neuro-pathy experimentally improves with administration of nasal insulin; and similarly,  individuals  with ApoE4  receiving nasal insulin improved their cognitive function, with the boost being higher in ApoE4 carriers than folks with any other alleles of ApoE.

    Higher amounts of Alzheimer amyloid  formed tangles are seen in Type 2 diabetics and in those with ApoE4; leading to the conclusion that "normal" ApoE3 fortuitously forms a complex with brain amyloids.
    Apparently ApoE iso-forms other that ApoE4 can more readily bring an amyloid to where the molecule LRP-1 (lipo-protein related protein 1) can move that amyloid out across the brain blood barrier .

  • Might-o'chondri-AL

    8/2/2011 5:31:26 PM |

    Hi Melinda,
    Thanks for repost, looks like Doctor D hammered his server into shape again.

  • Dr. Jack Kruse

    8/3/2011 4:57:17 PM |

    With regards to the large LDL content.  Again I am not a cardiologist, but a neurosurgeon.  The heart and brain work on the same principles of biochemistry.  And since these two organ take up much of the CO in the body they share much in common.  It is also why when we see neolithic disease affect the heart their is also a similar effect in the brain.  The Apoe4 story is one such case.  But so is the large LDL story.  Cardiology CW today believes that LDL matters.  In neurosurgery today its clear in neurodegenerative disorders we are lacking LDL and cholesterol more often than not.  This is incongruent to biochemistry.  Dr davis has said here in this thread the jury is out on large LDL in his field.  I am submitting that LDL matter little in any field.  Why?  If it did the body would have a specific detailed regulatory control method in place to deal with it and it does not.  In nature, with the consumption of organic, unprocessed parent essential fats rather than adulterated oils (PUFA's) and transfats, LDL cholesterol is supposed to be made up of significant amounts of properly functioning “parent” omega-6, linoleic acid (LA), and is not supposed to be harmful. It is the natural transporter of parent omega-6 and parent omega-3 into the cells. It is thus not critical to lower LDL cholesterol, nor is the absolute LDL number as important, if the diet contains sufficient unadulterated parent essential fats. These are unadultered PUFA's of both the omega 6 and 3 variety for clarity sake.  Also take note that the body has no natural “cholesterol sensor” in the bloodstream—it would if its levels had to be maintained within exact limits; such as, sodium, calcium, and glucose levels are monitored in many systems. For example, glucose levels are maintained to an amazingly tight 0.1% in each of us!  So Nature implemented biological mechanisms if required. There is no need for a cholesterol sensor because the absolute number is irrelevant.  That was my advice to Jack Kronk three weeks ago when he posted his VAP numbers and when I blogged about his numbers.  I understand that Dr Davis may not want to go out on a limb as I have here.  But I dont view it as a limb when the biology and biochemistry support my beliefs fully that LDL cholesterol levels are completely irrelevant to heart disease propagation.  This is why I advocate copious amounts of coconut oil to patients with heart disease and all neurodegenerative disorders including brain tumors and seizure patients.  In fact, my literature is loaded with thousands of papers supporting my belief made here.  I think its long over do that cardiologists start reading "other pathways" of data to reach conclusions that their own field muddies.  As a neurosurgeon, I read Dr Davis literature quite a lot and in comparing the two it is clear that our two fields are on a collision course from two different paths.  I got extreme clarity reading circulation over the last thirty years that cholesterol has nothing to do with heart disease.  Dr Davis has reach conclusions that are quite different from most of his fellow cardiologist as well.  I applaud him.  I just think he is still caught in the lipid hypothesis nightmare and that is the only reason he is not traveling down the road with me in unison.  Since he is a fine doc and one who clearly is ahead of his peers......i'll gladly wait for him on that road because we need him to alter what ails his branch of medicine to get to where we both need to be going for all patients.

  • Davide

    8/4/2011 2:24:29 AM |

    Dr. Kruse,

    What is your response to the fact that people with familial hypercholesterolemia (FH) have an exaggerated risk of CVD versus those who are not lacking ldl receptors? Why do so many of them have cardiac events in their 20's and 30's? Surely, you would not relegate this phenomenon to increased consumption of PUFA's and/or higher insulin?

  • Dr. Jack Kruse

    8/4/2011 4:21:16 PM |

    There are five major classes of FH due to LDLR mutations.  FH is a collection of genetic defects.  Many believe that the end result of these defects (IE high LDL or cholesterol) cause the diseases associated with it.  I do not.  Why?  When these people live past their 6th decade they have extremely low levels of neurodegeneration.  I believe the cause of the early on set  CAD is tied to secondary effects of what the primary genetic disease does to the liver to alter its function.  If one looks at FH patients and their VAP results one sees a pattern of chronic gut inflammation that is the real source of the atherosclerosis that causes higher incidences we see in FH.   These patients all have altered gut biofilms and some of the lowest levels of Vit K2 and vit D.  They also have extremely low DHEA S and pregnenolone levels are pointing to a chronic inflammation......due not to the high cholesterol level but to an altered gut axis.  Read my blog on this here.    http://jackkruse.com/your-vap-brain-love-not-war/   My views on this topic are radically different because even with severe LDL lowering treatments the disease patterns these people face remain unchanged.  Why?  because their gut remains the source of the inflammation that damages their arteries for their entire life.  We need to focus our efforts on the gut side of the equation and not the LDL side.  Ironically Dr Davis has done this with his assault on wheat.  Wheat drives sdLDL via what mechanism?  It screws up the liver and increases gut permeability to cause issues.  His current ideas and mine are very close.......but no one is tying this together.  I think my VAP post on the gut provides you the link.

  • Might-o'chondri-AL

    8/4/2011 10:55:40 PM |

    Genetic high total cholesterol is related to the over 50 amino acid variations of PCSK9 (pro-protein conertase subtilisn/kexin 9,  which comprises 692 amino acids). Individuals producing an excess of PCSK9 more extensively degrade their cholesterol receptors with surface defects; and so don't readily take up LDL out of circulation, which lets blood levels of LDL rise higher. Conversely, those making sparse PCSK9 can't degrade their LDL receptors, which pull lots of cholesterol into a tissue cell where it can pile up over time in that cell's lysosome; and blood levels of LDL seem to drop.


    PCSK9's worst version is D3744; where total cholesterol trends to 4 times normal and risk of death is estimated to be even +/- 10 years sooner than even other problematic PCSK9 genetic variations that affect maybe 1 in 500 westerners and account for +/- 5% of all pre-mature coronary heart disease. As regards the "older" age survival ability of those with familial high cholesterol  this may be due to the way over time plaque holds less lipid content and acquires more collagen with calcium infiltration. In other words younger plaque is less stable and more likely to burst free and be perilous.

    If fretting about plaque be aware that the average duration of carotid plaque is +/- 9.6 years; according to Carbon 14 dating from autopsies. Plaque may even form multiple times during one's life and the statistically dangerous symptoms take 5 - 15 years to manifest. Increased levels of circulating plasma insulin accelerate the rate that plaque forms; and also adds to a plaques instability (ie: potential to rupture) due to insulin's interaction with genes involved in the immune response;  like how those with insulin resistance make more pro-inflammatory cytokines. This bolsters Doc Davis' insistance to control glucose, since the down stream result is a more stable plaque.

    Noteably, there is the so called "protective cytokine" TGF beta which can allay plaque rupture. This is hard to predict for individuals because we have no way to assess who has what types of TGF beta receptors around , since normal and then plaque ridden blood vessels can harbor different TGF beta receptors. TGF  is considered a vital player inside vascular smooth muscle cells because it forms part of the interactive sequence that stops the smooth muscle cells from altering; and it bears mentioning that excess cholesterol can inhibit some TGF beta pathways.

  • jegesq

    8/5/2011 4:28:04 AM |

    For those who asked (Jack Kronk, Peggy, et.al.) about where and how one can get tested for ApoE it's simple:   Virtually any large commercial lab in the U.S. can do the test, e.g., Labcorp, Quest, etc.   Also, Atherotech (VAP) and Berkeley Heart Labs will do the test as well.   Since it's a genetic test, it's only run once during a person's lifetime.  The test can run anywhere from around $100 on up, depending on which lab runs it for you.

  • Dee

    8/5/2011 1:49:05 PM |

    In my last lipotropen test, I do not absorb chol not do I make it.  Am I a closed system?  My lp[a] is 41.  I am very puzzled.

    Dee

  • Dee

    8/5/2011 2:20:34 PM |

    That was from the Boston Heart lab.  I am a AP03/3.

  • George Zachary

    8/6/2011 12:21:32 AM |

    Super interesting!

    Do you know what SNP is PCSK9 ?  I'd like to look up it in my 23andme info.
    Thanks,
    George

  • Dee

    8/6/2011 12:29:15 AM |

    Plasma PCSK9 levels correlate with cholesterol in men but not in women
    Purchase
    $ 41.95


    References and further reading may be available for this article. To view references and further reading you must purchase this article.


    Janice Maynea, , , Angela Raymonda, Anna Chaplinb, Marion Cousinsb, Nadine Kaefera, Charles Gyamera-Acheamponga, Nabil G. Seidahc, Majambu Mbikaya, Michel Chrétiena and Teik Chye Ooia, b

    aHormones, Growth and Development Program, Ottawa Health Research Institute, The Ottawa Hospital, University of Ottawa, Ottawa, Ont., Canada

    bClinical Research Laboratory, Division of Endocrinology and Metabolism, Department of Medicine, The Ottawa Hospital, University of Ottawa, Ont., Canada

    cLaboratory of Biochemical Neuroendocrinology, Clinical Research Institute of Montreal, Montreal, Que., Canada

    Received 29 June 2007.  Available online 18 July 2007.

    Abstract
    Proprotein convertase subtilisin kexin-like 9 (PCSK9) is a secreted glycoprotein that negatively regulates low density lipoprotein receptor (LDLR) levels. Several single nucleotide polymorphisms (SNPs) in PCSK9 have been linked to autosomal dominant hypercholesterolemia (ADH). Conversely, hypocholesterolemia associates with both ‘loss of function’ nonsense and missense SNPs in PCSK9. We examined the association of plasma PCSK9 with lipoprotein parameters in 182 normolipidemics. For men (n = 98) plasma PCSK9 averaged 6.08 ± 1.96 μg/ml and Spearman analysis revealed significant correlation between it and total cholesterol (TC), LDLC, and TC/high density lipoprotein (HDLC) (r = 0.276, 0.282, and 0.228, respectively). For women (n = 84) plasma PCSK9 averaged 6.46 ± 1.99 μg/ml having no correlation with TC, LDLC or TC/HDLC. The ratio of plasma PCSK9/LDLC increased in men carrying ‘loss of function’ PCSK9 variations. Our results suggest a gender difference in PCSK9 regulation and function with PCSK9 correlated to TC and LDLC in men but not women.

    Keywords: Plasma PCSK9; Loss of function; Hypocholesterolemia; Hypercholesterolemia; Single nucleotide polymorphisms

    Article Outline
    Materials and methods
    dI found this on the internet, I'm not sure if this is what you need?  

    Dee

  • Dr. K

    8/6/2011 8:27:02 PM |

    All patients with FH need to have their thyroid optimized.  This issue was hashed out at the Ancestral Health Symposium on August fifth at UCLA.  Jack Kronk's VAP is helping many patients learn how to raise their HDL to increase endotoxin clearance from the portal circulation to prevent oxidation of slow moving cholesterol because of A lack of their LDL receptor.  Thyroid optimization can overcome this to a degree but it requires a physician who knows precisely how to do this and not create an unsafe situation.  Their diets has to be a strict low carb moderate protein paleo diet high in coconut oil.

  • Dr. K

    8/6/2011 10:05:56 PM |

    This too can be assessed by looking at thyroid beta receptors......it is associated with down regulation or resistance of this specific thyroid receptor.  A company in Denmark has a clinical trial on going about this specific receptor.  Thyroid hormones bing to both thyroid alpha and beta receptors.  But disease that affect the LDL receptors seem to preferentially knock out the thyroid beta receptor.

  • Dee

    8/6/2011 11:28:44 PM |

    I apologize if I sent the wrong ifo.  Didn't read it through.
    Dee

  • Jack Kronk

    8/8/2011 2:28:15 PM |

    Dr K. -

    I am inquiring with the my Doc about getting tested for ApoE. I will let you know how that goes.

    Regarding hypothyroidism, yah the issue that I'm running into is that "it requires a physician who knows precisely how to do this and not create an unsafe situation".

    This is the problem with our medical system in America. I live in San Diego, one of the biggest, most advanced cities on earth, and I am having trouble finding anyone over here that can truly help me with this. My doctor situaiton is pathetic. Sorry to say that, but I'll call a spade a spade. All they want to do is put me on Lipitor and go low fat whole grain. So then I am stuck with doing my own diligent research, and appyling knowledge that I can learn from people who actually know what they are talking about, and right now, for me, that means the internet. Incredible when you think about it.

    When you say low carb, do you mean no starch as well, not even potatoes? By the way... the name of this post is "The Exception to Low Carb". So... that's why this is so confusing. Some very knowledgable people think it's best to raise my intake of starches and lower my fats. If my body is creating more LDL (even small dense) because of my saturated fat intake, then it makes sense to replace sat fats with something else. I already get enough protein, so then I am left with carbs. If it has to be carbs, isn't safe starch my only real option? It can't be 'sugar'. It can't be 'fructose', or grain starch, right? Should I eat loads of salads? Or I am on the wrong track completely? Should I look at upping my mono fats in place of saturated, like using mac nut oil for cooking? Or would mono fats be just as problematic?

    You see? Honestly, I know this stuff stone cold. I know what *most* people do well with, but if we don't figure out how being pre-disposed to having issues with LDL receptors really changes things, we are going to (deservedly) get hammered by the low-fat whole grain camp when a fair amount of people who thought they had it all figured out are dropping dead from eating fats because they are ApoE and had no idea.

    I'm genuinely glad that my example is helping people. No doubt I am. But I'd be alright with feeling like I'm getting somewhere with all this in my personal case as well. At the moment, I can't really say that I feel that way just yet.

  • Dr. K

    8/11/2011 12:38:34 AM |

    Patients with apoe4 have a higher rate of AD and AD is associated with a cholesterol deficiency in the brain.  So for me apoe4 is a signal to load with the MCT of coconut oil which has massive benefits to the brain metabolically.  I find it hard to believe this is bad for the heart at any level because CAD tends to mirror CVD across all measures.  I think only cardiologist have this problem with Larger particle LDL because of the faulty lipid hypothesis.  cAD is an inflammatory condition.  It ha little to do with cholesterol itself.  If the cholesterol is oxidized then there are issues but this can be followed by acute phase reactants from the liver like HS CRP.  When it's up HDL tends to be low......and it's low because the liver is being bombard by gut endotoxins and this is a direct measure of the oxidation potential of an overwhelmed portal circulation.  To further the point......thyroid hormone, testosterone, estrogen, and high vitamin D levels all raise liver HDL and this is how they protect against heart disease.  I maintain large LDL confers no risk without inflammation.......and a low HDL is a great way to know if your liver is being overwhelmed in the portal circulation.  This is why vitamin K2 confers a great cardiac benefit.......it comes from a healthy gut biome.  vAP tells you a ton about your portal circulations inflammatory burden.

  • majkinetor

    8/14/2011 2:59:37 PM |

    M-Al, just copy your text prior to the post, or write it in the editor. I don't know which browser you use, but in Chrome if you use "back" on "server error", it will return what you typed in a reply.

  • Peter Silverman

    8/16/2011 5:08:49 PM |

    Following your diet I took an NMR last summer and this summer.  The small LDL particles went down (835 to 709) but the total particles went up (1800 to 2100).  Should I stick with your diet (low carb, no wheat, D, omega3's), one Walmart glucometer) or go back to rice and beans?

  • Jack Kronk

    8/24/2011 7:29:11 PM |

    I got quote at $390 for just an ApoE genetic test. Is that normal?

  • Adriana

    10/5/2011 12:33:30 PM |

    Have you seen any reduction in your LDL following this diet?

  • Eric

    7/9/2012 6:43:01 PM |

    I've been eating paleo/primal for about a year, dropped 10 pounds, and brought my triglycerides down from a high of 325 three years ago to 130. Unfortunately, my LDL-p is over 2600 (first time it was checked), and I found out I'm APO e4/e4.

    The doctor says e4/e4 should go vegan, which seems about as anti-primal as you can get.

    Any suggestions for where to start looking for eating guidelines?

  • Gary Mullennix

    5/4/2013 4:38:16 AM |

    My goodness, how very confusing!!  I'm hypothyroid.  My HDL is 95. My total C is 285. Ny LDL is 186. But my LDL fractions are mostly big and plumb and my small total 23. So, I think I'm ok...buy my doc thinks I should go vegan. I want coconut oil, little red meat.  I evercise 5x week. My heatt stress tests were all 'well within'   So, it sounds as though I need to get the E4 tested   More?

  • Mario

    3/9/2014 9:46:46 AM |

    I would be deeply grateful for your advice. I am doing my best to understand how to cope with my aPOE 3/4 status. I have Alzheimer's on both sides of my family, which has killed or is in the process of killing several relatives, including my father and maternal grandmother. Unsurprisingly, I have received much conflicting data.

    I am 46. I eat a strict Paleo diet (grass-fed, wild-caught, etc.) except for some resistant starch in the form of parboiled rice and unmodified potato starch. I consume approximately 50-60% fats (majority saturated fats including daily MCT oil), 30-40% protein and 10-20% carbs. I exercise vigorously and non-vigorously -- but not every day. (Incidentally, over three years I naturally increased my testosterone by 38% using this approach, going from the low 3's to 5.3.)

    My LDL is 128. My HDL is a distressingly low 33. Triglycerides are 59.

    MY NEXT MOVE: Seek out an LDL particle-size test. If that reveals my LDL particles to be of an unhealthy size then I will need to consider a different approach in regard to sat fats. Also, looking  to improve my sleep, which has been my Achilles' heel (consistently get only around six hours). Finally, using super-consistent exercise and increasing oyster intake to boost the HDL.

    I would appreciate any guidance.(!)

    Best / Mario

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