Lessons from the 20-year statin experience

Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI.
"

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.

Wheat "debate" on CBC

"Many Canadians plan warm buns, stuffing and pie for their Thanksgiving meals tonight. But I'll speak with a cardiologist who thinks we have no reason to be thankful for any food that contains wheat. William Davis says our daily bread is making us fat and sick."

That's the introduction to my recent interview and debate on CBC, the Canadian public radio system, aired on the Canadian Thanksgiving. Arguing the other side was Dr. Susan Whiting, an academic nutritionist. (I use the word "arguing" loosely, since she hardly argued the issues, certainly hadn't read the book, but was content to echo the conventional line that whole grains are healthy and cutting out a food group is unhealthy.)

I do have to give credit to the Canadian media, including the CBC, who have been hosting some rough-and-tumble discussions about the entire wheat question despite Canada being a world exporter of wheat. I recently participated in another debate with a PhD nutrition expert from Montreal who, in response to my assertion that the genetically-altered high-yield, semi-dwarf strains have changed the basic composition of wheat, argued that the creation of the 2-foot tall semi-dwarf strain was a convenience created so that farmers could see above their fields--no kidding. I stifled my laugh. (The semi-dwarf variants were actually created to compensate for the heavy seed head that develops with vigorous nitrate fertilization that buckles 4 1/2-foot tall wheat stalk, making harvesting and threshing impossible, a process farmers call "lodging." The 2-foot tall semi-dwarf thick, stocky stalk is strong enough to resist lodging.)

In short, debating the nutrition "experts" on this question has been tantamount to arguing with a school age child on the finer points of quantum physics. There has not yet been any real objection raised on the basic arguments against modern genetically-altered wheat. Modern semi-dwarf wheat is, and remains, an incredibly bad creation of the genetics laboratories of the 1970s. It has no business on the shelves of your grocery store nor on the cupboards in your home.

Carrot Cake

This is among my favorite recipes from the Wheat Belly book. I reproduce it here for those of you who read the Kindle or audio version and therefore didn't get the recipes.

I made this most recently this past weekend. It was gone very quickly, as even the 13-year old gobbled it up.

(I reduced the sour cream in this version from 8 to 6 oz to reduce cooking time. Also, note that anyone trying to avoid dairy can substitute more coconut milk, i.e., the thicker variety, in equivalent quantities.)

Makes 8-10 servings



 

 

 

 

 

 

Ingredients:
Cake:
2 cups carrots, finely grated
1 cup chopped pecans
1 cup coconut flour
1 tablespoon ground flaxseed
2 teaspoons ground cinnamon
1 teaspoon allspice
1 teaspoon nutmeg
1 teaspoon baking powder
2 tablespoons freshly grated orange peel
Sweetener equivalent to ½ cup sugar (e.g., 4 tablespoons Truvia)
½ teaspoon sea salt
4 eggs
1/2 cup butter or coconut oil, melted
2 teaspoons vanilla extract
½ cup coconut milk
6 ounces sour cream

Icing:
8 ounces cream cheese or Neufchâtel cheese, softened
1 teaspoon lemon juice
1 tablespoon Truvía or 1/8 teaspoon stevia extract powder or ¼ cup Splenda

Preheat oven to 325° degrees F. Grate carrots and set aside.

Combine coconut flour, flaxseed, cinnamon, nutmeg, baking powder, orange peel, sweetener, and salt in large bowl and mix by hand.

Put eggs, butter or coconut oil, vanilla coconut milk, and sour cream in mixing bowl; mix by hand. Pour liquid mixture into dry pecan/coconut flour mixture and blend with power mixer until thoroughly mixed. Stir carrots and pecans in by hand with spoon. Pour mixture into greased 9- or 10-inch square cake pan.

Bake for 60 minutes or until toothpick withdraws dry. Allow to cool 30 minutes.

Place Neufchâtel cheese in bowl. Add lemon juice and sweetener and mix thoroughly. Spread on cake.

Why wheat makes you fat

How is it that a blueberry muffin or onion bagel can trigger weight gain? Why do people who exercise, soccer Moms, and other everyday people who cut their fat and eat more "healthy whole grains" get fatter and fatter? And why weight gain specifically in the abdomen, the deep visceral fat that I call a "wheat belly"?

There are several fairly straightforward ways that wheat in all its varied forms--whole wheat bread, white bread, multigrain bread, sprouted bread, sourdough bread, pasta, noodles, bagels, ciabatta, pizza, etc. etc.--lead to substantial weight gain:

High glucose and high insulin--This effect is not unique to wheat, but shared with other high-glycemic index foods (yes: whole wheat has a very high-glycemic index) like cornstarch and rice starch (yes, the stuff used to make gluten-free foods). The high-glycemic index means high blood glucose triggers high blood insulin. This occurs in 90- to 120-minute cycles. The high insulin that inevitably accompanies high blood sugar, over time and occurring repeatedly, induces insulin resistance in the tissues of the body. Insulin resistance causes fat accumulation, specifically in abdominal visceral fat, as well as diabetes and pre-diabetes. The more visceral fat you accumulate, the worse insulin resistance becomes; thus the vicious cycle ensues.

Cycles of satiety and hunger--The 90- to 120-minute glucose/insulin cycle is concluded with a precipitous drop in blood sugar. This is the foggy, irritable, hungry hypoglycemia that occurs 2 hours after your breakfast cereal or English muffin. The hypoglyemia is remedied with another dose of carbohydrate, starting the cycle over again . . . and again, and again, and again.

Gliadin proteins--The gliadin proteins unique to wheat, now increased in quantity and altered in amino acid structure from their non-genetically-altered predecessors, act as appetite stimulants. This is because gliadins are degraded to exorphins, morphine-like polypeptides that enter the brain. Exorphins can be blocked by opiate-blocking drugs like naltrexone. A drug company has filed an application with the FDA for a weight loss indication for naltrexone based on their clinical studies demonstrating 22 pounds weight loss after 6 months treatment. Overweight people given an opiate blocker reduce calorie intake 400 calories per day. But why? There's only one food that yields substantial quantities of opiate-like compounds in the bloodstream and brain: wheat gliadin.

Leptin resistance--Though the data are preliminary, the lectin in wheat, wheat germ agglutinin, has the potential to block the leptin receptor. Leptin resistance is increasingly looking like a fundamental reason why people struggle to lose weight. This might explain why eliminating, say, 500 calories of wheat consumption per day yields 3500 calories of weight loss.

And, as in many things wheat, the whole is greater than the sum of the parts. Despite all we know about this re-engineered thing called wheat, eliminating it yields health benefits, including weight loss, that seem to be larger than what you'd predict with knowledge of all its nasty little individual pieces.

Just who is "Real Facts 2000"?

This is an example of what seems to be developing over at Amazon.com, posted as a "book review":

The author has no credentials, no credibility, just a small cult of terribly misinformed followers. Don't be fooled by the high volume screech against wheat and grains. Allegations of "secret ingredients in wheat" to make you eat more, or comparisons to cigerettes. Seriously?! For over 8000 years wheat has sustained and grown human kind, oh and it tastes good when mixed with a little water and yeast. Every nutritionist and serious medical professional will tell you that bread is the most economical and safe source of essential nutrients. In fact, bread is handed out in natural disasters because it sustains life without food safety issues or requiring refrigeration. And now, suddenly it will kill you. Comical! This book is such a bone headed, misinformed way to just scare people into not eating.

As for secret ingredients, humm, apparently the author is ignorant of the food laws that regulate everything that goes into food and on food labels. Unlike some enforcement agencies, the FDA has some serious teeth behind its enforcement. As for frankenwheat, again seriously?! Wheat, due to its ubiquitous presence in the world is treated as sacrosant from any GMO research or development.

If you need real, science based information on healthy eating, check out [...] and leave this book and its cult in the compound.


If you recognize the wording and tone, you will readily recognize the footprints of the Wheat Lobby here. "Terribly misinformed followers"? . . . Hmmm. "Food laws"? I didn't realize that eating more "healthy whole grains" was a . . . law?

Make no mistake: There are people and organizations who have a heavy stake in your continued consumption of the equivalent of 300 loaves of bread per year. There are people and organizations (read: pharmaceutical industry) who have a big stake on the "payoff" of your continued consumption of "healthy whole grains."

This is not a book review; this is part of a concerted, organized campaign to discredit a message that needs to be heard.

Anybody from the media listening?
Track Your Plaque challenges

Track Your Plaque challenges

Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

Comments (31) -

  • Nigel Kinbrum BSc(Hons)Eng

    12/1/2009 5:19:32 PM |

    As LDL-c is produced by the liver (I don't know where Lp(a) is produced but I'd hazard a guess that it's the liver), could the secret lie in the liver?

    See Cirrhosis and corn oil.

    Has the effect of beef fat & MCT's on small LDL-c percentage & Lp(a) been investigated?

  • David

    12/1/2009 5:30:54 PM |

    Dr. Davis,

    Could some of the non-response be be caused by underlying food sensitivities (other than wheat), without acute allergic reactions, that contribute to underlying chronic inflammation?  I.e., a gluten like effect but specific to another food in their diet.

    -David

  • bender645

    12/1/2009 6:02:29 PM |

    Hello Dr.

    I have read elsewhere (LA Vida Low Carb, Free the Animal, Hyperlipid)that saturated animal fat intake can positively impact LPa and LDL particle size.  Particularly that of pastured-grass fed animals.  

    I am not 100% familiar with your program or dietary recommendations, but it might be worth investigating.

  • Dr. William Davis

    12/1/2009 10:30:38 PM |

    Hi, Nigel--

    To my knowledge, not beef fat specifically but various fatty acid fractions, such as stearic acid, and percent fat intake have been examined; MCTs I believe have not been investigated.

    However, the effects of adding fats to the existing strategies in the Track Your Plaque program tend to be small, since the diet is not fat restricted.

  • Dr. William Davis

    12/1/2009 10:31:34 PM |

    Hi, David--

    Don't know for certain.

    However, these are generally slender, athletic types with no bowel symptoms, arthritis, etc. So I suspect an allergic theme does not tie them together.

  • Anonymous

    12/2/2009 3:06:57 AM |

    Consider an epigenetic effect as a possible cause for the resistant patients' failure to respond.

  • Dr. William Davis

    12/2/2009 3:18:03 AM |

    Anon--

    Please elaborate.

  • Anonymous

    12/2/2009 10:02:48 AM |

    If the idea is to reduce plaque...

    http://www.lef.org/LEFCMS/aspx/PrintVersionMagic.aspx?CmsID=115645

    After one year, the group receiving the drugs, but not pomegranate showed a significant 9% increase in intima-media thickness. In contrast, the group receiving the pomegranate plus drugs showed a reduction in carotid intima-media thickness as follows:

    After three months: 13%

    After six months: 22%

    After nine months: 26%

    After one year: 35%

    Carotid artery blood flow (as measured by end diastolic velocity) improved in the pomegranate plus drugs group as follows:

    After three months: 16%

    After six months: 20%

    After nine months: 31%

    After one year: 44%

  • P

    12/2/2009 3:00:03 PM |

    hmmm, interesting.
    Such epigenetic effects have resulted in reducing diabetic moratality during famine times previously. Should be interesting if someone studied similar gene expression for your Lpa problem.

  • Scott Miller

    12/2/2009 9:56:25 PM |

    Dr. Davis, I think your diligent quest to reverse heart disease needs to embrace two important additions:

    [1] Have your patients seriously reduce inflammation-causing polyunsaturated fats (primarily, any oil with a poly content greater than 10 percent, which means olive oil barely ducks under the bar, but not many other vegetable oils do, including the oft touted as healthy canola oil).

    [2] Have them consume more saturated fat, especially coconut oil. In effect, low HDL is a symptom of saturated fat deficiency. A great source of coconut oil is cold-processed virgin coconut oil (should smell like coconuts), and full-fat coconut milk (an excellent base for sauces, and smoothies mixed with frozen berries and whey protein powder).

    The main key, IMO, is to reduce processed vegetable oils, a highly inflammatory food ingredient that has a half-life in the body of 2-4 years, so the effects of reduction may take a while to notice.

  • Peter

    12/2/2009 11:11:50 PM |

    Dr Davis,
    Since hormones have such a profound effect on lipoproteins, could there be a connection between DHT levels and resistance to treatment here?  I recently read that early baldness is a risk factor for heart disease, and that DHT opposes estrogen much more strongly than testosterone.  Since estrogen is so heart protective, is it possible that this would be another avenue of attack?  If a person had high levels of the 5 alpha reductase enzymes, testosterone normalization as a treatment avenue might be neutralized in these cases (I am assuming that all hormones have been optimized in your resistant patients).
    I was thinking about this recently as I just came across a patent application for the use of finasteride in heart disease.  You had also mentioned the use of tamoxifen in one of your earlier posts, which would obviously relate here as tomaxifin binds estrogen receptors.

  • Anonymous

    12/3/2009 3:50:01 AM |

    It's so funny that Cheerios has targeted your site for its google ads.

    Cheerios® Cereal
    Improve Your Heart's Health With Cheerios® Cereal Today
    www.Cheerios.com

  • Nigel Kinbrum BSc(Hons)Eng

    12/3/2009 4:05:09 AM |

    Dr William Davis said "However, the effects of adding fats to the existing strategies in the Track Your Plaque program tend to be small, since the diet is not fat restricted."

    I was thinking more along the lines of substituting MCTs for omega-6 fats rather than adding fats.

  • Francis

    12/3/2009 5:22:29 AM |

    I may be wrong but there seems to be an emphasis on treating potentially benign lab values in your post.

    What do the heart scan scores show for the patients you mention? Isn't reversing their plaque the ultimate heart-goal of the program? If their plaque is reversing, so what if some lab values aren't perfect?

    The interesting question is what happens to the risk of having a heart attack or a stroke when plaque is under control, but small LDL or Lp(a) are not.

  • András

    12/3/2009 10:59:53 AM |

    Dr Davis,

    What about Pauling's old protocol for Lp(a) that involves Vitamin C and Lysine? Is it good?

  • Dr. William Davis

    12/3/2009 1:45:48 PM |

    Andras--

    I WISH the Pauling/Rath protocol worked.

    We've tried it and I've had a number of patients try it on their own. I have never witnessed any effect whatsoever on Lp(a), though diarrhea is a predictable result (from the high-dose vitamin C).

  • Kent

    12/3/2009 6:48:29 PM |

    In January of 09 I started out with LP(a) of 198 nmol/L. After finding Dr Davis and reading his book, I started applying his principles by bumping my Niacin from 1500mg to 2000mg, fish oil dosage of 7200mg to 9600mg combined EPA and DHA, Coq10, flaxseed, oatbran, little to no wheat diet, etc.

    However, with Dr Davis suggestions, I also followed the Pauling Therapy of 6g of Vitamin C and L-Lysine along with 2g of l-proline daily. In 3 months my LP(a) went from 198nmol/L to 105nmol/L. In 9 months my LP(a) was down to 45nmol/L, A 77% reduction from January! If you look on Dr Mercola's site, he also states that kind of documented results from the Pauling Therapy.

    I give credit to both Dr Davis and Linus Pauling, but most of all my Lord and Saviour Jesus Christ for answered prayer.

  • Anonymous

    12/3/2009 11:34:16 PM |

    Dr. Davis,

    thats interesting. How long did you try?

    As I understood him, he didn't recommend vitamin C and L-Lysin in isolation, but together with a Multivitamin, additional vit A, Bs, D, E, K, amino-acids arginine, carnitine, taurine, magnesium,..

    I myself started Pauling's protocol against a PAD - and within a half year my walking distance doubled from below a km.

    Short before this improvement I also got to experience the 'predictable' result of diarrhea, due to increasing from the usual 6 grams of vit C daily by titrating up to bowel tolerance (which, with 50 grams, proved quite high).

    Beside that, I experienced some other unexpected effects:

    # a rush on my back I had for a year healed right away
    # my seasonal strong hay fever ceased
    # a strong chest pain, for which I've been to hospital for one week 3 years ago without any diagnosis or treatment - particularly painful in physical or mental stressful situation - is gone now too.

    So already these 'minor' side-effects make me very grateful. Not to talk how glad I am about being able to walk faster than a snail again..
    However, in this respect there's still much improvement potential for me.

    Therefore, any clarifications - why it could have failed in your case - would be highly appreciated.

    Kind regards..

  • Dr. William Davis

    12/3/2009 11:53:19 PM |

    Hi, Kent--

    I'm glad it worked for you. Perhaps there are subsets of Lp(a) that respond, as Lp(a) is subject to great individual variation in behavior.

    It's also possible that it's the high-dose fish oil. We've seen such delayed responses to high-doses of EPA + DHA that take over a year to develop.

  • Dr. William Davis

    12/3/2009 11:55:44 PM |

    Hi, Anon--

    The experiences have been scattered, but all involved only C, lysine, and proline, though everyone here takes fish oil and vitamin D. Many also take magnesium. Most tried for about 6 months.

    So it's hardly a systematic study. But any hint of an effect would have been encouraging, but I have yet to see it.

  • David

    12/4/2009 2:24:47 AM |

    Hi Dr. Davis,

    What about exercise-induced hypertension? Do you still find that to be a persistent problem when all other biomarkers are optimal?

    Thanks,
    David

  • David

    12/4/2009 2:27:26 AM |

    Also, is there a way to know one has exercise-induced hypertension? Would one get headaches?

  • Dr. William Davis

    12/4/2009 3:14:39 AM |

    Hi, David--

    Yes and no. Following all the components of the program will reduce blood pressure. However, some people just don't respond as readily and hypertension with exercise and emotional stress persists. A simple stress test remains the best way to assess this.

  • Kent

    12/4/2009 6:20:49 PM |

    Dr. Davis,

    I've thought about that concerning the high dose of fish oil. I'm wondering possibly if it's a synergizing effect of all the supplements, including the C, Lysine and Proline.

    I also wanted to mention that I split the doses up throughout the day. I've been informed that Vit C and L-Lysine only stay in the system for a short time, therefore, if you take it only once or twice a day, it's not going to have near the effect as splitting it up. I take 2g of the proline, lysine and C in the morning, then take the remaining amounts of C and Lysine throughout the day every 2 hours or so at 1g each, with my last dose at 5:00pm. I try to take my last dose a couple of hours before taking my Niacin, as I've heard the C can sometimes have a negative effect on the Niacin.

    My brother has high LP(a) as well, without seeing it go down. He was taking pretty much everything I was, with the exception of proline and only 4-5g of fish oil. And he was only taking the lysine and C twice a day. He has altered it to match more of what I'm doing, so we're anxious to see what his next blood test reveal.

    By the way, thanks to applying the principles you laid out in the book and here on your site, my other blood levels have been improved drastically. For that I am extremely greatful!

  • Anonymous

    12/4/2009 11:30:22 PM |

    Dr. Davis,

    thanks for your clarification. I appreciate that you remain open to possibly more positive results with Pauling's protocol in the future..


    Hi Kent,

    what is the negative effect of vit C to Niacin you heard of? I'm aren't aware of any, though I too take the biggest part of vit C separate from meals, during which I use the Niacin.

    thanks..

  • StephenB

    12/6/2009 5:11:30 AM |

    For non-responders doing everything correctly but still holding on to lots of small LDL, what's happening to their heart scan scores?

    I was wondering if there were any possibility that small LDL is more associative of heart disease than causative.

  • Kent

    12/7/2009 4:11:09 PM |

    Hi Anon..

    The negative effects I've heard about Vit C to Niacin are spotty. What I've heard is that there is a possibility of any anti-oxident to diminish some possitive effects of Niacin, such as reducing it's HDL raising ability a bit. I don't know anyone personally that has experienced this, I just try not to the two together if possible.

  • Anonymous

    12/8/2009 3:08:01 AM |

    I try to filter out the "faith" based claims and stick with scientifically backed information.  Niacin improved my very low HDL by 30% but complete elimination of the exercise induced angina I had suffered disappeared for me when I subjected myself to high dose K2 for 6 months.  Nothing I have tried (including wheat elimination) enables me to stay off reasonably high dose statins

  • Anonymous

    12/8/2009 11:33:01 AM |

    Thanks for the reply, Kent. Though my HDL did raise about 18% within one year of 1.5 gram Niacin use, at 33 now it's still much too low.

    On your suggestion I'll try to take them more separated, beside raising the dose of Niacin. Which I think is advisable in my case due to Lp(a) anyway (57).

    What is the advised upper limit of the daily dose of Niacin at TYP?

  • Kent

    12/9/2009 6:17:13 PM |

    Anon..

    I really noticed a huge jump in my HDL, when I bumped Niacin from 1.5g to 2g, introduced high intake of fish oil, at least 7200mg to 9600mg, got vitamin D levels up, and alomost eleminated wheat. I went from HDL's of 40's/50's to 86.

    I believe the upper limit of Niacin depends on the type, wheter it be immediate, sustained, or slow release. Perhaps Dr. Davis could address that.

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