Are there any alternatives to niacin?

In the Track Your Plaque program, we tend to rely a great deal on niacin. When used properly, 90-95% of people will do just fine and achieve their lipid and lipoprotein goals with the help of niacin, along with their other efforts.

Unfortunately, around 5% of people simply can't take niacin without intolerable "hot flush" effects, or occasionally excessive skin sensitivity--itching, burning, etc.

Why does this happen? These 5% tend to be "rapid metabolizers" of niacin, i.e. they convert niacin (nicotinic acid, or vitamin B3) into a metabolite called nicotinuric acid. Nicotinuric acid is the compound responsible for the skin flush. Most people can slow or reduce the effects of nicotinuric acid by:

--Taking niacin with dinner, so that food slow tablet dissolution.

--Taking with plenty of water. Two 8-12 oz glasses usually eliminates the flush entirely in most people.

--Taking with an uncoated 325 mg tablet of aspirin in the first few weeks or months. Eventually, you will need to revert back to a better stomach tolerated dose of 81 mg, preferably enteric coated. But a full 325 mg uncoated can really help in the beginning, or when you have any niacin dose increases, e.g., 500 mg to 1000 mg.

But even with these very effective strategies, some people still struggle. That's when the question arises: Are there any alternatives to niacin?

Well, it depends on why niacin is being used. If you and your doctor are using niacin for:

Raising HDL--Then weight loss to your ideal weight; reduction of processed carbohydrates, especially wheat products; avoidance of hydrogenated ("trans") fats; a glass or two of red wine per day; dark chocolates (make sure first ingredient is chocolate or cocoa, not sugar), 40 gm per day; fish oil; exercise; other prescription agents (fibrates like Tricor; TZD agents for diabetes; cilostazol (Pletal)). Niacin is by far the most effective agent of all, but, if you're intolerant, raising HDL is still possible through a multi-faceted effort.

Reduction of small LDL--The list of effective strategies is the same as for raising HDL, but add raw almonds (1/4-1/2 cup per day), oat bran and other beta-glucan rich foods like oatmeal. Reduction of processed carbohydrates is especially important to reduce small LDL.

Reduction of Lipoprotein(a)--This is a tricky one. For men, testosterone and DHEA are effective alternatives; for women, estrogen and perhaps DHEA. Hormonal preparations of testosterone and estrogen are stricly prescription; DHEA is OTC. I have not seen the outsized benefits on lipoprotein(a) claimed by Rath et al by using high-dose vitamin C, lysine, and profile, unfortunately. We are clearly in need of better alternatives to treat this difficult and high-risk disorder.

Reduction of triglycerides/VLDL/IDL--I lump these three together since they all respond together. If you're niacin intolerant, maximixing your fish oil can be crucial for reduction of these patterns using doses above the usual starting 4000 mg per day (providing 1200 mg EPA+DHA). Reduction of processed carbohydrates, eimination of processed foods that contain high-fructose corn syrup, and weight loss to ideal weight are also very effective. "Soft" strategies with modest effects include green tea (>6 cups per day) or theaflavin 600-900 mg/day; raw nuts like almonds, walnuts, and pecans; exercise; soy protein.

Reduction of LDL--Lots of alternatives here including oat bran (3 tbsp per day), ground flaxseed (3 tbsp per day), soy protein (25 grams per day), Benecol butter substitute (for stanol esters), soluble fibers like pectin, psyllium, glucomannan; raw nuts like almonds, walnuts, and pecans.

In future, should torcetrapib become available (by prescription), this will add to our available tools for these areas when niacin can't be used. Until now, the alternatives to niacin depend on what you and your doctor are trying to achieve. In the vast majority of cases, HDL, small LDL, triglyceride, etc. goals for heart scan score control can be achieved, even when niacin is not well tolerated.

Is flaxseed oil a substitute for fish oil?


This question comes up so frequently that it's worth going over.

Flaxseed oil is a wonderful oil rich in linolenic acid, which may provide health benefits all by itself. Some authorities have speculated that the substantial reduction in heart attack seen in the Lyon Heart Study, the study that demonstrated the healthy power of the Mediterranean diet, is due to linolenic acid.

Flaxseed oil is also rich in monounsaturates and low in saturates, both desirable qualities. Of course, I'm talking here about flaxseed oil, to be distinguished from flaxseed , which are the intact seeds. The seeds themselves also contain the same oils, but contain other components, specifically lignan, a plant fiber with suspected health benefits like reduction in cancer risk.

Despite all flaxseed oil's wonderful properties, it is definitely not a substitute for fish oil. Why do we use fish oil for our coronary plaque control program (trying to reduce your heart scan score)? Several reasons. Fish oil:

--Dramatically reduces triglycerides, usually by 50% or more.
--Dramatically reduces specific lipoprotein classes like VLDL
--Dramatatically reduces, often eliminates, abnormal postprandial (after-eating) lipoprotein patterns, like IDL (intermediate-density lipoprotein)
--Has been conclusively shown to reduce risk of heart attack and death from heart attack (GISSI Prevenzione Trial).
--Has been shwon to reduce risk of stroke.
--Modifies blood clotting parameters, particularly a 20% reduction in fibrinogen.

Flaxseed oil, or linolenic acid concentrate for that matter, do not accomplish any of these effects, all crucial if you are to gain control over your coronary plaque.

Flaxseed oil and flaxseed remain wonderful nutritional agents for their own reasons. But they will not substitute for fish oil in your program. Only fish oil--the real thing--does the job.

If you have coronary artery disease . . . do you know why?

This conversation is aimed primarily at non-followers of the Track Your Plaque program, because if you were a follower, you’d already know the answer!

I saw a woman in the hospital today. She’d just survived her second heart attack one week earlier. At 51 years old, she was understandably shaken, perhaps terrified. She felt that her future was uncertain and, in fact, had discussed with her husband what he should do to prepare for a future without her.

One week earlier, she’d received three stents that successfully aborted her heart attack. But, as is always the case, the modest delays of ambulance transport, the emergency room preliminaries, then of mobilizing an available cardiologist and catheterization laboratory team, totaled nearly two hours before her stent procedure. Inevitably, a moderate amount of damage had been done to her heart.

Her first “event” had been very similar: very little warning, then 911 and the flurry of activity. Both times, the cardiologists (two different physicians) complimented the patient on her prompt action. Both also called her heart attacks “close calls”.

She defied the odds with two near-death events. So, when I met her a week after her last heart attack, I asked an obvious question: “Has anyone told you why you’re having these heart attacks?”

She looked completely puzzled at first. She then said, “No, not really. I just assumed it was genetic. My mother went through the same thing when she was my age. But she didn’t get as far as I have, since they didn’t have these procedures back then.”

To me, this seems inexcusable: This woman had experienced two brushes with death and no doctor had established a cause. Could this woman’s belief be true, that it’s just genetic?

While there are, indeed, genetic causes for heart disease, the vast majority of these genetic causes are 1) identifiable, and 2) correctable. Genetic does not necessarily mean hopeless. It just means that the usual equation of heart disease risk management (heart disease = LDL cholesterol = need for Lipitor) has limited value. It would be like giving penicillin to people for any and all infections. It will work occasionally, but it will fail miserably in a great many cases. Treating LDL cholesterol with statin drugs is just like that.

Perhaps this woman has lipoprotein(a), a serious genetic trait that predicts heart disease at a young age and is largely unaffected by statin drugs. Or, she may have a severe excess of small LDL, only partially suppressed by statins. If she has the combined pattern of lipoprotein(a) and small LDL, that means she has two statin-unresponsive and significant genetic traits. But they respond to niacin, specific nutritional strategies, and several other agents.

The message: If you have coronary disease, you need to insist on knowing why. “It’s genetic” is not an acceptable answer. “There’s no proof of any heart disease causes beyond cholesterol” is also nonsense. “Everyone gets heart disease, or “hardening of the arteries”, eventually. You just got it a little before everyone else” is also patently ridiculous.

Identifying the causes of your coronary disease (or coronary plaque if you’ve had a CT heart scan) is the first step in developing a program of treatment that provides you with control over this disease.

Have you tried inulin yet?

If you haven't yet tried it to facilitate weight loss, it's really worth giving the new inulin-containing product, Fiber Choice "Weight Management", a try.

Recall (from a prior Heart Scan Blog) that inulin is a vegetable-based fiber found in celery, green peppers, etc. that, when exposed to water, expands to many times original volume. This simple phenomenon yields satiety--a feeling of fullness.


The manufacturer of the product has also added green tea, which has been shown in two small clinical studies to enhance weight loss, though by a different route.

We've been advising patients to chew two of the strawberry flavored tablets one hour before every meal (or with breakfast if you eat immediately in the morning). You'll be satisfied with less food and you'll experience less intense food cravings.

Though no one so far has achieved a huge drop in weight, it does seem to enhance a slow, gradual weight loss larger than achieved by diet and exercise alone. And it's very safe and inexpensive. If you give it a try to help you lose weight, let us know what kind of results you've obtained.

Fish oil update on Life Extension

An article of mine came out in Life Extension Magazine and is available on the online version at:

http://www.lef.org/magazine/mag2006/sep2006_report_omega1_01.htm

This is an update on the heart health applications of fish oil.

Or, go to to www.lef.org and put fish oil into your on-site search and you'll come back to it in future.

Of course, it comes with Life Extension's promotion of its supplements.

Although it's not yet available online, the hard copy version of an article I wrote on homocysteine is available in the October, 2006 Life Extension Magazine. If you're not a member of their program, they'll send you a free copy just for signing up for it without obligation. Go to the home page of www.lef.org to do so. Or, Life Extension is available at newstands if you're in a rush or don't want to sign up for a free copy.

More on Vitamin D

If you haven't done so already, you should subscribe to Dr. John Cannell's free newsletter on vitamin D issues. His newest issue is available at:

http://www.vitamindcouncil.com/newsletter/2006-aug.shtml

A sign-up to subscribe is available on the same page.

I continue to be shocked and amazed at the prevalence and magnitude of vitamin D deficiency in the people I see every day. It's been a beautiful summer with very little rain. Most days have been in the 70-80 degree range--very comfortable to be outdoors in the sun and getting skin expoxure to activate vitamin D in the skin.

Yet, in the vast majority of people I see, summer blood levels of vitamin D are virtually indistinguishable from winter levels. Both hover around the 30 ng/ml range. Summer levels in Wisconsin people seem to be no more than 10 ng/ml higher than winter levels. This remains true even in people who spend a lot of their day outdoors gardening, walking, etc. wearing shorts and a short-sleeved shirt, i.e. with plenty of skin surface area exposed.

I'm at a loss to explain precisely why. Yes, it is Wisconsin. But a direct sun overhead, 75 degree day should be providing plenty of sun. My suspicious is that a combination of factors are at work: people are not spending as much time outdoors as they claim; they often seek shade; use sunscreen; and they're overweight. (Excess weight decreases vitamin D blood levels dramatically, yet another reason not to get fat!)

Read more about vitamin D by checking out Dr. Cannell's insightful comments on the unfolding vitamin D story. He holds nothing back.

Why not just get "perfect" lipids and call it a day?

What if you achieved the Track Your Plaque lipid targets: LDL cholesterol 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl?

After all, these are pretty stringent standards. Compared to national guidelines (the ATP-III Guidelines of the National Cholesterol Educational Panel), the Track Your Plaque 60-60-60 goals are laughably ambitious. There's a lot of wisdom hidden in those numbers. The triglyceride level of 60, for instance, is a level at which triglycerides become essentially unavailable for formation of triglyceride-containing lipoprotein particles such as small LDL and VLDL.

If you get to the 60-60-60 target, isn't that good enough? What if you just held your values there and went about your business? Will coronary plaque stop growing and will your CT heart scan score stop increasing?

Sometimes it will. But, unfortunately, many times it will not. The experience generated through clinical trials bear this out. Studies like the St. Francis Heart Study and the BELLES Trial both showed that just reducing LDL cholesterol is insufficient to stop plaque growth. Beyond the Track Your Plaque experience, there's no clinical trial experience that shows whether the 60-60-60 approach does any better.

In our experience, achieving 60-60-60 is indeed better than just reducing LDL. That makes sense. Just raising HDL from the average of 42 mg/dl for a male, 52 mg/dl for a woman adds advantage. Compound this with triglyceride reduction from the plaque-creating equation, and you've doubled success.

But there's even more. What if you had hidden patterns not revealed by conventional lipids? How about lipoprotein(a)? Small LDL? Postprandial (after-eating) abnormalities? Hypertensive effects (more common than you think)!

In 2006, stopping the increase in your heart scan score is, for most of us, not just a matter of taking Lipitor or its equivalent and sitting back. For nearly all of us, stopping the progression of your score is a multi-faceted effort.

Hospitals: Then and Now

It's 1920. The hospital in your city is a facility run by nuns or the church. It's a place for the very ill, often without hope of meaningful treatment, but nonetheless a place where surgeries take place, babies are born, the injured and chronically ill can find care. No one has health insurance and there's no Medicare. Everyone pays what they can. The hospital is accustomed to doling out plenty of care without compensation. For that reason, they welcome donations and sometimes will build new additions or other facilities in honor of a major donor.

Volunteeers are common, since the wards are understaffed and generally suffering from a shortage of trained nurses and personnel associated with the church. Drugs, such as they are, are often prepared from basic ingredients in the hospital pharmacy. Product representatives hawking medicines and devices are virtually unheard of.

Though their therapeutic tools are limited, the physicians are a proud group, dedicating their careers to healing. The majority of the medical staff volunteer large portions of their time to care for the poor who come to the hospital with very advanced stages of disease: metastatic tumors, advanced heart failure, debilitating strokes, overwhelming septicemia, etc.

Hospitals are usually governed by a board of clergy and physicians who make decisions on how to apply their limited resources and continually seek charitable donations.


Fast forward to present day: Hospitals are high-tech, professional facilities with lots of skilled people, complicated equipment,and capable of complex procedures. While they still house people with advanced illnesses, the floors are also filled with people with much earlier phases of disease. In general, they do a good job, with quality issues scrutinized by a number of official agencies to police practices, incidence of hospital-related infections, medication errors, care protocols, etc.

The hospital of 2006 is a more more effective place than the hospital of 1920. But its aims and operations are different, also. Though some churches are still involved in hospitals, more and more are owned by publicly-traded companies that answer to shareholders--shareholders who want share value to increase. Though donations are still sought, much of the revenues are obtained by concentrating on profitable, large-ticket procedures. More procedures are often generated by advertising.

Because they operate to generate profits, several hospitals in a single city or region compete with one another. The 21st century has therefore witnessed the phenomenon of hospital-owned physicians: more and more practicing physicians are employees of their hospital. That way, the physician brings all his patients and procedures to his hospital, not to a competitor. The top of the funnel is the primary care physician, who tends to see all disease when it first occurs. The primary care physician then sends the patient to the specialist, who is obliged (by contract) to perform his/her procedure in the hsopital paying their salary.




Representatives from companies manufacturing and selling expensive hospital equipment and drugs are everywhere, falling over themselves to gain attention of the physicians using their equipment and the hospital buyers who make purchasing decisions. Millions of dollars can be transacted with just one sale.

The number of volunteers has dwindled. The poor and uninsured are commonly diverted elsewhere, often to a government-funded, and often second-rate, institution. Hospitals measure success by comparing annual revenues and numbers of major procedures.

The hospital of 2006 is a vastly different place than 1920. If you're expecting charitable treatment, compassion, and selfless care, you're in the wrong century. In 2006, the hospital is a business. You don't expect charitable treatment at Wal-Mart or from your car dealer. Don't expect it from your hospital. They are businesses and you are a customer. Recognize this fact, lose the nostalgia for the hospitals of yesterday, and a lot more will become clear to you.

The dreaded small LDL particle

Brian is a 59-year old landscape architect whose starting CT heart scan score was 276.

Brian's food choices at the start were deplorable: a pound of sausage per week, sometimes more; butter on anything and everything; up to two pounds of cheese per week; hot dogs; etc. His lipoproteins were accordingly just as miserable: low HDL, high triglycerides, excessive (postprandial, or after-eating) IDL. Small LDL was a particularly stand-out pattern, with 95% of all LDL particles in the small category.

Brian made a dramatic turnaround in lifestyle and corrected all of his patterns--except for small LDL. After one year, small LDL still occupied 95% of all LDL particles, even though the quantity of LDL had been reduced. In order to help convince Brian that correction of his small LDL was going to be necessary to achieve control oover coronary plaque, I suggested that he undergo another heart scan. His score: 435, or a 57% increase.

Each day that passes, I gain more and more respect for small LDL as a cause for coronary plaque growth. Conventional thought among lipid experts is that small LDL should no longer be a factor if total LDL (e.g., LDL particle number) is reduced. But our experience suggests otherwise: when small LDL persists, we tend to see continued, sometimes frightening, plaque growth.

I therefore asked Brian to intensify his efforts: additional weight loss off his somewhat prominent abdomen (since visceral fat increases small LDL), further reduce wheat products and processed carbohydrates, increase niacin (to 1500 mg per day), and use more raw almonds and oat bran.

Don't let small LDL get the best of you. It is a nasty, sometimes persistent abnormality that has impressive effects on plaque growth.

Winning Through Intimidation

Do you remember the book, Winning Through Intimidation by author Robert J. Ringer?



In his 1984 bestseller, author Ringer details how to succeed in business by overwhelming clients and competition by appearing hugely successful and powerful. Rather than a business card, he'd hand out an elegant book to represent himself. He'd show up in a limousine to a meeting, even when he could barely afford it. He used these tactics, even when he was a small-fry, in commercial real estate and built a successful business following such techniques.

This reminds me a lot of what happens in conventional medical practice: The large and successful hospitals, filled with trained staff and technology, exude legitimacy and success. How can they possibly be wrong? Such overwhelming know-how and multiple levels of expertise mustbe right!

Let's be grateful that we do have access to such high-tech, capable care. Unfortunately, just as Mr. Ringer used deceptive practices to appear something he wasn't, this is also true in hospitals. Not all physicians have your best interests in mind. Their principal concern is how profitable your care can be for them--can you be persuaded to have your stent, bypass, etc.. After all, look around you: Aren't all this equipment and personnel impressive? Aren't you intimidated?

The patient that most recently drove home this issue for me recently was a smart and capable executive who came in for consultation. He had been told by his internist that a surgery (to replace his aorta, a HUGE procedure) was probably necessary. In my view, it was not--his process was simply not that far progressed. The risks for danger over the next several years was virtually nil. Unfortunately, this man, now confused and worried, sought an opinion from the chief of thoracic surgery (in the usual white coat and with professorial demeanor, I'm sure) in a major metropolitan hospital (in Chicago), who promptly rushed him off to the operating room.

The pathology report, cleverly not mentioned in any other of the hospital documentation, showed what I had suspected: this man had mild disease that wasn't even close to requiring surgery. But, with all that technology, $100,000 or so of costs, chief of surgery who looked the part, etc.--they must be right!

Robert Ringer's concepts only ring too true for hospitals and some of the unscrupulous physicians in practice. Don't allow yourself to be intimidated.
Unforgiving small LDL particles

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.

Comments (39) -

  • ChrisB

    10/21/2011 3:45:39 PM |

    Great Article.  As I'm sure you know by now, I've been kind of a lipidpanelaholic since having a MI 2 yrs ago.  The hardest information to find is that of how long it takes for lipids to respond to diet changes and how sensitive they can be to even the smallest amount of carbs.

  • Howard

    10/21/2011 4:44:48 PM |

    Are you sure that sort of response is not due to gluten/gliadin/lectin/transfat? Four crackers doesn't sound to me like much of a carb load, but for a gluten-sensitive person like me, that could set off some inflammation.

  • Marc

    10/21/2011 7:08:35 PM |

    Dr. Davis,
    How does alcohol fit in to the above "equation"? Specifically wine.

    Marc

  • Sam Sinderson

    10/22/2011 12:12:39 AM |

    I have been on a wheat-free and carb restricted diet for about 7 weeks, and being concerned that I might be Apo E4, and therefor need to also limit saturate fat as you explained in an earlier blog, I asked my doctor to order a small LDL test.  No independent lab here that I consulted knew what that was, nor obviously did my doctor, since he just ordered "small LDL".  The local hospital lab finally found the following, which is what I will have blood drawn for tomorrow:
    Lipoprotein Fractionation Panel 1, Ion Mobility
    Which includes:
    Choesterol; HDL Cholesterol; Triglicerides; :Lipoprotein (a); Lipoprotein Fractionation Panel 2, Ion Mobility (LDL, Total; LDL, Medium and Small; LDL, VerySmall; HDL, Large; LDL Peak Diameter, LDL Phenotype)

    I hope that this is what I need.  Probably it is overkill, but in this case apparently my Medicare Advantage plan will cover it since it has been more than 3 months, since I had a simple panel done.

    Is there a simpler test for small LDL?  By the way the CPT codes are 80061, 83695, 83704

  • Fat Guy Weight Loss

    10/22/2011 4:41:38 AM |

    Sounds like cheat days may not be that good of an idea...

  • Dr. William Davis

    10/22/2011 12:39:39 PM |

    Yes, it does cast cheat days in a new light!

  • Dr. William Davis

    10/22/2011 12:45:11 PM |

    That's it, Sam.

    It shouldn't be that hard. The information is actually fairly straightforward and provides crucial information.

  • Dr. William Davis

    10/22/2011 12:51:45 PM |

    Hi, Marc--

    Alcohol does indeed slow or stop weight loss, especially if more than a serving or two are consumed. So it pays to minimize during a weight loss effort.

  • Dr. William Davis

    10/22/2011 12:56:34 PM |

    Probably not, Howard, since those components have not been associated with triggering of small LDL. The trans fat component can indeed trigger small LDL, but it seems to occur even with foods minus trans fats.

    However, I am impressed that gluten/gliadin/lectin rolled off your tongue!

  • STG

    10/22/2011 1:36:14 PM |

    The problem is carb creep. I experienced this a few months ago when I received the results of my HbA1c test. I was still in the prediabetic range and it was higher than the HbA1c test I had a few years earlier. I didn't get it? I thought I was consuming less carbs then I was. When I actually looked at my diet there were carbs creeping in: dark chocolate and small "safe starches" (e.g, potatoes, yams). Another factor that may have impacted my blood sugar was the stress of travel/visiting family during that three month time period. My understanding is that elevated cortisol levels can raise blood sugar. In any case, my recent HbA1c is in normal range. I think this is because I eliminated even small amounts of dark chocolate and "safe starches" (see Jimmy Moore's comments about safe starches).

  • jethro

    10/22/2011 2:01:01 PM |

    How low should we go in carbohydrates to avoid increasing small LDL?

  • Davide

    10/22/2011 3:01:26 PM |

    I'm not sure that wheat has this acute effect on everybody. In fact, I know it doesn't happen with me. I keep a close eye on my lipids and my small LDL particles remain "relatively" low despite the fact that I consume wheat/sugar products. Then again,  my blood sugar does not significantly rise after carbohydrates, so maybe that's why. If I eat a massive plate of pasta, a glass of fruit juice, and dessert, my blood sugar may (keyword, "may") rise to 120, if that, but then it goes down to about 80 about 45 minutes after the meal. No joke. In other words, I'm thinking this effect may have to do with the degree of people's volatility to rising blood sugars. Just a guess.

    Fyi, I'm the apo E/4 person who's LDL amount/particle number (226, 2,000) is extremely sensitive to saturated fats and thus I'm always lost in the conundrum of balancing fats with carbs. Difficult!

  • Teresa

    10/22/2011 3:05:34 PM |

    I know that if weight loss is involved, it can take a few months after weight stabilizes for lipids to normalize.  If minimal or no weight loss is involved, how long does it take?

  • Fat Guy Weight Loss

    10/22/2011 5:31:19 PM |

    With the example about 4 crackers would be as low as 10g carbs.  Curious of the overall effects of say 10g carbs of sweet potatoes....

  • Dr. William Davis

    10/23/2011 11:49:09 PM |

    Then it depends on which parameter you are talking about, Teresa.

    Small LDL requires just days to respond, while triglycerides require weeks to months, while HDL requires months to years.

  • Dr. William Davis

    10/23/2011 11:51:13 PM |

    Hi, Davide--

    No doubt: Individual tolerances to various foods, including carbohydrates, can differ. And the apo E4 person has a tougher time of it.

  • Dr. William Davis

    10/23/2011 11:53:40 PM |

    Unfortunately, Jethro, there's no quick and easy way to decide this, since individual sensitivity varies.

    Although imperfect, you can use HbA1c, an index of glucose and not of small LDL, to gauge whether you've been triggering higher blood sugars that often parallel the triggering of small LDL particles. You could, of course, obtain lipoprotein testing 48 hours after ingesting a known amount of carbohydrates, e.g., 20 grams, but that is logistically difficult.

    That all said, most people can get away with 15 grams carbohydrates per meal, while some can't tolerate more than 10, yet others do fine with 30+ grams.

  • Dr. William Davis

    10/23/2011 11:54:15 PM |

    Excellent point, STG! And I like the "carb creep"!

  • Barbara

    10/24/2011 12:14:06 AM |

    Did you see this, Dr. Davis?

    http://medicalxpress.com/news/2011-10-common-link-autism-diabetes.html

  • Teresa

    10/24/2011 1:14:14 AM |

    And it takes years to unlearn all the inaccurate stuff learned in school, and to find and learn the good stuff that is out there.  Thanks.

  • Stephanie

    10/24/2011 2:27:52 PM |

    How does one check to see if they are apo E4?

  • ChrisB

    10/25/2011 1:19:25 PM |

    How does it affect lipid results?

  • steve

    10/25/2011 10:52:06 PM |

    Dr Davis:  What is the small LDL profile for native populations that consume tons of of carbs and no signs of heart disease; also, the Japanese consume lots of carbs- easily 3 cups of rice per day which is about 120 carbs from rice alone.  Low level of CAD; what are their levels of small LDL.  I know for myself ApoE 3/3 that carbs do affect the small LDL level i have and in any event in the absence of a statin i produce tons of LDL particles large or small depending upon carb levels.  I believe genetics plays a large role.
    Thanks

  • Dr. William Davis

    10/26/2011 3:19:22 AM |

    No doubt, Steve.

    However, I'm unaware of lipoprotein assessment done to answer these questions. That would be interesting, however.

  • Dr. William Davis

    10/26/2011 3:21:50 AM |

    Yes, agreed, Teresa: New lessons to learn every day in this Information Age!

  • Dr. William Davis

    10/26/2011 3:23:44 AM |

    Thanks, Barbara. No, I hadn't seen this. But I'm not the least bit surprised!

    I find it wonderfully satisfying that the puzzle pieces are falling in place, just like that 1000-piece jigsaw puzzle we struggled to put together, with the last few pieces fit just perfectly!

  • Dee

    10/28/2011 1:57:49 PM |

    Dr. Davis,
    Have you heard or read about Lumbrokinase helping to lower small "a" particles?
    Just wondering.
    Dee

  • Tim

    10/28/2011 7:14:08 PM |

    Dr. Davis,

    There seems to be a lot of mention of the E4 ApoE genotype.  What about those of us that are E2/E4?  Any different instructions for us?

    Thanks.

  • Dr. William Davis

    10/29/2011 10:48:39 PM |

    With this very tough pattern, you are best following lipoproteins and glucose measures like HbA1c to gauge response to various dietary manipulations. The basic diet approach, however, is largely the same; it just may require some adjustments, e.g., fat intake.

  • Dr. William Davis

    10/29/2011 10:49:12 PM |

    Sorry, Dee, no info.

    Where did you hear this?

  • Dee

    10/30/2011 5:20:26 PM |

    Here is the quote.  Appently it just helps lower the LP[a]  and does not have any terrrble side effects.  I may try it, nothing else is working.  My little a is 43 and rising in spite of all I do.

    "The one nutraceutical that has shown promising clinical results in actually lowering Lp(a) is a lumbrokinase product made by Canada RNA Biochemical called Boluoke. Like its chemical cousin nattokinase, lumbrokinase is an enzyme that helps break up fibrin—a fibrous protein that helps form blood clots—to avoid too much clotting and keep blood flowing optimally."

    :

    Dee

  • Sam Sinderson

    10/31/2011 7:32:29 PM |

    I have my results.  My PCP reported these to me "for my records" with no further comment.  Maybe he can't interpret them?
    Total Cholesterol: 231 (My PCP surely would think this is high.)
    I find it strange that they did not report LDL direct, though perhaps it is not done because of the breakdown below.  
    Calculated LDL: 133 H MG/DL
    HDL: 85 Mg/dl  This is higher than I have ever had measured.
    Triglycerides: 64 Mg/Dl  Even Simvastatin only got it down to 84.  I conclude that I am not Apo E4.
    The range after \ below  is the range they cite, I presume, as normal.
    Lipoprotein Innocent: <10  NMOL/L \ <75  I presume this is a good result.
    LDL, Total: 2268 H NMOL/L  \ 440-1600
    LDL, medium and small: 651 NMOL/L \ 144-787
    LDL, Very Small: 277 NMOL/L \ 75-419
    HDL large: 9315 H NMOL/L  \ 469-5258
    LDL Peak Diameter: 227.5 Angstrom  \216.-234.3
    LDL Phenotype A  Pattern A     I believe this to be the preferred pattern, low small LD and Triglycerides.  Ref: Obesity (2009) 17 9, 1768–1775. doi:10.1038/oby.2009.146--Reversal of Small, Dense LDL Subclass Phenotype by Normalization of Adiposity
    Patty W. Siri-Tarino1, Paul T. Williams2, Harriet S. Fernstrom1, Robin S. Rawlings1 and Ronald M. Krauss1

    Does this calculate to large LDL = 2268-651 =1617 (Not including medium)?
    When should I do this test again?
    Comment?

  • Dr. William Davis

    11/1/2011 2:03:32 AM |

    Hi, Sam--

    The "pattern A" comment is misleading. About 40% of your LDL particles are small, too much.

    It means going back to the strategies to reduce small LDL, such as wheat elimination and limiting carbohydrate exposure. It is worth repeating about 2 months after weight has stabilized following a diet change.

  • Sam Sinderson

    11/1/2011 12:49:43 PM |

    I have been on a no-wheat, limited, very-low carb, diet now for 6 to 7 weeks already.  I cringe to think of what the numbers may have been before.  I initially lost about 12 pounds in less than 2 weeks to get to 148, I am 72-in tall, and have stabalized there by eating more high-fat non-carb stuff.  You say 40% small.  You must be using the medium and small (640) over total (2268) to get 40%.  Apparently medium and small includes the very small, which must be a fraction of small?  How long should it take for the very small to approach zero?  Isn't that the more important number?  I will be out of the country for 2 weeks.

    Thanks

  • Dr. William Davis

    11/2/2011 1:43:14 AM |

    Yes, exactly, Sam: Combine medium and small.

    Dietary and weight changes usually exert effects on small LDL within a few weeks, much faster than most other parameters.

  • pb

    2/6/2012 3:47:25 PM |

    Get a VAP test....this measures your small particle/large particle LDL.
    labcorp code 804500

  • pb

    2/6/2012 3:51:39 PM |

    I am going to try to get a VAP test.  No doctors know of it....only folks on the web.  Why?  It seems like a very important test to measure your LDL properly.  Can someone elaborate on this further?

  • Dr. William Davis

    2/7/2012 3:18:11 AM |

    Easy, Pb: There are no drugs--read: "no financial incentive"--to treat the abnormalities generally uncovered by lipoprotein testing like VAP. Thus, no push to get it tested.

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