Can natural treatments "cure" or "treat" any disease?

According to current FDA policy, the answer is a flat "NO!"

No natural treatment, whether it be fish oil (as a nutritional supplement), l-arginine, vitamin D, magnesium, various flavonoids like theaflavin or resveratrol, can be declared to treat or cure any disease. That's why you see the evasive and vague wording on nutritional supplements, nutraceuticals, and various foods, like "Supports heart health" or "Supports healthy cholesterol". Claiming, for instance, that taking 6000 mg per day of a standard OTC fish will reduce triglycerides and stating so on the label of a supplement is unlawful and prosecutable.

Think what you will of Mr. Kevin Trudeau (author of Natural Cures They Don't Want You to Know About"): visionary, consumer advocate, David vs. the Goliath of the FDA and "Big Pharma", or huckster, scam artist, and one-time felon. But Trudeau got it right on one important issue: The FDA dictates what claims can be made to treat disease. On one of his ubiquitous informercials, Trudeau states:


"...the way the system works today, you have the Food and Drug Administration—the FDA, and you have the drug industry. They really work in tandem. Unfortunately, there’s an unholy alliance there. People don’t know that the majority of commissioners of the FDA, which allegedly regulates the drug industry, and the food industry—Food and Drug Administration, the commissioners of the FDA—the majority of them—go to work directly for the drug companies upon leaving the FDA and are paid millions and millions and millions of dollars. Now in any other format, that would be called bribery; that would be called a conflict of interest; that would be called payoffs. That’s exactly what’s happening right now. So what has occurred is the Food and Drug Administration is really working in tandem with the drug industry to protect their profits. Example: The Food and Drug Administration says that only a drug can diagnose, prevent, or cure any disease."


He goes on to say that

"...the Food and Drug Administration says only a drug--nothing else--can cure, prevent, or diagnose a disease. Therefore the Food and Drug Administration continues to call more and more and more things diseases. Therefore they eliminate all-natural remedies. No one can say what a natural remedy can do if it’s been classified as a disease. So Attention Deficit Disorder is now a disease. Therefore only a drug can cure, prevent, or diagnose it. Cancer is a disease. Acid reflux is now a disease. Obesity is now a disease."

(PLEASE do not construe this as an endorsement of Mr. Trudeau's overall opinions. But I do think he's right on this one point.)

The stated purpose of this restrictive policy is to protect the public. Indeed, in years past before protective legislation, ineffective and even poisonous products were commonly sold as therapeutic treatments. (Remember cocaine and morphine in cold remedies? Lead and other toxic agents were also common.) Unfortunately, a huge gap has emerged as clinical data accumulates that support the efficacy of nutritional treatments and other non-traditional methods to treat or alleviate diseases. Any disease, or anything construed as disease as Trudeau points out, can onlybe treated by a drug.

In the FDA's defense, they have made slow progress in allowing "claims" of benefits for several supplements and food substances, such as the beta-glucan of oat products, soy protein, and most recently barley (for cholesterol reduction). The scrutiny is quite thorough and the wording of the policy is quite specific. Regarding oat products, for instance, the policy states:

"FDA concluded that the beta-glucan soluble fiber of whole oats is the primary component responsible for the total and LDL blood cholesterol-lowering effects of diets that contain these whole oat-containing foods at appropriate levels. This conclusion is based on review of scientific evidence indicating a relationship between the soluble fiber in these whole oat-containing foods and a reduction in the
risk of coronary heart disease.

Food products eligible to bear the health claim include oat bran and rolled oats, such as oatmeal, and whole oat flour...To qualify for the health claim, the whole oat-containing food must provide at least 0.75 grams of soluble fiber per
serving. The amount of soluble fiber needed for an effect on cholesterol levels is about 3 grams per day."


(Source: FDA Talk Paper which can be viewed in its entirety at http://www.fda.gov/bbs/topics/ANSWERS/ANS00782.html.)

In light of the boom in nutritional and non-traditional research that validate or refute efficacy, is such a policy still necessary? Or does it inhibit the open dissemination of information and result in a extraordinary monopolization of health treatment for the drug companies?

This debate will likely rage for the next two or more decades, particularly as drug companies are increasingly viewed as profit-seeking enterprises and more validation is gained by non-drug treatments.

For the moment, don't dismiss a "treatment" because it doesn't come by prescription. But don't reject a drugjust because it is a prescription. We need to strike a healthy, rational balance somewhere in between.

Can procedures alone keep you alive?

My days in the hospital remind me of what heart disease can be like when no preventive efforts are taken--what it used to be like even with my patients before taking a vigorous approach to prevention (though over 12 years ago).

Several cardiologists in my hospital, for instance, express skepticism that heart disease prevention works at all. Yes, they know about the statin cholesterol drug trials. But they claim that, given their experience with the power of coronary disease to overpower an individual's control, statin drugs are just "fluff". Coronary disease is a powerful process that can only begin to be harnessed with major procedures, i.e., a mechanical approach.

So these cardiologists routinely have their patients in the hospital, often once a year, sometimes more, for heart catheterization and "fixing" whatever requires fixing: balloon angioplasty, stents, various forms of atherectomy. Year in, year out, these patients return for their "maintenance" procedures. Their cardiologists maintain that this approach works. The patients go on eating what they like, taking little or no nutritional supplements, and medications prescribed by their primary care physicians for blood pressure, etc. But no real effort towards heart disease prevention beyond these minimal steps.

Can this work? Very little at-home, preventive efforts, but periodic "maintenance" procedures?

It can, perhaps, for a relatively short time of a few years, maybe up to 10 years. But it crumbles after this. The disease eventaully overwhelms the cardiologist's ability to stent or balloon this or that, since it has progressed and plaque has growth diffusely the entire period that maintenance procedures have been performed. In addition, acute illness still occurs with some frequency--in other words, plaque rupture is not affected just because there's a stent in the artery upstream or downstream.

Not to mention this can be misery on you and your life, with risk incurred during each procedure. It's also terribly expensive, with hospitalization easily costing $25,000-$50,000 or more each time. (Compare that to a $250 or so CT heart scan.)


As people become more aware of the potential tools for prevention of heart disease, fewer are willing to submit to the archaic and barbaric practice of "maintenance" heart procedures in lieu of prevention. But it still goes on. If you, or anybody you know, are on this pointless and doomed path, find a new doctor.




Bloodletting, another antiquated health practice

Support your local hospital: HAVE A HEART ATTACK!

I'm kidding, of course. But, in your hospital's secret agenda, that's not too far from the truth. Catastrophes lead to hospital procedures, which then yields major revenues.

Prevention, on the other hand, yields nothing for your hospital. No $8,000 to $12,000 for heart catheterization, several thousand more for a stent, $60,000-plus for a bypass, $25,000 or more for a defibrillator. In other words, prevention of heart attack and all its consequences deprive your hospital of a goldmine of revenue.

The doctors are all too often conspirators. I heard of yet another graphic example today. A man I didn't know called me out of the blue with a question. "I had a heart scan and I had a 'score' that I was told meant a moderate quantity of plaque in my arteries, a score of 157. My doctor said to ignore it. But I got another scan a year later and my score was 178. So I told this to my doctor and he said, 'Let's get you into the hospital. We'll set up a catheterization and then you'll get bypassed.' Of course, I was completely thrown off balance by this. Here I was thinking that the heart scan was showing that my prevention program needed improvement. But my doctor was talking about bypass surgery. Can you help? Does this sound right?"

No, this is absolutely not right. It's another tragedy like the many I hear about every day. Heart scans are, in fact, wonderfully helpful tools for prevention. This man was right: he felt great and the heart scan simply uncovered hidden plaque that should have triggered a conversation on how to prevent it from getting worse. But the doctor took it as a license to hustle the patient into the hospital. Ka-ching!

This sort of blatant money-generating behavior is far from rare. Don't become another victim of the cardiovascular money-making machine. Be alert, be skeptical, and question why. Of course, there are plenty of times when major heart procedures are necessary. But always insist on knowing the rationale behind such decisions, whether it's you or a loved one.

Hospitals contain experts in ILLNESS

Hospitals contain many experts in sickness. This seems obvious. But walk down the hallways of any hospital, and you'll quickly be convinced that hospitals contain almost no experts in health.

People (hospital staff, that is, not the patients) in hospitals are especially good at identifying and treating disease. They lack knowledge of health.

If your nurse is 100 lbs overweight and struggles to walk down the hall because of arthritis in both knees, would you entrust her with health advice?

If your doctor sits down in the cafeteria and eats his lunch of a ham sandwich with cheese on a bun, fried onion rings, and a milkshake and pastry, can you believe that he/she possesses any insight into health and nutrition?

If your physical therapist or cardiac rehabilitation counselor struggles nearly as much as you while climbing a single flight of stairs, can you accept their advice on how to regain your stamina and use exerise to full health advantage?

The answer to all these questions is, of course, no. Hospital staff are generally expert at dressing surgical wounds, stopping bleeding, identifying infections, and providing the support services for surgical and diagnostic procedures. In contrast, they are generally miserable at conveying genuine health advice. They certainly fall short in being examples of health themselves.

To hospitals and their staff, health is a temporary situation that persists only until you become ill. Illness is an inevitability in the hospital staff mindset. Health is a temporary state in between illnesses.

We need to shake off this perverse mentality. Health is the state of life that should dominate our practices and philosophies. Illness via the occasional catastrophe, e.g., broken leg from skiing, car accident, etc., is the province of hospitals. We should gravitate towards this philosphy and away from the over-reliance on hospitals that has come to dominate our present perceptions of health. Hospitals are not glamorous. They are, for the most part, profit-seeking businesses intent on portraying themselves as champions of health.

When I walk down the halls of hospitals, I am shocked and ashamed at the extraordinary examples of ill-health presented by hospital staff. Yet they falsely paint themselves as experts in both illness and health. Don't believe it for a second.

Are there still unexplored causes of heart disease?

I met a woman today. She had her first heart attack at age 37. She just had her 2nd heart attack this morning, at age 40.

Several issues are surprising about her story. First, she's pre-menopausal. Heart attacks before menopause are unusual. We'll occasionally see women have a heart attack before or during menopausal years only if they're heavy smokers and/or they have had diabetes (either type I or type II) for many years. But this young woman had neither. She is slender and has never smoked.

Even more surprising are her basic lipid values: LDL cholesterol 35 mg/dl, HDL 150 mg/dl, triglycerides 317 mg/dl. This is a very unusual pattern.

Unfortunately, this is all developing acutely in the hospital. (I've just met her today--she's not a Track Your Plaquer!) Lipoprotein analysis would be extremely interesting. In particular, I'd like to see whether she has any other markers besides elevated triglycerides of a "post-prandial" abnormality, i.e., persistence of abnormal particles after eating. The high triglycerides make this quite likely.

If this proves true, the omega-3 fatty acids from fish oil will be a lifesaving treatment for her, since they dramatically reduce both triglycerides as well as persistent postprandial particles like intermediate-density lipoprotein (IDL). (Track Your Plaque Members: See the Special Report on Postprandial Abnormalities on the present home page at www.cureality.com for a more in-depth discussion of this fascinating collection of patterns that is just started to be explored.)

In the real world, especially acute care medicine, there's always a kicker: she speaks no English. Unfortunately, communicating the intricacies of a powerful program like ours that aims to identify all causes of heart disease, then corrects then and aims for coronary plaque regression, is difficult if not impossible.

I also do occasionally worry that, given this woman's extraordinary risk at a young age, and overall very unusual lipid patterns (HDL 150?!), if there are causes presently beyond our reach. We have to make use of the tools available to us for now.

Everything causes heart attack!

The media are presently gushing about a recent study that associates caffeine intake with heart attack.

CBS News: That cup of coffee you're craving might not be such a good idea. Research in the September issue of Epidemiology suggests coffee can trigger a heart attack within an hour in some people.


Some reporters and their quoted sources are musing about whether it's the caffeine, cream vs. other whiteners, time of day, interaction with other risk factors, etc.

My advice: Get a grip! How many relatively benign, every day factors in life can be blamed for dire health risks?

The problem with many of these studies is that they are cross-sectional. They do not enroll participants, then "treat" with coffee (or other substance in question) vs. placebo. In other words, it is not a randomized trial, the sort of trial necessary to prove a hypothesis. That's all that can be generated by a study like this one: a hypothesis.

Perhaps there's a bit of warning for the person with uncorrected lipids and lipoproteins, has no idea that they have extensive coronary plaque because they've never had a heart scan, and have a slovenly lifestyle. Maybe that person might have exaggerated risk from a cup of coffee.

But for us, involved and intensively addressing all causes of coronary plaque to the point of stabilizing or reducing it, coffee is likely a non-issue.

For more conversation on coffee and this report, go to the www.cureality.com home page.

Excessive Heart Procedures Makes New York Times Headline


One example of flagrant cardiac procedure excess has made New York Times headlines:


Heart Procedure Is Off the Charts in an Ohio City
The number of angioplasties performed in Elyria is so high that Medicare is starting to ask questions.

(The full article can be accessed through the New York Times website at http://www.nytimes.com/2006/08/18/business/18stent.html?pagewanted=2&ei=5094&en=b81be5f43f98a99b&hp&ex=1155960000&partner=homepage)



Cardiologists in little Elyria, Ohio, about a 30-minute drive west of Cleveland, do more coronary angioplasties and insert more stents than any other location in the U.S.--four times more than the national average, three times more than the Cleveland average. They perform even more than the recently-indicted cardiologist in Louisiana, who performed twice the national average of procedures.


The Times article, part of a series about financial incentives in medical care, provides a responsible and incredibly balanced report on the situation in Elyria. I have to give them credit, because from the eyes of a colleague (myself), this looks like blatant and extreme profiteering: "cathing for dollars".

I find it outrageous that this group of cardiologists claims that they have some special insight into heart care that justifies this extraordinary reliance on heart procedures. There's bound to be variation in practice patterns, but this is so outside the norm that I believe criminal behavior will be exposed. In fact, I believe that even the "norm", or average, rate of procedures is also excessive.

This is symptomatic of the perverse equation in heart disease care. If there's money to be made in major heart procedures, who wants to bother with prevention? Programs like the Track Your Plaque program present real potential to stop coronary heart disease in its tracks for many, if not most, participants--but don't expect to hear about it from your cardiologist. Don't expect to hear about it from the increasingly hospital-employed primary care physician.

Hopefully, media exposure like that in the New York Times is just the beginning of a public re-analysis of not only what's wrong with medicine today, but recognition of the tremendous power in preventive strategies when everyone stops being so enamored with hospital-based procedures. CT-based heart scanning that ignites your heart disease prevention program is your way to dodge the mainstream obsession with procedures.

More on "Bio-identical hormones" and Wyeth Pharmaceuticals

In October 2005, Wyeth petitioned the FDA, requesting that it completely ban the bioidentical alternatives that women have been using in ever-increasing numbers to achieve optimal hormone balance. With bioidentical replacement therapy clearly reducing its market share, Wyeth asked the FDA to outlaw all compounded bioidentical hormone formulations that compete with its own discredited drugs. If Wyeth is successful, then menopausal women will have no choice other than to take potentially life-threatening hormone drugs or to forgo hormone replacement therapy altogether, thus enduring the physically and emotionally debilitating effects of menopause-induced hormone depletion.

Dave Tuttle
Life Extension Magazine
August, 2006



For more commentary on Wyeth Pharmaceutical's outrageous and brazen petition to the FDA to bar prescription "bio-identical" hormones, i.e., hormones that are identical to natural human forms, read Life Extension's article, Health Freedom Under Attack!
Drugmaker Seeks to Deny Access to Bioidentical Hormones





This well-researched article is in the August, 2006 issue of Life Extension Magazine. The article can also be accessed online at http://www.lef.org/magazine/mag2006/aug2006_cover_attack_01.htm

or go to www.lef.org and click on the August, 2006 issue.

The author, Dave Tuttle, details the baseless arguments raised by Wyeth, a pathetic and amazingly selfish act in the name of protecting profits for Premarin, their prescription agent. It's bad enough to be selling this worthless drug. It's even worse--criminal, in my mind--to try to stamp out our right to have a physician write a prescription for a pharmacy to mix up hormones identical to that humans produce, individualized to our needs.

If you are as angry about this as I am, please go to the Life Extension online reprint that provides access to the International Academy of Compounding Pharmacists website to send the FDA an e-mail describing your opinion, or go to www.iacprx.org.

How accurate is LDL cholesterol?

Watch TV and you'd get the impression that the world revolves around LDL cholesterol: Commercials for Lipitor, Zetia, Vytorin, etc., all drugs to reduce cholesterol (total and LDL). Your doctor looks first and often only at LDL cholesterol.

If there's so much attention paid to LDL, how accurate is it? 100%? 90%? 80%?

Well, it varies widely. Occasionally, it's truly accurate, but most of the time it's miserably inaccurate . Every single day, I see people with LDL cholesterols that underestimates true (measured) LDL by 40%, 50%, and even over 100%. In other words, LDL cholesterol might be 120 mg/dl by the conventional method, but the genuine measured value might be 160 mg/dl, or even 240 mg/dl. It can be that far off--and it's not rare.

The converse can occasionally be true, though rarely in my experience: that conventional LDL overestimates true LDL. I saw someone in the office today like this, with a conventional LDL of 142 mg/dl but a true measured LDL of 115 mg/dl. I may see one or two more people like this the rest of this year.




Why is LDL so inaccurate? Several reasons:

--LDL in most labs is calculated, not measured. The "Friedewald calculation" derives LDL by substracting HDL and triglycerides (divided by 5) from total cholesterol. The higher triglycerides are, especially above 150 mg/dl, the more inaccurate the calculation becomes. As HDL drops below 50 mg/dl, this also introduces greater and greater inaccuracy.

--LDL particles vary in size. A more accurate representation and measure of LDL's dangers are therefore found in measures of LDL particle number , rather than a weight-based measure or calculation. LDL particle number can be measure as just that, LDL particle number (NMR), or as apoprotein B, the protein in LDL that occurs one apoB per LDL.

I liken conventionally calculated LDL cholesterol to a broken speedometer. You simply won't have an accurate measure of how fast you're going, though you may have a ballpark sense. But try telling that to the state patrol.

Or, as a cardiologist colleague said to me in a similar conversation about LDL: "Well, it's better than nothing!"

The lesson: If you're interested in plaque control, and control or reduction of heart scan score, you need a measured LDL, preferably LDL particle number by NMR or an apoprotein B. Another option is "direct" LDL.

Green tea: friend or faux?

The www.HealthCastle.com website is a helpful website on healthy eating that sends out a free newsletter. The content is all produced by licensed dietitions and nutritionists. Although I don't agree with everything said on the site, there's still some good information.

I'm a fan of green tea. Although I believe the effects are relatively modest (weight reduction, cholesterol reduction, anti-oxidation, etc., with theaflavin and/or green tea as a beverage,) they alerted me to the fact that the Lipton Green Tea product is one you should steer clear of. Here are their comments:



"More like Soft drink than Green Tea!With 200 calories, 13 teaspoons of added sugar and a long list of artificial ingredients, Lipton Iced Green Tea is more like a bottle of soft drink than tea, in our opinion."


The Lipton website lists the ingredients:

Water, high fructose corn syrup, citric acid, green tea, sodium hexametaphosphate, ascorbic acid (to protect flavor), honey, natural flavors, phosphoric acid, sodium benzoate (preserves freshness), potassium sorbate (preserves freshness), calcium disodium edta (to protect flavor), caramel color, tallow 5, blue1.

An 8 oz serving yields 21 grams of sugar. If you drink the full 20 oz. bottle (not hard to do!), that yields 52.5 grams of sugar! You will also notice that the second ingredient listed after water is high fructose corn syrup. This ingredient, you may recall, causes triglycerides to skyrocket, causes an insatiable sweet tooth, and is a probable contributor to obesity and diabetes.

In their defense, the Lipton people do also offer a sugar-free alternative without the excessive sweeteners and empty calories.

Do the Lipton products offer the same kind of benefits from green tea catechins (flavonoids) offered by freshly brewed teas? This product has not been formally tested by an independent lab to my knowledge, though, in general, commercially prepared and bottled teas tend to have dramatically less catechin/flavonoid content compared to brewed. (The USDA website provides access to an extraordinary collection of flavonoid food content at their USDA Database for the Flavonoid Content of Selected Foods - 2003. You'll find it at http://www.ars.usda.gov/Services/docs.htm?docid=6231.)

I think the HealthCastle people got it right: Brew your own, making sure to steep for at least 3 minutes. Alternatively, a green tea or theaflavin supplement provides many of the benefits. (Theaflavin has been used in trials at doses of 375 to 900 mg per day.) An in-depth report on green tea will be coming in a future Special Report on the www.cureality.com Membership website.
Saturated fat and large LDL

Saturated fat and large LDL

Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles


For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Comments (44) -

  • Anonymous

    2/16/2010 10:02:36 PM |

    Is there an inexpensive way of finding out which form you have?

  • Anonymous

    2/16/2010 11:02:49 PM |

    is there any truth to the idea that if your trig/HDL ratio is under 2.0 that your LDL type is predominantly large/buoyant?

  • Laura

    2/16/2010 11:37:17 PM |

    Is there a way to determine whether small LDL production is carb- or genetics-caused?

  • Anonymous

    2/16/2010 11:43:41 PM |

    Is this the same for poly/mono unsaturated fatty acids?

  • Anonymous

    2/16/2010 11:46:43 PM |

    Dr. Davis,

    Does the form of saturated fat have any impact on this in the case of genetic predisposition to small LDL formation? For example, does it matter if the fatty acids are lauric acid and stearic acid versus something like palmitic acid?

    Rick Braden

  • Daniel

    2/16/2010 11:50:11 PM |

    Dr. Davis,
    That's very interesting!!  Any chance you could provide the reference?
    Thanks, Dan

  • jtkeith

    2/17/2010 12:26:14 AM |

    This naturally leads to the question about understanding our personal genetic coding.  Without that coding information it seems difficult make an informed decision about the consequences of lowering carbohydrate and increasing fat (and saturated fat) until the consequences are upon you!

  • David

    2/17/2010 12:38:19 AM |

    This definitely needs a follow-up post. I've not seen this distinction until now. If true, Dr. Davis, does it not present a difficult dilemma for those who have both genetic sdLDL and Lp(a)? If saturated fat needs to be restricted for genetically high sdLDL, would this not leave the Lp(a) (which responds best to saturated fat intake) unopposed? What is your proposal to address this?

  • Ellen

    2/17/2010 1:09:25 AM |

    Interesting post, Dr. Davis. How would one find out if they are genetically predisposed to react to saturated fat intake with an increase in small LDL?

  • Harold

    2/17/2010 1:38:12 AM |

    Do you have some specific references for LDLa and saturated fat? Is it essentially congenital hypercholesterolemia that reacts with the sat fat?

  • steve

    2/17/2010 1:49:56 AM |

    this is a long overview discussion. thank you!  What would dietary recommendation be for someone if small LDL is genetic in origin?  Also, wouldn't this pattern possibly require statins to get LDL particle count as low as possible since it is unlikely that diet will do the job?  In my case, i need Lipitor and Zetia; otherwise my particle count mostly small remains high despite Vit D, normal weight,no wheat cornstarch or sugar.  Great post!

  • Anonymous

    2/17/2010 1:50:56 AM |

    Doc -

    Good post but -

    Hard to understand post without the background basis on which the statement is made.

    Is your statement based on clinical observations? Or is it based on opinion only?

  • switters

    2/17/2010 4:44:09 AM |

    Yes, references supporting your premise in this article would be very welcome.

  • Paul

    2/17/2010 9:46:22 AM |

    This post concerns me because as a low carber I find it difficult to maintain a low carb diet without saturated fat sources. Perhaps this is driving the concern and questions from others also.

  • Rabbi HIrsch Meisels

    2/17/2010 2:14:23 PM |

    Count me in those who are waiting to see data where this is coming from.
    Thanks for all your blogs posts.

  • zach

    2/17/2010 3:26:16 PM |

    Yes, I hope this isn't a hit and run post. Many learned people, such as Peter at hyperlipid would probably disagree. Do you have any references?

  • Alfredo E.

    2/17/2010 3:48:38 PM |

    So what do we do if we should not eat but a few carbos and up to certain amount of protein?

    The rest have to be saturated fats, isn't it?

    Please, some more practical information before we all run over the cliff.

  • Anonymous

    2/17/2010 5:48:11 PM |

    Harold, I am also interested in the familial hypercholesterolemia question.  After a quick search, I found this http://www.jlr.org/cgi/reprint/23/8/1196.pdf with a quote: "LDL has been
    found to be cholesterol-enriched and triglyceride-poor
    (5, 6), and in one study, the peak flotation rate of FH LDL
    has been found to be higher than in normals (6),
    implying decreased density, increased size, or both.
    However, these results are difficult to assess, since there
    is considerable heterogeneity of LDL in normal subjects,
    although size, flotation rate, and composition"

    So, FH people may be predisposed to large, fluffy LDL.  However, I do not know whether FHs handle saturated fats better than normals, and this is an important question.  

    -Aaron

  • Anonymous

    2/17/2010 5:54:55 PM |

    A question on triglycerides...if high TGs are a trigger for small, dense LDL and should be minimized, are there any ways to reduce area-under-the-curve TGs after a meal (other than the usual low carb, omega-3, etc. recommendations).  Are large, infrequent meals better than small, frequent meals?  Does fiber change the shape of the post-meal TG curve?

    Also, does fasting TG tell the whole story?  Could one have, say, <50 mg/dL fasting TG but have elevated TG throughout the day as a result of large, high-fat meals?  

    -Aaron

  • Anonymous

    2/17/2010 7:04:29 PM |

    Thank you Dr. Davis!  Finally a voice of sanity in this whole sat fat hoopla.

    I for one, although not neurotic about it, do not favor saturated fats and will eat a good non-hydrogenated margarine (like Smart Balance) over butter any day.

    Please keep up this sane blog and give us the WHOLE enchilada, not just what some want to hear.

  • Dr. William Davis

    2/17/2010 7:47:07 PM |

    Search PubMed or Google Scholar and you will find NO data on this issue. To my knowledge, there are none that distinguish genetically -driven small LDL vs. lifestyle-induced.

    This is based on having tested lipoproteins in thousands of people over the past 10+ years.

    Prototypical "genetic small LDL" person: 5 ft 10 inch, 140 lb male who eats low-carb. In other words this person is at ideal weight and does not eat foods that trigger small LDL--yet has 90% small LDL by NMR (e.g., 1200 nmol/L, LDL particle number 1550 nmol/L). Should this person overindulge in saturated fat, small LDL will go up.

  • Scott Miller

    2/17/2010 8:46:27 PM |

    Dr. Davis, how do you know it is saturated fats that are the cause? For example, most low-carbers also have elevated intake of inflammatory polyunsaturated fatty acids, which I would be much more likely to blame.  But, in either case, it seems there are too many uncontrolled variables involved (as far as food intake) to pin any of them to the wall.

    It's very difficult for me to believe saturated fat is the cause, while other possibilities exist.

  • Anonymous

    2/17/2010 9:08:19 PM |

    For everyone worrying about this, just get yourself a VAP or NMR test.  If you have LP(a) or sdLDL, that will show it.  You don't need genetic testing.

  • Anonymous

    2/17/2010 10:27:45 PM |

    What's are the trig and HDL numbers for the prototypical "genetic small LDL" person?

  • Anonymous

    2/17/2010 11:09:09 PM |

    Thanks Dr. Davis for another insightful post from your clinical experience, giving the kind of information that helps elucidate why saturated fat works for some and not for others - and the kind of information you can't get anywhere else.  Ignore the pro saturated fat/anti-polyunsaturated fat zealots, who can't be persuaded by any evidence or logic.

  • Anonymous

    2/17/2010 11:10:11 PM |

    "What's are the trig and HDL numbers for the prototypical "genetic small LDL" person?"

    I'd like to second that - can one have high HDL and low trigs and still have a small LDL pattern?

  • Kurt G. Harris MD

    2/18/2010 12:56:55 AM |

    Hello Dr. Davis

    You said:

    "Should this person overindulge in saturated fat, small LDL will go up."

    Just to be clear, are you saying you have observed low carb subjects (how low?) that have added saturated fat to their diets and then on subsequent testing you have seen sdLDL rise in absolute and percentage terms?

    If they were truly LC, were they already high sat fat at the time of the NMR or were they high PUFA (South Beach?)

    May I ask how many such cases you have seen?

    You should definitely publish this, or if you don't think it is publishable maybe you could give us all the data in a blog post.

    Thanks, this is very interesting.

  • Dr. William Davis

    2/18/2010 1:52:52 AM |

    In people with presumptive genetically-determined small LDL, HDL can be 70 mg/dl or greater, triglycerides 45 mg/dl or less, yet small LDL persists, usually at 600 nmol/L (NMR).

    I have approximately 100 patients like this. They tend to be very thin with BMI's of 23 or so, yet small LDL persists.

  • Stephen

    2/18/2010 3:11:53 AM |

    Hi Dr. Davis,

    This post really intrigues me. I am a first year medical student (24 yo) with familial hypercholesterolemia. I am on a low carb paleo diet, taking omega 3, vit D and just recently added magnesium to the mix as well. I went off Lipitor two months ago just an experiment to go along with this new eating plan, and received blood work only a few days ago. Numbers about 450 on total and 285 for LDL. My CT scan already showed plaque buildup in the coronary arteries, aorta, and one valve. While I am not looking for medical advice per se (since I know you prefer not to give it over your blog) I was just curious as to how your track the plaque plan and recommendations are effected with this type of genetic disorder. My cardiologist says if I dont go on drugs immediately I'll have a cardiac event at 40 years of age. I could use some advice and direction to persue. Is it impossible to avoid genetics, and the use of drugs are unavoidable? Thanks. Really appreciate it.

  • Anonymous

    2/18/2010 3:15:38 AM |

    How do you know how much small LDL you have?

  • Bonnie

    2/18/2010 3:53:00 AM |

    ""I'd like to second that - can one have high HDL and low trigs and still have a small LDL pattern?""

    Well - just speaking for myself, I have high HDL and low trigs, and always had a mix of small/large (A/B) pattern LDL.  When I stopped eating wheat, my LDL all became large.  

    I also have high Lp(a), which was uneffected by my eliminating wheat.

    You can drive yourself crazy figuring out what's OK to eat and what's not.  I don't worry about it anymore.  I rarely eat wheat because I've seen results from Not eating it, try not to overdo the sugar and fruit, get plenty of veggies and protein.  

    I get my VAP test once or twice a year to make sure everything is where it should be, more or less.

    I'm just not going to worry about it beyond that.  

    Bonnie

  • LeenaS

    2/18/2010 4:12:28 AM |

    Dr. Harris:

    Are these customers of yours lean lowcarbers eating plenty of LA or very, very much protein in their diet? If not, then what do they eat?

    With regards,
    LeenaS

  • Mike

    2/18/2010 4:26:28 AM |

    Interesting, and concerning, since I fit that description:

    Chol: 6.35mmol/L
    HDL: 1.88
    LDL: 4.2
    Triglycerides: 0.66
    Chol/HDL ratio: 3.4
    American Values:  TG 58.47 LDL 162.54 HDL 72.75
    Triglyceride/HDL ratio: 0.8
    Hieght: 6'0
    Wieght: 165lbs
    BF 8%

    I've had other opinions on these numbers; should I be pursuing more accurate particle numbers?  I go out of my way to consume large amounts of red meat, coconut oil, butter, and eggs.  I'm fitter and healthier (subjectively) than I ever have been at 36 than I was in my 20's.  I find it disconcerting than I could potentially be doing something detrimental.

  • Kurt G. Harris MD

    2/18/2010 4:43:49 AM |

    Hi Dr. Davis

    In the original post you said:

    "saturated fat will increase small LDL.  In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL."

    So, if I follow this correctly, you are saying that these 100 patients all had increases in their sdLDL after documented increases in saturated fat in their diets? In other words you had two data points for each subject, correct?

    If the subjects did not all have documented increases in sLDL then by "persist", do you mean their sdLDL went down with LC eating (like 800 to 600, say) or do you just mean that they had a single high value and it was only measured once, but it was high?

    If it is the latter, I could see how it's fair to say that some LC eaters have a higher sdLDL than we might predict (for whatever reason) but it seems like a non sequiter to conclude that the sdLDL would be made higher with more sat fat consumption.

    I just want to make sure I get this straight so I understand it correctly.

  • Paul

    2/18/2010 6:19:52 AM |

    Thin. Nice. I'm less concerned. lol

  • Anonymous

    2/18/2010 1:22:06 PM |

    Does this group of people also have elevated blood sugar, as might be predicted by another of your blog postings?

    http://heartscanblog.blogspot.com/2009/12/to-track-small-ldl-track-blood-sugar.html

  • David

    2/19/2010 3:10:43 AM |

    Dr. Davis,

    I concur with Dr. Harris in that more details would be nice to better understand exactly what you're saying.

    Are other variables accounted for? Were many, most, or all of these patients on statin drugs, which could have prevented a shift in particle size if triglycerides were low and insulin sensitivity was high?

    Again, if there is such a phenomenon going on, is the "genetic sdLDL" clearly atherogenic in the same way that "environmental sdLDL" seems to be?

    If so, I ask again, what is the solution for someone who is afflicted by both Lp(a) and genetic sdLDL? The "profile" for genetic sdLDL is similar to the profile for those with Lp(a), and there is probably a lot of crossover. Saturated fat lowers Lp(a), but (presumably) raises genetic sdLDL. This is a fierce dilemma! Would not the better choice be to choose the diet that opposes the more vicious of the two, which is Lp(a)? What is the priority?

    Has a high SFA diet only increased sdLDL per NMR, or has it also clearly been shown to increase CAC scores? In other words, does it clearly progress the disease itself?

    David

  • pmpctek

    3/7/2010 5:50:15 PM |

    Saturated fats not linked to heart disease: Meta-analysis - American Society for Clinical Nutrition (January 13, 2010). doi:10.3945/ajcn.2009.27725 © 2010

    It would really be interesting to know what the primary sources of saturated fat are for these "100 patients".  There may be a single (widely available) common source of sat fat that these specific patients are consuming, do we even know that?  I agree, by what has been revealed, that there are too many variables to know conclusively that saturated fat is the cause of their persistently elevated small LDL.

    Mark me down as someone who is not convinced that CLA, n3 rich organic, free range, and wild animal sources of fat could possibly in any way be detrimental to anyone.

  • Anonymous

    4/19/2010 1:45:33 PM |

    When will people stop worrying about cholesterol numbers? They really don't mean anything.

    Until someone explains a plausible mechanism through which lipoproteins directly kill me I will ignore it any suggestion that they do. This is what a good scientist would do.

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    11/3/2010 6:55:04 PM |

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