Calculus of the cardiologist

I call this the "calculus of the cardiologist":

Heart procedures = big money

More procedures = more big money

You do the math. If you do more procedures, you get more money.
What if your patients don't need more procedures? That's easy. You lower the bar on reasons to do procedures. You scare the pants off people and lead them to think that all heart disease or questions about heart disease are potentially life-threatening. You could even appear to be doing the patient a big favor. "My Lord! This is potentially dangerous. We need to perform a procedure without delay!"

There are incentives beyond direct cash payment. A patient of mine today showed me a memo to employees in his company that showed why certain hospitals are targeted for care. The criteria for choosing centers was based on number of procedures performed. In other words, the more procedures performed at a hospital, the more procedures will be directed there. Of course, this makes sense at some level. More procedures can also mean greater skill.

But have we lost sight of the fact that the mission is not more procedures and more money, but to get rid of a disease? If the intensity of effort devoted to heart procedures were re-directed to early detection, prevention, and reversal of disease, we'd have half the hospitals we now have. We'd also chop a huge chunk out of the national healthcare budget.

Lipoprotein(a) treatment alternatives

A question from a reader:


Two years ago, my doctor recommended a comprehensive lipid screening because both of my parents had heart disease. My only blood component way out of line was LP (a) [lipoprotein(a)]. It was 130. According to the lab that conducted the screening, Berkeley Heart Lab, a level above 30 should be cause for concern. I was stunned that mine was more than quadruple the danger level.

I began taking two grams [2000 mg] of niacin a day in addition to the Lipitor I was already taking. The next reading, a few months later, was 87. Over a period of about 18 months, I had a total of four readings from Berkley Heart Lab. My LP (a) fluctuated in the 80-130 range – still way above normal. My doctor said there was little else I could do to control it.

That doctor has since retired. I now see another doctor who uses a different lab. My first LP (a) reading with him a few months ago was 17, which is normal. I am still taking the same amount of niacin and Lipitor and I can’t think of anything that would account for the huge discrepancy. I’m going to have another test again soon.

Is one of the labs giving erroneous readings? If so, how can I tell which? If Berkeley Heart Lab is correct, is there anything I can do about my increased coronary risk due to high LP (a)?

Tom D.

Tom's frustration on the variation of Lp(a) is due to the fact that laboratories run the Lp(a) test by several different techniques and will generate tremendous variation in values. The key is to stick to the same measure over and over from the same lab, else you'll be terribly confused and frustrated. Tom essentially should ignore the value obtained that was unexpectedly low.

Another issue: Lp(a) is a turtle. It responds very slowly. In fact, we rarely check it more than once or twice a year. Check it too soon after a treatment change and it won't fully reflect the effect. You've got to wait at least several months before re-checking.

How about treatment alternatives? They are:

--More niacin. Not my favorite choice, since niacin >2000 mg per day begins to generate more side-effects, but it is a choice. You can go to 4000-5000 per day, but only with your doctor's supervision due to liver effects.

--Testosterone for males. We use topical testosterone from Women's International Pharmacy in Madison, Wisconson. Prescription patches like Testim are also effective.

--Estrogen for females. This is less "clean" than testosterone, introducing questions about endometrial and breast cancer risk, but it is a choice.

--DHEA--A small effect but every little bit can help. We use 25-50 mg per day, depending on blood levels and only if you're 45 years old or older.

--l-carnitine--In my experience, a small effect. It requires 2000 mg per day, which is expensive. Sometimes, an expected large effect develops, so it's worth a try if it fits in your budget.

--Fibrates--These are the drugs Tricor and Lopid. I don't like these agents very much because I think they're weak, including the effect on Lp(a) reduction. But they are choices for you and your doctor.

Lastly, you can simply be guided by your heart scan score. For example, if Tom's initial heart scan score is 200, and he continues his current program and one year later his score is 300, then alternative treatments are worth considering. But what if Tom's score is 189--he's regressed his coronary plaque. Then, who cares what his Lp(a) is?

Another issue to keep in mind is that, in the presence of Lp(a), keeping LDL to very low numbers (e.g., 60 mg/dl) may added value in preventing coronary plaque growth.

Trapped in a low-fat world

If you would like to...

--Reduce (good) HDL

--Raise triglycerides, sometimes by hundreds of points

--Raise blood sugar into the pre-diabetic range

--Raise blood pressure

--Accelerate coronary plaque growth

then go on a low-fat diet like the one promoted by long-time super low-fat advocate, Dr. Dean Ornish. Every day I have to educate patients that a low-fat diet as advocated by Dr. Ornish is a destructive, counter-productive process that makes coronary plaque grow and increases your heart scan score.

If you want to gain control over coronary plaque, do not follow the Ornish program or anything resembling it. The Ornish program is a dead end.

Instead, the crucial components of a healthy diet for plaque control are:

--Low saturated and hydrogenated fat, but not low all fats.

--High monounsaturated and omega-3 fats

--Low glycemic index (i.e., slow sugar release)

--High fiber

That simple. An excellent program to put these limits to practical use is the South Beach Diet. Or, follow the more detailed guidelines on the Track Your Plaque website (open content section).

Blame the niacin

Despite the fact that niacin is:

1) A vitamin--vitamin B3

2) One of the oldest cholesterol-reducing agents around with a long-standing track record of effectiveness and safety

3) Available as a prescription drug as well as a variety of "nutritional supplements"

most physicians remains shockingly unaware of its benefits, effects, and side-effects. Most, in fact, are either ignorant or frightened of advising their patients on niacin use. As a result, I commonly have to tell my patients to resume the niacin that their primary care physician has (wrongly) stopped because of itchy feet, grumpiness, groin rash, urinary tract infections, nightmares, diarrhea, hair loss, runny nose, etc. All of these are REAL reasons doctors have advised patients to stop niacin (though none were actually due to niacin).

Is niacin really that troublesome? No, it's not. In fact, if used properly, it's among the most effective and safe tools available for correction of low HDL, small LDL and other triglyceride-containing lipoproteins, lipoprotein(a), and dramatic reduction of heart attack risk. If added to a statin agent, the heart attack risk reduction can approach 90%.

Statins are just too easy for doctors to prescribe. Niacin, on the other hand, requires a good 15-20 minutes to describe how to use it. It could generate an occasional phone call from a patient who struggles with the annoying but largely harmless and temporary "hot-flush" feeling, a lot like a hot blush. Given a choice, most doctors would simply choose not to be bothered. For this reason, I'll commonly see many, many people with uncorrected low HDLs and other patterns.

Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

Here are the steps we advise that really make taking niacin easy and tolerable:

1) Take with dinner.

2) Take with 2 extra glasses of water. If you experience the hot-flush later on, drink an additional 2 8-12 oz glasses of water i.e., a total of 16-24 oz). Extra hydration is extremely effective for blocking the hot-flush.

3) Take a 325 mg, uncoated aspirin. This is only necessary in the beginning or with any increase in dose, rarely chronically for any length of time.


This is not to say that there aren't occasional people who are truly and genuinely intolerant to niacin. It does happen. But those people are a small minority, less than 5% of people in my experience. Niacin is far more effective and safe than most physicians would have you believe.

Eat fish three times a day

Patients commonly ask, "Why can't I get vitamin D from food? I drink milk and eat fish."

They're absolutely right: both vitamin D and some oily fish contain vitamin D. However, it's a matter of quantity. An 8 oz. glass of milk contains 100 units of vitamin D (at least it's supposed to; this is not always true). A serving of oily fish like salmon or herring may contain up to 400 units. Thus, if you ate fish three times a day like the Eskimos or the Inuit, you might obtain sufficient vitamin D to prevent the broad and alarming spectrum of phenomena associated with deficiency.

I suspect that most people don't want to eat fish three times a day, nor drink the 20 to 50 glasses of milk per day that would be required to obtain a truly healthy quantity of vitamin D.

The vocal and outspoken Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) has written eloquently on the potential relationship between influenza and vitamin D deficiency. He and his co-authors on a recently published paper point out that the peculiar and unexplained seasonality of influenza corresponds to vitamin D levels. Read his eloquent discussion in Medical News Today at http://www.medicalnewstoday.com/medicalnews.php?newsid=51913.

In the article, Dr. Cannell explains:

"The vitamin D steroid hormone system has always had its origins in the skin, not in the mouth. Until quite recently, when dermatologists and governments began warning us about the dangers of sunlight, humans made enormous quantities of vitamin D where humans have always made it, where naked skin meets the ultraviolet B radiation of sunlight.
We just cannot get adequate amounts of vitamin D from our diet. If we don't expose ourselves to ultraviolet light, we must get vitamin D from dietary supplements...Today, most humans only make about a thousand units of vitamin D a day from sun exposure; many people, such as the elderly or African Americans, make much less than that. How much did humans normally make? A single, twenty-minute, full body exposure to summer sun will trigger the delivery of 20,000 units of vitamin D into the circulation of most people within 48 hours. Twenty thousand units, that's the single most important fact about vitamin D. Compare that to the 100 units you get from a glass of milk, or the several hundred daily units the U.S. government recommend as “Adequate Intake.” It's what we call an “order of magnitude” difference.

"Humans evolved naked in sub-equatorial Africa, where the sun shines directly overhead much of the year and where our species must have obtained tens of thousands of units of vitamin D every day, in spite of our skin developing heavy melanin concentrations (racial pigmentation) for protecting the deeper layers of the skin. Even after humans migrated to temperate latitudes, where our skin rapidly lightened to allow for more rapid vitamin D production, humans worked outdoors. However, in the last three hundred years, we began to work indoors; in the last one hundred years, we began to travel inside cars; in the last several decades, we began to lather on sunblock and consciously avoid sunlight. All of these things lower vitamin D blood levels. The inescapable conclusion is that vitamin D levels in modern humans are not just low - they are aberrantly low."


Like Dr. Cannell, I am absolutely convinced that vitamin D deficiency plays an important role in a number of illnesses, including coronary disease. The more we mind our patients/participants vitamin D status (blood levels of 25-OH-vitamin D3), the more easily we gain control over LDL cholesterol, pre-diabetic patterns, blood pressure, blood sugar, and coronary plaque. In fact, I am becoming rapidly convinced that vitamin D deficiency is an extremely important coronary risk factor.

Because I live in Wisconsin (bbrrrrr!) where seeing the sun is a cause for celebration and sun exposure is possible three months a year, I take 6000 units per day vitamin D. This is the amount necessary to raise my blood levels into the true, physiologic range of 50-70 ng/ml. My wife takes 2000 units per day, and each of my kids takes 1000 units per day, though I believe that my 14-year old son (my size now) should take more. We'll judge by blood levels.

If there is a little-known secret to reducing heart scan scores, vitamin D is that "secret".

To read more from Dr. Cannell or to subscribe to his free and very informative newsletter, go to Vitamin D Council

What if I had a cure for coronary disease?

If I had a cure for coronary disease, what would it look like? What would constitute cure? Would you recognize it if I showed it to you?

In the strictest sense, "cure" means an absolute elimination of any sign of coronary plaque, as well as elimination of any and all dangers associated with coronary disease. It would also mean elimination of the factors that created coronary atherosclerotic plaque in the first place.

In a more practical sense, you could argue that "cure" means a reduction of the amount of material that constitute coronary disease along with a dramatic reduction of the associated risks (i.e., heart attack).

You might call this second, more lax definition "regression" or "reversal".

Is "cure" in the strictest sense possible? No, not to my knowledge in 2006. Yes, there are many (kooks) who claim this is possible, but there's no objective evidence of this occurring.

Regression, or reversal, however, is indeed possible. In fact, I've seen it countless times following the participants in the Track Your Plaque program. If your heart scan score goes from 1000 (a bad score with high risk for heart attack) to 750, you've experienced a large reduction in the amount of atherosclerotic plaque that is behind coronary disease. You've also reduced your risk of an "event" like heart attack to near zero (provided you remain on the program that achieved regression in the first place).

Unfortunately, with present technology regression or reversal does not mean that the original causes of coornary plaque are eliminated. They're just controlled. Fish oil, for example, powerfully reduces triglyceride-containing lipoproteins that trigger coronary plaque growth. But if you stop fish oil, the evil lipoproteins come right back and start injuring your coronaries, causing more plaque growth.

The Track Your Plaque program is the closest thing I know of to a "cure" for coronary disease, that is, "cure" in the sense of regression or reversal. Perhaps in future we'll have a "cure" in the strict sense. Until now, this program is the best there is.

Alternatives to fish oil capsules

Occasionally, someone will be unable to take fish oil due to the large capsule size, excessive fishy belching, or stomach upset. The easiest solution is usually just to try a different brand, e.g., Sam's Club (Makers' Mark brand) enteric-coated.

However, sometimes liquid fish oil preparations may be preferred. Here'a list of products we've used successfully. All cost more than plain old fish oil capsules, but fish oil is so crucial to your heart scan/coronary plaque control efforts, that it really pays to search out alternatives.



Liquid fish oil alternatives to capsules:

Liquid fish oil--e.g., Carlson's liquid fish oil. Most liquid fish oil comes flavored either lemon or orange.



Frutol--A very clever re-formulation of fish oil that makes it water-soluble and non-oily. The Pharmax company has put their fish oil into a fruit flavored base that tastes pretty good and is not too expensive.
Go to www.pharmaxllx.com for more information. Unfortunately, I do not believe it's available in stores.





Coromega--another non-oily preparation, though available in some health food stores. Coromega comes in little single-serving foil dispensers. It tastes kind of fruity (though I personally like the Frutol better for taste and consistency). It's kind of pricey ($1.40 per day for two packets).



Regardless of what preparation you choose, you can determine the dose needed by adding up the EPA+DHA content. For the basic prevention effect, the starting dose for the Track Your Plaque program, you need a total of 1200 mg per day of EPA+DHA. Higher doses, e.g., 1800-2400 mg per day, may be required for correction of high triglyceres or postprandial (after-eating) abnormalities.

Ignoring your heart scan is medical negligence

I continue to be dumbfounded that many doctors continue to pooh-pooh or ignore CT heart scans when people get them.

I can't count the number of people I've seen or talked to through the Track Your Plaque program who've been told to ignore their heart scan scores. The most extreme example was a man whose physician told him his heart scan score of nearly 4000 was nothing to worry about!


A real-life story of a retired public defense attorney whose heart scan score of 1200 was ignored, followed two years later by sudden unstable heart symptoms and urgent bypass prompted us to write this fictitious lawsuit. Though it's not real, it could easily become real. To our knowledge, no single act of ignorance about heart scans has yet prompted such a lawsuit, but it's bound to happen given the number of scans being performed every year and the continued stubbornness of many physicians to acknowledge their importance.



Major Malpractice Class Action Lawsuit Looms for Doctors Who Ignore Heart Scan Tests

It's been several years since new medical discoveries have debunked old theories regarding heart disease and heart attack and have verified the efficacy of CT heart scans for detecting both early and advanced heart disease. Doctors who fail to keep apprised of these finding or refuse to change their practice for financial reasons put themselves at risk for becoming defendants in a major malpractice class action lawsuit. The plaintiffs will be a growing class of persons who were debilitated by avoidable heart attacks and heart procedures and the heirs and estates of those who have died.
Milwaukee , WI (PRWEB) November 29, 2005 -- This press release outlines a template for a potential class action lawsuit that may be on the horizon for the medical industry. The class of plaintiffs for this theoretical action remains latent but is growing on a daily basis. However, it requires only one such plaintiff to find an attorney who recognizes the scale and magnitude of the potential damages and move forward on a contingency basis. In real terms, this class could include 80% of those who had a heart attack, underwent a heart procedure, or subsequently died. According to the latest American Heart Association statistics, this number is estimated to be a least 865,000 persons and the entire class could easily be 10 times that number. Using a conservative estimate of $500,000 in damages per class member, the total damages could exceed $400 billion.

The plaintiffs, defendants, third parties, and facts surrounding the following moot complaint represent an actual incident. The names, specific health information, and dates have been changed to protect potential litigants.

Plaintiff, through his attorneys, brings this action on behalf of himself and all others similarly situated, and on personal knowledge as to himself and his activities, and on information and belief as to all other matters, based on investigation conducted by counsel, hereby alleges as follows:

NATURE OF THE ACTION

1.Plaintiff brings this class action on behalf of himself and all other persons who suffered physical damages or mental distress as a result of receiving a medical diagnosis indicating they had no identifiable heart disease, elevated risk for heat attack, or who were prescribed medications not suited to treat their heart disease once detected.

2.Substantial and irrefutable medical evidence has established that cardiac stress testing is an ineffective method for detecting heart disease of the type that is the root cause in over 90% of all heart attacks and other complications of heart disease that result in death or debilitating injury. A readily available and well-publicized test known as “CT heart scanning” is capable of detecting virtually all heart disease of this nature. It has also been established that simple cholesterol testing often fails to detect persons like likely to develop serious heart disease and prevents them from receiving common treatments capable of reducing or eliminating the source of their undetected heart disease. Readily available blood testing techniques exist that are capable of detecting non-cholesterol related sources of heart disease.

3.The medical community has made significant investments in outdated methods of detecting and treating heart disease. They rely on the revenue streams generated by providing these treatments to persons whose heart disease has progressed to the stage that intervention is required to prevent death or debilitation. Any change in diagnostic or treatment methods resulting in the prevention of heart disease would require substantial investments in new technologies and would severely reduce the market for current treatments. Plaintiffs believe this is a motivating factor in the neglect and willful suppression of readily available technology capable of detecting and preventing heart disease and represents gross medical malpractice.

SUBSTANTIVE ALLEGATIONS

On January 23, 1999, Plaintiff underwent a CT Heart Scan which was interpreted by a cardiologist at the ABC Scan Center . Plaintiff received a report from the Scan Center cardiologist indicating that his “calcium score” placed him in the top 1% for heart attack risk among men in his age group. The report also included the comment “Patient has a high risk of having at least one major stenosis (50% or greater blockage) in his Left Anterior Descending (LAD) artery and is urged to consult with a physician regarding this finding.”

On March 3, 1999 Plaintiff presented Defendant with the results of the January 23, 1999 CT Heart Scan. Defendant told Plaintiff to disregard the CT Heart Scan Results and ordered a physical including a stress test and cholesterol blood test.

On April 1, 2005, Plaintiff had a heart attack and a subsequent coronary angiography that confirmed multiple obstructive coronary plaques in his LAD. Plaintiff received an emergency balloon angioplasty to relieve his acute condition. Substantial damage to plaintiff's heart was incurred before emergency angioplasty could be instituted.

On April 3, 2005, per Defendant's recommendation, Plaintiff underwent open heart surgery to insert three bypasses in his LAD to resolve substantial obstructive heart disease, the same artery identified as having likely obstructive heart disease over 5 years earlier via CT heart scan.

On July 7, 2005, Plaintiff independently obtained additional blood testing not ordered by Plaintiff and was found to have several additional blood abnormalities not discovered by Defendant that are known to contribute to the development of heart disease and were readily treatable using lifestyle changes, nutritional supplements, and prescription drugs.

As early as September, 1996, the American Heart Association (AHA) issued a “Scientific Statement” to health professionals acknowledging the strong link between heart attacks and high calcium scores in asymptomatic patients. Extensive studies and references have confirmed the ineffectiveness of stress testing to reveal early heart disease in asymptomatic patients.

Plaintiff alleges that Defendant failed to utilize readily available medical tests and protocols to identify, aggressively treat, and potentially delay, halt, or reverse advanced heart disease that later resulted in extensive physical and emotional trauma to the Defendant.

PRAYER FOR RELIEF

WHEREFORE, Plaintiff herein demands judgment:

A. Declaring this action to be a proper class action maintainable pursuant to Rule 23 of the Federal Rules of Civil Procedure and declaring Plaintiff to be a proper Class representative;

B. Awarding damages against each defendant, joint and severally, and in favor of Plaintiff and all other members of the Class, in an amount determined to have been sustained by them, awarding money damages as appropriate, plus pre-judgment interest;

C. Awarding Plaintiff and the Class the costs and other disbursements of this suit, including without limitation, reasonable fees for attorneys, accountants, experts; and

JURY DEMAND

Plaintiff hereby demands a trial by jury.

Light the fuse of heart disease

Father Bob, despite his calling as a priest and counselor, led a stressful life. His average day was packed tightly with commitments: counseling members of his congregation, visiting the hospital, more official priest and church duties.

At age 53, his heart scan score of 799 came as a complete surprise. Even more of a surprise, his stress test was dramatically abnormal showing poor flow in the front of his heart at a level of exercise that wouldn't challenge most 75 year olds. His blood pressure with exericse: 230/100. Bob was shocked.

A few stents to the LDL later, Bob was trying to turn a new leaf on lifestyle. His life prior to the diagnosis of heart disease was driven by convenience. Because his day was so filled with commitments, he simply grabbed what he could from hospital cafeterias, fast foods, etc.

But after his procedure, Bob committed to choosing healthier foods, walk every day, and resist the food temptations presented by convenience.

However, temptation defeated him twice in the first few weeks after his stents. On the first occasion, Bob gave into eating a cheeseburger. On the second, Bob was at a fish fry (this is Wisconsin, after all) and ate a large serving of deep-fried fish.

On both occasions, Bob started feeling awful within minutes after eating: foggy, bloated, gassy, and fatigued. He took his blood pressure after each incident: 210/90, even though his blood pressure had more recently been trending down towards 130/80.

What happened? Grotesquely unhealthy foods like the deep-fried fish and cheeseburger provoke an abnormal constrictive process body wide. Some call this "endothelial dysfunction". Regardless, it is a graphic and frightening demonstration of the power of these sorts of unhealthy foods to wreak immediate and dangerous effects. Father Bob's response was more exagerrated than most, but it happens to all of us.

Eat badly and your body will pay the price. Even that occasional hot chocolate sundae or Egg McMuffin will yield cumulative injury, among which will be a rise in your heart scan score.

"I don't know what I'm doing here"

Jim came to the office at the prompting of his wife.

At age 52, Jim was semi-retired, having to work only a few hours a week to maintain his business. He'd had a high cholesterol identified about 10 years earlier and had been taking one or another statin drug ever since.

However, Jim's wife was a pretty savvy girl and understood the inadequacies of the conventional approach to heart disease prevention. Nonetheless, when Jim came in, he declared, "I feel great. I don't know what I'm doing here!"

I persuaded Jim to undergo a heart scan. His score: 2211, in the 99th percentile (the worst 1% for men in his age group). However, it was worse than that. Any score above 1000 carries a heart attack risk of 25% per year unless prevention issues are fully addressed.

Indeed, Jim proved to have far more than a high LDL cholesterol. Among the patterns uncovered with his lipoprotein analysis were small LDL, the postprandial (after-eating) abnormality of intermediate-density lipoprotein (IDL), and high triglycerides and VLDL. All would require correction if Jim is to hope to gain control of his extensive coronary plaque.

The message: Trying to discern risk for heart disease from cholesterol is complete folly. This man was going to die or have an urgent major heart procedure within the next year or two, all while taking his statin drug.

Discard the silly notion that cholesterol tells you everything you need to know about heart attack risk. It does not. It helps a little but leaves vast voids in risk determination. Fill those gaps with a heart scan, plain and simple.
Butter and insulin

Butter and insulin

In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Comments (83) -

  • Miki

    3/19/2010 5:48:56 PM |

    I wander if the effect is due to the milk solids or the type of fatty acids. If it is the milk solids making ghee will solve the problem.

  • Anonymous

    3/19/2010 5:54:39 PM |

    So the low fat control meal of pasta and bread gives the LEAST amount of insulin response!

    So, to avoid insulin spikes you must minimize all types of fats.

    Fat+Pasta seem to trigger the insulin.  The glucose response does not seem to matter all that much.

  • jd

    3/19/2010 5:54:39 PM |

    Thanks for the great info as always.

    Is it correct to say, in view of the graphs, that this type of dairy-induced insulin elevation is not mirrored by blood glucose readings, so we couldn't check for it at home with a glucose meter?

  • John

    3/19/2010 5:56:08 PM |

    butyric acid causes an insulin response, as does casein...interestingly, although i can't find it, i saw a paper that showed the insulin response to white bread was actually less when combined with butter...

  • daniel the smith

    3/19/2010 6:06:21 PM |

    What if you eat it without any carbs (e.g., like I do with my eggs in the morning)? If there's nothing to trigger the insulin in the first place, butter can't make it worse, right? Or am I wrong?

  • Lucy

    3/19/2010 6:16:20 PM |

    That's an interesting study indeed.  It seems to indicate that eating no fat at all (the control meal) provided better results in every category except glucose rise, and then it was only with the rest of a fairly tight pack.  Adding any fat at all spiked the insulin significantly higher.   This is consistent with the charts in your post "The Timing of Blood Sugars".  Yet you concluded there that carbohydrates should never be consumed without fat.  Based on these studies, it sure looks like a person is trading a little glucose rise for a larger insulin spike when consuming fat.  Which begs the question, which is worse?  Does insulin cause more problems than glucose?   You did say it was the insulin that triggered weight gain...

    I remain unconvinced that I should rush out and follow Ornish.

  • Diana Hsieh

    3/19/2010 6:34:54 PM |

    Interesting post -- and my experience confirms it.  Here's something that I recently posted to the OEvolve e-mail list:

    As folks might know, I've been struggling with my weight due to my hypothyroidism.  Even though many of my symptoms have improved, I continued to gain weight at the very consistent rate of 3 pounds per month.  Sometimes, mostly due to a bit of fasting, I'd be down a pound or two, but then I'd suddenly gain back all that weight plus more within a day or two, so that I'd be on that steady upward slope again.  

    In late February, I was up to just over 150 pounds; that was my pre-paleo weight.  That's not so terrible in and of itself -- although I hated it -- but the continued upward progression was really alarming.  Plus, I'd outgrown almost all my pants!

    After listening to Robb Wolf talk about the growth-promoting, insulin-spiking effects of dairy, I realized that I'd been eating a huge amount of dairy lately -- far more than ever before.  I've been buying those huge blocks of cheese from Costco, not to mention those delectable half gallons of cream.  So instead of eating meat-and-veggie leftovers for lunch, I was usually eating some high-fat dairy.  And for breakfast, I would eat cheese rather than meat with my eggs.  

    A few weeks ago, I decided to cut my dairy down dramatically -- to basically just one serving per day at most.  So I'll have a cup of raw milk kefir or cheese on meatza, but not much more than that.  That was really hard for me to do for the first week, as I really was used to eating it as a staple.  I'm also not eating nuts, absent some "must have food as I run out the door" emergency, as I know they can hamper weight loss for me.

    The results have been good so far.  I've not gained any more weight in the last two weeks.  Instead, I've lost four pounds.  Given what I had been experiencing, that's pretty remarkable.

    I'm not sure how much more weight I'll lose just due to cutting back the dairy.  I definitely think my metabolism isn't quite up to speed yet due to the hypothyroidism. However, my experience suggests that eating boatloads of dairy -- even good-quality, high-fat dairy -- is an excellent way to gain weight.

    That being said, I don't think that it's necessary to cut out all dairy to lose weight.  I'm still eating some dairy, and I'm losing weight.  Plus, I lost my original 18 pounds with my 1.5 shares of raw milk -- that's 1.5 gallons per week.  (I'm now down to just 1/2 shares, meaning 1/2 gallon per week.)  I just think dairy is something to consider reducing if you're not meeting your weight loss goals.

    ***

    I've not lost much more weight since writing that, but I'm definitely not gaining any weight.  That's huge: I was petrified that I'd be 200 pounds by next summer.  

    I've probably stalled in that weight loss because my metabolism is still screwy due to my not-yet-fully-managed hypothyroidism.  Plus, I'm not seriously trying to lose weight right now: I don't want to stress my already over-stressed body.  But perhaps cutting out dairy entirely would make a difference.

    Anyway, thanks for putting some science behind my experience, Dr. Davis!  I'll definitely add a link to it in the discussion of dairy on the principles page of Modern Paleo.

    -- Diana Hsieh (Modern Paleo)

  • StephenB

    3/19/2010 6:40:08 PM |

    My working assumption has been that I don't need to worry about any increased insulin resistance with high saturated fat intake since I don't eat foods which spike my glucose. Am I correct?

  • Darrin Carlson

    3/19/2010 6:47:03 PM |

    Yikes! Never would have thought butter could do this. Are there any other non-carbohydrate foods that are known to cause insulin secretion?

  • Christian W

    3/19/2010 6:47:03 PM |

    If anything, it seems like the study supports the idea that all fats are bad, doesn't it?

    The zero fat control meal does better than all the fatty meals. Look at insulin for instance.

  • howardh

    3/19/2010 7:54:46 PM |

    I notice that you conveniently ignored the pasta (sugar/gluten) in the study, and attributed ALL of the negative effects to butter. Try again, this one failed.

  • Anonymous

    3/19/2010 8:35:11 PM |

    Hmmmm, Wheat Pasta and Wheat Bread?
    All bets are off. Would be curious to have conducted tests without either of those included.

  • Andrew

    3/19/2010 8:46:58 PM |

    Could butter still make you fat if you're eating below BMR?  It seems to me that if you were eating 1000 calories per day consisting of only butter, and your BMR was 1800, you would still lose weight.  Is there anything that scientifically proves this to be false?

  • Nostril Damus

    3/19/2010 9:00:35 PM |

    Any ideas why ?

    I believe insulin drives the rate of ageing, and this would certainly make me scale back my butter consumption.  

    But what part of butter causes this ?

  • Marielize

    3/19/2010 9:02:16 PM |

    Dear Dr Williams, I find this topic very interesting, but being a lay person would like to know a bit more. What would the "meal" they talk about be? Would that be grains? Is the resuls they got from combining grains with cream or butter? Would butter or dairy products have the same effect in the absence of grains?

  • Donald Duck

    3/19/2010 9:35:38 PM |

    Doesn't this study mainly show that butter is a bad idea when eaten together with lots of carbs?

    Is it really likely you would get the same insulin response if the butter was eaten without all that carbs?

  • Mark

    3/19/2010 9:44:04 PM |

    After removing dairy, grains, and anything else processed. I'd imagine it would be hard to eat too many calories when all you're left is meat, veggies, and fruit but not too much. Just curious, is that all we have to choose from?

  • K Walt

    3/19/2010 10:26:25 PM |

    Interesting.

    But the meals were carb-heavy, too.

    "The subjects then ingested, within 15 min, a fat-rich meal consisting of dietary fat [50 g/m2 body surface area of butter, refined olive oil (ROO), high-palmitic sunflower oil (HPSO) or a mixture of vegetable and fish oils (VEFO) along with a portion of plain pasta (30 g/m2 body surface area), one slice of brown bread, and one container of skim yogurt.

    I wonder if the same effect would be noted if were JUST butter, or oil.

    Is it the butter? Or the wheat pasta, brown wheat bread and lactosey yogurt?

  • sonagi92

    3/19/2010 10:26:26 PM |

    Thanks for taking the time to post a response to inquiring commenters.

  • pyker

    3/19/2010 10:26:26 PM |

    Interesting. Here are the numbers from the study for insulin AUC:

    19960 +- 2766 control
    27970 +- 2107 VEFO
    29619 +- 4975 MUFA
    34749 +- 1167 HPSO
    37582 +- 4364 SFA (butter!)

    Unless I've misread the study, the "control" meal has no fat at all, and is not isocaloric with the test meals. "the macronutrient profile was as follows: 72% fat, 22% carbohydrate, and 6% protein (see Table S1 under "Supplemental data" in the online issue). The subjects also consumed the same test meal containing no fat as a control meal". So the butter test meal has nearly 4x as many calories as the control meal. The AUC for insulin between the two is about double for the butter, but that seems like a useless measure.

    Comparing like-for-like, the spread between average insulin AUC for butter meal and the isocaloric alternate fat meals  shows the butter to be about 34% higher than VEFO and only 8% higher than HPSO. (I have to be pedantic here and point out the spread between averages is not as good as would be the average spread, but I can't get that unless I have the raw data from the study.)

    If you want to claim that butter has some unique ability to raise insulin vs. other fats, this is not strong support.

    You say "butter's insulin-triggering effect, doubling or tripling insulin responses", and "butter makes you fat". I don't see support for either claim when I read that study.

  • Neonomide

    3/19/2010 10:44:24 PM |

    Why ?

    How about cream and fatty milk, or other dairy products ?

    I guess coconut is again the safest bet here...

  • Beth@WeightMaven

    3/19/2010 10:58:06 PM |

    I'm not an MD nor a research scientist. But decades ago, I was a math major. If I read the study and do my math right, the subjects ate an 800 kcal meal of which 72% was fat, for 576 kcals worth of fat (the other control meal components were pasta, bread, and skim milk yogurt).

    576 kcals worth is nearly 6T of butter -- or 3/4 of a stick! To me, that is important additional context for the increased AUC for both the insulin and the triglycerides.

    Considering my typical use (~1T/meal) and considering the potential downside of replacing carb calories with more PUFAs (and omega 6s -- even 1T of EVOO has over 1g of omega 6), I'm not ready to throw out my ghee just yet.

  • Cheryl

    3/19/2010 11:43:30 PM |

    Is it the milk solids that do it?  if so, then ghee may be an alternative.

  • Anonymous

    3/20/2010 12:52:10 AM |

    as a  personal anecdote - eating butter (even in amounts of 200 g. a day) speeds up my fat loss - i feel as if i'm burning inside (elevated metabolism?)...

  • Dr. William Davis

    3/20/2010 12:56:53 AM |

    I see that I touched a nerve.

    This study is not meant to stand on its own, but taken in the context of other studies.

    I think that you should eat butter . . . in small quantities and occasionally. I do not believe that the data argue for liberal use every day, or else you chance triggering insulin. Remember: It's the interpretation of the data in the context of the broader experience that leads you to practical conclusions.

  • Catherine

    3/20/2010 1:39:53 AM |

    What about coconut oil as a butter substitute? There is a lot of hype and hoopla about it being a "safe" medium-chain saturated fat to use as a butter substitute.  Anyone tested if it spikes glucose?

  • zach

    3/20/2010 3:57:00 AM |

    Pastured butter rocks. My belief with butter is "a stick a day keeps the doctor away."

    It's as though the more butter I eat the leaner I get!

    The anthropological evidence really contradicts the data you and loren cordain cite. The pancreases of many people in traditional cultures carried them toward 100 years old, reacting to dairy every day, multiple times per day.

    Here is a 112 year old woman from a very long lived people who use dairy as a staple.

    http://news.bbc.co.uk/2/hi/europe/8550374.stm

  • Sue

    3/20/2010 7:49:50 AM |

    "Fat, in general, does not make you fat. But butter makes you fat."

    Why make such a comment in regards to butter?

  • Adam

    3/20/2010 8:18:10 AM |

    Dr Davis.

    First of all, thank you for your wonderful site and your willingness to impart life changing and saving advice for anyone to access.

    Peter at hyperlipid has written a counter on this particular blog entry of your.

    Would you care to comment?

    http://high-fat-nutrition.blogspot.com/2010/03/butter-insulin-and-dr-davis.html

  • CK

    3/20/2010 8:42:10 AM |

    So let me get this straight: Ingesting carbohydrates including the bad guy wheat does not do much to blood glucose levels and insulin response. But adding fat to the mix at least doubles, or, in the case of butter, quadruples the peak insulin response? That seems like the best refutation of all the low carb/paleo/primal/ef approaches I've ever seen. So where is the catch?

  • Anonymous

    3/20/2010 9:15:05 AM |

    The last sentence made me cry.

  • Donald Duck

    3/20/2010 9:54:54 AM |

    It seems like butter (or cream) without carbs does not create insulin spikes according to the study that Peter at Hyperlipid discusses here:

    http://high-fat-nutrition.blogspot.com/2010/03/butter-insulin-and-dr-davis.html

  • Anonymous

    3/20/2010 10:39:02 AM |

    If you eat fat, ASP levels will rise, which will make you gain fat. ASP levels increase in response to an oral fat load, and ASP is one of the most potent stimulant of triglyceride synthesis.

    So, if you eat carbs, insulin secretes and you store it as fat, if you eat fat, ASP levels rise and you store it as fat. Why is it only the insulin's fault?

    http://www.jlr.org/cgi/content/abstract/30/11/1727

  • But I thought...

    3/20/2010 11:03:43 AM |

    The oracle's take on your post doc:

    http://high-fat-nutrition.blogspot.com/2010/03/butter-insulin-and-dr-davis.html

  • Lori Miller

    3/20/2010 2:08:13 PM |

    I don't know about the effect of butter, but when I eat a fatty meal (like a cheesy omelet with an avacado), my BG goes down several points.

  • kilton9

    3/20/2010 2:23:42 PM |

    Here's a study that isolates cream and shows a very small insulin response: http://drbganimalpharm.blogspot.com/2009/12/insulin-and-aging-how-paleo-works.html

  • Alfredo E.

    3/20/2010 3:01:02 PM |

    This is becoming more confusing by the minute. First, no carbs,only fats and protein.

    Now, no butter, no dairy, no, carbs, just a few drops of fat and protein.

    I am going to cry, like the previous poster.

  • Hilary

    3/20/2010 3:05:41 PM |

    "Fat, in general, does not make you fat. But butter makes you fat."

    This seems wrong. When I eat more butter, I lose fat/weight. Eat more carbs, gain fat/weight. Been noticing this for years. Sure, put a load of butter on noodles or rice, and you'll gain plenty, but just keep the carbs low and there's no problem. This seems like a case of being blinded by science. Maybe the science isn't exactly wrong, but just incomplete or misapplied.

  • pmpctek

    3/20/2010 3:05:41 PM |

    I think I fugured it out...

    The AMA or AHA has kidnapped Dr Davis and they are forcing him to post these confusing refutations.

    What will we see next?  Studies that show how Cocoa Puffs actually will help reach our 60-60-60 goal after all?

  • Joseph

    3/20/2010 3:07:15 PM |

    After reading your post and the hyperlipid post I'm left with a few questions.

    1.The big one, why is butter raising insulin so much? I had previously thought it was only high GI carbs that did that. Hyperlipid seems to think it was the small amounts of casein.

    2.Is it right to say that since the control carb meal only contained 174 calories compared to the butter meal which contained 800 this study is fairly useless? It raises some interesting questions but you can't conclude anything until you have a proper control containing the same amount of calories.

    3. Are there any studies which measure insulin secretion after a pure butter meal with no carbs?

    Even though the study is inconclusive, I'm lowering my butter consumption until I'm sure it isn't causing an agrovated insulin response. Even though butter causes much higher levels of FFA's which mean more of the fat is being burned, insulin levels that high can't be healthy

  • Miles

    3/20/2010 3:52:22 PM |

    All this information hurts my brain...ugh. All I know is when I eat low carb... I lose weight... feel better and more energetic. Sometimes there's just too much analysis and information about what constitutes a healthy diet. It's all opinion and based on research. Then other research refutes that idea.

    My Grandma used to say, "Eat when you're hungry and drink when you're dry."

    BTW... Grandma lived to be 95.

  • Helen

    3/20/2010 3:54:17 PM |

    Dr. Davis,

    I'm not too sure this is right.  I don't have the time to hunt down the links right now, but there was a study on Swedish children recently that showed those eating full-fat dairy (butter fat) were leaner than those who ate low-fat dairy.  Also, butter contains a lot of CLA, which is now being sold as a fat-loss supplement.  I can't parse this study on its own merits like Peter or Pyker (though I thank them for doing so), but I remain unconvinced.  

    I also agree with other posters about the in-vivo, long-term evidence of dairy-reliant cultures and their longevity.  

    Again, with so many cautions of what not to eat, I'd love to see a Dr. Davis-approved diet plan.  If I were just following all the Don'ts, I'd go crazy (and hungry).

  • Anonymous

    3/20/2010 5:39:12 PM |

    The palmitic acid content of the butter would probably trigger  insulin when there is an abundant source of glucose in a meal.  But, if you look at this post by Stephan you will see that the body stores dietary fats when there is a glucose source of energy available.  

    http://wholehealthsource.blogspot.com/search/label/fats

    As the glucose is depleted the fat is released to be used as energy.  The graph in Stephan's post clearly shows the cycling that occurs in normal metabolism.


    The information Dr. Davis presented showed an insulin spike, not continual high levels of insulin that would inhibit the release of FA as an energy source.
    I believe it was Dr. Eades who recently posted about the constant exchange of fats in and out of storage, and the implication is that storage is only a problem when cells remain saturated with glucose.  The fat never comes out because it isn't needed.  In this scenario insulin resistance and fat storage is protective.

    http://high-fat-nutrition.blogspot.com/2010/03/getting-fat-is-good-official.html

    My understanding of this subject is, by limiting carbs, especially the sugar surrogates that are refined grain products, you can keep the normal cycling of energy sources going.

    When everything is working right, your body signals hunger and satiety appropriately, and the body runs at an equilibrium level of energy intake and energy expenditure.

    I suspect that the FA composition of butter makes it available as an energy source sooner than the other FA's tested in the study.  Hence the higher insulin level.


    I don't see where a moderate amount of butter, when there is a limited or low availability of glucose sources will make you fat, expecially if you are VLC or on a ketogenic diet.  I can see where it could be a problem if you were eating 150 or more grams of carbs per day and have metabolic syndrome.  Then high levels of insulin would spike even higher prompting the liver to pump out more glucose, and the fat just has no where to go except into storage.

    Take your vitamin D3 to get your adiponectin levels up.  Take fish oil while limiting Omega-6's to normalize inflammatory responses. Limit carbs, and get the glucose-FA cycle working for you.

  • Nigel Kinbrum

    3/20/2010 6:19:20 PM |

    Eating carbs with butter produces a big insulin response because butter induces temporary insulin resistance (IR) which means that more insulin has to be secreted to get the same net effect. Looking at the blood glucose response, the net effect is the same. So stop panicking. The temporary IR lasts for only a few hours.

  • Gretchen

    3/20/2010 7:49:28 PM |

    "Fat, in general, does not make you fat. But butter makes you fat."

    If you based your conclusion on the graph in this study, all fats make you fat.

    Protein also stimulates insulin, so protein makes you fat.

    Carbs stimulate insulin, so carbs make you fat.

    Conclusion: Food makes you fat.

    It's known that fatty acids acutely stimulate insulin synthesis. With chronic exposure to fatty acids (as occurs in obesity), insulin synthesis is blunted.

    I've never understood the body's rationale for this, unless a sudden infusion of fat makes it think it had better store the fat for the future, but with chronic stimulation it figures it has enough.

    I don't know how ingested fat is related to fatty acids in the blood, whether or not this is linear.

    Whatever, it doesn't look to me as if butter is much different from the other fats, and as others have pointed out, the amounts used in this study (on top of about 44 g of carb, which I wouldn't call a low-carb meal) were enormous.

    The other odd thing is that usually fats slow down a carb-stimulated blood sugar peak, and they didn't in this study.

  • Neil

    3/20/2010 10:33:31 PM |

    This is what is considered 'butter' in the study you refer to above Dr Davis and ultimately what this study uses to prove its point:

    "The subjects then ingested, within 15 min, a fat-rich meal consisting of dietary fat [50 g/m2 body surface area of butter, refined olive oil (ROO), high-palmitic sunflower oil (HPSO) or a mixture of vegetable and fish oils (VEFO) along with a portion of plain pasta (30 g/m2 body surface area), one slice of brown bread, and one container of skim yogurt]."

    Yep, that would be my definition of 'butter' as well!

    If that pile of c**p didn't raise your insulin levels what would?

    In addition: "The average total energy provided by the meals was 800 kcal (10 kcal/kg), and the macronutrient profile was as follows: 72% fat, 22% carbohydrate, and 6% protein"

    Only 22% carbohydrate, no chance of that increasing insulin levels either I suppose!

    It has to be the 'butter'

  • Peter

    3/21/2010 12:02:51 AM |

    @Helen: I couldn't have said it any better myself. I too remain unconvinced.

    You get fat from pasta, bread and butter in combination? Not really groundbreaking work.

  • Peter

    3/21/2010 12:19:14 AM |

    @Helen: I found the study you are referring to I believe.

    "BMI correlated strongly to fat mass and leptin was the best marker of overweight and fat mass in 8-year-olds. Food choice was similar to that at 4 years of age. An intake of fat fish once a week was associated with higher serum concentrations of n-3 fatty acids. The intake of saturated fat and full fat milk were inversely associated with BMI."

    The study was made at the University of Gothenburg.

    http://gupea.ub.gu.se/dspace/bitstream/2077/20457/2/gupea_2077_20457_2.pdf

  • Sue

    3/21/2010 12:51:41 AM |

    I'm sorry Dr Davis but you really didn't analyse this study properly before jumping to conclusions.

  • Anonymous

    3/21/2010 2:24:49 AM |

    Just wondering if you had seen this recent study about higher levels of Vit D being associated with increased arterial calcification in the African American population: http://www.eurekalert.org/pub_releases/2010-03/wfub-vdl031110.php

  • Mike

    3/21/2010 3:44:28 AM |

    Looking at insulin alone can be very misleading. If glucagon is released along with the insulin ,as happens when eating protein, then the fat storing effects of insulin are negated.

    For low carbers, the study is meaningless as it was done with lots of carbs. I will continue to eat butter and cheese until I see a meaningful study that shows that they cause a real problem.

  • PRIDE MAFIA

    3/21/2010 6:02:42 AM |

    Maybe DR Davis saw something on that "low carb cruise" that didn't sit well with him and he's rethinking certain principles?

  • W. Bacon

    3/21/2010 8:19:58 AM |

    Dr. Davis' goof is discussed here:

    http://high-fat-nutrition.blogspot.com/2010/03/butter-insulin-and-dr-davis.html

  • Anonymous

    3/21/2010 5:25:38 PM |

    No, Neil, the 'butter' was just butter. They didn't have "that pile of c**p" at one time: each item in the list was a separate meal & separate data point. Unfortunately, the wording of the paper is in places not very good.

  • Helen

    3/21/2010 8:28:26 PM |

    "Anonymous said...

    Just wondering if you had seen this recent study about higher levels of Vit D being associated with increased arterial calcification in the African American population: http://www.eurekalert.org/pub_releases/2010-03/wfub-vdl031110.php"

    I saw it, and was hoping to discuss it in the pro-D blogosphere.

    I have two ideas why this might be the case.

    (1)  Because people of African descent are adapted to live nearer the equator, where the sun is all you need for enough vitamin D, they may not be as adapted as Europeans to use dietary vitamin D (supplements being an analogue), which Europeans probably relied on during winter months.  Thus, too much supplemental vitamin D may be harmful to African Americans, at least in the case of arterial calcification.  (I hedge, because I've also read recently that African American children with low D status have higher rates of asthma. http://www.sciencedaily.com/releases/2010/03/100317112055.htm)

    (2) There is also the possibility that somewhat different dietary patterns between European Americans and African Americans may offer some explanation.  I can't imagine what this might be, but maybe something having to do with vitamin K2, which helps prevent calcium deposits in the arteries?  There are two possibilities here:

    (a) Maybe African Americans consume (or produce in the gut - from eating greens, a traditional part of the African American diet) more K2 than European Americans, and this is why they have less arterial calcification with lower D status - they don't need the D as much for arterial health, and more dietary D just upsets the balance.

    (b) Maybe they eat less K2 than European Americans (maybe eat less hard cheeses?), and thus vitamin D supplementation, which may require a certain level of K2 to be beneficial, might be harmful instead.

    This sentence leads me to believe it's more likely to be (a):  "Despite these lower vitamin D levels and dietary calcium ingestion, blacks naturally experience lower rates of osteoporosis and have far less calcium in their arteries."  The strong bones and clear arteries make me think African Americans may have better K2 status.  

    It's possible that vitamin A status also plays a role.

  • Helen

    3/21/2010 8:56:30 PM |

    Another thought on the question of African Americans and vitamin D - perhaps *because* they consumed less calcium their vitamin D requirements were lower, so the supplemented amounts were excessive.

  • Dr. William Davis

    3/21/2010 9:55:55 PM |

    The point is not whether glucagon is stimulated. That is, in my view, immaterial.

    The point is that your poor, tired pancreas, likely operating at a fraction of its original beta cell capacity from the years of the beating it took while you ate Cheerios and Cocoa puffs, ate sandwiches, and drank Coca Cola with your pizza, is being stimulated to produce more insulin.

  • Nigel Kinbrum

    3/22/2010 9:05:25 AM |

    Regarding calcification, I think that Helen has hit the nail well & truly on the head regarding Vitamin K2. "If it calcifies, think K2" is what I always say (along with "If it spasms, think Magnesium").

    Taking large amounts of Vitamin D3 and nothing else probably exposes deficiencies in the other fat-soluble vitamins A, E & K2.

    Having cured Lumbar osteoporosis in three years using Ca, Mg, D3 & K2 (and no Alendronate), I will never stop taking Ca, Mg, D3 & K2.

  • Anonymous

    3/22/2010 8:15:10 PM |

    Why eat carbs together with fat?
    They ate 44 g glucose which means the P-glucose could reach >48 mM without insulin i 70 kg person. Of course the disaster hormone insulin increases to block all lipolysis as well as proteinolysis to try to burn off all the totally unnecessary carbohydrates they added.
    If contol diet (gluose) did not change glucose and thus insulin level it must be fake.

    Just another totally stupid study.

  • Anonymous

    3/22/2010 8:53:10 PM |

    I guess I am going to become a breatharian....someone who survives only on air.....since I have learned that butter and fat stimulates my insulin, protein stimulates my insulin, carbs stimulate my insulin and thus I am doomed to be fat....and leptin is stimulated by all three but my brain doesn't register that I am full.  

    Ingesting air is the only thing that will not make me fat.

    Go here to be a Breathairian http://www.breatharian.com
    You can even go to a $1 million dollar seminar that must be completed prior to Dec 21, 2012.

  • Dana Seilhan

    3/22/2010 10:20:44 PM |

    When I'm low-carbing, a favorite meal is a tenderloin cooked medium-rare, sliced thin, and dipped in butter.

    I lose weight anyway.

    Also, what kind of butter was used in the study?  Was it regular grocery-store butter, or was it organic and/or grass-fed butter?  The FDA claims there's no difference between dairy produced with rBGH and dairy produced without, but I'm given to understand that rBGH-produced dairy has higher levels of IGF-1.  What would be the effect on insulin of all that exposure to insulinlike growth factor?

    And I'll second Miki's question of whether the milk solids wouldn't make a difference.

    And to the person who mentioned "all that lactose-y yogurt"--if you make yogurt correctly, it should have hardly any lactose in it at all.

  • Dana Seilhan

    3/22/2010 10:22:01 PM |

    I suspect that the FA composition of butter makes it available as an energy source sooner than the other FA's tested in the study. Hence the higher insulin level.

    Fatty acids by themselves don't prompt insulin release.  Protein does (but the insulin is balanced out by glucagon), and of course carbs do, but there's nothing inherently dangerous in a fatty acid that would prompt the body to store it away immediately.

  • Anonymous

    3/23/2010 7:02:21 PM |

    It seems like no one has a handle on how the metabolic parts fit together to make the whole. My experience from converting from whole grains and no-fat dairy to full-fat dairy has been weight loss and increased energy, particularly after eating a selection of artisan cheese. I often get up, have a bowl of full-fat yoghurt or kefir with 100% chocolate nibs and fresh-roasted nuts, then sample several artisan cheeses, and go cycling 44 km before getting back to make everyone else breakfast. My body seems geared to fat as fuel and I never get blood sugar lows. If this is raising my insulin, it apparently does not affect my blood sugar.

    Murray

  • Apolloswabbie

    3/25/2010 7:38:15 PM |

    Usually, I learn all I need to from Dr. Davis' posts.  My thanks to the other contributors today for illustrating that context is everything.  We have reason to believe that dairy from the industrial food chain would not be as good a food as if we could get true grass fed dairy cow products - but this seems out of context with other info I've seen which shows only moderate insulin response to dairy fats.  Bottom line: measure the markers which indicate insulin levels over time as a gauge of whether your diet does/doesn't work (unless you are losing weight - in which case, you know it is working).

  • Anna Delin

    3/26/2010 9:42:22 AM |

    It seems that whatever butter does to my insulin levels, this does not curb the very positive effects I experience from eating butter. When I cut carbs and replaced them with generous amounts of cream and butter (organic preferably) I lost 14 kg. Moreover, when in "carb country", i.e. airports, airplanes, trains and the like, I can keep my energy up by eating the small amounts of butter and cheese available. Butter also has a way of keeping me feeling full for a very long time. This implies that the fat is not stored away in my fat cells but instead made available for burning. Perhaps other people are more sensitive.

  • ET

    3/26/2010 11:46:15 AM |

    While I often disagree with the conclusions you post, I always enjoy the discussions and research raised by your blogs.  It's one reason I keep coming back for more.  It's keeps me searching for answers.

  • Star Trek TNG

    3/28/2010 6:13:00 PM |

    I still prefer coconut oil for fat loss used in a no-carb diet. I'll find that ghee, which I've also tried, isn't so effective for weight-loss perhaps because it's not so fatty. But it does have to be in a no-carb diet, not a low-carb one. Everyone's got a switch which is triggered by carbs, but no-one knows where it is, not exactly. So unless a study is rabidly no-carbs, none at all, I don't really see what can be learned.

    BB

  • Nancy

    4/8/2010 12:53:02 AM |

    Dr William
    your response to the commentors seems to indicate that butter will make you fat IF you have abused your body with carbohydrates because of a compromised pancreas.  I am willing to suppose this could be true, but what about people who his ave not abused their bodies, what about children being raised low carb from the start, would butter be fattening for them?  Your response would lead me to believe your answer will be no.  I really appreciate your blog and recommend it to all, but please clarify this issue.  Maybe a whole new blog on this would be a good idea, since the entire low carb community is talking about it.

    To everyone else I have to say there is nothing like testing something for yourself.  If you have an insulin tester, have some butter and test yourself and make a chart.  See how YOU are affected.

  • Alejo Hausner

    4/9/2010 1:28:50 PM |

    The work was funded by the Fundación Centro de Excelencia en Investigación sobre Aceite de Oliva y Salud (“Center of excellence for research on olive oil and health”).

    Notice that they end up concluding that olive oil raised glucose and insulin less than butter. Had this study been done by French researchers and not Spanish researchers, it would have found that butter is better for you than olive oil!

    Alejo

  • jpatti

    5/7/2010 7:58:00 AM |

    Pasture-raised butter is a good source of vitamins A, D and K2 plus CLA.

    And it makes veggies yummy.  

    As Julia Child said... butter is better.

  • info

    5/16/2010 6:10:09 AM |

    Little test
    I'm a very low carber. 80% of my calory intake come from fat. I eat less than 20 grams of carbs. I did a little test. For a week I took tallow and coconut oil instead of butter. In that week I lost three pounds. Conclusion: Butter seem to have a sort of effect.

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  • buy jeans

    11/2/2010 8:24:56 PM |

    The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

  • Chester The Bear

    1/19/2011 10:55:45 PM |

    Um... Sorry... I see the data differently.
    In the fat meals in the study, the amount of fat intake was the same, yet butter delivers higher serum FFAs, indicating that fat might stimulate lipolysis, even though it appears to induce a short term insulin spike.
    Carbohydrate might promote a lower insulin response, but it blocks lipolysis.
    Finally, there's a lot more going on here than just insulin.  To take it out of context is meaningless.

  • racing games

    1/20/2011 11:15:13 AM |

    but my question is what is the reason behind this insulin triggering effect of butter? can anyone answer this?

  • liposculpture guide

    1/26/2011 7:18:57 AM |

    It's always good to challenge deeply held beliefs in case we are wrong. I do have a soft spot for butter and hope it is an outlier as far as blood glucose.

  • francisco camps

    2/5/2011 8:41:02 PM |

    I am scary with butter now...lol

  • ABBEY

    3/5/2011 6:27:47 AM |

    As people know, I've been struggling with my weight due to my hypothyroidism. Although many of my symptoms have improved, I kept the weight gain in very consistent rate of 3 pounds per month. Sometimes, mostly due to a little fast, would be a pound or two, but then suddenly I would like to recover all that weight plus more than a day or two, so it would be in this constant uphill again.

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  • Matt Titus

    5/6/2011 3:42:50 AM |

    I wonder if the results would be the same with raw butter?

  • Paula Nedved

    10/3/2011 2:30:40 AM |

    Peter over at Hyperlipid has done a critique of this post of your, Dr. Davis.
    Entitled "Butter insulin and Dr. Davis"    He dunna believe you.

  • Nancy

    10/20/2011 4:57:58 PM |

    I'm stunned by your absolute condemnation of butter based on this one study.  Geez, have you been paid off by Wesson or Crisco?   You need to consider all the confounding variables in this study.  Your blog post should be retracted and/or rewritten.  This is very disappointing after your carefully researched examination of wheat.

    In my experience, butter and butter fat are good for you.  I have lost considerable body fat and gained much muscle this year on an eating plan that involves a lot of raw milk and cream from grass-fed cows, 3 to 4 glasses of milk and up to a cup of cream per day.  Butter fat is not making ME fat, quite the opposite.

  • Karl Schmidt

    9/27/2012 6:35:46 PM |

    Insulin goes down faster because the vegetable fats are stored in the fat tissue faster..

    A better understanding of butter is here :

    http://high-fat-nutrition.blogspot.com/2012/09/protons-pancreas.html

  • Karl Schmidt

    12/1/2012 9:41:46 PM |

    There is another problem with that study - people do not keto adapt in 8 hours - it takes 4- 6 weeks to fully adapt to a low carb diet.

    Once adapted, low-carbers are BETTER able to clear FA as the liver revs up it's fat metabolic capabilities.  Low carbers also tend to eat less frequently - reducing the exposure to both BG and FA - only when both are elevated do we see the pronounced toxic effects of the fats.

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