Tell me your wheat elimination story and receive a copy of my new book, Wheat Belly

I'm looking for interesting wheat-free experiences.

For the past year, I have been writing my new book, Wheat Belly . After many, many late nights and soccer games missed, it's now finished. The book will be out in fall, 2011, to be published by Rodale, the Prevention Magazine people.

Wheat Belly will provide, in excruciating detail, the discussion of how wheat was transformed from innocent wild grass to incredible genetically-altered Frankengrain and why it has become such a health nuisance.

I am looking for interesting stories of wheat elimination for the online and special editions of the book. If you have an interesting tale of wheat-elimination successes, woes, or drama, I'd like to hear about it. Even better, if you would agree to be interviewed by phone (not for live use, just for comments and detail), the editors at Rodale will help tell your story.

If we use your story, I will have a free copy of the new Wheat Belly sent to you when it becomes available.

Please post your story in the comments here. I will then need to obtain your contact info, which we will do privately.

 

Real men don't eat carbs

Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen levels; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone and high estrogen, a cause for depression, emotionality, weight gain, and low libido.

--Sugar-provoking carbohydrates like wheat cause visceral fat to accumulate which, in turn, triggers prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and persistent lipoproteins, like chylomicron remnants and VLDL particles, that impair endothelial function literally within minutes to hours of ingestion. Impaired endothelial function underlies erectile dysfunction. This is why Internet spammers so enthusiastically send you offers for discounted Viagra.

--Carbohydrates increase blood sugar which provokes the process of glycation, glucose modification of proteins, that also contributes to endothelial dysfunction followed by erectile dysfunction.

Real men therefore avoid carbs.

Real men don't eat carbs

Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone, high estrogen, a cause for depressions, emotionality, and weight gain.

--Consume carbohydrates like wheat and visceral fat causes prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and prolonged lipoproteins like chylomicron remnants and VLDL particles that impair endothelial function. Impaired endothelial function underlies erectile dysfunction. Eat a bagel, become impotent.

Why do the Japanese have less heart disease?

We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0


Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."
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.

  • kimberly

    9/16/2010 1:46:12 AM |

    I love to prepare some recipe that contain many cream.  although i know that a person can gain weight I don´t matter because i love the taste, Simply delicous. And when i cook, my husband usually is very happy.
    Actually i was looking information about how tobuy viagra  but i reached this blog, i really enjoyed reading.

  • 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.

    people searches

  • 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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