The American Heart Association has a PR problem

The results of the latest Heart Scan Blog poll are in. The poll was prompted by yet another observation that the American Heart Association diet is a destructive diet that, in this case, made a monkey fat.

Because I am skeptical of "official" organizations that purport to provide health advice, particularly nutritional advice, I thought this poll might provide some interesting feedback.

I asked:

The American Heart Association is an organization that:

The responses:
Tries to maintain the procedural and medication status quo to benefit the medical system and pharmaceutical industry for money
240 (64%)

Doesn't know its ass from a hole in the ground
121 (32%)

Is generally helpful but is misguided in some of its advice
79 (21%)

Accomplishes tremendous good and you people are nuts
6 (1%)


Worrisome. Now, perhaps the people reading this blog are a skeptical bunch. Or perhaps they are better informed.

Nonetheless, one thing is clear: The American Heart Association (and possibly other organizations like the American Diabetes Association and USDA) have a serious PR problem. They are facing an increasingly critical and skeptical public.

Just telling people to "cut the fat and cholesterol" is beginning to fall on deaf ears. After all, the advice to cut fat, cut saturated fat, cut cholesterol and increase consumption of "healthy whole grains" in 1985 began the upward ascent of body weight and diabetes in the American public.

Believe it or not, my vote would be for something between choices 1 and 3. I believe that the American Heart Association achieves a lot of good. But I also believe that there are forces within organizations that are there to serve their own agendas. In this case, I believe there is a substantial push to maintain the procedural and medication status quo, the "treatments" that generate the most generous revenues.

I believe that I will forward these poll results to the marketing people at the American Heart Association. That'll be interesting!

Comments (17) -

  • Tuck

    3/1/2011 11:46:38 PM |

    Did the monkeys get to vote? ;)

  • reikime

    3/2/2011 12:11:04 AM |

    I would LOVE to read a response from the AHA!

  • Anonymous

    3/2/2011 12:15:46 AM |

    Come on Doc, these statistics are obviously bias. That's like asking the readers of an vegan/animal-rights blog, "Do you think meat is murder?" and trying to transpose the results as being all encompassing.

  • Rick

    3/2/2011 1:32:30 AM |

    I have to agree with Anonymous here. Nothing surprising in the fact that the majority of readers of a blog that regularly criticizes the AHA have a critical stance towards the AHA.

    Move along, these are not the droids you're looking for.

  • Harold

    3/2/2011 2:34:28 AM |

    I think you are being a bit generous to them. I certainly agree about the ADA. They seem to be in it for the money and they are getting plenty of it from drug companies. I am a physician and a diabetic and if I followed their advice my blood sugars would be out of control. As it is I am on a very low carb life style and in excellent control!
    Thanks for your posts.

  • Real Food RD

    3/2/2011 4:13:16 AM |

    certainly it's not a random sample, but nonetheless, I would have to agree that all of these organizations and government agencies are losing credibility with the public and fast.  As a health professional myself, I can only hope my colleagues may begin to soften their stance before our credibility is completely shot with the public.

  • Anonymous

    3/2/2011 1:14:17 PM |

    Tuck, the monkeys must make up the extra 18%.

    Doctor, I truly appreciate your blog, read it religiously and follow much of your advice, but before forwarding to the AHA, you might want to check the numbers.

  • renegadediabetic

    3/2/2011 1:59:02 PM |

    I think the AHA has done a lot of good in the treatment of heart attacks and keeping people alive.  However, I was thinking mainly of the "prevention" side when I voted "Tries to maintain the procedural and medication..."

    Likewise, the ADA and other diabetes orgs are no doubt doing some good research into causes and prevention of type 1 diabetes, but their nutritional approach is a disaster.  Again, just maintaining the status quo for so long that they would be afraid to admit they were wrong if they finally did see the light.

  • Might-o'chondri-AL

    3/2/2011 5:24:44 PM |

    Their heart is in the right place. In another 40 years scientists will be deriding the intriguing bloggosphere theories.

  • reikime

    3/2/2011 5:53:19 PM |

    I just dislike these organizations jumping on a bandwagon d'jour, and trying to apply it to everyone blanketly.

    People are not a " one size fits all " species!  When will the AHA, ADA, etc, stop aligning with big agriculture and pharma and think of individual people and their specific needs?  Is that just a pipe dream?

  • Tara

    3/2/2011 11:20:06 PM |

    Real Food RD, I'm with you!

    I was going to throw the other ADA in that stack too.  I've let them know several times how I feel about their corporate sponsors and partners.  Disgusted.

  • Brian Vickerman

    3/3/2011 2:12:54 AM |

    To be honest... after promoting such a lifestyle for so many years... wouldn't a sudden change in opinion open them to law suits?

    How can they respond to that?

  • reikime

    3/3/2011 3:14:54 AM |

    Great point Brian. I hadn't even thought of it.

    Wouldn't it be the same with any condition that current medical research might up- end the treatment protocols?
    ie..remember when patients with gastric ulcers were advised to drink milk and cream and avoid spicy foods etc?  
    Then enter H. Pylori...albeit some 10 years after published studies and much derision from U.S. gastros. Treatment standards changed dramatically. Never heard of lawsuits over that.

  • Anonymous

    3/3/2011 3:16:21 AM |

    Could people leave more than one response?  The percentages add up to more than a hundred.
    Bob

  • Bob

    3/3/2011 3:27:57 AM |

    OK, I did the math.  Apparently about 375 unique respondents, with 70 or so choosing more than one answer.

  • mongander

    3/3/2011 4:05:38 AM |

    My impression is that 'disease associations' exist primarily to ensure their continued existance.

    I have heard good reports on the Muscular Distrophy Assoc.

  • Anonymous

    3/3/2011 8:37:54 PM |

    Dr D, I don't think the AHA is sending you a Christmas card this year

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The origins of heart catheterization: Part II

The origins of heart catheterization: Part II

On the afternoon of October 30th, 1958, nearly 30 years after Werner Forssmann’s fumbling attempts, Dr. Mason Sones, a 5 foot 5 inch, plain-talking, cuss-every-few-words, cigarette-wielding radiologist at the Cleveland Clinic, was performing a routine angiogram of a patient’s aorta (the large vessel emerging from the heart) in a dark basement laboratory. (In Sones’ day, imaging methods remained primitive, disease diagnosis relying more than anything else on the physician’s powers of observation and crude diagnostic procedures. Abdominal pain was assessed with exploratory laparotomy, headaches with air injected into the brain and nervous system (“pneumoencephalography”), an excruciatingly painful ordeal. Being able to track the course of x-ray dye injected into specific internal organs, whether liver, biliary tree, aorta, lungs, or coronary arteries, represented a huge advance in diagnostic tools for human disease.)

In 1958, no one had yet injected dye directly into the coronary artery of a living human.


Just as the dye injector was triggered, Dr. Sones’ eyes widened in horror when the black and white monitor showed that the catheter had inadvertently jumped into the right coronary artery. The injection pump, already triggered to release its load, proceeded to pump 30 cc of X-ray dye straight into the artery. (Modern techniques usually require only 5–10 cc of dye.) Dr. Sones recounts the incident:

“It was late in the day and we were tired. I hit the switch to rev up the x-ray generator so I could see. As the picture came on, I could see that the damn catheter was in the guy’s right coronary artery. And there I was, down in the hole [a recess to shield him from radiation]. I yelled, “Pull it out! Pull it out!”*? By that time, about 30 cc of the dye had gone into the coronary artery. I climbed out of the hole and I grabbed a knife. I thought that his heart would fibrillate and I would have to open his chest and shock his heart. [In Sones’ day, modern CPR hadn’t yet been developed as a method of resuscitation.] But he didn’t fibrillate—his heart stopped. I demanded he cough. He coughed three times and his heart began to beat again. I knew at once that if the heart could tolerate 30 cc of dye, we would be able to safely inject small amounts directly into the coronary artery. I knew that night that we would have a tool to define the anatomic nature of coronary disease.”


*An observer, Dr. Julio Sosa, reported that Dr. Sones, in his shock, also blurted, “We’ve killed him!” After all, conventional wisdom of that era, based on observations from dye injections into the coronary arteries of dogs, was that injecting x-ray dye into human coronary arteries would result in immediate death from the electrical imbalance provoked in heart muscle momentarily deprived of oxygen-carrying blood.

Thus it was established that it was indeed possible to directly inject x-ray dye into human coronary arteries and reveal its internal contours. That’s not to say that the x-ray dyes of 1958 were innocuous. Far from it. In addition to briefly interrupting heart rhythm, as happened with Sones’ first accidental attempt, the dyes used then typically caused dizziness and the sudden urge to vomit. During the first 30 years of direct coronary catheterizations, it was common for hospital staff to run to the patient’s side, bucket in hand to catch the inevitable vomit, once the heart was jump-started by coughing.

Not surprisingly, Dr. Sones’ discovery set off both an avalanche of criticism and bold predictions of how the new technique might change the course of diagnosis in heart disease.

Over the subsequent weeks and months, Dr. Sones proceeded to purposefully insert catheters into coronary arteries and create angiograms that revealed the extent of coronary atherosclerosis. He learned how to fashion new catheter shapes to facilitate access to the arteries. Sones developed an impressive experience in the new technique. For the first time, clear images of the coronary arteries were routinely obtainable for the confident diagnosis of coronary atherosclerosis before death. Dr. Sones became an unlikely celebrity in Cleveland, entertaining physicians from around the world eager to learn about his methods, politicians and celebrities, even Middle Eastern nobility complete with bodyguards and food testers.

Dr. Sones continued to work in Cleveland, furthering the techniques of heart catheterization after his fortuitous error. He died of lung cancer in 1985, 17 years after his discovery.

Thus was born the modern age of heart catheterization.

Today, over 10,000 heart procedures are performed in the U.S. every day, 365 days a year, the vast majority of which involve heart catheterization or begin with a heart catheterization. Dr. Sones' fortuitous blunder was followed by 30 years of productive refinement and development before the blatant excesses of this technique really began to be exploited.


Copyright 2008 William Davis, MD
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Are endogenous nutritional supplements better?

Are endogenous nutritional supplements better?

Just a muse.

Endogenous substances are those that are already contained within our bodies. They are part of basic human equipment.

Exogenous substances are those that come from outside of our bodies. This includes various substances in foods, drugs (most, though not all), and pesticides.


I often mull over all of the tools we use in the Track Your Plaque program to achieve control over this thing called coronary plaque. It struck me that just about all the supplements we use that seem to provide outsized benefits are all endogenous substances themselves:

--Omega-3 fatty acids from fish oil
--Vitamin D
--l-arginine
--Niacin (vitamin B3)

Many of the other substances, though not directly relevant to our plaque-control efforts, but are among the most effective nutritional supplements, also supplement endogenous levels: calcium pyruvate, creatine, acetylcarnitine, DHEA, testosterone, progesterone, growth hormone, pregnenolone, phenylalanine, tyrosine, melatonin, etc.

Curiously, most drugs are not meant to directly supplement endogenous levels, but are designed either to enhance or block an enzyme (e.g., acetylcholinesterase inhibitors that block breakdown of acetylcholine; HMG CoA reductase inhibitors to block cholesterol synthesis; angiotensin converting enzyme inhibitors to reduce blood pressure), to exert toxic effects on an organism (antibiotics, antivirals), or to exert an entirely unique effect that does not ordinarily occur in the human body (some anti-cancer drugs, for instance). (This is an admitted, vast over-simplification.)

That's not to say that any endogenous substance is desirable or safe when supplemented. Cortisol, thyroid hormone, and estrogens are three examples of endogenous substances that have downsides when administered at slightly more than physiologic concentrations.

Nonetheless, it makes me wonder if the world of endogenous substance supplementation has not been fully explored. Are there other endogenous substances that are as potent and wonderful, for instance, as vitamin D but not yet fully appreciated? I'm sure there are.

Comments (6) -

  • Anonymous

    5/3/2008 11:20:00 PM |

    I don't know if this would qualify as an endogenous substance, but I've recently added the herb turmeric to my supplementation list. I take a capsule or two a day.  I'm on an e-mail list for supplement studies and marketing going on in health food circles, and it seems tumeric is receiving good press for its ability to help strengthen bones. Figure with the connection between brittle bones and heart disease, it's worth taking a little.

  • Jenny

    5/4/2008 12:43:00 PM |

    Dr. Davis,

    You mentioned that estrogen is a natural substance that causes problems if administered at higher than physiological levels.

    You do know, I hope, that all the data showing supposed problems from estrogen supplementation is from research studies where women were given MUCH too high doses. I've been using a dose of non-horse origen estrogen about 1/4 of what they used the studies and it makes a huge positive difference in my blood sugar, blood pressure, and weight with no negative effects on my endometrium (which my doctor has me get measured with ultra sound every so often.

    I'm very grateful that I have a good gynecologist who didn't react mindlessly to the research showing negative outcomes from estrogen.

    It appears to be protective against macular degeneration (which made my dad blind in his 90s) and for me it makes blood sugar control much, much easier.

    But the usual dose given women is much, much too high, and it isn't adjusted for body weight or titrated by observing symptoms. And hence the whole idea of supplementation has been nixed.

  • Anne

    5/4/2008 9:37:00 PM |

    That is interesting about the bones and tumeric. I recently added curcumin because my fibrinogen level was elevated. Maybe it will help with my bone loss too. That would be great.

    What is the difference between tumeric and cucurmin? Does it matter which I take? I could not find tumeric but I did find cucurmin 500mg.

  • Anonymous

    5/5/2008 1:57:00 PM |

    Hi Anne,

    I guess it is the curcumin found in the spice turmeric that is receiving positive press.  As mentioned I've seen some on bone health studies but have also seen heart health and diabetes write-ups too.  I'll post below a recent small rodent research paper on diabetes benefits of curumin:

    Curcumin may offer diabetes benefits: study
    By Stephen Daniells

    KEYWORDS

        * Phytochemicals, plant extracts

        * Diabetes

    GET THE LATEST MARKET REPORTS

        * curcumin
        * diabetes
        * cardiovascular health

    All market reports

    30-Apr-2008 - Curcumin, the natural pigment that gives the spice turmeric its yellow colour, could have benefits for diabetics, suggests a joint Korean-American study.
    A mouse model of diabetes was used to test the effects of curcumin on various variables and significant improvements were reported for insulin resistance and glucose tolerance, report the scientists from Sunchon National University and Kyungpook National University in Korea, and Columbia University in the US.

    Curcumin has increasingly come under the scientific spotlight in recent years, with studies investigating its potential benefits for reducing cholesterol levels, improving cardiovascular health, reducing the risk of Alzheimer's, and potential protection against cancer.

    If results of the new study, published in the journal Molecular Nutrition & Food Research, can be repeated in humans, it may suggest potential for the spice for diabetes management or prevention.

    Promising results for diabetic mice

    The researchers, led by Mi-Kyung Lee, used diabetic mice, so-called db/db mice, and non-diabetic controls, named db/+. The animals were fed diets with or without added curcumin (0.02 per cent) for six weeks.

    They report that the diabetic mice supplemented with curcumin experienced lower blood glucose levels, than the controls. The animals also lost less weight.

    Activity of the glucokinase enzyme in the liver was higher in the diabetic mice following the curcumin-supplemented diet than in the diabetic control group. This enzyme plays a key role in the conversion of glucose into glycogen, the body's main carbohydrate stores. This would blunt the glucose rise following the meal.

    The spice was also linked to reduced activity for other enzymes associated with the production of markers of cardiovascular health, such as free fatty acids, cholesterol, and triglyceride were also significantly lower following curcumin supplementation in the diabetic animals.

    Importantly, no effects were observed on blood glucose, plasma insulin, and glucose regulating enzyme activities in the non-diabetic animals, stated the researchers.

    "These results suggest that curcumin seemed to be a potential glucose-lowering agent and antioxidant in type 2 diabetic db/db mice, but had no affect in non-diabetic db/+ mice," they concluded.

    Potential market opportunities

    Significant additional research needs to be performed before anyone can contemplate recommending curcumin for diabetics, but if further studies support these preliminary positive findings, this may offer help for the estimated 19 million people affected by diabetes in the EU 25, equal to four per cent of the total population. This figure is projected to increase to 26 million by 2030.

    In the US, there are over 20 million people with diabetes, equal to seven per cent of the population. The total costs are thought to be as much as $132 billion, with $92 billion being direct costs from medication, according to 2002 American Diabetes Association figures.

    Source: Molecular Nutrition & Food Research
    Published online ahead of print 8 April 2008, doi: 10.1002/mnfr.200700184
    "Effect of curcumin supplementation on blood glucose, plasma insulin, and glucose homeostasis related enzyme activities in diabetic db/db mice (p NA)"
    Authors: K.-I. Seo, M.-S. Choi, U.J. Jung, H.-J. Kim, J. Yeo, S.-M. Jeon, M.-K. Lee

  • Richard A.

    5/6/2008 6:57:00 PM |

    Turmeric is about 4% curcumin. Turmeric and curcumin need fat like Vitamin d to be best absorbed. Lecithin also improves absorption.

  • Physical Therapy Supplies

    6/13/2011 7:46:31 AM |

    As much I know the large doses of cretin monohydrate are widely taken, particularly by athletes, as an endrogenic supplement; cretin supplements are also taken by patients suffering from gyrate atrophy, muscular dystrophy, and neurodegenerative diseases.
    Physical Therapy Supplies

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What's that in your mouth?

What's that in your mouth?




Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.


Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.

Comments (17) -

  • Aaron Blaisdell

    1/7/2010 7:58:19 PM |

    Amen, brother! This is the dirty little secret that proponents of the lipid-hypothesis of CAD continually try to sweep under the rug. Looks like the cat's out of the bag, though, thanks to the internet.

  • Anonymous

    1/7/2010 8:23:51 PM |

    But what can be done about post-meal elevated triglycerides?  Would it be best to avoid fats too, and just eat fruits and vegetables, if one had the will power to do it?

  • Kiwi

    1/8/2010 8:24:56 AM |

    Perhaps we should just give up eating altogether.

  • Nigel Kinbrum BSc(Hons)Eng

    1/8/2010 10:41:14 AM |

    I think that worrying about post-meal elevated triglycerides is probably shortening your life more than post-meal elevated triglycerides.

  • Lindsay

    1/8/2010 2:44:33 PM |

    so what does this mean?

  • Emily

    1/8/2010 4:31:21 PM |

    "It also remains true if you chronically consume fats."

    my understanding is that it is actually in support of normal metabolic functioning for us to "chronically" eat fat. low carb eating, in my lay-person's opinion, means therefore eating good fats (and i am of the un-pc standpoint that saturated animalfats are a-ok) , not just green veggies alone. low-car and low-fat would be no fun! but that's just my 2 cents.

  • ET

    1/8/2010 7:12:24 PM |

    I've had two non-fasting cholesterol tests performed in the last year.  My fasting triglycerides are around 40.  My triglycerides three hours after eating a meal with 10g carbs and 59g of fat were 91.  The time prior to that, they were 79 eight hours after breakfast and three hours after lunch (both were high-fat meals).

    Yeah, they go up, but not that much.

  • donny

    1/8/2010 7:37:28 PM |

    So what about the other side of the equation? Decreasing the absorption rate of fat (or spreading it out over more meals) might not help any. But if you can optimize the deposition of fat where it really belongs, in subcutaneous fat tissue-- that is, if fat is deposited in fat tissue where it belongs until needed, at a rate close to the rate at which new dietary fat is absorbed into the bloodstream-- then there shouldn't be a problem.
    Interventions that raise HDL generally increase adiponectin. Eating less wheat, beer, fructose, or adding in fish oil, niacin, vitamin d, even being born a woman. And they also associate with less wheat belly.

    http://www.springerlink.com/content/dpy09vbc0r8jxnm9/

    -----------------------------------
    Conclusion/interpretation. These data suggest that adiponectin concentrations are determined by intra-abdominal fat mass, with additional independent effects of age and sex. Adiponectin could link intra-abdominal fat with insulin resistance and an atherogenic lipoprotein profile.
    --------------------------------
    Maybe they've got cause and effect reversed here? I read a study in mice that were leptin-deficient. Adding extra adiponectin made the mice fatter. So adiponectin is probably not so much a reaction to deposited fat as it is a promoter, maybe a facilitator of proper fat storage.

    ?

  • Anonymous

    1/8/2010 7:44:30 PM |

    Thanks, interesting post. Just wondering: what about proteins?

  • Finn

    1/8/2010 8:58:31 PM |

    So if I eat cheese slices with butter as snacks all day, my triglys will be chronically high and I can get heart problems?

    Does this mean that intermittent fasting is very important if you eat low carb/paleo style?

  • Johnny M

    1/8/2010 10:41:07 PM |

    Where Oh Where can I find a Doctor like Doctor Davis in the New Jersey area?

    My doc who is a cardiologist referred to by local medicenter when it was found out my Trigs were 235 and Total Cholesterol were 295, LDL 195, HDL 57, promptly put me on 5 mg Crestor to lower trigs and LDL, never discussed diet or anything with me. His office plastered with Pfizer Lipitor posters and Crestor bags given by pharma reps.

    Heres the kicker, this was all done with blood work that was NON-FASTING. I had blood drawn an hour after I had eaten eggs and bacon. This was also around halloween time too when I was over indulging on ALOT of Sub sandwiches and bread and lots and lots of candy. I love peanut butter cups. But I know 5 a day is excessive, which was my intake.  Was I getting a DOUBLE Whammy increasing my Trigs?

    Since I found this blog, I've been taking my Crestor which I don't want too. But have taken up the no wheat diet and HFC out of my diet that Dr Davis suggests. Dropped 18 pounds in a matter of weeks.

    Took my own cholesterol with one of those home machines after 4 weeks of Crestor. Doctor wants to test after 3 months. But my Total Cholesterol was 151, calculated LDL 87, HDL 50 and Trigs 69. I wonder how much was the Crestor doing the change or the change in my diet and 18 pound weight loss?

    Sorry for the rambling, but Dr. Davis your blog does give great info and brings peace of mind to me.

  • Bryce

    1/8/2010 11:34:10 PM |

    Anonymous,

    Absolutely not. Having elevated triglycerides immediately after a meal is not a dangerous thing. It's only when they are chronically elevated that you are in danger. Same thing with insulin. Chronically elevated levels are the problem.

    Both of these are caused by excessive sugar/carb consumption.

    -Bryce Lee

  • Anonymous

    1/9/2010 2:37:00 AM |

    Bookmarked this. Sometimes non-standard due to you after sharing. Positively value my time.

  • Dennis

    1/9/2010 4:34:05 PM |

    Dr. Davis: a friend of mine recently had triglycerides trending up to 700 and more. I pointed him to your blog, recommended low carbs and fish oil, and after *one month* his TGs are around 200.

    Kudos to you.

  • Scott W

    1/9/2010 5:51:41 PM |

    Interesting series of posts. But keep one thing in mind: Excess blood glucose is converted to palmitic acid by the liver...a saturated fat.

    (This fact alone should give the anti-saturated-fat crowd pause...if the body could have evolved to convert glucose to any type of fat, why did it evolve to produce a saturated fat? Can't be too bad for you...)

    Anyway, if the body through DNL produces a saturated/healthy fat after only a very brief (and normal) spike in blood glucose - after which the glucose returns to a normal fasting level - then high starch (not fructose) diet appears to be quite healthy. This would answer the question of why a rice-base culture can maintain good health while consuming a diet high in starches...in effect, they are eating a high saturated fat diet.

    If they don't eat continuously, allowing their bodies time to eliminate the excess blood glucose and the attendant insulin spike before the DNL triglycerides (palmitic acid) hits their blood stream, then there is no insulin-driven storage of the fats. Instead, they have elevated blood-borne fats that remain available for a consistent energy source of over time, of a type that their body prefers and has evolved to produce.

    Can you get the same effect from eating saturated fat in the first place? Yes. But to assume that this is better than the starch-driven approach you have to accept that higher levels of ANY saturated fat in the bloodstream is unhealthy. Which runs counter to the viewpoint of paleo and low-carb eaters.

    As Stephen has pointed out, there is no evidence that post-prandial glucose spikes are dangerous to someone with a healthy metabolism (i.e. not a type I or II diabetic). So, if there is no evidence of danger from a post-starch-meal spike, why would your body care where it got its saturated fat? Either dietary or liver-produced, it’s all the same once it is in your blood.

    Following the chain of reasoning further, a high-starch diet that leads to DNL production of palmitic acid would be healthier than a high fat diet composed of vegetable oil or other undesirable fats.

    We have to be very careful about quickly latching onto bits of "evidence" that confirm our biases. Remain scientific, think it through. The human body is an amazingly complex organism; when we begin to isolate its responses to prove our points, we can start down a path that leads to conclusions that may satisfy our dietary worldview, but are not entirely accurate.

    Scott W

    Note: If we are being carefully scientific in our approach, we should be careful to distinguish our descriptive terms for non-fat and non-protein calorie sources. "Carbohydrates" is too general. It encompasses fructose, which as a much different effect on the liver than glucose. My discussion above focuses on starches for a reason; they break down to glucose, which the body has evolved to handle efficiently, even in large quantities. It can handle fructose, too, but did not experience it in large quantities prior to modern times. Even using the term "sugar" is inaccurate, since it is half fructose and half glucose. By extension of my discussion above, eating pure glucose powder (dextrose) would be as healthy for a rice-based culture as eating white rice itself. You are simply giving the body the end product of rice digestion (glucose), from which it can produce palmitic acid.

  • Dr. William Davis

    1/9/2010 9:19:15 PM |

    There's no question that postprandial triglyceride-rich lipoproteins are causally related to atherosclerosis, regardless of whether they were fat-driven or carbohydrate-driven.

    However, these brief posts are NOT meant to endorse low-fat diets. They are meant to show that a simple low-fat vs. low-carb approach is too simple-minded. There are other aspects of diet that count for substantial effects. Postprandial phenomena are one important class of effects that cannot be fully controlled by just controlling carbohydrate or fat content of the diet.

  • Anonymous

    1/9/2010 9:47:39 PM |

    You still haven't explained why the chart in your previous post (Di Novo Lipo-what?), where normoinsulinemic people have lower DNL on a high-fat diet, is in marked contrast to the chart of Gretchen in the post before that (Gretchen's postprandial diet experiment II) when she was eating high-fat.  From those two posts, it seems that peoples' postprandial triglyceride level is dependent on the amount of insulin they produce (and obviously how sensitive they are to that insulin).  Therefore a high-fat diet is not problematic unless one is also hyperinsulinemic.

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