Chocolate peanut butter cup smoothie

19. March 2011 William Davis (18)
Here's a simple recipe for chocolate peanut butter cup smoothie.

The coconut milk, nut butter, and flaxseed make this smoothie exceptionally filling. If you are a fan of cocoa flavonoids for reducing blood pressure, then this provides a wallop. Approximately 10% of cocoa by weight consists of the various cocoa flavonoids, like procyanidins (polymers of catechin and epicatechin) and quercetin, the components like responsible for many of the health benefits of cocoa.


Ingredients:
1/2 cup coconut milk
1 cup unsweetened almond milk
2 tablespoons cocoa powder (without alkali)
2 tablespoons shredded coconut (unsweetened)
1 tablespoon ground flaxseed
1 teaspoon almond extract
1 1/2 tablespoons natural peanut, almond, or sunflower seed butter
Non-nutritive sweetener to taste (stevia, Truvia, sucralose, xylitol, erythritol)
4 ice cubes

Combine ingredients in blender. Blend and serve.

If you plan to set any of the smoothie aside, then leave out the flaxseed, as it absorbs water and will expand and solidify if left to stand.

For an easy variation, try adding vanilla extract or 1/4 cup of sugar-free (sucralose) vanilla or coconut syrup from Torani or DaVinci and leave out the added sweetener.

The compromise I draw here is the use of non-nutritive sweeteners. Beware that they can increase appetite, since they likely trigger insulin release. However, this smoothie is so filling that I don't believe you will experience this effect with this recipe.
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Comments (18) -

  • Anonymous

    3/18/2011 11:28:11 PM |

    This is very good - just mixed up a large glass full (minus the flaxseed).  And, that's my question, do you use finely ground flax seed?  I also tossed in a fist-full of blueberries - should be able to tolerate them well; I just had a very intense resistance training session

    I'd love to see more recipes for some ideas.  I disagree with those who wrote in on the earlier post, characterizing smoothies as "not real food."  I'm a big fan for time-challenged mornings and post-workout nourishment.

    Bill

  • praguestepchild

    3/19/2011 12:11:34 AM |

    I can't believe you passed up a perfectly good opportunity to embed a cheesy 80's Reese's commercial in this post.

    http://www.youtube.com/watch?v=DJLDF6qZUX0

  • Dr. William Davis

    3/19/2011 1:36:19 PM |

    Anon--

    Yes, I used a finely-ground flaxseed.

    The berries are a great idea, provided quantity is small.

  • Kathryn

    3/19/2011 6:33:41 PM |

    Just a cautionary note -

    Sucralose/Splenda can have severe reactions.

    I seem to respond/react to things severely.  Sucralose has caused both allergic reaction (swollen mucus membranes) and severe migraine for me.  In fact, as a frequent migraine sufferer (tho much less now that i've removed gluten and sulfites), the migraine i got from sucralose was by far the worst i've ever had.  

    Personally, i am of the belief that if it effects me so strongly, it is probably not good for anyone, but the damage it does is much less pronounced in other people.

    I stick to stevia for a no-calorie sweetener.

  • Geoffrey Levens

    3/19/2011 8:43:16 PM |

    http://jstevens.wordpress.com/2008/02/20/how-sucralose-aka-splenda-is-made-and-why-you-want-to-avoid-it/

    "How Sucralose (aka Splenda) Is Made And Why You Want To Avoid It

    ...I wanted to comment on Splenda.  Splenda, also known as sucralose, was created accidentally when some chemists were trying to produce an insecticide.  Here is the process by which they produce the formula sold in stores:

    “1.  Sucrose is tritylated with trityl chloride in the presence of dimethylformamide and 4-methylmorpholine, and the tritylated sucrose is then acetylated with acetic anhydride.

    2.  The resulting sucrose molecule TRISPA is chlorinated with hydrogen chlorine in the presence of tolulene.

    3.  The resulting 4-PAS is heated in the presence of methyl isobutyl ketone and acetic acid.

    4.  The resulting 6-PAS is chlorinated with thionyl chloride in the presence of toluene and benzyltriethylammonium chloride.

    5.  The resulting TOSPA is treated with methanol in the presence of sodium methoxide to produce sucralose.”  (Note that methanol, wood alcohol aka paint remover,  is one of the questionable ingredients in aspartame.)

    In addition, the bags and packets of Splenda commercially available are not pure sucralose.  They also contain bulking agents.  All artificial sweeteners use bulking agents.  Do you know what they use?  Sugar.  Dextrose, sucrose, and maltodextrin.  (Maltodextrin is corn syrup solids composed primarily from fructose and glucose in a starch form.)   All sweetener packets are at least 96 percent sugar.  Splenda is 99% sugar.

    The packets are labelled calorie free as a result of manipulating a loophole in the food labeling laws.  The product can be described as sugar free if a serving contains less than 5 grams of sugar, and calorie free if a serving is less than 5 calories.  So they set the serving size on bags at .5 grams  and the packets contain a serving of 1 gram.  A one gram packet contains 4 calories.   This can be confirmed on the manufacturer’s website in the FAQ section:  â€œLike many no and low calorie sweeteners, each serving of SPLENDA® No Calorie Sweetener contains a very small amount of common food ingredients, e.g., dextrose and/or maltodextrin, for volume. Because the amount of these ingredients is so small, SPLENDA® No Calorie Sweetener still has an insignificant calorie value per serving and meets FDA’s standards for “no calorie” sweeteners. “

    To make matters worse, when sucralose was shown to not raise blood sugars, it was the pure substance that was tested, not the mixture that is sold to the public.  Dextrose, sucrose, and/or maltodextrin are definitely going to raise a diabetic’s blood sugar.  There is also a great deal of evidence that artificial sweeteners actually cause an increase in appetite, causing people who consume them to take in more calories than they would otherwise.

    Stevia, on the other hand, lowers blood sugar, making it a much better choice.  If you have tried stevia in the past and did not like the flavor, you might want to try another brand. ..."

  • Brandon Nolte

    3/19/2011 10:38:51 PM |

    If your looking for a more nutritious "sweetner" you should try adding half a cup of coconut water. Delicious!

    Ps. I love your blog. Keep up the great work!

  • bob412

    3/19/2011 11:34:59 PM |

    Tapioca starch in the almond milk, but not enough to hurt you.

  • Dr. John

    3/20/2011 2:49:18 AM |

    I enjoy your blog. You have a good thread about the hazards of hyperglycemia.
    However, this recipe is not one I would recommend to patients attempting to reverse metabolic syndrome, T2D, or IR.
    Their main concern is the inflammation caused by the above listed disorders. The omega 6 content of the peanut butter, sunflower seed, and to an extent, almond butter would exacerbate the inflammation mitigated by the hyperglycemia.
    In addition, sugar alcohols (xylitol, erythritol) tend to cause GI upset (gas, diarrhea). Also the hazards of Sucralose are intuitively obvious....it contains chlorine molecules....commonly found in many household cleaners, and of course used in WWI as a pulmonary choking agent.
    I would only use macadamia nuts/nut butter, and Stevia to sweeten.
    Dr. John

  • Dr. William Davis

    3/20/2011 1:28:28 PM |

    Thanks, Dr. John.

    I hear you on the sucralose issue. I've actually been having positive experiences with stevia, xylitol, and erythritol. The important thing is that people have some good choices nowadays, unlike 20 years ago when we had saccharine . . . period.

    There is no question that mannitol and sorbitol have greater potential for both GI distress (diarrhea) as well as increases in blood glucose, so these are clearly on the no-no list (unless you need a quick laxative).

  • Gabriella Kadar

    3/20/2011 7:23:42 PM |

    Sucralose is not metabolized.  Most of it is excreted unchanged in the feces.  A small percentage is absorbed and excreted unchanged in urine.  

    Sodium in food is more of a concern for a person who experiences migraine headaches.  Over-activity of muscles activated by the Trigeminal nerve due to airway resistance secondary to water retention is a greater concern.  Various factors are present both anatomically and physiologically in people who experience migraine.  The only way to determine if sucralose is actually the cause of a migraine is to consume sucralose on its own.

    What concerns me is what happens to the sucralose in the environment.  The addition of a chlorine atom, (not a molecule, Dr. John) results in a molecule which cannot be metabolized by bacteria.  If environmental degradation is possible, then sucralose excreted by human beings is not an issue.  But if it persists in the environment, then it is a pollutant.

  • Anonymous

    3/21/2011 3:22:42 AM |

    I am practically a fruitarian, so much of what I like would be off limits.
    Is there an article here on what IS recommended?

  • Dr. John

    3/21/2011 3:29:27 PM |

    Yes, atoms, not molecules...ie. precisely 3 atoms of chlorine/molecule of sucrose...

    An interesting thing about this selective halogenation of sucrose, is the fact that sucralose (being 600 times as sweet as sucrose), increases the HbA1c numbers in my patients. This demonstrates a lessening of diabetic control. Thus, hemoglobin gets glycated and fasting blood sugar increases....with the attendant hyperglycemia issues as mentioned, and this excellent blog site.

    For this reason I do not recommend sucralose for diabetics nor anyone wanting to keep blood sugar levels within normal limits. The current cost and future costs for diabetes will cripple our healthcare structure. Here are ADA numbers:

    $174 billion: Total costs of diagnosed diabetes in the United States in 2007
    $116 billion for direct medical costs
    $58 billion for indirect costs (disability, work loss, premature mortality)

    Dr. John

  • Gabriella Kadar

    3/22/2011 1:42:51 AM |

    Dr. John, is it possible that other factors contribute to higher H1ac levels in your type 2 diabetic patients?  

    Since sucrolose is not metabolically active and does not act as a laxative, then there could be other endocrinological and neurological reasons for higher glucose levels.

    Here's an abstract on sucralose and Type 2 diabetes:

    Grotz VL, Henry RR, McGill JB, Prince MJ, Shamoon H, Trout JR, Pi-Sunyer FX. Lack of effect of sucralose on glucose homeostasis in subjects with type 2 diabetes. J Am Diet Assoc. 2003 Dec;103(12):1607-12.

    OBJECTIVE: To investigate the effect of 3-months' daily administration of high doses of sucralose, a non-nutritive sweetener, on glycemic control in subjects with type 2 diabetes. DESIGN: A multicenter, double-blind, placebo-controlled, randomized study, consisting of a 6-week screening phase, a 13-week test phase, and a 4-week follow-up phase. SUBJECTS/SETTING: Subjects with type 2 diabetes (age range 31 to 70 years) entered the test phase of this study; 128 subjects completed the study. The subjects were recruited from 5 medical centers across the United States and were, on average, obese. INTERVENTION: Subjects were randomly assigned to receive either placebo (cellulose) capsules (n=69) or 667 mg encapsulated sucralose (n=67) daily for the 13-week test phase. All subjects blindly received placebo capsules during the last 4 weeks of the screening phase and for the entire 4-week follow-up phase. MAIN OUTCOME MEASURES: Glycated hemoglobin (HbA1c), fasting plasma glucose, and fasting serum C-peptide were measured approximately every 2 weeks to evaluate blood glucose homeostasis. Data were analyzed by analysis of variance using repeated measures. RESULTS: There were no significant differences between the sucralose and placebo groups in HbA1c, fasting plasma glucose, or fasting serum C-peptide changes from baseline. There were no clinically meaningful differences between the groups in any safety measure. CONCLUSIONS: This study demonstrated that, similar to cellulose, sucralose consumption for 3 months at doses of 7.5 mg/kg/day, which is approximately three times the estimated maximum intake, had no effect on glucose homeostasis in individuals with type 2 diabetes. Additionally, this study showed that sucralose was as well-tolerated by the study subjects as was the placebo.

    PMID: 14647086 [PubMed - indexed for MEDLINE]

    Now, I can understand how sugar alcohols taken in large quantities might have some effect on blood sugar because they are laxative and increase gut motility and cause discofort or pain, both of which will spike blood sugar values. the liver dumps glucose into the bloodstream when the body is under stress like this.  And of course, the pancreas reacts very sluggishly to endogenous glucose.

    I think type 2 diabetics should have routine sleep study screening to determine whether breathing issues during sleep may be upramping the sympathetic nervous system and causing high sugar levels during sleep. We can't just help these people improve their life quality by looking at only one parameter.

    They need otolaryngological evaluation for anything from deviated nasal septa to chronic allergies, enlarged adenoids and tonsils.  The size of their jaws, how they function and tongue posture also factors in.

    Not to mention, anyone with pulmonary issues would have increased effort on breathing...asthma, pulmonary hypertension etc.  The existance of chronic pain and anxiety conditions also influence how the body produces its own glucose.  

    Patient's require a multi-disciplinary workup to determine the multiple factors that result in the development of type 2 diabetes.  It's not merely diet because these people have an awfully hard time changing their diets without having other problems addressed.

  • Anonymous

    3/24/2011 7:01:46 PM |

    Excellent! Dr. Davis, you have had many posts of what not to eat but very few on what we should eat. Taking something out of our diet means we have to replace it with something. This post seems to be in the right spirit. I am going to try this soon. Now if only you can post a similar substitute for Keva Juice's Oreo Speedwagon smoothie! Yes, I know they are hazardous to your health but they are wickedly good!

    -- Boris

  • Dr. John

    3/25/2011 5:50:15 AM |

    I'm not totally convinced why sucralose, a chloro-carbon, similar to DDT and PCBs, would elevate the HgA1c levels. My guess would be a neurological response to an ingested poison. Sucralose does kill intestinal beneficial bacteria...lactobacillus, bifidobacteria, and bacteroides...of varying amounts of 37-67%...and the enteric nervous system would react by elevating cortisol/adrenaline/glucagon: while at the same time not delaying gastric emptying.
    Body perception is stress....glycation of RBCs result, with CVD and sudden cardiac death.

    Studies that use diabetic, and obese subjects in the assessment of A1c elevation are biased from the start. These individuals have already lost glycemic control and as a result would not have normal A1c levels to begin with...let alone studying their response 13 weeks later.

    McNeil Nutritionals, maker of SPLENDA® Brand products, stated it has provided the American Diabetes Association (ADA) with a sponsorship to support the Association's efforts to fund research, information and advocacy programs on behalf of people with diabetes.
    And McNeil Nuts. are owned by Johnson and Johnson, who are large contributors to the ADA...the journal of the previously listed biased study showing the sucralose doesn't affect A1c levels...in spite of the fact in clinical results showing the opposite.

    Anything, sucrose or sucralose, that elevates A1c levels is cardio-lethal...and is best avoided.

  • reikime

    4/2/2011 5:07:29 PM |

    Dr. D,
    Do you use regular coconut milk or the lite? Does it make a difference, except calorically?

    Thanks!

    Jeanne

  • Anonymous

    4/8/2011 1:09:56 AM |

    I am allergic to the artificial sweeteners. Thought I could tolerate sucralose but it just took a little time for a reaction. My mouth and throat became inflamed and I had sore bumps all over the inside of my throat and back of my mouth after about a week.

    I don't like stevia or the other natural no calorie sweeteners either...they just don't taste sweet to me or have odd flavors.

    But I found something.  It is not calorie free, but it has low glycemic index and tastes just like sugar.  It is "Organic Blue Agave". What are a few calories in exchange for some actual taste.

    I bought it at Costco.

  • Geoffrey Levens

    4/8/2011 1:30:13 AM |

    ""Organic Blue Agave". What are a few calories in exchange for some actual taste."

    High fructose corn syrup (HFCS) is about 55% fructose and cause inflammation, insulin resistance, and elevates triglycerides.  Agave syrup is often 70% or higher (possibly as high as 90%) fructose!  Marketing scam...

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Overweight, hungry, diabetic, and fat-free

15. December 2009 William Davis (52)
Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

10. December 2009 William Davis (32)
Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

8. December 2009 William Davis (15)
Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

4. December 2009 William Davis (0)
Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis

2. December 2009 William Davis (0)

Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil


Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

1. December 2009 William Davis (31)
Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

I'll supply the tar if you supply the feathers

30. November 2009 William Davis (13)
The results of the latest Heart Scan Blog poll are in.


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)


Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

What goes up can't come down

28. November 2009 William Davis (13)
According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)


Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of > or = 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Gretchen's postprandial diet experiment

27. November 2009 William Davis (11)
Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.









Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.



This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

After-eating effects: Carbohydrates vs. fats

25. November 2009 William Davis (17)
In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.