Organic really IS better

16. August 2009 William Davis (18)
If you have any doubts about the value of organic foods vs. conventionally-grown foods, then take a look at the findings from a USDA--Yes, USDA--sponsored study.

In this study, the nutritional content of organic vs. conventionally-grown blueberries were compared. Ironically, these observations come from the USDA's Genetic Improvement of Fruits and Vegetables Laboratory of the Produce Quality and Safety Laboratory.

Their findings (all values expressed as weight per 100 grams fresh weight blueberries, or a bit less than 1/4 cup):


Total phenol content (e.g, flavonoids):

Organic: 319.3 mg
Conventional: 190.3 mg

Organic blueberries had 68% greater phenol content.


Total anthocyanins (an important class of flavonoids):

Organic: 131.2 mg
Conventional: 82.4 mg

Organic blueberries had 59% greater anthocyanin content.


Antioxidant capacity (ORAC):

Organic: 46.14 mg
Conventional: 30.8

Organic blueberries had 50% greater antioxidant capacity.


Flavonoids suspected to carry unusually potent health effects--malvidin, delphinidin, myricetin, and quercetin--were all contained in greater proportions in the organically-grown blueberries, also. These flavonoids are demonstrating pharmacologic-level health effects in preliminary studies.

Why a genetics laboratory? After all , the study findings came out heavily in favor of non-genetic, organic farming methods of growing produce. It certainly must have at least given pause to the vocal group within agriculture and the USDA that have long argued that organic produce is no different. I suspect that the laboratory will now try to recreate the nutritional value of organic through genetic manipulation of cultivars grown using conventional methods.

Regardless of the motivations behind the study, we see that there is no comparison: organic blueberries are superior in nutritional value to those grown with conventional pesticides and herbicides. While the study addressed only blueberries, the dramatic difference makes it likely that similar differences exist in other fruits and vegetables.

Coming on the Track Your Plaque website: An in-depth Special Report on the health effects of anthocyanins.
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Comments (18) -

  • Anne

    8/16/2009 1:31:49 PM |

    Dear Dr Davis,

    A little off topic, but I take a good fish oil omega-3 supplement and I eat a lot of fish too (wild and therefore organic), but I've been finding disturbing reports on the net that omega-3s and fish are not so good for us after all because the oils are very easily oxidised in the body, and I'm wondering if you could comment sometime please. Here are some links about the 'dangers' of fish oil:

    http://www.paleonu.com/panu-weblog/2009/6/19/fish-oil-or-not.html

    http://high-fat-nutrition.blogspot.com/search?q=fish+oil

    http://raypeat.com/articles/articles/fishoil.shtml

    Anne

  • hb

    8/16/2009 7:37:23 PM |

    I guess there's no free link? Couldn't see it on the Lab's website.

  • moblogs

    8/17/2009 9:33:45 AM |

    Even if it wasn't better, some things definitely taste better, so the premium is apparent.

  • Nameless

    8/17/2009 6:18:17 PM |

    The problem with organic blueberries (for me) is simply finding them. Seems nobody locally sells organic blueberries.

    As for fish oil, oxidation is a potential issue, but hopefully vitamin E protects against that. There could be a concern though with very large dosing, or bad fish oils. It'd be interesting to see more krill oil vs fish oil studies, testing oxidation, lipid changes, plaque reduction, etc. Krill would, seemingly, avoid some of the oxidation problems fish oil may have.

    I would also be interested if Dr. David considered writing an article about oxidized cholesterol in the future, as it seems to get ignored a lot. But if fish oils did increase oxidized cholesterol in the body to such an extent as to increase plaque, I'd think he would have seen it by now, since most of his patients are probably taking fish oil.

  • Helena

    8/18/2009 11:54:50 PM |

    Dr Davis, I have been reading alot about blueberries and their power to lower LDL cholesterol. But we just went over the fructose and how bad that is for the cholesterol. Am I missing something special with the blueberries? I know they are high in Vitamin C and K, but is that it? I feel like I don't know what to believe regarding blueberries. Thankful for a reply. Regards, Helena

  • Dr. William Davis

    8/19/2009 1:10:31 AM |

    Hi, Helena--

    Blueberries are, on the whole, good. They have a wonderful complement of flavonoids and other nutrients.

    But, too much of a good thing . . . Then the fructose gets you. So, a modest quantity is good, just as in many other foods.

  • Dr. William Davis

    8/19/2009 1:12:11 AM |

    Anne-

    The fact remains: Large clinical studies that have looked at cardiovascular events and mortality, such as GISSI-Prevenzione, have demonstrated significant reductions.

    I agree that we must always question "conventional" wisdom. But sometimes conventional wisdom is correct.

  • Richard A.

    8/19/2009 4:02:36 PM |

    From what I understand, wild blueberries are higher in anthocyanins than are the standard blueberries. Wild blueberries are smaller in diameter than the standard.

    In southern California, Trader Joe's carries wild blueberries at a good price -- about $2.99 for 16 ozs. Indeed, TJ's has a good selection of berries at a good prices.

    http://www.wildblueberries.com/

  • Tom

    8/19/2009 4:37:04 PM |

    This website that Anne posted - http://raypeat.com/articles/articles/fishoil.shtml - raises some pretty frightening concerns about supplemental fish oils, and he includes references to studies that seem to confirm some of his points.

    Dr. Davis, have you had anopportunity to read his comments, and if yes, what is your thinking about his allegations?

    Thank you.

    Tom

  • David

    8/19/2009 4:39:26 PM |

    Hi Dr. Davis,

    Do you ever see patients that have a zero calcium score? I'm just wondering if your diet/lifestyle advice applies as well for prevention as it does for your sample of patients.  

    Thanks,
    David

  • karl

    8/19/2009 6:47:52 PM |

    Where can one find this study? Were both blueberries the same species?

    I've wondered if the smaller wild blueberries had more skin and thus more flavinoids?

  • Kismet

    8/19/2009 11:21:18 PM |

    Tom, if anything the risks of Omega-3 fatty acids might outweight their benefits in a select few: exceptionally healthy people with no risk factors whatsoever. (And never forget that dosis sola venenum facit.)
    I guess it certainly does not apply to Dr. Davis' patients and probably not to most of us.

    There may be pros and cons of taking high or moderate doses of fish oil but that is to be expected, isn't it? It's a matter of risk:benefit ratios. If large interventional trials show a mortality benefit in certain populations, then we can be sure of it.

    I've planned to read up on the issue of O-3 and those purpoted risks for quite some time (but haven't, so take my opinion FWIW).

  • Nameless

    8/20/2009 12:48:51 AM |

    I expect this will come up in the upcoming report on Anthocyanins, but a recent study has shown some nice lipid improvements using approx the equivalent to a cup of blueberries --

    http://www.ajcn.org/cgi/content/abstract/ajcn.2009.27814v1
    http://inhumanexperiment.blogspot.com/2009/08/anthocyanins-from-berries-increase-hdl.html

    The study used an extract, so they seemingly got around the fructose issue. But I think the benefits of blueberries would outweigh the relatively low levels of fructose anyway. It's really the only affordable way to get enough anthocyanins to match the study, until some pharmaceutical company gets wind of it, I guess. *Black Currant/Blueberry pills ala Lovaza*

  • Van Rensselaer

    8/20/2009 3:36:10 AM |

    Anne,

    I've read the blog posts from both Hyperlipid and Panu you've provided.  I think Peter at Hyperlipid raises some very interesting questions, but I'm really not prepared to get carried away with panic.  First, I think it's very important to keep in mind that the study Peter cites had the subjects consuming 30 ml of fish oil per day.  Total omega-3 content alone was in the neighborhood of 15 ml, if I recall correctly.  This is an enormous dose!  Furthermore, Peter makes the point that this is probably only an issue with concurrent consumption of excessive carbs and/or alcohol (and excessive omega-6, one suspects...), perhaps thus explaining why Eskimo on a traditional diet do not experience hepatic steatosis, etc... at such high levels of omega-3 intake.  As for the "raypeat" article you've provided, I can only say that I've checked out two of the papers he cites, and was left a bit puzzled.  For instance, the issue of liver toxicity he mentions (I first followed this issue based on the concern Peter @ hyperlipid raised) refers to a study using a rabbit model.  Very interesting, but it's critical to ask just how much fish oil you can force-feed a herbivore before something horrible happens.  We've seen very wrong and enduring dietary advice arise from studies using rabbit models before (ie the lipid hypothesis), so I say, let's not jump to conclusions.  The second study raypeat points us to "Mechanisms for the serum lipid-lowering effect of n-3 fatty acids" really doesn't have much to say about deleterious effects, as far as I can see.  Here's a quote for you: "The finding that n-3 fatty acids are transported from the liver as ketone bodies to a larger extent than n-6 fatty acids may thus explain that a high intake of n-3 fatty acids is not accompanied with hepatic steatosis."

    I'll keep reading up in the meanwhile.  This is a pretty fascinating subject to me.

    Oh, and I like my blueberries!  Lots of tasty organic options in the SF Bay Area.  I think Michael Pollan mentioned in one of his books that wild and organically raised plants tend to have a much higher antioxidant content because they're left to their own devices, having to fend for themselves rather than rely on the crutch of insecticides to protect them...

    Kind regards,

    Van Rensselaer

  • Van Rensselaer

    8/20/2009 3:58:24 AM |

    I forgot to say that Aronia, aka "chokeberry" is supposedly loaded with anthocyanins.  I've bought the juice from Trader Joe's before.  It's not very sweet at all and is astringent like unsweetened 100% cranberry juice.  Maybe an ideal candidate?  Low in sugar, high in anthocyanins.


    Van Rensselaer

  • Anonymous

    8/20/2009 1:26:56 PM |

    To the risks of O-3s... I understand that some genetic variants are linked to these risks.  I would very much like to know the good Doc's opinion on genetic testing and variation, and how it affects they way we metabolize certain nutrieints.  Perhaps there is no "one diet fits all" solution, but rather a "one diet fits a genotype."

  • robert

    9/3/2009 8:19:26 PM |

    Hello Readers and Dr. Davis,

    Let me try to clear up what may be a little confusion regarding the USDA organic vs conventional blueberry results for phenolic profile, total anthocyanins, and the ORAC value of each. Firstly, organic blueberries are grown and harvested from the wild and although they do get some management, they are supremely adapted to their cold northern environment and fare well enough left alone and are are "organic" by default (some managers do apply fertilizers and set fires for weed control). These wild northern bluberries are Vaccinium angustifolium. On the other hand, "conventional" blueberries are generally more southerly tetraploid and hexaploid species, Vaccinium corymbosum and V. ashei and interspecific hybrids developed for the fresh market and the emphasis on uniform, dry scar fruit with pleasing color and shelf life to withstand the rigors of the food system. The wild types have far more phenols and anthocyanins located just under their skins on a per gram basis than modern cultivars of V corymbosum and relatives. However, they also do not stand up well to the logistics of shipping fresh to millions of retail outlets and tend to "bleed" anthocyanin when disturbed. For this reason, most are canned or frozen. The point is that USDA did not really segregate their data properly if it was not a straight comparison between like species and known environments. Comparing V. angustifolium from Maine or Canada with V. corybosum used for the fresh market for these constituents does not give a clear picture that "organic" techniques automatically infer higher concentrations of components desirable for human consumption than "conventional" cropping. There is much more going on than production techniques and these conclusions do not hold as a consequence of technique when applied to the exact same cultivar. I work on the genetic improvement of blueberry and other small fruits so I have a bit of experience with this. If you want the antioxidants of blueberries on a year-round basis, buy the Dole frozen wild blueberries. BTW, I don't work for Dole. Hope this helps. Thanks.

    Robert C. Richardson, Ph.D.

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Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

2. April 2010 William Davis (12)
Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

1. April 2010 William Davis (11)
The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

28. March 2010 William Davis (16)
Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

26. March 2010 William Davis (20)
Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

23. March 2010 William Davis (24)
Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

21. March 2010 William Davis (19)
No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

Statin stupid

19. March 2010 William Davis (0)
If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

19. March 2010 William Davis (83)
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.

Vitamin D as a cardiovascular risk factor gains ground

18. March 2010 William Davis (0)
If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

18. March 2010 William Davis (74)
No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.