Fat Head: Tom Naughton's manifesto for low-carb eating

I just got back from Jimmy Moore's low-carb cruise to the Bahamas.

Among the many interesting people I met on the cruise was the creator of the documentary film, Fat Head, Tom Naughton.

Tom brings both creative insights into low-carbohydrate eating as well as humor. Low-carb eating can be a pretty contentious issue, but Tom made it fun. He will make you laugh about many of the odd notions we have about diet.

Among the best parts of Fat Head is Tom's portrayal of the effects of carbohydrates on insulin and fat metabolism:






Fat Head joins the ranks of films like Food, Inc, that make nutrition information entertaining. For anyone interested in a unvarnished look at diet, weight loss, along with a few laughs along the way, Tom Naughton's Fat Head is worth viewing.

Oatmeal: Good or bad?


You've heard it before: oatmeal reduces cholesterol. Oatmeal producers have obtained permission from the FDA to use a cholesterol-reducing claim. The American Heart Association provides a (paid) endorsement of Quaker Oats.

I've lost count of the times I've asked someone whether they ate a healthy breakfast and the answer was "Sure. I had oatmeal."

Is this true? Is oatmeal heart healthy because it reduces LDL cholesterol?

I don't think so. Try this: Have a serving of slow-cooked (e.g., steel-cut, Irish, etc.) oatmeal. Most people will consume oatmeal with skim or 1% milk and some dried or fresh fruit. Wait an hour, then check your blood sugar.

If you are not diabetic and have a fasting blood sugar in the "normal" range (<100 mg/dl), you will typically have a 1-hour blood glucose of 150-180 mg/dl--very high. If you have mildly increased fasting blood sugars between 100 and 126 mg/dl, postprandial (after-eating) blood sugars will easily exceed 180 mg/dl. If you have diabetes, hold onto your hat because, even if you take medications, blood sugar one hour after oatmeal will usually be between 200 and 300 mg/dl.

This is because oatmeal is converted rapidly to sugar, and a lot of it. Even if you were to repeat the experiment with no dried or fresh fruit, you will still witness high blood sugars in these ranges. Do like some people and pile on the raisins, dried cranberries, or brown sugar, and you will see blood sugars go even higher.

Blood sugars this high, experienced repetitively, will damage the delicate insulin-producing beta cells of your pancreas (glucose toxicity). It also glycates proteins of the eyes and vascular walls. The blood glucose effects of oatmeal really don't differ much from a large Snickers bar or bowl of jelly beans.

If you are like most people, you too will show high blood sugars after oatmeal. It's easy to find out . . . check your postprandial blood sugar.

In past, I recommended oat products, specifically oat bran, to reduce LDL, especially small LDL. I've changed my mind: I now no longer recommend any oat product due to its blood sugar-increasing effects.

Better choices: eggs, ground flaxseed as a hot cereal, cheese (the one dairy product that does not excessively trigger insulin), raw nuts, salads, leftovers from last evening's dinner.

Mustard: Super health food?

Could mustard--yes, the yellow condiment you smear on hot dogs--be a super heart healthy food in disguise?

Consider that mustard contains:

Vinegar

Turmeric

No appreciable sugar


The vinegar slows gastric emptying, resulting in slower absorption of any carbohydrates and a reduced glucose area-under-the-curve. Of the little fats contained (about 3 grams per 1/4 cup), most are desirable monounsaturates. Mustards are relatively rich in selenium, with 20 mcg per 1/4 cup, helpful for protection against cancer and thyroid disease, and magnesium, 31 mg per 1/4 cup.

Turmeric is added to most mustards. One of the constituents of turmeric, curcumin, the substance that confers the bright yellow color, has been a focus of interest for its anti-inflammatory effects. Curcumin has been documented to reduce activity of the inflammatory enzymes cyclooxygenase-2 (COX-2), lipoxygenase, and reduce activity of inflammatory signal molecules, tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1,2,6,8, and 12, and monocyte chemoattractant protein (MCP). Curcumin also has been shown to reduce LDL oxidation, a potentially important step in atherosclerotic plaque formation. Turmeric is used as a tea by Okinawans. (Hmmmm . . . )

Turmeric content of mustard can vary, of course. Likewise, sugar content. Look for mustards that are not sweetened, so avoid honey mustard in particular. Look for hot, brown, horseradish, Dijon, etc. If there is a downside to mustard, it's sodium content, though the 709 mg per 1/4 cup should only be a problem for those who are sodium-sensitive (African Americans, in particular).

So perhaps mustard isn't exactly a super health food. But it may have some bona fide health effects and should be used generously especially if you are concerned about blood sugar and inflammatory phenomena.

Exercise and blood sugar

There is no doubt that exercise yields benefits across a spectrum of health: reduced blood pressure,  reduced inflammation, reduced blood coagulation, better weight control, stronger bones, less depression, reduced risk for heart attack.

Exercise also influences blood sugar. Diabetics understand this best: Exercise reduces blood sugar 20, 30, 50 or more milligrams. A starting blood sugar, for instance, of 160 mg/dl can be reduced to 80 mg/dl by jogging or riding a bicycle. (I recently had brunch at an Indian restaurant with my family. Blood sugar one-hour postprandial: 134 mg/dl. I was sleepy and foggy. I got on my stationary bike and pedalled at a moderate clip for 60 minutes. Blood sugar: 90 mg/dl.)

Could the reduction of blood sugar with exercise be THE reason that exercise and physical activity provide such substantial benefits?

Think about it. Reduced blood sugar:

1) Reduces risk for future cardiovascular events.
2) Reduces glycation of proteins, i.e., reduced glucose binding to proteins like the ones in artery walls and the lenses of your eyes.
3) Reduces blood coagulation
4) Reduces endothelial dysfunction (abnormal artery constriction that leads to atherosclerosis)

This might explain why it doesn't require high levels of aerobic activity to derive benefit from exercise, since even modest efforts (e.g., a 15-minute walk after eating) reduce blood sugar substantially.

The incredible 33-year, 18,000-participant Whitehall study tells us that a postprandial (after-eating) blood sugar of an impossibly-difficult 83 mg/dl is required to erase the excess cardiovascular risk of blood sugar. Could this simply be telling us that physical activity or exercise is required to suppress blood sugars to these low levels?

It makes me wonder if an index of the adequacy of exercise is your post-exercise blood glucose.

The most important weight loss tool


Question: What is the most effective tool available to help you lose weight? 


A pedometer (walk 10,000 steps, etc.)?

A treadmill? 




A bicycle?






No. None of the above. 

The most important tool you can use to achieve weight loss is your glucose monitor:



Timing of blood sugars

Because different foods generate different blood sugar (glucose) responses, the timing of your blood sugar is an important factor to consider.

This question has come up a number of times. Commenters have asked whether the one-hour postprandial glucose is timed with the start of the meal or the conclusion of the meal.

In my view, if we simply ignored all aspects of meal composition, then blood glucose should be obtained one hour after the conclusion of a meal. This is because most mixed meals (i.e., mixed in composition among proteins, fats, and carbohydrates) yield peak blood glucose levels at 60-90 minutes after consumption. Timing blood glucose to 60 minutes after the conclusion of a meal puts the sample right about at the peak.

But this is an oversimplification. For instance, here is the blood glucose behavior after so-called "complex" carbohydrates wheat bread, rye bread, rye made with beta glucan, and whole wheat pasta (50 grams carbohydrates each) in slender, healthy volunteers, mean age 29 years:


From Juntunen et al 2002

Note that blood glucose peaks at 35 minutes postprandial. (To convert glucose in mmol/L to mg/dl, multiple by 18. Thus, whole wheat bread increased blood glucose from 94 mg/dl to 122 mg/dl. Also note the lower peak glucose for pasta, but sustained higher glucose levels hours later.)

In another study, older (mean age 64 years), overweight (BMI 27.9) females with diabetes were given 50 grams carbohydrate, 50 grams carbohydrate with olive oil, or 50 grams carbohydrate with butter:


From Thomsen et al 2003. Control meal of soup plus 50 g carbohydrates ({blacktriangledown}), the control meal plus 80 g olive oil ({circ}), and the control meal plus 100 g butter (•).

In this experience, note that postprandial glucose peaks 60-120 minutes after the meals (consumed within 10 minutes), delayed more when either oil is included. Blood glucose started at 144 mg/dl and peaked as high as 230 mg/dl with carbohydrates only; peaks were reduced (along with AUC) when oil was included. (Note the differential effect, olive oil vs. butter.)

These two sets of observations give you a range of blood glucose behavior. One side lesson: Carbohydrates should never consumed by themselves, else you will pay with a high blood sugar (not to mention the hypoglycemic response later for many).

Psssst . . . There's sugar in there

You non-diabetics who check your postprandial blood sugars already know: There are hidden sources of sugar in so many foods.

By now, everybody should know that foods like breakfast cereals, breads, bagels, pretzels, and crackers cause blood sugar to skyrocket after you eat them. But sometimes you eat something you thought was safe only to find you're showing blood sugars of 120, 130, 150+ mg/dl.

Where can you find such "stealth" sources of sugars that can screw up your postprandial blood sugars, small LDL, inflammation, blood pressure, and cause you to grow visceral fat? Here's a few:

Balsamic vinaigrette
Many commercially-prepared balsamic vinaigrettes, especially the "light" varieties, have 3 or more grams carbohydrates per tablespoon. Generous use of a sugar-added vinaigrette can therefore provide 12+ grams carbs. (Some, like Emeril's and Wish Bone, also contain high-fructose corn syrup.)

Hamburgers
I learned this lesson the hard way by taking my blood sugar after having a hamburger, turkey burger, or vegetarian burger (without bun): blood sugar would go way up. The effect is due to bread crumbs added to the meat or soy.

Tomato soup
If it were just tomatoes, it would still be somewhat high in sugars. But commercially-prepared tomato soup often contains added high-fructose corn syrup, sucrose, and wheat flour, bringing sugar totals to 12 to 20+ grams per half-cup. A typical 2-cup bowl of tomato soup can have upwards of 80 grams of sugar.

Granola
Sure, granola contains a lot of fiber. But most granolas come packed with sugars in various forms. One cup of Kellogg's Low-fat Granola with Raisins contains an incredible 72 grams (net) carbohydrates, of which 25 grams are sugar.


Given modern appetites and serving sizes, you can see that it is very easy to get carried away and, before you know it, get exposed to extraordinary amounts of sugar and carbohydrates eating foods you thought were healthy.

And don't be fooled by claims of "natural" sugar. Sugar is sugar--Just check your blood sugar and you'll see. So raw cane sugar, beet sugar, and brown sugar have the same impact as white table sugar. Honey, maple syrup, and agave? They're worse (due to fructose).

How low should blood sugar be?

What should your blood sugar (glucose) be after eating?

Take a look at the data from the Whitehall study reported in 2006. The Whitehall Study stands apart from other studies in that it was very large (over 18,000 participants) who were observed for an unusually long time (33 years). All participants were administered a 50 gram glucose "challenge" at the start with glucose levels checked after the glucose challenge.

Here's what they found:




From Brunner et al 2006.
Small LDL: Perfect index of carbohydrate intake

Small LDL: Perfect index of carbohydrate intake

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.

Comments (15) -

  • nitrile exam gloves

    12/8/2009 3:58:05 AM |

    Thanks for the knowledge sharing...it helps to be healthy.

  • x.ds

    12/8/2009 12:02:31 PM |

    Here is a link showing the atherogenicity in mice of different saturated fats in diets with 1% cholesterol. Look at page 1416 of the free full report that can be downloaded here:

    http://www.ncbi.nlm.nih.gov/pubmed/8409772

    On the opposite you can see bread not being atherogenic in baboons here:

    http://www.ajcn.org/cgi/content/abstract/33/8/1869

    By the way you can notice the effect of 0.1% cholesterol at the end of the article = 1 gm cholesterol per kg of food = 5 egg yolks.

    Does it look a lot ? "There is evidence from animal experiments showing that if atherogenic dietary factors are reduced to levels comparable to man's intake, the same vessel changes occur as with higher levels, but more slowly."

    Download the free full report here:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1938976/

    In this report you can also see butter to be highly atherogenic to swine without additional cholesterol to their diet.

  • Bobber

    12/8/2009 5:06:03 PM |

    What about rice?  Does it also increase small LDL particles?

  • Nigel Kinbrum BSc(Hons)Eng

    12/8/2009 6:54:52 PM |

    @x.ds: Humans aren't C57BL/6J mice (susceptible to diet-induced fatty streak lesions), baboons or pigs.

  • Future Primitive

    12/8/2009 7:34:20 PM |

    @x.ds

    The strain of mice in the first study are predisposed to diet-induced obesity, type 2 diabetes, and atherosclerosis.

    Likewise, here's an interesting quote from the last paper based on a porcine model: "Whenever there are three
    animals from the same litter, they are divided equally among the three groups (ie, "control", "butter", & "egg yolk" groups)  In the present experiment, this occurred once. These three pigs had the most aortic atherosclerosis in their respective groups. The control pig with the most atherosclerosis was the brother of the pigs with the most disease fed egg and butter."  

    The group of pigs with the highest rate of atherosclerosis was the egg yolk group - yet at most we see a vanishingly positive relationship, if any, in a large number of human epidemiological studies of moderate egg consumption and heart disease (too many to list here - many are recent and easy to locate, though).  Do we even have grounds to formulate a hypothesis of egg induced atherogenesis based on human observational studies? I don't know, really - though a casual glance suggests, "no".

    Looking forward to reading the other study you pointed us to when I get the time.

  • Anonymous

    12/8/2009 7:42:17 PM |

    x.ds:

    Often times these animal studies don't translate well when applied to humans.

    Also, like Dr. Davis pointed out in his blog, most (LDL) cholesterol lowering research doesn't use advanced lipoprotein testing like NMR so the data is misleading to say the least.

  • Anonymous

    12/8/2009 9:16:54 PM |

    x.ds:

    It would be nice for a change to see experiments on other than herbivorous (mice) or mostly vegetarian animals (both pigs and baboons on the wild).

  • Dr. William Davis

    12/8/2009 11:48:34 PM |

    Bobber--

    While all carbohydrates increase small LDL, the effect of wheat is the most extravagant.

  • Anon X

    12/9/2009 3:18:19 AM |

    I generally agree with those who deny the universal applicability of experimental results in mice and rats to men. However, I do so with this one caveat; there is one fact I cannot deny: Many women are convinced that most men are rats.

  • LynP

    12/9/2009 4:42:51 AM |

    Doc, does this mean that I ca sorta log my particle size by getting my apoB checked in quarterly labs? I'll never be able to convince primary to do the outright particle size test...yet (working on that). Thnx.

  • Anonymous

    12/9/2009 3:08:55 PM |

    I admit I do not understand VLDL-C. What I would really like to find is a simple range scale. Mine shows up VLDL-C..7  Non HDL ..70
    I do not know if that is good or bad. Is there such a chart showing like,  1 good ... 100 bad ??
    LP(a) shows up by itself and I understand that because there is a range showing bad ..over 30.
    Any help understanding appreciated

  • David

    12/10/2009 2:39:45 AM |

    Dr. Davis,

    I honestly think you are doing God's work and have learned to appreciate the value of heart scans through your site.  However, it still bugs me that so many people in Asia can live off of large quantities of white rice with minimal atherosclerosis.  For instance, this study shows that American Whites have much higher atherosclerosis than Japanese despite the Japanese having much higher LDL-cholesterol, blood pressure, fasting glucose, and smoking rates:

    http://ije.oxfordjournals.org/cgi/content/full/34/1/173


    This other study (below) tries to explain this difference based on the Japanese consumption of fish. However, if you look at the data, those Americans who consume the most fish oil consume about as much fish oil as those Japanese that consume the least fish oil, and yet between these comparable groups in terms of fish consumption, the Japanese still have vastly lower atherosclerosis on heart scans.  And the Japanese American group consumes more fish than the White American group and has more coronary calcium.

    http://content.onlinejacc.org/cgi/content/full/52/6/417


    And here is another study showing much lower CAC in Japanese than in Japanese-Hawaiians even after controlling for a bunch of risk factors including fish intake:

    http://aje.oxfordjournals.org/cgi/content/full/166/11/1280


    Although in this other study looking at only at Americans, the incidence of CAC appears to be similar to that in Japanese - so maybe there was something unusual about the US samples in the other studies?

    http://content.onlinejacc.org/cgi/content/full/49/20/2013

  • Anonymous

    12/10/2009 8:23:46 PM |

    Dr. Davis,
    What is your opinion of the LP-Pla2 test for arterial plaque?  If you've used the test, do any elements of your program reduce levels of this enzyme?

  • buy jeans

    11/3/2010 9:44:57 PM |

    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.

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