Unexpected effects of a wheat-free diet

Wheat elimination continues to yield explosive and unexpected health benefits.

I initially asked patients in the office to eliminate wheat because I wanted to help them reduce blood sugar and pre-diabetic tendencies.

A patient would come to the office, for example, with a blood sugar of 118 mg/dl (in the pre-diabetic range) and the other phenomena of pre-diabetes or metabolic syndrome (high blood pressure, high inflammation/c-reactive protein, low HDL, high triglycerides, small LDL), and the characteristic wheat belly. Eliminate wheat and, within three months, they lose 30 lbs, blood sugar drops to normal, blood pressure drops, triglycerides drop by several hundred milligrams, HDL goes up, small LDL plummets, c-reactive protein drops.

People also felt better, with flat tummies and more energy. But they also developed benefits I did not anticipate:

--Improved rheumatoid arthritis--I have seen this time and time again. Eliminate wheat and the painful thumbs, fingers, and other joints clear up dramatically. Many former rheumatoid sufferers people tell me that one cracker or pretzel will trigger a painful throbbing reminder that lasts a couple of hours.

--Improved ulcerative colitis--People incapacitated with pain, cramping, and diarrhea of ulcerative colitis (who are negative for the antibodies for celiac disease) can experience marked improvement. I've seen people be able to stop all their nasty colitis medications just by eliminating wheat.

--Reduction or elimination of irritable bowel syndrome

--Reduction or elimination of gastroesophageal reflux

--Better mood--Eliminating wheat makes you happier and experience more stable moods. Just as wheat is responsible for a subset of schizophrenia and bipolar illness (this is fact), and wheat elimination generates dramatic improvement, when you or I eliminate wheat, we also experience a "smoothing" of mood swings.

--Better libido--I'm not sure whether this is a consequence of losing a belly the size of a watermelon or improvement in sex hormones (esp. testosterone) or endothelial responses, but more interest in sex typically develops.

--Better complexion--I'm not entirely sure why, but various rashes will often dissipate, bags under the eyes are reduced, itching in funny places stops.


It's also peculiar how, after someone eliminates wheat for several months, re-exposure of an errant cracker or sandwich results in cramping and diarrhea in about 30% of people.

Obviously, people with celiac disease, who can even die of exposure to wheat, are even worse. What other common food do you know of that makes us sick so often, even occasionally with fatal outcome?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Do "Heart Healthy" sterols cause heart disease?

The sterol question continues to pop up.

Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia?

Below, I've reprinted a previous Heart Scan Blog post on sterols.


Sterols should be outlawed

While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

Higher blood levels of sterols increase cardiovascular events:
Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Why obese people can't fast

Why do obese people claim it is impossible to fast?

Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse.

Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.")

According to an LA Times article, fasting may be difficult to impossible for some people:

"Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'"
(Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)

Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt.

Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)

Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone.

Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.

Test your own thyroid

134 people responded to the latest Heart Scan Blog poll:


When I ask my doctor to test my thyroid, he/she:

Accommodates me without question 45 (33%)

Questions why, but orders the tests 49 (36%)

Refuses because you seem "healthy" 20 (14%)

Refuses without explanation 4 (2%)

Ridicules your request 16 (11%)



That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.

However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.

Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.

Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.

So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."

You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?

You could:

--Drink more coffee
--Exercise more in the hopes that it will snap you out of your lethargy
--Sleep more
--Take stimulants of various sorts

Or, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?

You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here.

This is yet another facet of the powerful revolution that is emerging: Self-directed health.

Trains, planes, and heart scans

A Heart Scan Blog reader posted the following question:

It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?

Good question. Think of it this way:

Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc.

A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.

It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300.

Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:

1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat.

2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk.


With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know.

D2 and D3 are two different things

Helena posted this instructive comment in response to the Heart Scan Blog post, Weight loss and vitamin D. It illustrates the confusion common among physicians and pharmacists on the differences between D2 and D3.

(Edited slightly for clarity.)

Not many weeks ago a colleague of mine (let’s call him Eric) asked me if I knew the difference between D2 and D3 and I told Eric that D2 comes from irradiated mushrooms and D3 comes from wool. In other words, D3 is the same kind of vitamin as humans get from the sun. Humans just don’t get enough and we can’t produce it on our own, like the sheep can. (D3 is natural for humans, D2 is not.)

After telling Eric this, he asked me how he would know what he is taking and I gave him the medical definitions of them both (D2 = Ergocalciferol; D3 = Cholecaliciferol). Since I was aware that he had gotten his Vitamin D by prescription, I told him “I am 99.9% sure that you are taking D2, but I would be thrilled to find out I am wrong.”

Eric called his pharmacy right away and got the answer I was expecting: ergocalciferol. On confronting the person Eric was talking to, the answer he got back was that Ergocalciferol is the only Vitamin D they are giving out.

A week later, Eric had a new appointment with his doctor and decided to ask him about the D2/D3 issue. The doctor said he knew that there was a difference in them both, but could not say what, not even the basic facts I mentioned above. But the doctor stamped a post-it with what he had sent to the pharmacy just to show Eric. “Vitamin D3; 50,000IU tab” is what the stamp said.

Eric, off course, got confused and was starting to believe that the pharmacy had made a mistake by giving him Ergocalciferol (D2) since the doctor had given him D3, or at least that is what was stamped on the little note he had.

Today, after getting a refill of his Vitamin D he also got and kept all his paperwork that came along with it. Still believing that stamp the doctor had given Eric earlier, he asked me to double and triple check that my definition of D2 and D3 was correct. I did, just for my own sanity, and I was still right.

One of the sheets Eric brought me today was the “Patient Education Monograph” sheet stating the drugs and how to use it and so on. The thing that jumped out the most to me was this:

Generic Name: Vitamin D – Oral
Common Brand name(s): Drisdol, Maximum D3
Identification: PA140 Green Oval Capsule

This is the Drug Eric was given: Vitamin D 1.25 MG softgel; Generic name: Ergocalciferol

My researching mind went into high concentration mood and I started to dig. And this is what I found:

The brand name Drisdol is Ergocalciferol (D2), not D3. The Brand name Maximum D3 seems to be hard to find out there in cyber space as a brand name. But the ones I found that were called Maximum D3 seems to be the real stuff, however none of them required a prescription.

When trying to find out through the identification number on the pills (PA140) I now know for sure that Eric is taking Vitamin D2 and not the preferred Vitamin D3. The brand name, Drisdol, had the identification W on one side and D92 on the other, but it is still Ergocalciferol.

The only conclusion I can draw from all this is that the medical industry does not know or care about the difference in D2 and D3 – it is all same to them. And as long as the pharmacies only give out D2 it does not matter what the doctor prescribe anyway.

I know that people are most likely to be prescribed a D2 pill than to be told to buy over-the-counter D3. But it was almost heart breaking to see the letter D and number 3 right next to the drug Drisdol, as we know is a D2 vitamin. It just didn’t make sense to me that they can be labeled as the same type of medication, when we know it is not!



Incredible.

Why prescribe plant form D2 when you can get perfectly reliable, safe, effective D3--the human form, at the health food store for about $6?

Once again, it's the peculiar false bias of physicians and pharmacists: If it's prescription, it must be good; if it comes from a health food store, it must be bogus.

Humans need human vitamin D. Plain and simple.

For more on the D2 vs. D3 issue, see the Heart Scan Post, The case against vitamin D2.

Weight loss: Different causes, different solutions

Heart Scan Blog reader, Kris, related this enlightening story of weight loss (slightly edited for clarity).

Kris learned that excess weight is gained through multiple causes. The solutions are therefore multiple, not just one change in diet or two.


I started studying about my thyroid issue much earlier and did lose some weight. But ever since I started following Dr. Davis’s blog, it has given me confidence that I was on the right track. I did have my thyroid and iodine figured out from other sources, but Dr. Davis helped me to understand the issues with not only the thyroid but vitamin D3, fructose, fish oil, niacin, wheat etc. I have lost 43lb in last 14 months.

It seems to me that there are certain percentages of weight connected with different issues. For example, after I gave up alcohol and sugar, I lost about 14lbs from total weight of 243lbs, weight came down to about 229lb. Then it stopped at 229lb, even though I was in the gym almost 5 to 6 days a week with full workouts.

After I changed my thyroid medication to natural thyroid hormones (took synthetic T4 for over 10 years), the weight dropped down further 13lbs or so in matter of few days, shape of the face changed from moon shape/double chin to ordinary long face. Then it kind of stopped at around 213-216 lbs.

After giving up wheat, reducing carbs, increasing protein intake (whey protein, chicken etc. no soya, no fructose) the weight came down another 14lbs. Now it is around 200-202lbs and I am over 6.2 tall with heavy set of bones.

I feel better than I have ever in my life. More stamina, more clarity/no fog, more confidence and 99% of the time relaxed and being able to see the situation from multiple angles.

I use to be able to drink a liter or more jack denial without a problem in one evening but now can’t stand half a can of beer (I miss JD). Drinking alcohol makes me sick. I sleep well and if I wake up in the middle of the night, I have no problem going back to sleep. No more out of breath stair climbing at all.

One other thing: I used to be the most attractive meal to the mosquitoes, but not anymore. This year I haven’t been bitten once. I take my dog to the park everyday and I do not use any mosquito repellent, what a relief. I don’t know if it is because of thyroid, iodine, wheat or something else. Skin texture has changed dramatically. I do not use full soap or shampoo, 20% borax, 10 percent of my soap or shampoo for scent and rest water, mixed in a 500ml bottle. No more dandruff, dry skin, pimples for me.

Dr. Davis I am thankful to people like you who have the ability to see beyond what you have been taught and have the guts to say the way it is. Most of us work to make living on daily basis but some make their living while spreading their knowledge to save lives. Dr Davis you are one of those few people. Please keep it going.

Calling all losers!

I'd like to invite anyone who has followed the Track Your Plaque Break the Weight Barrier program to consider posting their stories and photos on the Heart Scan Blog.

Because our focus is prevention and reversal of coronary heart disease, we have not made an effort to catalog the weight loss experience that people have while on the program. For many, weight loss has been substantial. (Several people this week alone have reported weight loss of 9 to 46 lbs in the past 6 months.)

It would be helpful to hear and see these results.

For those of you who don't mind having a story and photo on this Blog, please come back in future to post your results. You will find this post by entering "weight loss" into the site-specific search bar at the top of the page.

Weight loss and vitamin D

At the start of her program, Penny's 25-hydroxy vitamin D blood level showed the usual deficiency at 22 ng/ml.

She supplemented with 8000 units of vitamin D. Another 25-hydroxy vitamin D blood level several months later showed a level of 67.8 ng/ml, right on target.

But Penny also began our diet, including the elimination of wheat, cornstarch, and sugars, and, over 6 months, lost 34 lbs.

Now a much trimmer 146 lbs (still more to go!), another vitamin D blood level: 111 ng/ml.

Penny's weight loss means that the vitamin D is distributed in a smaller total volume, particularly a lower volume of fat.

This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.

Some references on this effect:

Men and women over age 65:
Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women.

Obese women:
Low 25-hydroxyvitamin D concentrations in obese women: their clinical significance and relationship with anthropometric and body composition variables

Obese children:
Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season.

African-Americans:
Relationship of vitamin D and parathyroid hormone to obesity and body composition in African Americans.

Although the bulk of the effect is most likely due to sequestration by fatty tissue, perhaps less sun exposure in obese people also contributes:
Body mass index determines sunbathing habits: implications on vitamin D levels.
One hour blood sugar: Key to carbohydrate control and reversing diabetes

One hour blood sugar: Key to carbohydrate control and reversing diabetes

Diabetics are instructed to monitor blood glucose first thing in the morning and two hours after eating. This helps determine whether blood sugar is controlled with medications like metformin, Januvia, Byetta injections, or insulin.

But that's not how you use blood sugar to use to prevent or reverse diabetes. Two-hour blood sugars are also of no help in deciding whether you have halted glycation, or glucose modification of proteins the process that leads to cataracts, brittle cartilage and arthritis, oxidation of small LDL particles, atherosclerosis, kidney disease, etc.

So the key is to check one-hour after-eating (postprandial) blood sugars, a time when blood glucose peaks after consumption of carbohydrates. (It may peak somewhat sooner or later, depending on factors such as how much fluid was in the meal; protein, fat, and fiber content; presence of foods like vinegar that slow gastric emptying; the form of carbohydrate such as amylopectin A vs. amylopectin B, amylose, fructose, along with other factors. Once in a while, you might consider constructing your own postprandial glucose curve by doing fingersticks every 15 minutes to determine when your peak occurs.)

I reject the insane notion that after-eating blood sugars of less than 200 mg/dl are acceptable, the value accepted widely as the cutoff for health. Blood sugars this high occurring with any regularity ensure cataracts, arthritis, and all the other consequences of cumulative glycation. I therefore aim to keep one-hour after-eating glucoses 100 mg/dl or less. If you start in a pre-diabetic or diabetic range of, say, 120 mg/dl, then I advise people to not allow blood glucose to go any higher. A pre-meal blood glucose of 120 mg/dl would therefore be followed by an after-eating blood glucose of no higher than 120 mg/dl.

No doubt: This is strict. But people who do this:

--Lose weight from visceral fat
--Heighten insulin sensitivity
--Drop blood pressure
--Drop HbA1c and fasting glucose over time
--Reduce small LDL and other carbohydrate-sensitive measures

By the way, if you inadvertently trigger a high blood sugar like I did when I took my kids to the all-you-can-eat Indian buffet, go for a walk, bike, or burn the sugar off with a 30-minute or longer physical effort. Check your blood sugar again and it should be back in desirable range. But then learn from your lesson: Eliminate or reduce portion size of the culprit carbohydrate food.

Comments (27) -

  • Might-o'chonri-AL

    8/2/2011 6:11:40 AM |

    Glyco-sylation occurs inside a cell's endoplasmic reticulum lumen when certain  carbohydrates  (in the form of N-linked oligo-saccharides) meld with a newly folded protein that gets translated into  a glyco-protein.  There are different rates of activation and de-activation  between glyco-sylated and un-glycosylated proteins; this affects how that protein migrates as it tries to perform it's job and how  glycation can induce degenerative states.  Tissue cells with endoplasmic reticulum stress can exasperate certain disease progression because such "stress" there promotes more glycosylation.

  • Annabel

    8/2/2011 12:40:42 PM |

    I couldn't agree more with the advice to test every 15 minutes as a means of discovering your own "sugar curve." When I tried this, I found that my own peak falls pretty consistently at 75 minutes after beginning a meal. Testing at 2 hours completely overlooks my highest blood glucose levels.

    It's a particularly good technique for those folks whose A1c levels are higher than their fingersticks would predict...it's almost surely because they're doing their sticks way past their glucose peak.

    When test strips cost up to a buck apiece, it may feel hard to justify using six or eight of them on a single meal--but what you learn may save tens of thousands in medical bills!

  • Curt

    8/2/2011 1:31:12 PM |

    Another great article - thank you! I'm curious about your thoughts on controlled 1 hour blood sugars (mine are rarely over 110) but baseline levels that aren't much lower. Typically in the 95-105 range. I will get something in the 80s occasionally, but 100 is more common. I never really spike - even a high carb meal will only get me to 130s or so and that never really happens as I don't eat much sugar/starch at all.

    Another quick question: You've mentioned a couple times recently about this way of eating being particularly good for VISCERAL fat. That is exactly what I've found. Tremendous benefits and I feel great. I have leveled out for a while (months) in fat loss, however, with a good amount of subcutaneous fat still present. Is there another protocol for getting after this type of fat? I'm already no wheat, low carb, paleo.

    Thanks again for your excellent articles! Always learning something new.......

  • ShottleBop

    8/2/2011 1:38:20 PM |

    Do you have citations to support your statement that glycation occurs at BGs of 100 or more?  This is one of the more-commonly discussed issues on diabetes discussion boards--but folks are wont to ask for backup.

  • Jeff C

    8/2/2011 1:47:11 PM |

    Regarding glycation specifically...

    1. Do you agree that fructose ("frucation") causes more AGE than glucose?
    2. What to you make of Ray Peat's assertion that poly-fats are much more glycalating than glucose?

    "The so-called "advanced glycation end products," that have been blamed on glucose excess, are mostly derived from the peroxidation of the "essential fatty acids." The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do." (Fu, et al., 1996)." - Ray Peat

  • Richard

    8/2/2011 3:21:55 PM |

    Thanks for the great article!
    I've just begun tracking blood sugars closely, changed my diet to one very low in carbs and no grains, and am determined to find ways to keep at it. I've started a blog just track my progress and keep me honest: http://transformation-transformative.blogspot.com/
    I'll also try the 15 minute testing to see where my personal peak in blood sugar occurs.
    Again, many thanks!

  • steve

    8/2/2011 3:31:08 PM |

    Hi Dr. Davis:  What is the relationship between fasting BG taken at the Dr's office and A!C?  My fasting BG level is 73.5 but my A1C is 5.4.  I would have expected the A1C to more correspond to the fasting measurement; in the case of my wife it does.  Is it related more to the red blood cells lingering around longer or lipoprotein particles which increases the chance of glycation?  Recently had a larger than normal amount of carbs in a meal- rice and blueberries and BG spiked to 119, not to bad, but will experiment with carb portion to keep under 100 as BG may be a contributing factor to my CAD.  I am also a hyperabsorber of fat despite being an ApoE 3/3.

    As an aside, i have sent around a link of one of your interviews regarding Wheat Belly and many eyes have been opened as well as many looking to buy the book.  Might not be a bad idea to have a link to any of your interviews on Wheat Belly posted to this site.
    Thanks for the enlightening good work!

  • Dr. William Davis

    8/3/2011 12:23:09 AM |

    Hi, Shottle--
    This will be the topic of an upcoming discussion. The documentation of this effect is quite extensive. It is no longer a matter of "if" but "how much."

  • Dr. William Davis

    8/3/2011 12:25:11 AM |

    Hi, Jeff--
    This is one of oranges and apples comparisons.
    Fructose does indeed induce flagrant glycation. Glucose induces glycation, though less vigorously.

    However, there is a separate but very poorly named process called exogenous glycation which has less to do with glycation than with oxidation of fats.

    This will be the topic of future discussions.

  • Dr. William Davis

    8/3/2011 12:26:22 AM |

    My first thought is that, if weight loss is ongoing, there is a temporary situation of insulin resistance that generally dissipates with weight stabilization.

    It's also possible that your pancreas has inadequate baseline production of insulin. I'm hoping it's the first possibility.

  • Dr. William Davis

    8/3/2011 12:28:05 AM |

    Hi, Steve-

    You will find that, if you did frequent fingersticks around the clock, the highish A1c reflects the higher blood glucose values that occur after meals.

    Thanks for the feedback on the Wheat Belly project. I will indeed crosslink some of the more relevant discussions.

  • Might-o'chondri-AL

    8/3/2011 2:39:31 AM |

    Advanced glycation end products (AGE) involve some of haemoglobin's hydro-carbon Beta side chain valine residue linking up to non-polar "glucose" aldehyde compounds and certain non-"glucose" aldehydes. Various pathological kinds of AGEs can occur from distinct events; in one situation it is macrophage activity producing enzymatic myelo-peroxidase, which can activate hypochlorite favoring a serine amino acid wing to form up to make the AGE called glyco-aldehyde.

    Probably the AGE called methyl-glyoxal is the one most relevant to diabetes prevention; since Type 1 diabetics blood serum levels of methyl-glyoxal is +/- 6 times higher than normal. This AGE can be formed when the byproduct triose-phosphate (triose = subset of carbs) is generated from the glycolytic pathway called  Embden-Meyerhof; this  byproduct risks being made into methyl-glyoxal.

    Maybe the most well known AGEs are the non-enzymatic Amadori products formed via hydrolysis; one is called glyoxal coming from glucose oxidation. And the other Amadori type AGE is 3-deoxy-glucosone (3DG), which requires fructo-selysine and the fructos-amine 3 kinase cascade to shuffle together 3DG.

  • Might-o'chondri-AL

    8/3/2011 2:40:38 AM |

    Diabetes reveals the problem with AGEs; this is because diabetics risk incurring kidney nephro-pathy, One of the pathological results is oxidative kidney stress, which limits sodium (Na) excretion thereby fostering  hyper-tension . When AGEs like 3DG, glyoxal & methyl-glyoxal  (among others, like pentosidine ) circulate into the kidneys their carbonyl compounds  are hard to clear by the kidneys; the side effect is to engender  uric uremia problems and meanwhile levels of carbonyls build up in what is called "carbonyl stress".
    Japan research of the plant compound chamaemeloside found that in humans it lowered levels of the AGEs 3DG & pentosidne better than any other natural remedy; optimal response was reduction of down to 1/5 th of subject's starting levels.  Chamaemeloside is the active compound in chamomile (Anthemis noblis); the extraction formula was 1 Kg of chamomile flowers steeped covered in 20 Lt. water for 3 hours at 80* celcius ( a lab temperature probably not critical for home remedy preparation).

  • Peter Silverman

    8/3/2011 12:56:13 PM |

    Volek and Phinney in their new book about carbohydrate restriction think that as you increase  fat from 30% to 60% of your diet, insulin resistance increases, then it drops when you go above 60%.  It seems that among the most experienced researchers of carbohydrate restriction, there's little consensus about the optimal amount of fat or carbs.  Ron Krausse, for instance, thinks 35% to 45% is optimal.

  • steve

    8/3/2011 5:23:50 PM |

    Peter:
    When these researchers talk about carb levels are they considering vegetables to be carbs, or just fruits, grains, potatoes?

  • frank weir

    8/3/2011 6:41:32 PM |

    You must mean, "can exacerbate certain disease progression...." meaning: to increase the severity, violence, or bitterness of; aggravate

  • frank weir

    8/3/2011 6:59:22 PM |

    This is wonderful information BUT I wonder if it might be unfortunate if folks who routinely have post-prandials of 120 to 140 take your 100 level as a sign of "failure"...things are seldom so cut and dried, black and white. I don't know if I'm hitting 100 or less  after every meal, but my A1C has dropped from 7.5 to 5.8 since last November restricting carbs. And I've lost 30 pounds. I will begin to be more dogmatic about one-hour glucose checks but my rough sense is that I'm not at 100 or less a majority of the time. But I might be wrong about that. Do you see what I'm getting at? Glucose control is an ongoing process that includes lots of self education since most GP's are not keen AT ALL on restricting carbs, including mine. When I read your post, my initial feeling was, "Cripes, 100 after EVERY meal? Don't think I can do that...."

  • Might-o'chondri-AL

    8/4/2011 1:05:26 AM |

    From another commentator here, in an  earlier thread of Dr. Davis' here is how to use HbA1c to determine your average blood glucose level (note: this is not a morning "fasting" level) .
    1st: multiply your HbA1c by 28.7
    2nd: subtract 46.7 from 1st amount
    3rd: take last number as your average waking hours mg/dL blood glucose over last  few months  
    ex:  HbA1c of 5.4 x 28.7 = 159.98 minus 46.7 = 108.28 mg/dL of average blood glucose level

  • Peter Silverman

    8/4/2011 2:24:31 AM |

    They don't count non-starchy vegetable as carbs.

  • ShottleBop

    8/4/2011 3:15:11 AM |

    Thanks for the heads up!

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  • Stephanie

    8/4/2011 2:13:27 PM |

    Dr. Davis,
    I have found that if I take my carb level too low (below 50g per day) that my fasting blood glucose levels actually go up rather than down.  If my carb intake is closer to 70-80, my fasting glucose is lower.

    Have you had this experience with some of your patients?  Can you shed any light onto what might be happening?

    Thanks!
    Stephanie

  • Anne

    8/4/2011 2:34:11 PM |

    Non-starchy vegetables do have carbs and I do have to count them. A half cup of broccoli can have about 6 carbs and since I limit my carbs to no more than 15g/meal, that broccoli on my plate is significant.

    I found getting a scale that reads carbs too was an important tool for me. I found I was ofter overestimating how much of a low carb veggie I could eat. If my blood sugar starts to rise, I go back to measuring and that seems to get me back on track.

    Anne

  • majkinetor

    8/14/2011 1:25:56 PM |

    I think thats normal, its commonly encountered on paleo forums/blogs. It has something to do with physiological insulin resistance, Petro @ Hyperlipid talked about. Look here:

    http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html

  • majkinetor

    8/14/2011 1:38:24 PM |

    I wouldn't suggest that everybody blindly follow CHO < 50g / day. As always, its about the context. People usually forget that. We mostly extrapolate from results of people who already have metabolic problems.

    Anyway, I am currently perfectly healthy apart from some minor dermatology problems (eczema).
    When I have prolonged periods of reduced CHO input (around 50g / day), I eventually start having some mucus problems. Dry eyes particularly, but also joint pain. I am not 100% sure if its about low carb diet, but it looks like it. Now I target 75g < CHO < 100g per day by adding small potato and a bit more chocolate to my diet.

    I think overemphasizing carb reduction is not good thing for most people. Carbs should go down by pretty big amount for most people, but not to extreme. In anyway, its better to measure then to guess. My sugar is never above 110 after meal and fasting is always around 95.

  • John F

    8/13/2012 9:48:10 AM |

    I decided to take this advice and have been tracking my 60 mins postprandial blood glucose for the past two days to see if all the years I've been low carbing have been making any difference. Especially working my way through different foods to see how they affect me and I've ranged from 64 mg/dl to 97 mg/dl so I'm pretty hapy.

    However this evening 60 minutes after my dinner of panfried steak with a creamy cajun sauce I got a reading of just 55 mg/dl. A lot of websites say this is too low. I'm 32, healthy male, 5,9", weigh 160 lbs, not diabetic and I don't feel sick so I'm not sure what to make of this low reading. The only thing I did was finish a hard CrossFit workout about 30 mins before I had dinner... so a total of 90 minutes before the blood glucose test.

    Any advice on what this "low" reading means? I'm hoping it's normal and means I'm burning fat!

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