author">William Davis(38)
Take a look at these glycemic indexes (GI):
White bread 69 Whole wheat bread 72 Sucrose 59 Mars bar 68 White rice 72 Brown rice 66
I've made issue in past of whole wheat's high GI--higher than white bread. Roughly in the same glycemic league as bread are shredded wheat cereal, brown rice, and a Mars candy bar.
With few exceptions, wheat products have among the highest GIs compared to the majority of other foods. For instance:
Kidney beans 29 Chick peas 36 Apple 39 Ice cream 36 Snickers Bar 40
Yes, by the crazy logic of glycemic index, Snickers is a low-glycemic index food.
While I do not believe that low GI makes a food good or desirable, since low GI foods still provoke high blood sugars, small LDL particles, trigger glycation, and other abnormal phenomena, they are clearly less obnoxious than the items in the first list.
Starches that are dried and/or pulverized, such as cornstarch, potato starch, rice starch, and tapioca starch (cassava root) will increase blood sugar even more than wheat. Foods with these starches have GI's of 80-100.
Cornstarch, potato starch, rice starch, and tapioca starch: Sound familiar? These are the main starches used in "gluten-free" foods. A hint of the high GI behavior of these dried starches is seen in the GI for cornflakes of 80.
So remember: Wheat-free is not the same as gluten-free. Gluten-free identifies junk carbohydrates masquerading as healthy because they don't contain one unhealthy ingredient, i.e. wheat.
Dr. Colin Campbell caused a stir with publication of his 2005 book, The China Study. Dr. Campbell, after extensive animal and epidemiologic research conducted in China over 20 years, concluded that a diet high in animal protein, especially casein, was associated with increased cancer, osteoporosis, and heart disease risk.
Denise's analysis is nothing short of brilliant, absolutely "must" reading for anyone interested in nutrition.
Her comments on the relationship of wheat to heart disease:
Why does Campbell indict animal foods in cardiovascular disease (correlation of +1 for animal protein and -11 for fish protein), yet fail to mention that wheat flour has a correlation of +67 with heart attacks and coronary heart disease, and plant protein correlates at +25 with these conditions?
Speaking of wheat, why doesn’t Campbell also note the astronomical correlations wheat flour has with various diseases: +46 with cervix cancer, +54 with hypertensive heart disease, +47 with stroke, +41 with diseases of the blood and blood-forming organs, and the aforementioned +67 with myocardial infarction and coronary heart disease?
Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins (chylomicrons, chylomicron remnants, VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles.
The list of reasons why small LDL particles are more atherogenic, i.e., plaque-causing, is long:
--Small LDL particles, being smaller, more readily penetrate the endothelial barrier of the arterial wall. --Small LDL particles are more adherent to glycosaminoglycans in the artery wall. --Small LDL particles are poorly taken up by the liver LDL receptor, but enthusiastically taken up by macrophage receptors of the sort in your artery walls. --Because of their poor liver clearance, small LDL persists in the bloodstream far longer than large LDL. --Small LDL particles are more oxidation-prone. Oxidized LDL are more likely to trigger inflammatory phenomena and be taken up by macrophages in the artery wall.
Let me add another reason why small LDL particles are more likely to cause plaque: They are more likely to undergo glycation. (More on glycation here.)
Glycation occurs when glucose (sugar) molecules in the blood or tissue modify proteins, usually irreversibly. Small LDL particles are uniquely glycation-prone. (This is likely due to a conformational change of the apoprotein B in the small LDL particle, exposing lysine residues along apo B that become glycated.)
Here's a great demonstration of this phenomenon by Younis et al:
"LDL3" is the small type. Note that small LDL particles are 4-5 times more glycated than large LDL. That's a big difference.
Once glycated, small LDL is especially resistant to being taken up by the liver. Like annoying in-laws, they hang around and hang around and . . . The longer they hang around, they more opportunity they have to contribute to plaque formation.
So, carbohydrates trigger formation of small LDL particles. Once formed, small LDL particles are glycated when blood sugar increases. While LDL can be glycated even when blood sugars are in the normal range (90 mg/dl or less), glycation goes berserk when blood sugars go higher, such as a blood sugar of 155 mg/dl after a bowl of steel-cut oatmeal.
We know that foods that trigger insulin lead to fat storage. Putting a stop to this process allows you to mobilize fat and lose weight. If you're starting out from scratch, rapid and dramatic weight loss can be experienced, as much as one pound per day.
So how can you stop triggering insulin?
The easiest way is to eliminate, or at least minimize, carbohydrates. My favorite method to restrict carbohydrates is to eliminate wheat and minimize exposure to other carbohydrates, such as oats, cornstarch, and sugars. All these foods, wheat products worst of all, cause blood sugar and insulin to skyrocket.
Another way is to check your blood sugar one hour after completing a meal and keep your after-eating, or "postprandial," blood sugar 100 mg/dl or less. Let's say you are going to eat stone ground oatmeal, for example. Blood sugar prior to eating is, say, 90 mg/dl. One hour after oatmeal it's 168 mg/dl--you know that this is going to trigger insulin and make you fat. Oatmeal should therefore be eliminated.
Keeping blood sugar to 100 mg/dl or less after eating teaches you how to avoid provocation of insulin. A shrinking tummy will follow.
To do this, you will need:
1) A glucose meter--My favorite is the One Touch Ultra Mini ($13.42 at Walmart). It's exceptionally easy to use and requires just a dot of blood. Drawback: Test strips are about $1 each. Accuchek Aviva is another good device. (We've had a lot of problems with Walgreen's brand device.) 2) Test strips--This is the costly part of the proposition. Purchased 25 or 50 at a time, they can cost from $0.50 to $1.00 a piece. 3) Lancets--These are the pins for the fingerstick device that comes with the glucose meter. A box should be just a few dollars.
No prescription is necessary, nor will insurance pay for your costs unless you're diabetic. To conserve test strips, use them only when a new, untested food or food combination is going to be consumed. If you had two scrambled eggs with green peppers, sundried tomatoes, and olive oil yesterday and had a one hour postprandial glucose of 97 mg/dl, no need to check blood sugar again if you are having the same meal again today.
1) A free T4 thyroid hormone at the low end of normal, or even in the below normal range, along with a highish TSH (usually >1.5 mIU/L) are the most frequent patterns that signal iodine deficiency. Occasionally, a low free T3 value will also increase, though this is the least frequent development.
2) At a dose of 500 to 1000 mcg iodine per day, it requires anywhere from 3 to 6 months to obtain normalization of thyroid measures.
3) Reversal of small goiters also occurs over about 6 months.
4) Iodine intolerance is uncommon. If it occurs, using a low starting dose, e.g., 100-200 mcg per day, usually works. The dose can be increased gradually over the ensuing months.
5) Perceptible benefits of iodine occur only occasionally. The most common perceptible effects are increased energy and increased warmth, especially of the hands and feet.
6) Some people who have taken thyroid hormones for years will develop reduced need for their medication with iodine supplementation. In other words, their physician was inadvertently treating iodine deficiency with thyroid hormone replacement. Anyone already on any thyroid preparation(s), e.g., Synthroid, levothyroxine, Armour thyroid, Naturethroid, etc., should watch for signs of hyperthyroidism when iodine is added. But having your own thyroid gland make its own thyroid hormones is better and healthier than relying on the prescription agents. Just be sure to monitor your thyroid measures.
7) Iodine toxicity can occur--Two people in my clinic population developed iodine toxicity by taking 6000 mcg iodine per day for 6 or more months. (Both patients did it on their own based on something they read). Iodine toxicity is evidenced by shutting down your thyroid, i.e., marked increase in TSH, e.g., 15 mIU/L.
Most of the people in my clinic obtain their iodine from kelp tablets. Some use potassium iodine (KI) drops. A handful have used the high-potency Iodoral (12.5 mg or 12,500 mcg iodine per tablet); this was also the form that generated the toxic effects in the two females.
All in all, iodine deficiency is actually far more common than I ever suspected. Not everybody is iodine deficient. But a substantial minority of the Midwest population I see certainly are.
