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Postprandial Responses: Part 3 - Carbohydrates and postprandial blood sugar
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While fats determine postprandial triglycerides,
carbohydrates determine postprandial blood sugar.

Higher postprandial blood sugars, more than fasting blood sugars,
are associated with up to several-fold increased risk for cardiovascular events.

Managing carbohydrate intake is therefore
a crucial aspect of your Track Your Plaque program.

I'm not diabetic.  Why do I need to check my blood sugar?

Checking blood sugar (glucose) is proving to be a powerful means to construct a diet that is individualized to your own unique responses. It is now easy and inexpensive to assess blood sugars. Knowing the blood sugar consequences of your meals can provide unexpected insights into your response to diet.

If you’re not a diabetic, why bother checking blood sugar? Increased levels of blood sugar below the diabetic range are associated with increased risk for plaque growth and cardiovascular disease. Even more than fasting blood sugars, after-eating blood sugars are proving to be an important predictor of heart attack and plaque growth: the higher the after-eating blood sugar, the greater the risk for heart disease.

We apply blood glucoses to help construct a better diet, one that does not contribute to plaque growth. We therefore view blood glucose from a different perspective than the way blood sugars are used by people with diabetes. While diabetics will often check fasting and before meal blood sugars to dose insulin or assess medication response, we will be using after-meal (postprandial) blood sugars to assess tolerance to various foods.

Beyond plaque control, gaining control over postprandial blood sugar levels also helps construct a diet that:

  • accelerates weight loss
  • reduces inflammation
  • reduces small LDL
  • reduces triglycerides
  • reduces blood pressure

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20, occasionally even free (with rebates or similar offers). (We have had good experiences with the UltraTouch Mini, Bayer Contour, Walmart Relion, and the Accu-Chek devices.) You will also need to purchase the fingerstick lancets, calibrating solution, and test strips; the test strips are the most costly part of the project, usually running $0.50 to $1.00 per test strip. But since people without diabetes will need to check their blood sugar only occasionally, the cost of the test strips is, over time, modest. Health insurance will cover your costs only if you are diabetic. Instructions for use of the glucose monitor are included with the device. It should require only a few minutes to become familiar with your particular device.

Some practical tips to obtain reliable blood glucose values:

  • Hydrate well to ensure obtaining an adequate blood sample.
  • Use a depth setting on your fingerstick device that easily provides the necessary sample size.
  • Use the sides of the fingertips, not the pads. Wash and dry your hands beforehand.
  • Twirl your arms at your sides or hang them down in front of you while you bend over to encourage pooling of blood in the fingertips.
  • Avoid “milking” the finger except for slight milking at the base of the finger (where it attaches to the hand). “Milking” is a frequent cause for falsely increased blood sugars.
  • Be sure to have fresh batteries if your device is older. Also note that test strips have an expiration date (listed on the test strip package).

How blood glucose injures arteries

High blood sugar contributes to atherosclerotic plaque growth via several fundamental mechanisms.

Surges in blood glucose trigger endothelial dysfunction, the abnormal constrictive effect that characterizes early atherosclerosis (De Caterina 2000). This effect is concentration-dependent, i.e., the higher the blood glucose, the greater the endothelial dysfunction. This occurs via increased levels of oxidizing agents, superoxide anion and peroxynitrite, that reduce arterial nitric oxide and increase oxidative stress (Cosentino 1997).

Higher blood glucose causes glycation of LDL particles (i.e., glucose molecules become attached to proteins in LDL) and formation of advanced glycation end-products in the arterial wall (Lyons 1992).

Increased blood glucose activates blood coagulation: platelet activation; activation of clotting factor VII; and activation of the clotting protein, fibrinogen (Ceriello 1995). Increased blood glucose activates adhesion factors, such as intercellular adhesion molecule-I (ICAM-I) and vascular adhesion molecule (VCAM) that permit inflammatory blood cells to enter artery walls, as well as inflammatory molecules, such as cytokines and c-reactive protein (Ceriello 2004).

Fasting glucose vs. postprandial glucose

In World Health Organization definitions, impaired fasting glucose (IFG) refers to blood glucose ≥110-126 mg/dl after an 8-hour fast. Impaired glucose tolerance (IGT) refers to blood glucose ≥140 but less than 200 mg/dl after a test 75-g glucose load (a “glucose tolerance test”). These definitions were based on blood glucose levels associated with eye and kidney disease, not cardiovascular disease (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus 2002). Thus, these cutoffs may have limited relevance to cardiovascular issues.

While the groups of people with higher fasting glucose (“impaired fasting glucose,” IFG) and those with increased postprandial glucose (“impaired glucose tolerance,” IGT) overlap, the two measures also identify different groups of people: only 45% of subjects with IFG have IGT; conversely, <25% of subjects with IGT have IFG (Gabir 2000) when IFG is defined as 126 mg/dl or greater, IGT defined as 140-200 mg/dl.

While fasting glucose is primarily a reflection of liver resistance to insulin and impaired pancreatic insulin production, glucose levels following a meal or glucose challenge better reflect the level of insulin resistance in muscle and reduced beta cell function (pancreatic cells that produce insulin), features also found in diabetes. 5-10% of people with impaired glucose tolerance will convert to diabetes each year (Abdul-Ghani 2006). Thus, impaired glucose tolerance is “closer” to diabetes than impaired fasting glucose.

In actuality, the risks from high blood sugar after a meal are likely continuous, i.e., there is no distinct cutoff below which there is no risk and above which there is risk; risk develops gradually the higher the after-eating blood glucose.

Also, note that the “capillary whole blood glucose” value obtained by fingerstick can differ from the venous plasma sample that is obtained by a conventional blood draw in the lab; variation is greater in postprandial samples and can also vary from device to device. As a practical solution, whenever you have a blood draw for glucose, take your glucose meter with you and run a side-by-side sample to gauge the variation.

High blood glucose leads to plaque growth

Studies looking at atherosclerosis from a number of different directions have shown that higher levels of both fasting and postprandial blood glucose are associated with atherosclerosis.

Two-hour glucose values of 104-109 mg/dl or greater after glucose challenge are associated with greater likelihood of arterial retinopathy, i.e., abnormal arteries in the retina, a marker for atherosclerotic potential (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus 2002). However, the Expert Committee set 140-200 mg/dl as the abnormal “impaired glucose tolerance” cutoffs after glucose challenge.

Two-hour glucose values of 110 mg/dl or greater are associated with greater carotid intimal-medial thickness (CIMT), a reflection of increased cardiovascular risk; 2-hour glucose values after glucose challenge also proved a superior predictor of CIMT compared to fasting glucose and HbA1c (Temelkova-Kurktschiev 2000).

Angiographic studies have demonstrated greater progression of coronary atherosclerotic plaque and more diffuse disease in people with impaired glucose tolerance (≥126 mg/dl) and diabetes (Kataoka 2005; Mellen 2006; Saely 2008).

High blood glucose leads to coronary events - which measure is best?

Numerous studies have demonstrated that high blood sugars are associated with increased risk for cardiovascular events.

Which measure of blood glucose is best? Of all methods to measure blood sugar—fasting, postprandial, HbA1c (hemoglobin A1c, or glycated hemoglobin, a measure of the preceding 60-90 days of blood sugars)—postprandial measures stand out as the most potent predictor of cardiovascular events like heart attack (Meigs 2002; Gerstein 1999)

Although HbA1c purportedly measures around-the-clock glucose exposure over an extended period and is associated with cardiovascular events, postprandial blood glucose is more strongly associated; the two values are correlated by approximately 50% (Temelkova-Kurktschiev 2000). Even when HbA1c is factored out, 2-hour post-challenge glucose remains a predictor of events (Meigs 2002). This likely develops because HbA1c represents an average of preceding blood glucose, while postprandial or post-challenge glucose represents the extremes of blood glucose excursions.

Sorkin et al (Sorkin 2005) collected all major experiences looking at fasting and postprandial (glucose challenge) glucose levels that measured total (all-cause, including cardiovascular) mortality.

For fasting glucose:

(The values shown represent “relative risk” (RR), or the increased risk compared to a control population.)

The analysis suggests that mortality begins to increase with fasting glucose as low as 93 mg/dl, clearly increased above 110 mg/dl; RR for mortality increases 0.43 to 2.80-fold at 126 mg/dl and higher. Another recent study (not included in the above analysis) comparing people after a first heart attack compared to normal controls showed that a fasting glucose of 88 mg/dl distinguished people with heart disease from controls (Gerstein 1999).

Note that mortality is increased in the range ordinarily considered as impaired fasting glucose or “pre-diabetes,’ i.e., 110-126 mg/dl.

For postprandial (postchallenge) glucose:

With 2-hour post-challenge (usually 75 g glucose) glucose, there is greater disparity among studies. Some studies show a trend towards increased risk with post-challenge glucose slightly below 100 mg/dl (Hoorn Study; de Vegt 1999), with unquestionably increased risk beginning at 120 mg/dl.

The 33-year, 18,000-participant Whitehall Study (published after the above analysis and therefore not included) showed that post-challenge (50 g) 2-hour blood glucose as low as 83 mg/dl increased mortality from cardiovascular disease, although 5-10 years were required for the difference to be observed (Brunner 2006):

From Brunner et al 2006. Survival by baseline glucose tolerance status. Age-adjusted survival and 95% CI. Glucose intolerance (GI), 5.3-11.1 mmol/l (95-200 mg/dl) 2-h glucose. Newly diagnosed diabetes (T2DM), 2-h glucose ≥ 11.1 mmol/l (≥200 mg/dl).

The continuous nature of risk posed by both fasting and postprandial glucose was shown by Coutinho et al (1999) in a pooled (meta-) analysis of 20 studies involving over 95,000 participants from data available up until 1999:


From Coutinho 1999. The curve and 95% confidence intervals are shown for fasting glucose and 2h post-challenge glucose. Note that mmol/l are converted to mg/dl by multiplying by 18. Thus, 4 mmol/l = 72 mg/dl, 5 mmol/L = 90 mg/dl, 6 mmol/l= 108 mg/dl.

Cardiovascular risk therefore begins to develop at surprisingly low levels of both fasting and postprandial glucoses.

Checking your own blood glucose

Assessing your own blood glucose is easy and inexpensive. It can frequently provide unexpected insights into your response to diet.

We use blood glucose checks in a way that is different from the way used by diabetics. Diabetics usually check fasting blood glucose in the morning and before meals to manage insulin or assess effects of drug treatment. That’s NOT how we will use blood glucose.

We use blood glucose to assess the effects of diet. Because our aims are different, we approach the use of blood glucose in an entirely different way. We use: 1) glucose just prior to a meal, and 2) glucose 1 hour after finishing a meal. Glucose levels after a meal reveal the effect of a specific food or meal on blood glucose and provides feedback on its blood sugar-increasing effect.

Consider checking blood glucose whenever your response might be in question, e.g., a change in meal composition or a previously untested food. If you’ve previously tested the effect of a breakfast of scrambled eggs, then there’s no need to test it again after the same meal.

For example, say you want to test your blood glucose response to stone-ground oatmeal in skim milk with raisins and walnuts. Blood glucose prior to meal: 102 mg/dl; blood glucose one-hour after the meal: 157 mg/dl—far too high and sufficient to add to plaque growth and coronary risk.

When does blood glucose peak after a meal? The time to peak glucose differs in individuals and by the composition of the meal. Adding oils/fats or proteins, for instance, will delay the peak. “Simple” carbohydrates, like white flour products, will accelerate the peak, while more “complex” carbohydrates will delay the peak. At least once, it may be helpful to check blood sugars every 30 minutes over 2 hours to gauge your individual peak. As a practical compromise, we recommend checking your blood sugar at 60 minutes after completing a meal, unless your individual response pattern suggests otherwise.

What are ideal blood glucose levels? From the above discussion, you can see that a perfect consensus does not exist. It is also clear that risks from both fasting and postprandial glucose are continuous with no clear cutoff between no risk and the beginning of risk. However, for our working purposes, the data suggest that ideal fasting blood glucose is 90 mg/dl or less; one-hour postprandial 100 mg/dl or less. At the start of your program, before weight loss, exercise, and the improved insulin responses of the Track Your Plaque diet have taken hold, one-hour postprandial blood glucose of ≤110 mg/dl is a good starting point. Long-term, ≤100 mg/dl is a better target that likely provides maximum plaque control and reduction of risk.

Should you undergo a 2-hour oral glucose tolerance test (OGTT)?

The OGTT, in which you drink a 75-gram glucose challenge, followed by blood sugars checked every 30 minutes over 2 hours, is the conventional method to diagnose impaired glucose tolerance and diabetes. However, if you will be checking your own post-challenge blood glucoses, the OGTT may be superfluous, since your own blood glucose checks reflect the real-world experience, while the OGTT reflects the response to glucose only, an artificial situation that is only meant to mimic the real-world experience.

What if your postprandial glucose is high?

If postprandial glucoses exceed your target value (e.g., 110 mg/dl), then there are three general strategies to follow to reduce blood glucose:

1) Reduce or eliminate the foods that cause the hyperglycemia
2) Increase sensitivity to insulin at the liver and muscle level
3) Increase pancreatic release of insulin

(This is an oversimplification; there are other actions to consider, e.g., glucagon and other regulatory hormones, that also impact blood sugars. However, for our purposes, the above serves as a useful model to help us manage blood sugars without use of medications.)

The first choice is obviously easiest and most natural. There are also reasons beyond blood sugar to reduce intake of foods that provoke high blood sugar, e.g., reduction of triglycerides and small LDL. Increased sensitivity to insulin is also a desirable goal; the prototypical strategies for enhanced insulin sensitivity are exercise and weight loss, both of which exert substantial effects.

The third strategy, enhanced insulin release from the pancreas, remains an effect of uncertain benefit and may be harmful. There is some suspicion that such strategies may increase cardiovascular risk, increase body weight, and even degrade pancreatic insulin release over the long-term (Bianchi 2009). This uncertainty has been cast over the sulfonylurea class of diabetes drugs (tolbutamide, glipizide, glyburide); while they reduce blood sugars, they also induce weight gain and may increase cardiovascular risk. In other words, forcing the pancreas to release insulin may not be a desirable phenomenon. We should bear this lesson in mind as we discuss nutritional supplements.

If your postprandial blood glucose is higher than your desired level, here are steps to consider to reduce it:

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