Postprandial Responses:
Part 3 - Carbohydrates and postprandial blood sugar
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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