who are in the sub-clinical phase (age 35-45) and clinical phase of aging (age
45 and above) have a one in three chance of getting this syndrome and not knowing
Perhaps the following signs are more recognizable: feeling sluggish
physically and mentally, especially after a meal. Gaining a pound here and a pound there
-and having increasing difficulty
losing them. Having blood pressure
creep up year after year. And
finding that the blood cholesterol, triglycerides, and blood sugar levels are
doing the same. These are all accepted signs
of aging. They are also all of the symptoms of Syndrome X.
Syndrome X can explain why you feel lousy
today -- such as being tired and fuzzy-minded. It can explain why you have high
triglycerides, high cholesterol or high blood pressure, why you are feeling
lousy after meals
, and why you are seeing your health spin out of
control without knowing why. It can also explain why you are aging faster than
your peers. More importantly, Syndrome X sets
the stage for catastrophic health problems, such as heart disease, diabetes,
Alzheimer's, cancer, and other age-related diseases.
It is estimated that this syndrome afflicts
over 60 million Americans and one in four adults over age 35.
cigarette smoking, hypertension, and obesity are the main culprits for the development
of artherosclerotic coronary artery disease (CAD). However, these account only
for half of the cases of CAD. The other pathologic processes underlying atherosclerosis
remain unknown. Syndrome X may be the cause
of up to fifty percent of all heart attacks.
It is an epidemic of
do you develop Syndrome X?
Syndrome X develops slowly
over time, often over a course of 20 years
It is the end result from years
(often decades) of taking in a modern day diet high in refined carbohydrates
such as breads, starches and sweets.
These foods, once taken, trigger
a rapid increase in blood sugar levels, and the body responds by raising levels
of insulin secretion that in turn helps to move the sugar out of the blood stream
into the cells. Insulin is a hormone secreted by the pancreas. It helps the
body utilize glucose (blood sugar) by binding with receptors on cells like a
key would fit into a lock. Once the key - insulin - has unlocked the door of
the cell, the glucose passes from the blood into the cell. Inside the cell,
glucose is either used for energy or stored for future use in the form of glycogen
in liver or muscle cells.
The more carbohydrates you eat, the more your pancreas releases insulin to lower
the excessive blood sugar. This is especially so with simple or refined carbohydrates
that are converted into sugar quickly (the high-glycemic index foods like white
bread and white flour) once inside your body. While insulin levels rise and
fall with each meal and is part of the normal metabolic process, chronic carbohydrate
overload causes chronic insulin overload. The cells of the body, be they the muscles
or the fat tissues, recognize that excessive
sugar is toxic.
They try to shut down the influx of sugar into the
cells and therefore go through a down-regulation process to resist the command
of insulin. This state is called insulin resistance. The pancreas, in response
to the insulin resistance and resulting lowered transport of glucose out of
the blood stream to the cell, puts out even more insulin in order to avoid too
high a blood sugar level. This compensatory
increase in insulin output continues until the pancreas fails to keep up.
Some people produce two, three or four times the normal amount of insulin. Yet,
because the cells have lost their sensitivity to insulin, they require even
more of it to maintain normal glucose levels. In advanced stages of insulin
resistance, when the pancreas becomes exhausted and can no longer maintain the
insulin production, insulin production drops, resulting in adult onset diabetes
mellitus (also called type 2 diabetes). Insulin
resistance plus compensatory hyperinsulinemia is nature's way of preventing
the evolution into type 2 diabetes.
It is often referred to as a
As long as there is insulin resistance, the
blood sugar and blood insulin levels are both high.
Over time, high
blood sugar and high insulin cause a myriad of destructive damages to almost
every tissue they touch. It is important to recognize while insulin resistance
or high blood sugar is each bad for health on its own, it takes both insulin
resistance and compensatory hyperinsulinemia, to result in the various manifestations.
These manifestations represent the resultant
damage and surface as a compilation of symptoms representative of multi-system
dysfunction. This includes the cardiovascular system, muscular system, kidney
system, reproductive system, and lipid metabolic system, just to name a few.
These symptoms, when grouped collectively
in a setting of insulin resistance, is called Syndrome X.
It can go undetected for up to 40 years, and a family history of type
2 diabetes, CHD, or hypertension increases the risk for Syndrome X.
X as explained by Dr Reaven
Syndrome X was first discovered by Stanford University Professor and researcher
Gerald Reaven, MD. In 1988, he first presented the results of twenty years of
study that showed that the effect of an array of changes around a little known
medical condition called insulin resistance to increased heart disease.
In his book Syndrome X
, Dr Reaven describes the condition as follows:
This deadly heart ailment begins in the bloodstream, shortly after we eat.
That's not a startling idea, for we know that eating fatty or cholesterol-laden
foods can be bad for our hearts. However, the Syndrome X culprit isn't red meat
or butter, it's carbohydrates. Yet these carbohydrates are reluctant, inadvertent
Before entering the body proper, our food is broken down into various constituent
parts in the intestine. One of these is glucose (blood sugar) from carbohydrates.
Upon entering our cells, some of the glucose is put right to work providing
the energy that cells need to perform their various tasks. The rest is stored
in certain cells for later use. But the glucose doesn't simply flow into the
storage cells. Instead, it must be guided in by insulin, a protein secreted
by the pancreas.
Insulin acts like a shepherd, herding its precious flock into the cellular "corrals".
Unfortunately, in many of us, glucose behaves like a group of errant sheep,
stubbornly refusing to go where the shepherd directs. When that happens, the
pancreas pumps out more and more insulin. That's the biochemical equivalent
of sending out more and more "shepherds" to get the "sheep"
into the "corrals". Imagine hundreds of shepherds chasing thousands
of sheep across a pristine field covered with thick, beautiful green grass.
Those hundreds of feet and thousands of hoofs will quickly tear up the field,
ripping out or flattening down clumps of grass. Soon, the field that once looked
so green and lush will be trampled and scarred, brown and dirty.
Something similar happens inside your body when glucose refuses to move into
the storage cells at the insulin's command. The interior linings of your arteries,
like the grassy field, are "ripped" and "trampled" as the
body attempts to overcome this problem.
Eventually, the insulin "shepherds" corral the glucose, and order
is restored in the body. But all is not well, for the "field" (the
lining of your coronary arteries) has been damaged, and there's other damage, as well.
This damage sets the stage for heart disease.
of Syndrome X
The fundamental defect in patients with Syndrome X is insulin resistance
in both adipose and muscle tissue.
The net result is hyperinsulinemia. The
term hyperinsulinemia refers to higher-than-normal levels of insulin in the
Each cell reacts to insulin differently. Some organs are highly sensitive to
high insulin, while others are less so. Insulin
resistance per se therefore does not cause damage, but it is the reaction of
the various tissues to chronic high insulin that is the main problem
An example is the kidney. The ability of insulin to stimulate sodium re-absorption
by the kidney could be very normal but at the same time the muscles in that
individual could be quite resistant to insulin action. The kidney is therefore
an "innocent bystander" of the increased insulin secretion in this
person due to the muscle insulin resistance.
Excessive insulin causes damage to the whole body, including:
The inner lining or endothelium
of the arterial walls comes under attack by excess insulin. The risk of arterial
blood clots, which can cause heart attacks or strokes, is increased
pathophysiology is very complicated. It is clear, however, that the damages
include reduced nitrous oxide activities (which could lead to hypertension),
increased platelet and monocyte adhesion, increased pro-coagulant activity,
impaired fibrinoloytic activity, and impaired degradation of glycosylated fibrin.
The net result: increased blood pressure,
increased formation of atherosclerotic plaques, increased thrombus formation,
angina, and heart attack.
The risk of cardiovascular disease is significantly
increased when the endothelium is damaged.
Pancreas. Type 2 diabetes
when the pancreas ultimately "burns itself out" from the excessive
demand for insulin production which it cannot keep up in an insulin resistance
state. Only 20% of people with excessive insulin due to insulin resistance develop
diabetes. The rest continues to produce enough insulin to meet the demand.
The ovary, being exposed to consistently
higher levels of insulin, increases its testosterone secretion accordingly,
the ovary being
sensitive. It is a major factor in the development of polycystic
Some research indicates it might also
increase the risk of prostate, colon and breast
Syndrome X also generates high
levels of cell-damaging free radicals and causes premature aging. Some researchers
believe it can also increase the risk of Alzheimer's
Excessive insulin leads to sodium retention.
Fluids follow sodium, resulting in excessive fluid in the body and ultimately
, a condition that is present in 50%
of those with Syndrome X
of Syndrome X
The manifestations of Syndrome X can be broken down into eight major categories:
1. Glucose intolerance:
Not all individuals with
Syndrome X have diabetes by definition. However, their blood glucose concentration
is usually higher than those individuals who do not have Syndrome X.
people who are insulin resistant produce large enough quantities of insulin
to maintain near normal blood glucose levels. In Syndrome X, VLDL, chylomicrons
and their metabolic remnants (chylomicron and VLDL remnants) are removed more
slowly from the plasma by virtue of their increased concentrations, resulting
in increased postprandial lipemia. Unfortunately, the increased VLDL also reduces
the ability to remove postprandial newly absorbed chylomicrons. More often than
not, they have impaired glucose tolerance
A glucose tolerance test, where insulin and blood glucose
are measured, can help determine if someone is insulin resistant.
The characteristic findings are
high plasma triglycerides and low HDL cholesterol.
This combination is a hallmark of Syndrome X. The pathway is quite
interesting. With high blood insulin level, the liver produces more triglyceride
rich VLDL, a carrier of fat. The amount of triglycerides therefore increases.
Cholesterol ester transfer protein (CETP) transfers cholesterol from HDL to
VLDL, exchanging it for triglycerides. As a result, the HDL ("good")
In addition, there is a shift in the LDL particle diameter to smaller and
denser LDL cholesterol fractions, which is the most potent and damaging kind.
The dense LDL cholesterol will attack the endothelium, causing inflammatory
responses that ultimately results in fatty streak and plaque formation characteristic
3. Uric acid metabolism:
There is a decrease in
the ability of the kidney to excrete uric acid, so renal uric acid clearance
is decreased and the blood uric acid concentration
4. Kidney manifestation:
It appears that half
the patients with hypertension are insulin resistant
. This is due
to fluid retention caused by high insulin level.
5. Hemodynamic manifestations:
There is evidence
that the sympathetic nervous system activity is increased in insulin resistant
individuals. Systolic pressure is often greater than 140 mmHg, and diastolic
pressure higher than 90 mmHg. This further
contributes to hypertension.
6. Fibrynolytic changes:
There is an increase in
Plasminogen activator inhibitor 1 (PAI-1). When PAI-1 is high, dissolution of
blood clot is reduced, and fibrinogen and thrombus formation increases. The
increase in fibrinogen tends to increase coagulation. This plays a role in the
development of coronary heart disease.
Obesity is a common feature. The body
mass index (BMI) is often greater than 25
kg/sq.m. Until recently, insulin resistance was thought to cause obesity only
in adults, because it is considered an age-related condition. This is clearly
wrong. A 1998 evaluation of more than 2,000 Finnish men led to the finding that
insulin resistance is associated with obesity beginning in early childhood and
middle age. The researchers also noted that each five percent weight increase
at age 20, over the average for that age, was associated with a nearly 200 percent
greater risk of full-blown Syndrome X by middle age.
High insulin itself does not cause obesity.
On the contrary, obesity leads to increased insulin resistance.
are all born with a certain degree of insulin resistance or sensitivity. As
one gains weight, one's body becomes more insulin resistant. Studies have shown
that tissue sensitivity to insulin is decreased by about 30-40% in people who
are 35% over their ideal body weight.
Why obesity makes us more insulin resistant is not totally clear. It may
be related to the fact that people who are obese because of their increased
levels of body fat release more fatty acids from their fat depots, which in
turn can inhibit insulin action.
8. Antioxidant Depletion. Low levels of antioxidant
vitamins and DHEA (dehydroepiandrosterone) and high cortisol levels are commonly
found in people with Syndrome X.
It is likely to due to the increased free
radical activity, and concurrent reduction in the endogenous antioxidant level
as the body tries to neutralize the free radical activities. It has been shown,
for example, that atherosclerotic plaques
not only contain cholesterol but also oxidized ascorbate (vitamin C).
body deposits the antioxidant ascorbate there in an attempt to overcome the
free radical damage.
Fortunately, no complicated tests are needed
to diagnose Syndrome X
. Very simple measurements and good
interpretive skills and careful attention in history taking are needed
have an accurate diagnosis of insulin resistance. It comes down to the clinician's
knowledge of metabolism and endocrinology. Abnormal
test results include elevated blood pressure, triglycerides, uric acid and glucose
levels accompanied by a low HDL count. If these results are all
normal, the chance of being insulin resistant is very low. Let us take a closer
Fasting triglyceride level above 1.9 mmol/L (170 mg/dl)
is a very good
marker of the increase in postprandial lipemia, the appearance of small dense
LDL, and the increase in PAI-1 levels. A high fasting triglyceride is a key
marker for Syndrome X (or insulin resistance)
HDL cholesterol level that is less than 1.0 mmol/L (38 mg/dl)
a good indicator of insulin resistance.
Fifty percent of individuals with hypertension
have insulin resistance.
Systolic pressure is often greater than 140 mmHg and diastolic pressure greater
than 90 mm/Hg without medication.
Fasting glucose above 5.5 mmol/L (100 mg/dl)
indicates that a person
is at risk of insulin resistance. The higher the blood glucose within the normal glucose
range, the greater the insulin resistance. A two hour glucose concentration
post glucose load of greater than 7.8 and less than 11.1mmol/L (140 and 198
mg/dl respectively) may not merit the diagnosis of type 2 diabetes, but will
suggest insulin resistance.
Triglyceride to HDL cholesterol ratio of more than 2
is a warning sign.
If the ratio is over 4, it is a good indicator of insulin resistance.
Interesting, fasting insulin level may not
be the best indicator.
The measurements are hard to do, and the values
are going to differ from lab to lab. One can have a high insulin level and not
have syndrome X.
It should also be noted that a high LDL in
itself is not a key marker for Syndrome X.
LDL in most laboratories is derived
from calculations. The formula is:
LDL = total cholesterol
- HDL cholesterol - (triglyceride / 5).
It should be noted if the triglyceride level is above 300 mg/dl, the LDL
calculation will not be accurate because of correlation problems.
case, the actual measured LDL level should be obtained. While a high LDL is
a good indicator of cardiovascular risk, a low HDL cholesterol level is even
more significant, as well as a low (<4.5) total cholesterol/hdl cholesterol
ratio. Furthermore, advanced cardiovascular
indicators such as lipoprotein (a), homocysteine, and C reactive protein (an
indicator of endothelial inflammatory response) should be part of the routine
workup of anyone suspected of Syndrome X.
X in a Nutshell
underlying cause of Syndrome X is insulin
resistance - a diet-caused hormonal logjam that interferes with your body's
ability to efficiently burn off the sugar you eat
. The more sugar
you eat, the higher the risk for syndrome X.
Syndrome X occurs when the
high insulin level damages our bodies' internal systems, producing a crop of
symptoms. Specifically, this group of health problems includes insulin resistance
(the inability to properly deal with dietary carbohydrates and sugars), abnormal
blood fats (such as elevated cholesterol and triglycerides), being overweight,
and high blood pressure.
Symptoms of Syndrome X include:
Abnormalities of blood clotting
Low HDL and high LDL cholesterol levels
High triglyceride levels
Central obesity (excessive fat tissue in the abdominal region)
Impaired glucose tolerance
High blood pressure
Low levels of antioxidant vitamins and DHEA, with high anti-inflammatory and
anti-stress hormone cortisol
If you have 3 or more of the above, you should
consider yourself either having or at high risk of Syndrome X
The term "cardiac Syndrome X" refers to a heart condition where chest
pain and electrocardiographic changes suggest that ischemic heart disease are
present, but without angiographic findings of coronary disease.
has shown that people with cardiac Syndrome X also have lipid abnormalities.
This suggests that Syndrome X and cardiac Syndrome X may be one and the same.
of Syndrome X
No one knows for sure what causes syndrome X. Some scientists think that a defect
in specific genes may cause insulin resistance
and intensive research is now underway. What we do know so far is:
Insulin resistance is aggravated by obesity
and physical inactivity;
both of which are increasing in the U.S.
The more sugar you take in, the higher the chance of you developing Syndrome
The fact that many obese people have high insulin levels but do not develop
diabetes or syndrome X is interesting. Many obese people have high insulin sensitivity
and do not have insulin resistance at all. There is evidence of a widespread
variability in insulin mediated glucose disposal by muscle in non-diabetic individuals.
In a study conducted by Dr.Reaven on 500 individuals, there is an apparent ten-fold
difference between the most insulin sensitive and the most insulin resistant
X and Type 2 Diabetes
There are over 60 million people in the United States alone who have Syndrome
X. There are an additional 24 million people that have glucose intolerance,
a pre-diabetic state. In addition, there are over 16 million people who have
adult onset diabetes mellitus (Type 2 diabetes) and only half of these individuals
knows they have diabetes. Some diabetics have had their disease for over 8 to 10
years before the physician even makes the diagnosis. This may account for the fact
that over 60% of their diabetic patients already have major cardiovascular disease at the time
of diagnosis of diabetes.
Science has not yet determined why some people with insulin resistance eventually
develop diabetes and others do not. Type 2 diabetes develops in a relatively
small number of individuals who are insulin resistant. Most
individuals who are insulin resistant continue to secrete large amounts of insulin
and do not get type 2 diabetes
. We do know that insulin resistance
is the body's natural defense against chronic high sugar load. It is the body's
defense against the evolution to diabetes. In other words, type 2 diabetes
is often the advanced stage of insulin resistance.
The point to remember is that while most insulin
resistant patients do not get diabetes, they are still at risk for coronary
Ideal fasting blood sugar level
The easiest way to measure the status of sugar in your body is through a simple
fasting blood sugar laboratory test. A fasting serum glucose level of more than
125 mg/dL is the current threshold for identifying patients with diabetes. This
was based on the incidence of diabetic retinopathy. Now physicians are increasingly
focused on the diabetes-related risk of coronary heart disease. In a cross-sectional
study of 2,440 people, researcher Dr. Dennis Sprecher reported that people with
a fasting serum glucose level of 100-125 mg/dL had an adjusted, 2.8-fold higher
risk of having a coronary heart disease event than people with a fasting glucose
level of less than 79 mg/dL. This finding suggests that patients
with high levels of serum glucose in the nondiabetic range (100-125 mg/dl) also
face a substantial risk of having coronary heart disease. In fact, the Cleveland
Foundation now uses a fasting serum glucose of 90 mg/dL or
higher as a biomarker of coronary heart disease risk. Ideal
fasting blood sugar should be no higher than 90mg/dl, regardless of age.
X and Coronary Heart Disease
Individuals with Syndrome X have an increased risk of heart disease
according to the American Heart Association (AHA). The relationship is not Syndrome
X leading to CHD or one factor being responsible for the increased risk, but
rather that, taken as a cluster, there is increased prevalence of CHD in people
with insulin resistance and the various manifestations. Those afflicted with
syndrome X is akin to have been injured by a shotgun blast, with multiple bullet
wounds. While none of the multiple bullet wounds may by itself lead to death,
the collative damage caused by the multiple bullet wounds raises the chances
of death significantly. In real-life terms, we are talking about increasing
risks of cardiovascular disease, cancer, stroke, and pre-mature aging.
Only one study has shown that in people followed prospectively, insulin resistance
increases the risk of CVD. There are multiple studies showing that insulin level,
as a predictor or surrogate measure of insulin resistance, predicts CHD. We
also know that a low HDL is a powerful predictor of CHD. There is more and more
evidence that small dense LDL particles and increased remnant lipoprotein concentrations
due to the increased postprandial lipemia are linked to CHD.
X and Aging
Vladimir M. Dilman, M.D., co-author of The Neuroendocrine Theory of Aging, refers
to insulin resistance as an "age-related pathology." In fact, it is
one of the few consistent indicators of longevity. Centenarians have a lower
blood sugar and blood insulin level relative to their age.
In the mid-1970s, biologist Anthony Cerami discovered that chronically high
blood glucose levels was the main trigger in a chemical process that produced
advanced glycosylation end products (AGES), which were implicated in normal and
advanced aging and age-enhanced diseases. AGEs
form at accelerated rates whenever blood-sugar levels are high as with age.
AGEs damage to the body is extensive.
Referred to as a carmelization or browning reaction, cross-linking by AGEs involve
a chemical reaction between sugar and protein molecules. No one part is spared.
Serious damage to cell membranes and collagen
fibers is near universal.
This cross-linking leads to the stiffening
of connective tissue and hardening of arteries, leading to pre-mature aging
and hypertension. As cross-links increasingly reduce the flexibility and permeability
of tissues and cells, cellular communications and repair processes also begin
to break down. A compensatory inflammatory response may be launched by the body,
especially in the endothelium. This leads to a cascade of damaging events resulting
in fatty streaks and atherosclerosis. Eventually, the tissues of the body
become irreversibly transformed, and the inevitable result is aging, disease
and finally death.
It is well known that bathing your cells in high sugar (as in diabetics)
causes premature aging.
This is because this sugar-driven damage acquires
breakneck speed, raising their levels of AGE-infused collagen to those of elderly
people. Diabetics suffer a very high incidence of nerve, artery and kidney damage
because high blood sugar levels in their bodies markedly accelerate the chemical
reactions that form advanced glycation products. The endothelium of diabetic
patients also secretes unwanted growth factors that leads to blood vessel hypertrophy
and reduced lumen size.
This reduces the blood flow, exacerbating the already
compromised insulin delivery and further increases the chances of insulin resistance.
The reduced blood flow leads to reduced oxygen delivery to needy tissues,
resulting in increased peripheral neuropathy commonly seen in diabetes.
Treatment of Syndrome X
Physicians have been concentrating on treating the symptoms of
Syndrome X such as hypertension and dyslipidemia rather than concentrating on
the underlying problem, which is insulin resistance.
Since over 50% of the
prescriptions filled in the United States are for hypertension, elevated cholesterol
levels, heart disease, and diabetes, you can get a glimpse of the economic importance
of this problem.
Syndrome X is usually totally reversible without
. The key is to slow down carbohydrate absorption while increasing
insulin sensitivity. This can be done by lowering
your carbohydrate intake (the low-carb diet), together with a nutritional supplementation
program designed to slow carbohydrate absorption, increase insulin sensitivity,
and normalize blood sugar levels.
However, human nature (and human metabolism) being what it is, the majority
of patients with syndrome X cannot accomplish these goals
. In these cases,
each metabolic disorder associated with syndrome X needs to be treated individually,
and aggressively. A short-term treatment
with drugs is seldom but may be needed.
Treating the lipid abnormalities.
The lipid abnormalities seen
with syndrome X (low HDL, high LDL, and high triglycerides) respond nicely to
weight loss and exercise. Treatment should be aimed primarily at reducing LDL
and triglyceride levels, and raising HDL levels. Successful drug treatment
usually requires treatment with a statin or one of the fibrate drugs, or a combination
of a statin with either niacin or a fibrate
. It should also be noted that
the use of statin drugs is not without its
Treating the clotting disorder.
Patients with syndrome X have
several disorders of coagulation that make it easier to form blood clots within
blood vessels. These blood clots are often a precipitating factor in developing
heart attacks. Patients with metabolic syndrome X should generally be placed
on daily aspirin therapy to help prevent such clotting events.
Treating the hypertension.
High blood pressure is present in more
than half the people with metabolic syndrome X, and in the setting of insulin
resistance, high blood pressure is especially important as a risk factor. Recent
studies have suggested that successfully treating hypertension in patients with
diabetes can reduce the risk of death and heart disease substantially. Low
should be used according to Dr.Reaven. No more than
12.5 mg of hydrochlorathiazide should be prescribed. People
with Syndrome X should not be prescribed the anti-hypertensive dosages of thiazides
that have been recommended in the past
cases should be controlled with ACE inhibitors.
ACE inhibitors increase
levels of nitrous oxide (a potent endothelium generated vasodilator), resulting
in vasodilatation and blood pressure reduction. ACE inhibitors also have
been shown to improve endothelial function, and so have HMG-CoA reductase inhibitors
(such as lovastatin and pravastatin), and to a lesser degree, calcium channel
blockers (such as verapamil and nifedipine).
Treating High Blood Sugar.
High blood sugar must be normalized.
Traditionally there are four points of intervention to reduce blood sugar:
Two major classes of drugs are the sulonylureas
and the meglitinides.
Sulfonylureas have been used for more than
4 decades. Their primary goal is to increase the level of endogenous insulin
by stimulating the pancreatic secretion. These agents have no direct effect
on insulin resistance. They may decrease the resistance slightly by reducing
plasma glucose level. The meglitinide class, of which repaglinide is approved
in the U.S., also stimulates insulin release from the pancreas. Clearly, these
should be avoided
with Syndrome X who already have a high insulin level. Further insulin will
only worsen the problem.
Alpha-glucosidase inhibitors are currently
represented by acabose. The primary mechanism of action of these agents is to
inhibit specific enzymes that break down carbohydrates in the small intestine.
Absorption of carbohydrates is delayed, resulting in a reduction of postprandial
hyperglycemia. No specific action on insulin resistance has been reported.
The biguanides, of which metformin
is the agent used in the U.S., mainly decrease hepatic glucose production, They
also increase peripheral insulin sensitivity, leading to reduced plasma glucose
level. They also have some effect in reducing intestinal glucose absorption.
Clearly this is a better drug to use than
the previous two.
This class of oral agents is known as the
of which troglitazone is approved for use in
the U.S. It reduces insulin resistance by increasing the uptake of glucose by
peripheral tissues such as skeletal tissue. It is therefore uniquely
designed to attack insulin resistance.
Treatment of Syndrome X
While there are no drug treatments that can directly reverse the insulin resistance
that causes syndrome X; there is, in fact, a way to reverse the insulin resistance
- and that is through diet, exercise, and nutritional supplementation.
Clearly, the following goals should be met in any diet for Syndrome X sufferers:
a. Reduction of carbohydrates. With less carbohydrates
around, there will be less insulin needed.
b. Reduction of LDL cholesterol which can lead to heart disease
c. Reduction of blood glucose level
d. Increase in insulin sensitivity
The question is: If you reduce carbohydrate,
and reduce fat, then how are you going to get enough calories? I
one food group is reduced, the calories must be supplied by another food group.
The strategy is clear - reduce carbohydrates, especially simple refined carbohydrates.
How you make up the calories is less clear. There
are only two options available: carbohydrates can be replaced with proteins
or with fats.
Clearly saturated fats should be restricted to reduce
the risk of cardiovascular disease and to lower LDL cholesterol level. Therefore,
part of the carbohydrate should be replaced with "good" fat.
Replacing carbohydrates with proteins ignores
the fact that protein, once in the intestinal tract, converts to amino acid.
Amino acids increase insulin secretion. It is unclear, however, whether proteins
are as potent as carbohydrates in stimulating insulin secretion.
Dr Reaven's Syndrome X diet derives 45 percent
of calories from carbohydrates, 15 percent from proteins and a hefty 40 percent
from fats. I
n contrast, American Heart Association recommends
keeping fat intake to no more than 30 percent of your total calories and boosting
the carbohydrates to at least 55 percent.
What makes Dr Reaven's diet different from
the latest run of carbohydrate diets is that his eating plan is
low in protein.
This is very different from Dr Atkins'
diet that is high in protein.
diet high in protein is suitable for those with normal insulin sensitivity,
but inappropriate for those with syndrome X. It is important to note that
there are good fats and there are bad fats. The
fats recommended by Dr.Reaven are mostly heart-friendly unsaturated fats from
plant and vegetable sources such as olive oil and nuts, not from the artery-clogging
saturated fats present in steaks.
Dr Reaven suggests replacing saturated fats with and mono- and poly -unsaturated
fats will equally benefit LDL cholesterol lowering as compared to replacing
saturated fats with carbohydrates. This is confirmed in multiple studies.
Mono- and poly-unsaturated fats do not
raise insulin levels, so you get the benefit of both LDL cholesterol and Syndrome
X control. Unsaturated fats are found in foods such as vegetable
oils (olive oil in particular is high in mono-unsaturated fats) nuts, and
avocados, whereas saturated fats are abundant in fatty cuts of meat and whole
milk dairy products.
It has been postulated that use of low glycemic-index carbohydrates will
avoid worsening the manifestations of Syndrome X due to its slow glucose release
and absorption rate. There is little doubt that low glycemic-index carbohydrates
such as fruits and vegetables are superior when compared to high glycemic-index
carbohydrates such as white flour and white bread. Dr Reaven studied this
by increasing the fiber intake to the level recommended by the ADA for diabetics,
and it had almost no effect. In a recent paper, substantial increases in the
fiber level (exceeding the ADA recommendation) resulted in improved metabolic
characteristics, as compared to a high carbohydrate/low fat diet. No comparison
was made between the very high fiber diet vs. a diet low in carbohydrates
and high in unsaturated fats.
The simplest and most effective approach
is to replace the carbohydrates with poly- and mono-unsaturated fats and restrict
saturated fat intake, to achieve both
lower LDL cholesterol and improve Syndrome X.
2. Nutritional Supplementation.
A variety of natural non-toxic food based compounds can be used.
The goals are to normalize blood sugar,
and increase insulin sensitivity.
Treating the lipid abnormalities. For Dyslipidemia, the following can
be considered: pantethine (300 -1,200 mg),
panthothenic acid (300-1,300 mg), guccolipid (50-150 mg), polycosinol (5-10
mg), mineral ascobates (2-5 grams), lysine (2-5 grams), proline (1-2 grams),
chromium polynicotinate (400 -1200 mcg), and fish oils (1000 to 4000 mg).
Treating the clotting disorder. To reduce the blood clot risk, natural
compounds such as vitamin E (300 to 1200
I.U.) and gingko biloba extracts (30 to 150 mg) have blood thinning
properties and help promote circulation. Antioxidant therapy with optimum
doses of Vitamin A, C, and E helps to stabilize plaques, improve vascular
tone, and reduce thrombus.
Treating the hypertension. To lower blood pressure, antioxidant
therapy helps to stabilize plaques and improve vascular tone by
inhibiting oxidation of LDL cholesterol.
Treating high blood sugar. For glucose normalization and to increase
insulin sensitivity, natural non-toxic compounds that have sugar modulation
effects include chromium polynicotinate
(400 -1200 mcg), venadyl sulfate (25 -100 mg), lipoic acid (100-300 mg)
can be considered.
For rebalancing the internal terrain to enhance digestive balance and
digestive enzymes, green foods such as
chlorella, spirulina, algae, soluble fiber, and probiotics should
For antioxidant deficiency: a strong
multi-vitamin with at least 10,000 I.U. of beta carotene, 500 mg of vitamin
C, 200mg of selenium, 100 mg of grape seed extract, 30 mg of co-enzyme Q10.
For normalization of adrenal function,
pantethine 300-900 mg, pantothenic acid 400-1,200 mg should be
Because of tremendous individual variation,
the use of nutritionals should therefore be personalized for your
body. One person's nutrient can be another person's toxin. If you
have a specific health concern and wish my personalized nutritional
recommendation, write to me by clicking
studies have shown that modest exercise is beneficial. However, unequivocal
metabolic benefits from exercise will not be achieved from a casual walk a
couple of nights a week. Significant, regular, chronic exercise is required
to see improvements in insulin action, triglycerides, and HDL cholesterol.
Exercise is as powerful a tool as weight loss.
4. Weight Management.
Every attempt should be made to reduce total body weight to
within 20% of the "ideal" body weight calculated for age and
height. If this is done Syndrome X will improve significantly. There is little
question about its effectiveness.
5. Other lifestyle Factors:
a. Alcohol. In population-based studies, moderate drinkers are found
to have lower insulin levels as compared to non-drinkers. Our small-scale
studies have shown moderate drinkers to be more insulin sensitive. There have
been no intervention studies to show that initiating alcohol consumption in
individuals who are insulin resistant with low HDL is beneficial. So it
is not reasonable to suggest that non-drinkers should start to drink 1-2 drinks
per day. On the other hand, we do not have the evidence to recommend abstaining
b. Smoking. Smoking is unequivocally bad, asspciated with high
triglycerides, low HDL cholesterol and insulin resistance.
Two of the key factors that affect our health is glucose (also known as
blood sugar) and the hormone insulin.
Because of the high carbohydrate
foods we, as a whole population, now eat, our bodies' levels of glucose and
insulin have gone out of control. Such high carbohydrate foods probably include
cereals, muffins, breads and rolls, pastas, cookies, donuts, and soft drinks.
Quite simply, we are overdosing on glucose
-- two substances which in high doses will accelerate
the aging of our bodies and encourage the onset of diseases. Insulin resistance
is the body's way to resist excessive sugar and carbohydrate levels, and 60
million Americans have this problem. When insulin resistance is accompanied
by compensatory hyperinsulinemia- (not explained in article), the systemic
damage is collectively known as Syndrome X.
Fortunately, Syndrome X can be reversed
with dietary, lifestyle, and nutritional supplements. Dr
Reaven, the acknowledged father of Syndrome X, advocates a diet high in unsaturated
fat (45%), low in protein (15%), and moderate in carbohydrate (40%).
weight management, and optimum nutritional supplements such as chromium polynicotinate,
vitamin C, proline, lysine, and other antioxidants help to normalize sugar
and increase insulin sensitivity.
Dr. Lam was first to coin the term, ovarian-adrenal-thyroid (OAT) hormone axis, and to describe its imbalances. He was first to scientifically tie in Adrenal Fatigue Syndrome (AFS) as part of the overall neuroendocrine stress response continuum of the body. He systematized the clinical significance and coined the various phases of Adrenal Exhaustion. He has written five books: Adrenal Fatigue Syndrome - Reclaim Your Energy and Vitality with Clinically Proven Natural Programs, The Five Proven Secrets to Longevity, Beating Cancer with Natural Medicine (Free PDF version), How to Stay Young and Live Longer, and Estrogen Dominance. In 2001, Dr. Lam established www.DrLam.com as a free, educational website on evidence-based alternative medicine for the public and for health professionals. It featured the world’s most comprehensive library on AFS. Provided free as a public service, he has answered countless questions through the website on alternative health and AFS. His personal, telephone-based nutritional coaching services have enabled many around the world to regain control of their health using natural therapies.
For the latest Anti-Aging and Adrenal Fatigue related health issues, visit Dr. Lam at
Feel free to email Dr. Lam by clicking
here if you have any questions.
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