A NEW APPROACH TO METABOLIC SYNDROME
By: Michael P. Ciell, R.Ph.,
The Greatest Healthcare/Financial Crisis
Metabolic Syndrome (aka Syndrome X) with its four hallmark symptoms
of obesity, hypertension, dyslipidemia and hyperglycemia is devastating
our country as well as the whole of North America. In March of 2005 the
National Institutes of Health and the New England Journal of Medicine
published a paper stating that because of this epidemic the current
generation is projected to have a shorter life expectancy then the
previous one…for the first time in recorded history! Since that paper
things have become much worse. Worse, despite the fact we have changed
the USDA “Food Pyramid”, developed many new classes of pharmaceutical
agents (especially ones for pre-diabetes and diabetes Type II), have
taken soda machines out of schools, and even the First Lady’s top
priority is the obesity epidemic. This syndrome, with all of its
comorbidities (cardiovascular disease, stroke, many cancers, kidney
failure, blindness, amputations ,etc.), accounts for the majority of
healthcare dollars spent. If the tide is not turned, Metabolic Syndrome
will bankrupt our country. This is a fact.
The Pathophysiology of Metabolic Syndrome
In 1987 the late Gerald Reaven, MD, Professor of Medicine at Stanford
University’s College of Medicine, first demonstrated that the four
hallmark symptoms shared a commonality: hyper-insulinemia coupled with
insulin resistance. He coined the term “Syndrome X” to illustrate the
point: the four legs of the “X” represent the symptoms (hypertension,
central obesity, hyperglycemia and dyslipidemia) and the nexus of the
“X” being the causal agents of too much insulin along with insulin
resistance (the cells’ do not respond to normal physiologic amounts of
insulin). This is the standard, accepted medical model of this disease.
The Failure of Current Treatments
We are being ravaged by this syndrome due to the simple fact that we
have ignored the model! Instead of focusing our attention on the root
cause we have decided to treat each of the symptoms as separate,
unrelated diseases. Thus we have new dietary recommendations and “diets
d’Jour”, as well as a plethora of exercise regimens prescribed for
obesity and of course, the “diet pills”. There too are the myriad of
prescription drugs to ‘control’ the other three symptoms. If our
attention is on ‘controlling symptoms’ we have admitted, by default,
that there is NOTHING WE CAN DO FOR THE CAUSATIVE FACTORS and we will
just have to LEARN TO LIVE WITH OUR DISEASE (i.e. ‘it will always be
with us, we’ll just control it’). This attitude of acceptance is bad
enough and unaffordable in the long run, but that’s the least of it. If
we understand the pathophysiology of this syndrome we readily can see
why many of these treatments actually make the other symptoms much
worse! Hyper-insulinemia means the patient’s pancreas is secreting an
exaggerated amount of insulin in response to rises in blood glucose.
This can easily be confirmed by doing a fasting insulin level OR the
standard glucose challenge test and ordering insulin levels along with
glucose levels at time zero, one hour and two hour intervals post
challenge glucose administration.
Sadly, the vast majority of
practitioners do not even think about such an important marker. So we
dwell on just the glucose level or Hemoglobin A1c (merely symptoms ) and
prescribe drugs such as the sulfonylureas (i.e. glyburide, glipizide,
glimperide) which cause the pancreas to secrete EVEN MORE INSULIN or we
actually give them INSULIN ITSELF in an aggressive attempt to control a
symptom. If the model is correct then this therapy should make the
syndrome worse……and it does! This is the fundamental reason why we have
failed to stem the tide (or actually reverse) this seemingly insidious
malady.
The Concept of Homeostasis
If insulin just mediated glucose uptake by our cells and did nothing
else, we probably would not have this problem. However this is not the
case and when the amount of insulin remains consistently elevated it
does other things…..and these things are NOT good. Before discussing
the effects of hyper-insulinemia, a review of the fundamental concept of
homeostasis should be addressed.
The body is an organism that strives
to maintain a constant internal environment in the face of constantly
changing, often hostile, external factors. Blood pressure, blood
glucose, body temperature, acid / base balance, etc. must remain within a
relatively narrow range in order to survive. It does so by means of
the action/reaction principle, or mechanisms that exert opposite effects
so that a balance may be
achieved. Examples are: vasodilation / vasoconstriction, oxidation /
reduction, anabolism/catabolism, assimilation / elimination, etc. These
systems are exquisitely regulated primarily by the nervous system and
the endocrine (hormonal) system. So if the environmental temperature
is 125 degrees, our internal temperature remains at 98.6 degrees.
Likewise if the temperature drops to 20 degrees, certain mechanisms are
in place to make certain our internal temperature remains a constant
98.6. Glucose homeostasis is essential for life as certain cells in the
body can only use glucose as an energy source (certain brain cells, the
adrenal medulla, red blood cells, etc.). Whether in times of feast or
famine, blood glucose must remain in a certain range and insulin and
glucagon are the master hormones that control this process (forget about
ghrelin, leptin, incretins and all these ‘new mini-hormones’ that are
in the literature today…these are subservient to the two masters). The
body needs BOTH of these “master hormones” to maintain balance ( as they
have exactly opposite physiological functions….if you know what insulin
does, then you automatically know what glucagon does…the exact
opposite!) and if an imbalance occurs, dysfunction or “disease” will
arise.
The Physiological Effects of Insulin
Insulin’s primary function is mediating glucose uptake to muscle cells,
and in this way, helps regulate blood glucose homeostasis. However
insulin binds to many other receptors in the body and affects MANY other
physiological parameters. And here’s the “rub”. If insulin receptors
on the muscle cells become resistant to insulin’s effect (and do not
uptake glucose in an effective manner) the pancreas will produce more to
ensure glucose uptake will occur. But if we increase insulin levels,
what happens to OTHER receptors that are not “resistant” yet and
modulate other bodily functions? This scenario becomes way more
complicated, in that, these receptors become ‘insulin resistant’ at
different times. So a ‘typical Syndrome Xer’ presents to the physician
with some central obesity, slightly elevated blood pressure, slightly
elevated blood glucose and a less than stellar lipid panel. He is told
to lose some weight by eating more fruits and vegetables, cut down on
fats and cholesterol (have oatmeal instead of bacon and eggs) and do
some light exercise. This is standard, first line therapy of lifestyle
changes and sounds very reasonable. This compliant patient makes these
changes and returns in two months, shocked and disappointed that his
symptoms have become worse! Now he is given a low dose ACE inhibitor
coupled with a diuretic for his hypertension and placed on metformin and
glyburide to help control hyperglycemia. The glyburide tells the
pancreas to secrete even more insulin and he gains more weight. Insulin
also “ramps up” the enzyme HMG-Co A reductase which basically tells the
body to produce even more cholesterol.
Excess insulin also drives the
kidneys to retain sodium and waste magnesium,
which is an essential element for insulin receptor sensitivity.
Hypertension and insulin resistance worsen. Usually at this point (if
not done sooner) a statin is added along with niacin and another oral
hypoglycemic and we ‘start the march’ to insulin therapy. This is why
many of these patients will find themselves on six to nine prescription
drugs and this is the current “Standard of Care” for this syndrome.
Let Your Food Be Your Medicine
Let us now suppose that the above patient visited a Chiropractic
physician first. This particular physician is skilled in the use of a
‘muscle sparing’ protein diet, not a hyper protein diet ala Atkins.
This diet is also low in fat, particularly saturated fat and is very
carbohydrate restrictive (providing about 40 grams of carbohydrates
daily mainly from fibrous vegetables). The physician explains the
“medical model” of Syndrome X and relates how the overproduction of
insulin can contribute to all his symptoms.
Correcting hyperinsulinemia
is very straightforward: all carbohydrates (with the exception of
fiber) will eventually be turned into glucose….sometimes quickly,
sometimes slowly. As the glucose is absorbed the pancreas begins to
secrete insulin (in this case, too much insulin). By restricting the
carbohydrates the production of insulin is immediately reduced. The
patient is interested but confides that he can be hypoglycemic at times
and is afraid of such a restrictive protocol. The physician relates
that hypoglycemia is usually the consequence of an overproduction of
insulin, not a lack of carbohydrates. He further explains the body has
“three tanks of energy” from which to draw. Glycogen (or our stored
glucose), muscle, which can be broken down via gluconeogenesis to supply
glucose and fat (triglycerides) which can be turned into glucose (from
the glycerol) and ketonic bodies which most of the cells In the body can
use for fuel. But the body draws on these compartments in a very
specific order. It will always use the glycogen first and only when
‘that tank’ is empty, will it then begin to simultaneously burn muscle
and fat.
The physician tells the patient if he keeps “putting fuel in
the glycogen tank”, he will never be able to access his fat reserves,
thus the restriction of carbohydrates. He also says that we never want
to lose muscle, thus the inclusion of the adequate amount of protein to
replenish what is lost to gluconeogenesis. During the first three days
of this protocol the patient may feel a little tired or weak (as the
body depletes its glycogen) but once this is gone and the body ‘switches
over to muscle and fat’, he will have plenty of energy and hypoglycemic
episodes will be a thing of the past. His patient is interested but
asks: “ketonic bodies”, does that mean ketosis…I thought that was bad?”
Again the physician explains that ketoacidosis is bad and that is why a
Type I diabetic would never be placed on this program. In this case
ketosis just means ‘living off your reserves’ and is the reason human
beings were able to survive times of famines. His concerns allayed, the
patient begins the program.
Under The Influence Of Glucagon
Six weeks later the elated patient returns to his Chiropractor. He is
thirty pounds lighter and says that his medical doctor told him his
blood work was fantastic! In layman’s terms the physician tells him:
“Well you have actually reset your pancreas, it no longer is pumping out
too much insulin and now you can start to put fruits, grains and dairy
back into your diet”. After this patient’s glycogen reserves were
depleted and carbohydrates continued to be restricted, the body had to
ensure proper blood glucose levels were maintained. Under these
conditions the pancreas produces more glucagon (which raises blood
sugar) and much less insulin (whose primary function is to lower blood
sugar).
But there is more to glucagon than this primary function.
Glucagon stimulates two adipocyte (fat cell) enzymes (HSL and ATGL) and
inhibits a third (Lipoprotein lipase). The result is the release of
trigylcerides from the fat cell (to be used a fuel) as opposed to
insulin’s effect which is to store fat. Glucagon enhances the entry of
free fatty acids across the mitochondrial membranes so they can be used
as fuel (insulin inhibits this). Glucagon also greatly inhibits the
action of HMG-CoA reductase (along with all the other enzymes necessary
for cholesterol synthesis) and forces cells to pull cholesterol from the
blood stream via ‘ramping-up’ LDL receptors (1983 Nobel Prize in
Medicine). This is why this patient’s lipid panel came back stellar.
Finally in the kidneys the retention of sodium (caused by excess
insulin) has now been corrected and his hypertension has resolved. The
pathophysiology of Syndrome X is predictable. The reversal of this
syndrome is also predictable and repeatable! As a matter of fact this
exact method is being employed by over 700 chiropractic practices in the
United States and Canada as well as many medical practices. Tens of
thousands of patients have experienced same benefits described here.
The Chiropractic physician (because of his/her training and philosophy)
can become a leading force in helping to reverse this terrible syndrome.
Let this article be a call to action!
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