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Scientists have known that calorie restriction, when accompanied by optimum
nutrition ( also known as C.R.O.N.) can extend lifespan of animals 30 to 230
%, depending on the species. Primate studies are in process. It will be another
10 years before we known the final results, and no doubt, results will then
lead to even more questions. What we do know, from major studies of centenarians
already underway, is that the demographics have nothing much in common.
Many centenarians are smokers, for example. They come from all over the world
without a favoring any geographic location in particular. However,
there are 3 consistent blood metabolic indicators of
all centenarians that are relatively consistent: low sugar, low triglyceride,
and low insulin. All three are relatively low for age. Among these
three variables, insulin is
the common denominator. The level of insulin sensitivity of the cell is one of the
most important markers of lifespan.
Insulin
When
we eat, the food we consume turns into sugar once inside the body. This is particularly
true of carbohydrates such as potato or rice. This sugar circulates within us,
and under the influence of insulin, is absorbed into the surrounding cells and
tissue where it is metabolized into energy, or in the case of excessive sugar,
stored for future use.
Insulin is commonly known as a hormone secreted by the beta cells of the pancreas
that lowers the blood sugar by promoting their transport from the blood stream
to the cell. Cells, in turn, use sugar as fuel to generate ATP, the energy currency
of the body. Insulin's real purpose in our body is to help the body store excess
nutrients.
When we take in excessive sugar and once the body sense that there is too
much, insulin is released to take the excess sugar out of the bloodstream
and store it by converting it into glycogen. The amount of glycogen stored in
the liver is small. The entire reserve cannot last more than a day of activity.
Excess sugar above and beyond what can be stored as glycogen is then stored
as palmitic acid, a saturated fatty acid. Now you see how excessive sugar (calorie) intake leads to extra fat
in the body.
Carbohydrates and Insulin
Carbohydrates we eat fall into two groups -complex
and refined. Examples of complex carbohydrates include whole grains,
vegetables, whole fruits, nuts, and legumes. Examples of refined carbohydrates
include white flour, white rice and sugar. All
carbohydrates are broken down into sugar once inside the body. Some are broken
down slower than the others. The ones that break down slowly are
called low-glycemic carbohydrate, such as legumes, apples , cherries, above
ground vegetables. Other carbohydrates break down faster into sugar. These are
called high glycemic carbohydrates. Examples are wheat, rice, tubers vegetables
(potatoes), watermelon, and banana.
Excessive consumption of high glycemic index carbohydrate causes the most
sugar storage in the body. Excessive intake
of all carbohydrate, especially the high-glycemic type, is the primary culprit
in the development of insulin resistance.
Carbohydrates, once broken down into sugar inside the body, promote insulin
release from the pancreas. Each time there is a surge of sugar in the diet
(as in taking a big bowl of noodles), there is a corresponding surge in blood
sugar, and an immediate surge in insulin as the body tries to move the excessive
sugar out from the blood and store it somewhere else. This
process is an automatic one as
the body balances itself to maintain a constant blood sugar level.
While sugar is a good source of energy, it was
never designed to be the primary source of energy. Sugar is meant
to be an emergency short-term fuel, like when you are running away from
a tiger. Yes our brain will burn sugar for energy, but it doesn't have to. It
can do very well from burning ketones from fats. Fats and triglyceride can then
be converted into sugar for emergency use. The
body prefer fat as the energy source.
Furthermore, the body can survive very well without simple refined carbohydrate
provided that adequate protein and fat is on board to provide the calories required
for metabolic functions. Our body is designed to run on fats as a fuel and
not sugar. In fact, excess sugar is stored as fat because fat is the preferred
source of fuel. The body can store a lot of fat but only limited amount of sugar.
Sugar is a recognized toxic as far as the body
is concern if present in excessive amounts. The body's job is to get
rid of these excessive sugars. The best way is to burn it. What it cannot
burn will be stored as glycogen, and when that fills up, it turns into fats.
When you eat sugar, the body will burn sugar first and you stop burring fat.
First sugar from the blood stream will be used, and then stored sugar in the
form of glycogen is next. Last, sugar from the muscle will be used. When these
supplies are exhausted, energy is obtained from burning the saturated fats in
our adipose that originated as sugar.
When you take a high carbohydrate diet such as pasta, the carbohydrate changes
into sugar inside our body. Our blood sugar goes up quickly. The body does
not welcome this rush. It panics. The pancreas is immediately signaled to release
insulin in order to facilitate the movement of sugar away from the blood stream
into the cell, thereby lowering the blood sugar. This reaction is
a back up plan for something that should not happen too often in our body, as
our body was never designed to process sugar in large quantities in a short
time. The pancreas tries to do its best to lower sugar through the release
of the hormone insulin. But it generally overcompensates and
secretes more than we need at times, especially when the pancreas is chronically
stressed. The result - your blood sugar goes down excessively.
At this time, our body secretes sugar-raising hormones such as cortisone
and epinephrine to raise the blood sugar back up to normal level
as a compensatory mechanism. This yo-yo effect happens each time there
is a sudden sugar load, and it is one of the biggest stressors in our body.
With the release of sugar raising hormones, our
blood sugar is finally stabilized, but it comes at a price. The epinephrine makes us nervous. It also stimulates the heart
to beat faster. Cortisol is a catabolic hormone and causes breakdown of peripheral
tissues. This yo-yo effect of unstable blood sugar signals the brain to crave
more carbohydrate as a way to increase sugar anyway it can for survival, not
know what is coming next. Signals from the brain creates a craving soon after
a meal is finished, telling us to eat more carbohydrate, like a big bowl
of cheerios, or a pie between meals. This in turn causes a surge in our
blood sugar. This never ending viscous cycle of
sugar feeding on more craving on sugar turns our body into a carbohydrate
addict and makes us fat.
Insulin Resistance
The cycle of sugar spikes mentioned above cannot go on forever. Each
time it happens, the body is stressed. In response, the body puts out anti-stress
hormones from the adrenals called cortisol. In
time, the adrenals becomes exhausted from this production, just as
the pancreas is exhausted from the constant
insulin output which it is not able to keep
up with. A metabolic dysfunction is
created. The pancreas takes a beating and ultimately becomes exhausted. When
this happens to the pancreas, the amount of insulin secretion is reduced and
resulting high blood sugar rises out of control, creating a condition called
adult onset diabetes mellitus (also called Type 2 diabetes) that affects over
16 million Americans.
While the pancreas is being stressed,
the adrenal glands are also becoming exhausted from putting
ever increasing amount of cortisol needed to raise blood sugar from the transient
hypoglycemic episode after each high carbohydrate meal The result is adrenal
exhaustion. The production of cortisol and a wide variety of sex
hormones, including progesterone, is reduced as well. The symptoms include chronic
fatigue, hormonal imbalance, estrogen dominance, and reduced sex drive, among
many other symptoms.
But before we get to this stage of
exhaustion both in the adrenals and the pancreas, the cell has a self-protecting mechanism in place. It
has an internal braking mechanism. This is a protective function to avoid the
toxic effects of high insulin and high sugar. The cell is trying to close
itself from the entry of sugar and glycogen. In other words, the cell, when
flooded with insulin chronically, start to down-regulate itself and start shutting
itself off from responding to insulin. Their receptor activities and the
number of receptors decrease so they don't have to deal with the undesirable
insulin effect. Instead of following insulin's instruction to allow sugar into
the cell, they refuse to listen to insulin's command and keep the sugar out.
In this state, the blood insulin level is high as the pancreas is on an overdrive
to produce more insulin. The blood sugar level is also high as the cells refuse
the entry of sugar. This state is called insulin
resistance. It is the fundamental a metabolic dysfunction, and
may be considered a pre-diabetic state. This state of insulin resistance
alone, evidenced by a high blood sugar level and high blood insulin level, is
commonly known as Syndrome X or Metabolic Syndrome,
is accompanied by other hyperinsulinemia symptoms such as high blood
pressure, high LDL "bad" cholesterol, low HDL "good" cholesterol, and high triglyceride.
However, it is important to note that not all people who have high insulin and
high blood sugar level have Syndrome X.
The difference between adult onset diabetes mellitus ( also called Type 2 diabetes)
and insulin resistance is simple. The key problem leading to type 2 diabetes is insulin
resistance coupled with the inability to secrete enough insulin to overcome
that resistance. The blood sugar level is
high due to insufficient insulin. With insulin resistance, both blood sugar levels and blood insulin
levels are high. Type 2 Diabetes is the end stage result of metabolic dysfunction
in the processing of sugar in our body.
Cellular
Response to Insulin Resistance
Different cells respond to insulin differently. Some cells
are more resistant than others, as some cells are incapable of becoming very
resistant. The liver becomes resistant first, followed by the muscle tissue
and lastly the fats.
The sugar in our blood is determined by the amount we eat from our diet and
the amount of sugar from the liver. During the night, in the case of insulin
resistance, the liver is putting out sugar as a way to keep the body going,
as it is not listening to the command of insulin. In the morning, the fasting
blood sugar is therefore elevated. In the muscles, insulin resistance means
that sugar is not transported into the muscle cells for metabolism and energy
generation. More sugar is therefore outside, further contributing to an increase
in blood sugar.
The more you expose the cell to insulin, the more
the cell becomes insulin resistance in a bid to protect itself. This
process progresses through life as our cells progressively become more insulin
resistant. It cannot be avoided, and that is why one of the prominent signs
of aging is insulin resistance. Those who are able to reduce the rate of insulin
resistance will live longer. In order words, the rate of insulin resistance
determines our rate of aging.
Results of Insulin Resistance
When the cell resists insulin to come in, the insulin level outside the cell
increases. This increased circulating insulin level has many negative effects,
including the following:
1.
Hypertension and Cardiovascular Disease. Magnesium
is an important muscle relaxant and a critical mineral required for over 300-enzymatic
reactions in the cell. When the cell is insulin resistant, magnesium cannot
be stored. The intracellular magnesium level declines. Without the
relaxing effects of magnesium, muscles of the blood vessel contracts, leading
to hypertension, and further reduction of glucose and insulin delivery
to the cell as peripheral vascular circulation is compromised. Without
this, blood vessels also contract. Increased insulin in the blood also leads
to sodium retention and increase in fluid, worsening
the hypertensive state. The combination
of hypertension and fluid retention is a deadly combination, leading to angina
and congestive heart failure. Separately, without sufficient intracellular
magnesium, the energy production cycle at the cellular mitochondria is less
efficiently, and the body becomes more tired and fatigued easily. Insulin
production is also reduced as magnesium is necessary for insulin production.
2. Angina. Increased Insulin also reduces the
production of nitrous oxide, a potent vasodilator, from the endothelium.
With less nitrous oxide, the vascular system is in a state of vasoconstriction,
further worsening the hypertensive stated cause by reduced magnesium mentioned
above. Severe constrictions can lead to angina
(chest pain) and heart attack.
3. Altered Lipid Profile. Insulin mediated lipid level in the blood.
The amount of triglyceride in the blood is a direct reflection of the amount
of sugar intake in the diet. There is almost a direct correlation between triglyceride
and insulin levels. Insulin resistance is characterized by high triglyceride, low HDL ("good") cholesterol, high LDL ("bad")
cholesterol levels.
4. Artherosclerosis. The
initiation of atherosclerosis is thought by many researchers today to result
from injury to the layer of endothelial cells which normally form the luminal
surface of blood vessel walls. A blood environment high in sugar is laddened
with free radicals. These free radicals cause the endothelium to be damaged.
The damaged endothelium becomes inflamed. This inflammatory process can be measured
in the blood and evidence by the elevation of a substance called C Reactive Protein.
As the endothelium's structure is inflamed, it becomes permeable to lipoproteins,
particularly low-density lipoproteins (LDL) and macrophages. These particles
will enter into the site of injury, accumulate cholesterol as cholesterylester
and develop into foam cells. Being adhesive, the cells will attract other unwanted
substances , initiating the arthersclerosis process with a fatty streak, eventually
leading to plaque formation. The unwanted plaque consist of lipids (fats), complex
carbohydrates, blood, blood products, fibrous tissue and calcium deposits. Plaques
have a large amount of deposits comprising LDL-cholesterol and a variety of
cholesterol carrier such as lipoprotein (a). A high LDL or lipoprotein (a) therefore
is an important risk factor for atherosclerosis.
5. Thrombus. Increase platelet adhesiveness and increase
coagulation of the blood leads to thrombus formation.
6. Osteoporosis. Insulin is a master hormone that
controls many anabolic hormones such as growth hormone, testosterone, and progesterone.
In insulin resistance, the anabolic process is reduced. Bone is build upon the
command of such hormones. When these hormones are reduced, the amount of bone building is reduced, and the amount of calcium excreted
is increased.
7. Reduced Sexual Function. Insulin helps control
the manufacture of cholesterol that is the precursor of all sex hormones, including
estrogen, progesterone, and testosterone, and DHEA. The more insulin resistance,
the lower the DHEA level
8. Inflammatory Response. Excessive sugar leads to
an oxidative process called glycation. Glucose is glycagted and becomes a sticky
substance called advanced glycated end products (AGE) when it is combined with
protein and oxygen. This glycation damages the protein to the extent that adhesive
white blood cells are attracted to the area to carry it away as it is undesirable.
White blood cells imitate an inflammatory reaction, leading to arthritis and other inflammatory diseases.
9. Hypothyroidism. The conversion from T4 to T3 in
the liver is lowered, leading to hypothyrodism.
Treatment Goals in Insulin Resistance
1. Laboratory : Reduce insulin level as much as possible.
There is no limit on how low. Fasting insulin
level should be taken and should be less than 10
mU/ml
. It has been shown that a fasting
insulin level of greater than 15 mU/ml
carries a
four-fold increase risk of heart disease. Triglyceride should also be reduced to less than 100
mg/dl, and fasting blood sugar no more than 90mg/dl. Lp(a), if elevated, should
be reduced to less than 20 mg/dl, and
homocysteine, another risk factor, should be reduced to less than
8 umol/l. C-reactive protein should be reduced
to less than 3 mg/dl. While fasting
insulin is a good measurement of insulin level, it is not widely used because
of high variability among people. You can have high insulin level
and not be in insulin resistance state. There is a variety of insulin secreting
tumors that can attribute to high insulin state, for example.
2. Weight: Control. 90% of those with insulin resistance
are obese. Central obesity and increased abdominal girth is a hallmark of
insulin resistance. Maintain the ideal body weight . Total body fat
should be less than 20% for men and less than 27% for women.
Diet and Lifestyle Interventions
Insulin resistance is a reversible condition. Follow
these steps:
1. Reduce intake of refined carbohydrates will reduce sugar
load. This is the most effective way. A low
carbohydrate diet low in refined and high glycemic index should be
the focus. Complex and low glycemic index carbohydrates are also acceptable.
2. Resistance training exercise increases insulin sensitivity.
While any exercise is good for the body, resistance training exercise increase insulin sensitivity. Aerobics
exercise also facilitate the buring of excessive sugar in the body and reduce
insulin requirement. To be effective, exercise should be consistent. A
total of 30 minutes of moderately intense aerobics exercise as tolerated
( broken down in to 10 minute blocks is acceptable) is the minimum.
3. Use fat as the primary fuel and not protein. Maintain
neutral protein balance with 1-2 grams of protein per kg weight. Approximately
15% of your calories should be from protein.
Animal proteins are acceptable as long as they are not grain fed ( contain up
to 50% saturate fat) but grass fed ( contain less than 10% saturated fat and
high in omega-3 oils.). Protein use is not encouraged because its breakdown
product, amino acid, enhances insulin secretion. Fats do not do this.
Excessive proteins also cause acidity in the body. If you eliminate the need
to burn sugar, you don't need much sugar in your diet even if you are insulin
resistant. Therefore, you want to convert from a sugar burner to a fat burner.
Carbohydrates are still necessary (40% of calories),
but you have chosen the right kind - low glycemic complex carbohydrates such
as green leafy vegetables. Get 45%
of your calories from fats (mostly unsaturated), but not from saturated fats.
It should be a low saturated fat diet because
we already have a plentiful supply. Focus on mono-unsaturated fat such as that
from olive oil and nuts.
Nutritional Interventions: Supplementation
Available
information and clinical experience suggests that some substances positively
influence insulin resistance. Minerals, including magnesium, calcium, chromium,
and vanadium, appear to have associations with insulin resistance or its management.
Amino acids, including L-carnitine, also might play a role in the reversal of
insulin resistance. Additional nutrients such as coenzyme Q10, and lipoid acid
appear to have therapeutic potential.
1. Chromium
Chromium is an essential trace mineral nutrient. Like iron, zinc, selenium,
copper, and several other essential trace minerals, chromium plays a critical
role in maintaining normal health and well being.
Chromium helps insulin to work efficiently. Many well-controlled clinical studies
through the years show blood glucose improvements in the patients tested.
Important studies include one from the Human Nutrition Research Center of the
United States Department of Agriculture conducted in 1996. Researchers in the
study randomized 180 adult-onset diabetics into 3 groups of 60 each: one group
received placebo twice per day, the second received 100 mcg twice daily of chromium
as chromium picolinate and the third received 500 mcg of chromium as chromium
picolinate twice daily. Their blood work was examined at baseline, at 2 months
and at 4 months. The patients were told to remain on their anti-diabetic medications
and continue with their diets and activity levels as before. The
results were impressive: blood glucose, insulin levels, cholesterol and Hemoglobin
A1C all decreased, with the higher dose generally (but not always) more effective
than the 200 mcg.
Dietary Intake of Chromium
Few foods are rich sources of chromium in the Western diet, the best being organ
meats, mushrooms, wheat germ, broccoli and processed meats. Data from U. S.
Government sources show that the great majority of Americans get less chromium
in their daily diets than the amount recommended by nutrition experts. The RDA
Committee recommends 50-200 mcg of chromium/day; the vast majority of Americans
get less than 50 mcg/day. It is estimated that as high as 80% of all Americans
is deficient in this mineral and may not know it.
Unfortunately, it is not possible to get enough
chromium by food alone without excessive calories and obesity. To obtain 200
mcg by food alone, one has to take in over 8,000 calories a day. A
large part of the problem has to do with processed food and the increase consumption
of sugar. The modern American consumes an average of 120 pounds of sugar per
year from all sources. These ingested sugars (such as table sugar and products
made with it) bring insulin and chromium into the blood and cause chromium to
be excreted in the urine after it's through working with the insulin on the
increase in blood sugar.
Inadequate chromium intakes from processed food, increased chromium losses due
to increased sugar consumption, decreasing chromium tissue levels as we age
are the main reasons as to why the majority of Americans and diabetics are deficient
in chromium. Improvements in blood sugar in significant numbers of diabetics
and pre-diabetics with modest chromium supplementation were observed. It should,
however, take place alongside the two other proven ways of normalizing sugar:
low-fat, high complex-carbohydrate of low glycemic index type diets for weight
loss/weight maintenance and regular exercise.
Assessment of Chromium Status
Deciding whether or not someone is chromium deficient cannot be done easily.
Routine blood test is generally not accurate. The only generally accepted method
for assessment of chromium status is to supplement an individual who has abnormalities
of blood sugar, cholesterol, triglycerides or all three with the trace clement.
If the laboratory values improve, then chromium insufficiency is presumed.
Safety of Chromium
Chromium comes in various forms. The dietary form is called chromium tri-valent.
This is non-toxic and necessary for essential body function. Chromium in
its hexa-valent form is used in industries and is highly toxic.
It is extremely difficult to poison laboratory animals with oral dietary tri-valent
form of chromium. For example, cats fed 1,000 mg of trivalent chromium per day
showed no signs of toxicity. The equivalent daily dose for a 150 lb person would
be approximately 35,000 mg per day or 3.5 million mcg per day. In terms of the
number of 200 mcg tablets, this would be 175,000 tablets per day for a human.
Forms of Chromium
There are various forms of dietary chromium. These vary in bioavailability (absorption
and retention) and biological activity (ability to potentate and harmonize insulin).
Inorganic chromium such as chromium chloride is unfortunately poorly absorbed
(0.5-2%) and has little effect on insulin because it must first be converted
into a biologically active form, which the body has a limited ability to do.
The two most popular forms of organic chromium are niacin-bound chromium (also
called chromium polynicotinate) and chromium picolinate. Although picolinate
and polynicotinate sound alike, there are significant differences between the
two compounds.
Chromium Polynicotinate is actually
a family of niacin-bound chromium compounds. Niacin-bound chromium strongly
potentiates insulin - chromium's most vital function - while chromium picolinate
is less effective comparatively speaking.
Niacin-bound chromium such as chromium polynciotinate is also more bioavailable
than chromium picolinate. An Animal study at the University of California found
that chromium polynicotinate is better absorbed and retained up to 311% better
than chromium picolinate and 672% better than chromium chloride. Such high bioavailability
means that chromium polynicotinate can deliver more benefits that chromium has
to offer.
2. Magnesium / Calcium
Magnesium: A deficiency in magnesium is a common occurrence in
patients with insulin resistance, especially those with hypertension.
Some doctors have discovered that among normotensive and hypertensive patients,
a higher magnesium level corresponded to a greater degree of sensitivity to
insulin. Magnesium deficiency results in impaired insulin secretion and magnesium
replacement restores insulin secretion.
In developed countries, magnesium seems to be lacking in a large majority of
the population. The recommended daily allowance for magnesium is 350 mg a day.
In America, 80% of the population fails to meet this standard. The recommended
dose is 500 to 1,000 mg, while maintaining a magnesium:
calcium ratio of 1:1.
Calcium: Calcium supplements have been found to be effective
in some cases. An experiment comprising of 20 non-diabetic and hypertensive
subjects was conducted. Subjects were given standardized diets consisting of
500 mg of dietary calcium per day for a period of four weeks. Following this
period, another 1,500 mg of calcium or placebo was given daily in a randomized,
double blind fashion for another eight weeks. After this intervention period,
treated patients were found to have decreased fasting plasma insulin levels
and a significant increase in insulin sensitivity.
3. Vanadyl
Sulfate
This is another trace mineral associated with sugar regulation.
Vanadium or vanadyl sulfate regulates fasting blood sugar levels and improves
receptor sensitivity to insulin. It is an effective mineral for treating type
2 diabetic individuals with insulin resistance.
Boden et al conducted a single-blinded, placebo-controlled study on the effects
of vanadyl sulfate on eight male and female subjects with type 2 diabetes. The
subjects were given 50 mg of vanadyl sulfate twice a day for a period of four
weeks, followed by a four-week placebo phase. The results showed slight improvements
in fasting glucose and hepatic insulin resistance following the treatment period.
However, the level of insulin resistance was maintained throughout for those
on the placebo.
In another study, Halberstam et al gave 100 mg of vanadyl sulfate daily for
three weeks to obese type 2 diabetic patients as well as non-diabetic subjects.
There was a significant decrease in fasting plasma glucose and a significant
improvement in insulin sensitivity in the treated patients. There was, however,
no change detected in the obese non-diabetic subjects.
Cohen et al also looked into the effects of vanadyl sulfate at 100 mg daily
in type 2 diabetic patients following a three-week intervention period. His
results showed a beneficial effect of vanadyl sulfate on improving both hepatic
and peripheral insulin sensitivity. These effects were even sustained for another
two weeks after the vanadyl sulfate supplements were stopped.
In another study, Halberstam et al gave 100 mg of vanadyl sulfate daily for
three weeks to obese type 2 diabetic patients as well as non-diabetic subjects.
There was an obvious decrease in fasting plasma glucose and a significant improvement
in insulin sensitivity in the type 2 diabetic patients. There was, however,
no change detected in the obese non-diabetic subjects.
We get about 50 to 60 mcg of vanadyl sulfate via our diet. If we have diabetes,
the dosage required may be 1000 times more.
Sad to say, the potency of vanadium compounds has not been extensively tested in
clinical trails. The dosage recommended
is therefore at 25 mg 1 to 3 times a day for a short-term use.
4. Fish
Oils
Omega-3 fatty acid increase insulin sensitively at the cellular
membrane by increasing the fluidity of the cell membrane. Omega-3
also have endothelial membrane stability benefits and reduces inflammatory
response.
Fish oils is rich in omega-3 essential fatty acids (omega 3 EFAs) and its active
ingredient EPA and DHA. Common fish oil capsules
found in health food stores contain approximately 180 mg of DHA and 120 mg of
EPA. 1000 -3,000 of DHA/EPA from fish oil is recommended. If you dont
like to take fish oil, consider eating Atlantic salmon, which contain about
2.5 grams of EPA/DHA per 4 oz serving. It is important to take some vitamin
E along with omega-3 fatty acid to prevent fatty acid oxidation which can be
counterproductive. If taking too much fish oil causes you to have a "fishy"
burp, consider taking flaxseed. It also contain DHA and EPA, though at a much
lower concentration.
5. Coenzyme Q10
Coenzyme Q10 (CoQ10) is a promising nutritional intervention for insulin resistance,
at least among subjects with hypertension. Singh et al conducted an eight-week
randomized, double blind trial comparing the use of a water-soluble form of
CoQ10 (60 mg twice daily) to a vitamin B complex in 59 hypertensive patients.
Their results indicated CoQ10 at this dose lowered
glucose and fasting insulin levels, suggesting possible improved insulin resistance.
CoQ10 supplementation also resulted in improvements in blood pressure, lipid
profiles, and blood levels of the antioxidant vitamins A, C, E, and beta-carotene.
Measured parameters associated with oxidative stress decreased with CoQ10 supplementation.
The only observed change in the group taking the B-vitamin complex was increases
in Vitamin C and beta-carotene.
6. Vitamin C , Lysine, Proline
High sugar level is a potent generator of free radicals. Vitamin C's antioxidative
effect in mopping up unwanted free radical and preventing them from attacking
the endothelium is well established. In addition to this, there is another important function of Vitamin C - that in the
formation of critical collagens responsible for keeping the vascular system
pliable and healthy. In the blood vessel, collagen, together with
elastic fibers, forms an integral part of the subendothelial connective tissue
just below the endothelium ( a single layer of very thin squamous epithelial
cell that lines all blood vessels), as well as the external elastic lamina.
During the aging process, the wear and tea of collagen fibers must be replaced
and maintained. These three nutrients ensure that the substrates needed for
optimum collagen building and maintenance is present. Furthermore, lysine
and proline have unique features of having a high affinity for sticky lipoproteins.
With high level of these two amino acids, plaques already formed can be dissolved
and washed out of the body. The end result - healthier vascular walls and reduced
risk of cardiovascular disease.
Summary
It is clear that insulin is a key determinant of the aging process. In
fact, it determines more about aging than almost any other indicators we have.
As we age, our insulin level increase. Those who can slow down the velocity
of this process are in effect extending their longevity.
Fasting blood sugar, together with complete lipid profile, will give
us a good status report on the level of insulin activity and insulin resistance
in the body. It is associated with almost all chronic degenerative diseases,
including hypertension, diabetes, cardiovascular disease, and stroke. Over 60
million Americans suffer from this a silent epidemic of massive proportions.
Fortunately, insulin resistance can be reversed
and cured through lifestyle adjustments, diet, exercise, and proper nutritional
supplementation of various natural non-toxic compounds.
Insuin and cortisol are two
catabolic hormones in the body. They are destructive and are pro-aging. Maintaining
a low insulin level is a key , if not the key to longevity.
About The Author
Michael Lam, M.D., M.P.H., A.B.A.A.M.
is a specialist in Preventive and Anti-Aging Medicine. He is currently the Director
of Medical Education at the Academy of Anti-Aging Research, U.S.A. He received
his Bachelor of Science degree from Oregon State University, and his Doctor
of Medicine degree from Loma Linda University School of Medicine, California.
He also holds a Masters of Public Health degree and is Board Certification
in Anti-aging Medicine by the American Board of Anti-Aging Medicine. Dr. Lam
pioneered the formulation of the three clinical phases of aging as well as the
concept of diagnosis and treatment of sub-clinical age related degenerative
diseases to deter the aging process. Dr. Lam has been published extensively
in this field. He is the author of The Five Proven Secrets to Longevity
(available on-line). He also serves as editor of the Journal of Anti-Aging
Research.
For More Information
For the latest anti-aging related health issues, visit Dr. Lam
at www.LamMD.com. Feel free to email
Dr. Lam at dr@LamMD.com if you have any questions.
Reprint Information
This article may, in its unabridged, unaltered form and in its entirety only,
be reprinted and republished without permission provided that it is for personal
and non commercial education use only and further provided that credit be given
to the author, with copyright notice and www.LamMD.com
clearly displayed as source. Written permission from Dr. Lam is required
for all other use.
©2002 Michael Lam, M.D. All Rights Reserved.
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Magnesium responsiveness to insulin and insulin-like growth factor I in erythrocytes
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Hua H, Gonzales J, Rude RK. Magnesium transport induced
ex vivo by a pharmacological dose of insulin is impaired in non-insulin-dependent
diabetes mellitus. Magnes Res 1995;8:359-366.
Nadler JL, Buchanan T, Natarajan R, et al. Magnesium deficiency produces insulin
resistance and increased thromboxane synthesis. Hypertension 1993;21:1024-1029.
Sanchez M, de la Sierra A, Coca A, et al. Oral calcium supplementation reduces
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