|
|
|
Insulin and Aging |
 |
(READING TIPS: For fast reading, scan through the topic headings in BOLD BLACK, important conclusions in BOLD BLUE, and " Must Know " in BOLD RED. To jump to specific sections in this article, click on the respective LINKS in the Contents.)
Contents
Insulin
Carbohydrates and Insulin
Insulin Resistance
Cellular Response to Insulin Resistance
Results of Insulin Resistance
Treatment Goals in Insulin Resistance
Diet and Lifestyle Interventions
Nutritional Interventions: Supplementation
1. Chromium
2. Magnesium / Calcium
3. Vanadyl Sulfate
4. Fish Oils
5. Coenzyme Q10
6. Vitamin C , Lysine, Proline
Summary
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.
Selected References
Dominguez LJ, Barbagallo M, Sowers JR, Resnick LM.
Magnesium responsiveness to insulin and insulin-like growth factor I in erythrocytes
from normotensive and hypertensive subjects. J Clin Endocrinol Metab 1998;83:4402-4407.
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
intraplatelet free calcium concentration and insulin resistance in essential
hypertensive patients. Hypertension 1997;29:531-536.
Striffler JS, Polansky MM, Anderson RA. Overproduction of insulin in the chromium-deficient
rat. Metabolism 1999;48:1063-1068.
Riales R, Albrink MJ. Effect of chromium chloride supplementation on glucose
tolerance and serum lipids including high-density lipoprotein of adult men.
Am J Clin Nutr 1981;34:2670-2678.
| ||||||||||
