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[IP] Article-Insulin Resistance

by Michael Lam, MD , MPH, ABAAM
Specialist in Preventive and Nutritional Medicine
Board Certified, American Board of Anti-Aging Medicine

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

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.
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

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.
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