I?ve gathered a number of resources for you regarding insulin
resistance/insulin levels. Some of them cover what you said you
already knew (But I don?t know what you know and what you don?t know!
Feel free to simply ignore the information you already know!)
Due to copyright restrictions, I am only able to post small amounts
of information-please check each web site for complete information.
Please note that all of my sources come from reliable and reputable
web sites, and not sites that sell supplements, books or snake oil.
Content posted on Google Answers is also copyrighted, and you will
need to check with the Google editors before sharing this information.
You may certainly post a link to this answer, or links to individual
snippets, but to copy the information, you will need permission. Send
an email to:
?Should there be any disturbances to the binding of insulin to the
receptors, or of the receptor response to insulin, there will be
reduced insulin activity, or insulin resistance. If insulin is not
functioning, there is reduced glucose entry into the cells, which is
detected by the pancreas as raised blood sugar (hyperglycaemia). The
pancreatic response is then to produce more insulin,
(hyperinsulinaemia) to compensate for the lack of cellular response to
the hyperglycaemia. Insulin resistance has been estimated to occur in
up to 25% of the ?normal? non-diabetic population of the USA5, at
least as commonly as obesity. Poor insulin activity and chronically
elevated blood insulin levels are associated with a number of serious
diseases. Among these, hypertension, obesity, ischaemic heart
disease9, dyslipidaemia10 and non-insulin-dependant diabetes
mellitis11 are major diseases in which insulin resistance has a
clearly demonstrated relationship with the aetiology and clinical
course of the disease. The cluster of findings of hypertension,
dyslipidaemia and hyperinsulinism has been labelled Syndrome X.?
?Several factors are known to promote insulin resistance. There is
a strong genetic component as illustrated in the Aboriginal
population, where insulin resistance has been found in small
populations still living a traditional lifestyle. This may well be
protective under conditions of feast-and -famine where efficient fat
deposition is advantageous, but when exposed to the Western lifestyle
results in NIDDM rates 10x the Australian population33. The same
predisposition may be present in Melanesian, Polynesian and
Micronesians, in whom obesity occurs in 70% of women and 65% of men.
Obesity, particularly central obesity, induces peripheral tissue
insulin resistance, and overeating produces hyperinsulinism which
promotes further weight gain. Thus a vicious cycle ensues of
increasing weight gain and increasing hyperinsulinism. However,
obesity itself does not necessarily create insulin resistance. There
is an interaction between obesity and lack of exercise. A sedentary
lifestyle, as is usual in Western society, predisposes to insulin
resistance. One third of Australians have no exercise, and only one
third exercise at a medium or high level35. Vigorous regular walking
has been shown to result in a 36% decrease in the ratio of
insulin/glucose concentrations with reduced endogenous insulin
requirements, and reduced fat stores36. Exercise training apparently
reverses insulin resistance by enhancing the recruitment of GLUT-4 to
the cell surface. GLUT-4 acts to promote insulin-stimulated glucose
transport in fast-twitch muscles37, and is an alternative glucose
transport for skeletal muscle.
Dietary factors are also implicated in the development of insulin
resistance. High carbohydrate diets decrease insulin receptor numbers,
probably as a result of the increased cellular contact with insulin
and resultant receptor down regulation.
A number of studies have shown that high carbohydrate diets increase
plasma triglyceride levels, VLDL cholesterol, insulin and glucose
concentrations in NIDDM40,41 and in post-menopausal women.?
?Diets high in saturated fats and trans-fatty acids have been shown to
decrease membrane fluidity and decrease insulin receptor binding, thus
promoting insulin resistance43. Interestingly, a high omega-6:omega-3
EFA diet is also detrimental to insulin receptor sensitivity. This is
seen in the Israeli diet where the high intake of soya oil which is
predominantly omega-6 EFA results in an omega-6 :omega-3 EFA of 25:1,
and there is a high prevalence of cardiovascular disease,
hypertension, NIDDM and obesity in addition to other diseases.?
?Insulin stimulates glucose uptake into tissues, and its ability to
do so varies greatly among individual persons. In insulin resistance,
tissues have a diminished ability to respond to the action of insulin.
To compensate for resistance, the pancreas secretes more insulin.
Insulin-resistant persons, therefore, have high plasma insulin levels.
The syndrome can be defined as a cluster of abnormalities, including
obesity, hypertension, dyslipidemia and type 2 diabetes, that are
associated with insulin resistance and compensatory hyperinsulinemia.
However, a cause-and-effect relationship between insulin resistance,
these diseases and the mechanisms through which insulin resistance
influences their development has yet to be conclusively demonstrated.?
?The lack of practical, inexpensive, reliable serum tests means that
the diagnosis of insulin resistance can, at best, be made on the basis
of strong clinical suspicion (Table 1). This is reasonable because the
goal is to identify a condition whose treatment is neither risky nor
expensive because it involves sensible lifestyle modifications and
careful monitoring for the component diseases of the syndrome.?
"Increases in body weight reduce insulin action (although in some
patients,insulin resistance precedes the obese state).
Physical activity reduces insulin resistance.
Weight loss reduces insulin resistance.
Alcohol reduces insulin resistance.
Saturated fat intake increases insulin resistance in animals.
Linoleic acid (18:2n-6) in muscle phospholipids is positively
correlated with hyperinsulinemia.
Long-chain polyunsaturated fatty acids (carbon chain length 20?22) in
muscle phospholipids are inversely related to hyperinsulinemia
andpositively related to insulin sensitivity.?
Here is a slide show that covers many of your questions:
?Insulin resistance appears to be a common feature and a possible
contributing factor to several frequent health problems, including
type 2 diabetes mellitus, polycystic ovary disease, dyslipidemia,
hypertension, cardiovascular disease, sleep apnea, certain
hormone-sensitive cancers, and obesity. Modifiable factors thought to
contribute to insulin resistance include diet, exercise, smoking, and
stress. Lifestyle intervention to address these factors appears to be
a critical component of any therapeutic approach. The role of
nutritional and botanical substances in the management of insulin
resistance requires further elaboration; however, available
information suggests some substances are capable of positively
influencing insulin resistance. Minerals such as magnesium, calcium,
potassium, zinc, chromium, and vanadium appear to have associations
with insulin resistance or its management. Amino acids, including
L-carnitine, taurine, and L-arginine, might also play a role in the
reversal of insulin resistance. Other nutrients, including
glutathione, coenzyme Q10, and lipoic acid, also appear to have
?Insulin resistance syndrome (IRS), also called metabolic syndrome,
is a clustering of risk factors for a number of disorders, including
type 2 diabetes mellitus, polycystic ovary syndrome (PCOS),
atherosclerosis, and cardiovascular disease (CVD). Collectively, these
conditions result in an enormous burden of morbidity and mortality and
billions in annual health-care expenditures, explains W. Timothy
Garvey, MD, chair of UAB's Department of Nutrition Sciences.
"In many patients, several ? and sometimes all ? of these conditions
coexist. In 1988, researchers recognized the common underlying
abnormality was insulin resistance," he says. "Because it usually
develops long before associated conditions appear, identifying insulin
resistance syndrome allows clinicians to recommend lifestyle
modifications that reduce risks of developing overt disease."
"Insulin resistance, which results from defects in insulin's
ability to stimulate muscle cell glucose transport, has complex
genetic and environmental causes. We now suspect the syndrome occurs
early in life, eventually producing the cluster of abnormalities that
confer disease risk," Garvey says.
Many IRS characteristics are independent risk factors for both type 2
diabetes and CVD. Studies show insulin resistance is the earliest
detectable prediabetic metabolic defect and is the most powerful risk
factor for subsequent progression to overt diabetes (Clin Cornerstone.
Insulin sensitivity varies widely among apparently healthy
individuals, and the degree of resistance positively correlates with
increased risk for associated diseases, Garvey explains. "Insulin
resistance syndrome provides the common ground for the pathogenesis of
?Insulin-resistance is defined as any condition in which the plasma
insulin concentration is higher than the blood sugar level suggests it
should be. It is therefore, not unreasonably, interpreted to mean that
insulin is not as effective at lowering the blood sugar level as it
should be, i.e. there is "resistance" to its action. The nature of
this "resistance" is a major unsolved problem in medicine and
physiology, although recents insights have dispelled much of the
mystery, and therefore opened the way for new and highly promising
?One way in which the tissues can become truly "resistant" to
insulin's actions results from the removal of insulin receptors from
the surfaces of their cells (so-called "down regulation" of insulin
?A new system for classifying carbohydrates calls into question
many of the old assumptions about how carbohydrates affect health.
This new system, known as the glycemic index, measures how fast and
how far blood sugar rises after you eat a food that contains
White bread, for example, is converted almost immediately to blood
sugar, causing it to spike rapidly. It's classified as having a high
glycemic index. Brown rice, in contrast, is digested more slowly,
causing a lower and more gentle change in blood sugar. It has a low
?Diets filled with high-glycemic-index foods, which cause quick and
strong increases in blood sugar levels, have been linked to an
increased risk for both diabetes (3, 4) and heart disease. (5, 6) On
the other hand, lower GI foods have been shown to help control type 2
?Digestible carbohydrates are broken down in the intestine into their
simplest form, sugar, which then enters the blood. As blood sugar
levels rise, special cells in the pancreas churn out more and more
insulin, a hormone that signals cells to absorb blood sugar for energy
or storage. As cells sponge up blood sugar, its levels in the
bloodstream fall back to a preset minimum. So do insulin levels.?
?Insulin resistance isn't just a blood sugar problem. It has also been
linked with a variety of other problems, including high blood
pressure, high levels of triglycerides, low HDL (good) cholesterol,
heart disease, and possibly some cancers. (10)
Genes, a sedentary lifestyle, being overweight, and eating a diet
filled with foods that cause big spikes in blood sugar can all promote
insulin resistance. Data from the Insulin Resistance Atherosclerosis
Study suggests that cutting back on refined grains and eating more
whole grains in their place can improve insulin sensitivity. (11)?
?The glycaemic index of food is another consideration in the
development of insulin resistance. High glycaemic index food produce a
more rapid rise in blood glucose levels, paralleled by a more marked
insulin response than low glycaemic index foods. If consumed
regularly, this results in insulin resistance. The glycaemic index is
determined by the saccharide type ? glucose is worse than sucrose
(glucose-fructose), which is worse than fructose45, and by the starch
type, with amylose being lower than amylopectin46. Amylose is an
unbranched glucose polymer, whereas amylopectin is a branched glucose
polymer, in which the glucose residues are more accessible to
In addition to these macronutrient factors, various micronutrients
have been shown to affect cellular insulin resistance. Calcium,
magnesium and sodium have been particularly implicated, with some
researchers believing that the imbalance of calcium and magnesium
intracellularly is the primary defect of insulin-resistance47, with
most of the dietary and lifestyle factors found to increase insulin
resistance inducing a calcium/magnesium imbalance intracellularly48.
Magnesium plays an important role in glucose homeostasis by affecting
both insulin secretion and action. Tissue levels of magnesium are
often low in diabetics49 and low intracellular magnesium results in
impairment of insulin action and a worsening of insulin resistance in
hypertension and NIDDM50,51. Sodium chloride induces insulin
resistance by causing magnesium loss and further disturbing this
calcium/magnesium ratio52. Chromium is another micronutrient necessary
for good insulin function.?
?Foods with a high glycemic-index value tend to raise your blood
sugar faster and higher than do foods with a lower value. However,
low-index foods aren't necessarily healthier than high-index foods.
Although the glycemic-index diet has some potential benefits ? such as
reducing blood sugar levels ? it is very complicated. Many factors
affect the glycemic-index value of a specific food, including how the
food is prepared and what is eaten with it. Also, the GI value for
some foods isn't known. For these reasons, the American Diabetes
Association has concluded that there isn't enough evidence to
recommend the general use of a low-glycemic-index diet for people with
?Habitual intake of diets with a high glycemic index and high
glycemic load or diets with a high content of total carbohydrate
including simple sugars was not associated with the probability of
having insulin resistance. Furthermore, intake of dietary fiber was
inversely associated with the probability of having insulin
?Examples of foods with a low glycemic index include those with
higher fiber content such as whole grain breads and brown rice.
Non-starchy vegetables are another example of foods with a low
glycemic index (for example, broccoli, green beans, asparagus,
carrots, and greens). Since foods are rarely eaten in isolation, it
can be argued that the glycemic index of each food isn?t as important
as the overall profile of the whole meal itself.?
?Conclusions Each therapeutic agent, as monotherapy, increased 2-
to 3-fold the proportion of patients who attained HbA1c below 7%
compared with diet alone. However, the progressive deterioration of
diabetes control was such that after 3 years approximately 50% of
patients could attain this goal with monotherapy, and by 9 years this
declined to approximately 25%. The majority of patients need multiple
therapies to attain these glycemic target levels in the longer term.?
?It was examined whether sodium sensitivity was associated with
insulin resistance, an important atherosclerotic cardiovascular risk
factor in essential hypertension. Fiftythree patients with essential
hypertension, who had normal (n = 12) and impaired (n = 41) glucose
tolerance, were placed on high (12-15 g NaCl/day) and low (1-3 g)
sodium diets for 1 week each to determine sodium sensitivity. Fasting
plasma glucose and insulin concentrations were measured on a regular
sodium diet. The homeostasis model assessment insulin resistance index
(fasting glucose [mmol/L] x fasting insulin [mU/L]/22.5) was 1.40 ±
0.10 and 1.47 ± 0.14 in non-sodium sensitive and sodium sensitive
The insulin resistance index was positively correlated with the
sodium sensitivity index, while was negatively correlated with
fractional excretion of sodium (FE[Na]) obtained during a high sodium
diet. In addition, the insulin resistance index had a positive
relationship with overall creatinine clearance. Sodium sensitivity
index was also negatively correlated with FE[Na] obtained during a
high sodium diet.
These results showed that insulin resistance might participate in the
genesis of sodium sensitivity in essential hypertension by enhancing
tubular sodium reabsorption, as reflected in decreased FE[Na] and
augmented creatinine clearance. Insulin resistance seemed elevated in
sodium sensitive state of essential hypertension, leading to future
?During high sodium intake, plasma renin activity and aldosterone
decreased and plasma atrial natriuretic peptide increased; these
changes did not correlate with the change in mean arterial pressure,
insulin resistance, or change in urinary nitrate excretion. To the
extent that urinary nitrate excretion reflects activity of the
endogenous nitric oxide system, these results suggest that the salt
sensitivity of mean arterial pressure may be related to blunted
generation of endogenous nitric oxide. The results also demonstrate
that insulin-resistant individuals have an impaired natriuretic
response to high sodium intake.?
?Insulin-resistance has been postulated to be responsible for
enhanced sodium retention in obese individuals; therefore,
insulin-resistance may be critical to the pathogenesis of
sodium-sensitivity in individuals with essential hypertension. This
article summarizes the data relating insulin and or insulin-resistance
to sodium sensitivity in obesity, diabetes, and in non-obese subjects
with essential hypertension.?
?There is also evidence that the amount and range of
carotenoid-like pigments in an individual's blood is inversely related
to fasting serum insulin levels,65 suggesting a diet low in vegetables
might contribute to insulin resistance. Epidemiological evidence does
not support a role of dietary vitamins E or C consumption having a
significant association with insulin sensitivity;66,67 Diets higher in
vitamin A, on the other hand, have shown an inverse relationship with
insulin resistance.67 Dietary micronutrient deficiencies might also
promote insulin resistance.
Chief among these deficiencies appear to be minerals including
calcium, magnesium, potassium, chromium, vanadium, and zinc.68-74
Intake of sodium, either too high or two low, appears to negatively
impact insulin sensitivity. Evidence presented by Donovan et al is
suggestive of high sodium intake possibly exacerbating insulin
resistance.75 At the other extreme, salt restriction also appears to
increase insulin resistance for most individuals. While moderate
dietary sodium reduction may lower blood pressure without a distinct
adverse effect on glucose metabolism in subjects with primary
hypertension,76 it appears that salt restriction does not improve
insulin resistance in hypertensive subjects.77 In fact, available
evidence seems to be in agreement that severe reduction of salt intake
may contribute to an increased serum lipid and insulin levels, and a
deterioration of insulin sensitivity in both healthy volunteers and
patients with hypertension.76,78,79 Evidence even suggests moderate
salt restriction can aggravate both existing systemic and vascular
This site also discusses vanadyl sulfate, vitamins, calcium,
magnesium, and chromium?s effect on insulin.
?We have shown recently that sustained elevations of cytosolic free
calcium in insulin target cells, such as are observed in patients with
obesity and non-insulin-dependent diabetes mellitus and in some
patients with hypertension, may lead to the development of insulin
resistance. Although the mechanisms that lead to such increases are
not yet well understood, they appear to include an enhanced influx of
calcium via calcium channels. We found that the presence of the
calcium antagonist nitrendipine in the incubation medium prevented
increases in cytosolic free calcium concentration and ameliorated the
insulin resistance induced by various mechanisms.?
Obesity and Diet
?Resistance of the body to the actions of insulin results in
increased production of this hormone by the pancreas and ensuing
hyperinsulinemia. Obesity beginning in childhood often precedes the
hyperinsulinemic state. Other components of the insulin resistance
syndrome are also present in children and adolescents.5,6 An
association between obesity and insulin resistance has been reported
in the young, as has the link between insulin resistance,
hypertension, and abnormal lipid profile.
There is an increasing amount of data showing that being overweight
during childhood and adolescence is significantly associated with
insulin resistance, dyslipidemia, and elevated blood pressure in young
adulthood. Weight loss by obese youngsters results in a decrease in
insulin concentration and improvement in insulin sensitivity.?
?What causes insulin resistance?
No one knows for sure. Some scientists think a defect in specific
genes may cause insulin resistance and type 2 diabetes. Researchers
continue to investigate the cause. What we do know is that insulin
resistance is aggravated by obesity and physical inactivity both of
which are increasing in the U.S.
Do all people with insulin resistance develop diabetes?
No. Science has not yet determined why some people with insulin
resistance eventually develop diabetes and others do not.
By maintaining an appropriate weight and a physically active
lifestyle many individuals are able to reduce their chances of
becoming insulin resistant and developing diabetes.
What is the best diet for people with insulin resistance?
Research indicates that low fat diets may aggravate the effect of
insulin resistance on blood lipids. Therefore, for individuals who
are insulin resistant, a diet low in saturated fat (less than 10
percent of total calories) and more moderate in total fat content (40%
of total calories) may be beneficial. This recommendation is
different from the low-fat, high-carbohydrate diet that many health
organizations recommend to help prevent heart disease. Specifically,
they recommend decreasing fat intake to less than 30 percent of
calories. Some groups recommend even lower levels of dietary fat.
It is also beneficial to maintain an appropriate body weight because
obesity can aggravate insulin resistance. To maintain an appropriate
weight, regulate caloric intake and maintain a physically active
lifestyle. A registered dietitian can assist with developing a proper
diet plan for people with insulin resistance, or a family history of
type 2 diabetes.?
?Can you reverse insulin resistance?
Yes. Physical activity and weight loss make the body respond better to
insulin. By losing weight and being more physically active, you may
avoid developing type 2 diabetes. In fact, a major study has verified
the benefits of healthy lifestyle changes and weight loss. In 2001,
the National Institutes of Health completed the Diabetes Prevention
Program (DPP), a clinical trial designed to find the most effective
ways of preventing type 2 diabetes in overweight people with
pre-diabetes. The researchers found that lifestyle changes reduced the
risk of diabetes by 58 percent. Also, many people with pre-diabetes
returned to normal blood glucose levels.
The main goal in treating insulin resistance and pre-diabetes is to
help your body relearn to use insulin normally. You can do several
things to help reach this goal.
Be Active and Eat Well
Physical activity helps your muscle cells use blood glucose because
they need it for energy. Exercise makes those cells more sensitive to
The DPP confirmed that people who follow a low-fat, low-calorie diet
and who increase activities such as walking briskly or riding a bike
for 30 minutes, five times a week, have a far smaller risk of
developing diabetes than people who do not exercise regularly. The DPP
also reinforced the importance of a low-calorie, low-fat diet.
Following a low-calorie, low-fat diet can provide two benefits. If you
are overweight, one benefit is that limiting your calorie and fat
intake can help you lose weight. DPP participants who lost weight were
far less likely to develop diabetes than others in the study who
remained at an unhealthy weight. Increasing your activity and
following a low-calorie, low-fat diet can also improve your blood
pressure and cholesterol levels and has many other health benefits.
Scientists have established some numbers to help people set goals that
will reduce their risk of developing glucose metabolism problems.
? Weight. Body mass index (BMI) is a measure used to evaluate body
weight relative to height. You can use BMI to find out whether you are
underweight, normal weight, overweight, or obese. Use the Body Mass
Index Table to find your BMI.
o Find your height in the left-hand column.
o Move across in the same row to the number closest to your weight.
o The number at the top of that column is your BMI. Check the word
above your BMI to see whether you are normal weight, overweight, or
obese. If you are overweight or obese, talk with your doctor about
ways to lose weight to reduce your risk of diabetes.
?Exercise training improves insulin sensitivity.19 Patients with
suspected insulin resistance should be advised to increase their level
of physical activity. Even regular, sustained, moderate increases in
physical activity, such as daily walking, can substantially decrease
insulin resistance.20 This is compatible with the standard
recommendation that everyone should accumulate at least 30 minutes of
moderate-intensity physical activity on most or, even better, all days
of the week.?
Very little research has been performed in humans, but studies are ongoing.
?Insulin sensitivity improves within a few days of caloric
restriction, before any significant weight loss occurs.13 Weight
reduction leads to further improvement. The amount of weight loss
needed for sustained decreases in insulin resistance is still unclear.
In obese women without diabetes, weight loss of approximately 15
percent has been linked to significantly lower insulin levels.22
Regaining even a modest amount of the lost weight, however, with a
body weight that was still 10 percent below starting values, resulted
in an increase in insulin levels to baseline. The women in this study
were very obese (mean BMI: 36.4 kg per m2) and remained obese even
with the loss of 15 percent of body weight (mean BMI: 30.5 kg per m2).
The implication is that all obese patients should be encouraged to
attain a healthy body weight. This can be accomplished and sustained
through dietary modification and exercise--a recommendation that is
easy to make, of course, but difficult to follow.?
?Unknown at this time. Neither the mechanisms by which life
extension takes place (in rodents) nor the mechanisms by which the
complex features associated with insulin resistance and the Metabolic
Syndrome X are prevented by CR are understood (Bodkin et al. 1995).
Clearly, advancements in this area will lead to better understanding
of this powerful nutritional tool. The estimate of changes induced in
mammals by the long-term application of CR is likely to involve
thousands of alterations, only a small portion of which causally
influence longevity and health. One step, the description of altered
functions and the protein changes underlying those, has been advanced
by several of the reports included in this symposium.?
?CR produces altered pathways of nutrient disposal, including
reduced plasma glucose, insulin and leptin levels (Hansen and Bodkin
1993, Hansen et al. 1996). Although glucose tolerance is retained at
normal levels under CR, there is evidence to suggest alterations in
the intermediary pathways of glucose metabolism. In detailed studies
of weight stable reduced individuals, energy efficiency was increased,
that is fewer calories per lean body mass were required to maintain
stable weight (Leibel et al. 1995, DeLany et al. 1999)?
?Skeletal muscle insulin sensitivity improves with a moderate
reduction in caloric intake. We studied possible mechanisms in
calorie-restricted [CR: 60% ad libitum (AL) intake] compared with AL
rats, utilizing a time-matched feeding protocol (3, 5, 10, or 20
?Our findings suggest that 2 biomarkers of longevity (fasting
insulin level and body temperature) are decreased by prolonged calorie
restriction in humans and support the theory that metabolic rate is
reduced beyond the level expected from reduced metabolic body mass.
Studies of longer duration are required to determine if calorie
restriction attenuates the aging process in humans.?
"These cross-sectional findings in nondiabetic men with coronary
artery disease suggest that increased consumption of saturated fatty
acids is associated independently with higher fasting insulin
"Research results posted on the Journal of Biological Chemistry's
Web site at www.jbc.org show that a saturated fat metabolite called
ceramide contributes to the development of insulin resistance in
cultured cell experiments. Furthermore, the lab studies indicate that
excess accumulation of ceramide in the body is a necessary link
connecting saturated fats to insulin resistance. The entire research
paper can be found on the Web site's papers in press section and is
expected to be published in the journal's April print edition.
"Our research team is making great progress -- we have determined that
ceramide is undeniably an important factor in the development of
insulin resistance in muscle tissue," said Scott Summers, assistant
professor in the Department of Biochemistry and Molecular Biology and
principal investigator of the study. "These findings suggest that
medication aimed to prevent ceramide accumulation in body tissue might
lessen or even prevent insulin resistance and lead to breakthroughs in
the treatment of type 2 diabetes."
?Very good studies indicate that trans fats interfere with insulin
receptors and therefore with insulin resistance. The saturated fats do
The recommendations regarding dietary saturated fats intake versus
trans fats intake for the past number of years have been very
confusing to the public, and judging from the articles, also confusing
to the researchers. Trans fats are mistaken by many of the health
professionals for saturated fats although they are not similar in
their effects on the human body, just similar in the manner of
stability in the baking or cooking realm.?
?Another example of inappropriate conclusions drawn from a research
project comes from Colorado State University, where researchers
decided that a "saturated fat byproduct" was a potential contributor
to type-2 diabetes. This so-called saturated fat metabolite is
ceramide. Ceramide is a lipid molecule made in the body from something
called sphingosine and a fatty acid (which could be oleic acid, a
so-called good fatty acid). This molecule is used to make
sphingomyelin, which is one of the structural elements in the lipid
bilayer, as well as being a cellular signal molecule. Sphingomyelin is
one of the lipid building blocks of the myelin sheath so important for
Ceramides are interesting molecules currently being studied for a role
in programmed cell death, and substances known to induce ceramide
production are components such as endotoxins and chemotherapeutic
agents more likely to be from the stress of trans fats than from the
normal saturated fats, which are such important building blocks of our
?To determine whether there is an association between diet and
plasma insulin concentration that is independent of obesity, we
studied the relation of dietary composition and caloric intake to
obesity and plasma insulin concentrations in 215 nondiabetic men aged
32-74 years with angiographically proven coronary artery disease.?
?CONCLUSIONS. These cross-sectional findings in nondiabetic men
with coronary artery disease suggest that increased consumption of
saturated fatty acids is associated independently with higher fasting
?Now research suggests that too much saturated fat may be
problematic, even if your cholesterol isn?t high, because of its
possible effects on insulin functions, potentially raising the risk of
diabetes, cancer, ovarian disorders and other health problems.?
Omega 3, Omega 3 and other fatty acids
?Omega-3 fatty acid treatment in type II diabetes leads to rapid
but reversible metabolic deterioration, with elevated basal hepatic
glucose output and impaired insulin secretion but unchanged glucose
disposal rates. Caution should be used when recommending omega-3 fatty
acids in type II diabetic persons.?
?The in vivo insulin stimulated glucose uptake was estimated by
determining the metabolic clearance rate (MCR) of glucose in the
steady state of a simultaneous infusion during 150 min of glucose (33
mumol/kg/min) and insulin (50 mU/kg/hr). The MCR of glucose increased
in all patients; from 3.93 +/- 0.55 - 4.69 +/- 0.74 ml/kg/min (mean
+/- SEM, p less than 0.05). Plasma triglyceride concentrations fell
from 1.9 +/- 0.3 - 1.2 +/- 0.2 mmol/l (mean +/- SEM, p less than
0.05). We conclude that in NIDDs dietary supplementation of omega 3
fatty acids improves in vivo insulin sensitivity and lowers plasma
triglyceride levels, while erythrocyte membrane fluidity remains
?Our studies are important because they demonstrate that
hyperinsulinemia can be rapidly reversed via the dietary provision of
small amounts of long-chain -3 fatty acids. However, this "insulin
sparing" action of acute dietary long-chain -3 fatty acids occurs in
the absence of an acute improvement in insulin sensitivity and
therefore at the expense of maintenance of glucose tolerance.?
?Omega-6: a polyunsaturated fat found in vegetable oils. The most
common one is linoleic acid. Omega-6 fat may reduce the risk of heart
disease by lowering total and LDL (bad) cholesterol, but it may lower
HDL (good) cholesterol as well. Omega-6 fat also reduces the effects
of insulin and the immune system. Most vegetable oils, especially
soybean, corn and safflower, are high in omega-6 fats. Other sources
include borage, evening primrose, and black currant oils.?
?Omega-3 PUFA reduce fasting and postprandial TG, may improve
insulin sensitivity (as shown in animal experiments), decrease
platelet and leukocyte reactivity, alter immunological functions, and
may slightly decrease blood pressure. Omega-3 PUFA may also
beneficially influence vessel wall characteristics and blood rheology.
Furthermore, both types of PUFA (omega-3 and omega-6) have been shown
to inhibit cardiac arrhythmias in animals. The role of omega-3 PUFA in
blood clotting and fibrinolysis still remains controversial, whereas
omega-6 fatty acids may lead to increased oxidation of lipoproteins.
Regardless of the effects on LDL oxidizability, both types of PUFA
have shown beneficial effects on the development of atherosclerosis.
As yet, little is known about the effect of specific omega-6 fatty
acids with respect to the IRS. Potential adverse effects of dietary
PUFA must not be neglected, but should be viewed in light of the
beneficial effects of these agents.?
Abstract only: ?We discuss the concept that the two essential (not
produced by the body and obtained exclusively through the diet)
polyunsaturated fatty acid families?n-6 and n-3?may play a role in the
pathogenesis of insulin resistance through inflammatory pathways.
Linoleic acid, the major n-6 fatty acid, is metabolized into
pro-inflammatory arachidonic acid, which, in turn, gives rise to
leukotrienes and protaglandins. N-3 fatty acids, found in plants and
in fish, reduce the levels of arachidonic acid, thereby lowering
inflammatory mediator concentrations and increasing insulin
sensitization. We discuss these findings and their implications for
insulin resistance and their possible effect on coronary heart
?Acute elevations of plasma free fatty acid (FFA) levels augment
glucose-stimulated insulin secretion (GSIS). Prolonged elevations of
FFA levels reportedly impair GSIS, but no one has previously compared
GSIS after prolonged exposure to saturated or unsaturated fat. Rats
received a low-fat diet (Low-Fat) or one enriched with either
saturated (Lard) or unsaturated fat (Soy) for 4 weeks.?
?These data indicate that prolonged exposure to saturated fat enhances
GSIS (but this does not entirely compensate for insulin resistance),
whereas unsaturated fat, given in the diet or by infusion, impairs
GSIS. Inferences regarding the impact of fatty acids on GSIS that are
based on models using unsaturated fat may not reflect the effects of
?Insulin resistance, when combined with impaired insulin secretion,
contributes to the development of
type 2 diabetes. Insulin resistance is characterized by a decrease in
the insulin effect on glucose transport in
muscle and adipose tissue. Tyrosine phosphorylation of IRS-1 (insulin
receptor substrate 1) and its binding to PI 3-kinase (phosphoinositide
3-kinase) are critical events in the insulin signalling cascade
leading to insulinstimulated glucose transport. Various studies have
implicated lipids as a cause of insulin resistance in muscle. Elevated
plasma fatty acid concentrations are associated with reduced
insulin-stimulated glucose transport activity as a consequence of
altered insulin signalling through PI 3-kinase.?
?Essential to the development of the disease is insulin resistance
of the peripheral tissues. Insulin resistance may be partly modified
by the specific types of dietary fatty acids. Trans fatty acids
(TFAs), created through the transformation of polyunsaturated fatty
acids from their natural cis form to the trans form, are abundant in
the Western diet. TFAs take on similar properties as saturated fats,
and appear to be more atherogenic.
High intakes of saturated fats may promote insulin resistance. It is
therefore reasonable to hypothesize that high intakes of TFAs would
have similar, or stronger, effects. In this review, all current
evidence on the topic of TFAs, insulin resistance, and type 2 diabetes
is summarized and interpreted. Although there is some support from
observational and experimental studies for the hypothesis that high
intakes of TFAs may increase the risk for type 2 diabetes,
inconsistencies across studies and methodological problems make it
premature to draw definitive conclusions at this time. More
experimental research in humans is needed to further address this
ALA (alpha linolenic acid)
An ongoing study, with no conclusion- ?To determine the influence
of an ALA enriched diet on lipoprotein-associated phospholipase A2
(Lp-PLA2) in individuals with impaired glucose tolerance or type 2
diabetes. Hypothesis 2: Those individuals on an ALA-enriched diet will
show a reduction in lipoprotein-associated phospholipase A2 (Lp-PLA2)
compared to those individuals not on an ALA-enriched diet.?
?Overweight patients who are insulin resistant often require high
dosages of insulin. These high dosages can cause weight gain, making
glycemic control more difficult.?
?Metformin decreases hepatic glucose output and improves peripheral
insulin sensitivity, which results in improved glycemic control in
patients with type 2 diabetes. With the use of metformin, blood lipid
abnormalities, particularly hypertriglyceridemia, improve, and weight
loss is often reported. These beneficial effects make the combination
of metformin and insulin an attractive treatment that allows patients
to avoid weight gain while achieving glycemic control.?
?The authors conclude that adding metformin to an intensified insulin
regimen results in a reduction of hemoglobin A1c level that is 11
percent lower than that achieved with insulin therapy alone, with less
total insulin used, a less complicated insulin regimen and no increase
in the incidence of hypoglycemia or weight gain.?
?Metformin (Glucophage) is a medicine which is used to help bring
down insulin levels and help keep blood sugar normal. It lowers
insulin levels by lowering the amount of glucose released from the
liver. It also makes your body more sensitive to insulin, so it
doesn?t have to make as much.
How do I take metformin?
If your doctor prescribes metformin, you need to take it before your
main meals (usually breakfast and dinner). Your doctor will tell you
to begin at a very low dose and slowly increase the amount of medicine
you take over a few months??start low, go slow.? It?s a good idea to
take a multivitamin every day when you are taking metformin because it
can decrease your digestion of certain vitamins (B12 and folate).?
?Two drugs from the biguanide class, metformin and phenformin, were
developed in 1957. Unfortunately, phenformin reached the U.S. market
first and resulted in several deaths from lactic acidosis. When this
risk surfaced, phenformin was pulled from drugstore shelves worldwide.
Metformin was eventually found to be 20 times less likely to cause
lactic acidosis, but it was tainted by the history of its cousin.
Metformin first became available in France in 1979 and has been widely
used in Europe since then, but it was not cleared for use in Type 2
diabetes in the U.S. until 1994.?
?Metformin lowers fasting blood glucose levels by an average of 25%
(17 to 37%), postprandial blood glucose up to 44.5%, and the A1c by an
average of 1.5% (0.8 to 3.1%). Metformin reduces raised plasma insulin
levels in cases of metabolic syndrome by as much as 30% and reduces
the need for injected insulin in Type 2s by 15 to 32%.
Metformin is available under the trade name Glucophage, or as an
extended-release tablet called Glucophage XR. It works well when
combined with sulfonylureas. A combination of glyburide and metformin
is available as Glucovance. Combined therapy leads to a greater
reduction in blood sugar than can be attained by either class alone.
Generic metformin is available at a reduced cost.?
?Metformin (Glucophage) is a medication that is used for treating
diabetes. It has two mechanisms of action that help to control blood
glucose levels. It prevents the liver from releasing glucose into the
blood, and it increases the sensitivity of muscle and fat cells to
insulin so that they remove more glucose from the blood. Because of
these actions, metformin reduces blood insulin levels. The DPP studied
the effects of metformin in addition to diet and exercise on the
prevention of diabetes in insulin resistance. Metformin reduced the
development of diabetes by 31%. (Note, however, that the benefit was
not as great as with diet and exercise!)?
?Low-Dose Flutamide-Metformin Therapy Reverses Insulin Resistance
and Reduces Fat Mass in Nonobese Adolescents with Ovarian
?Another study, the STOP NIDDM (Study to Prevent Non-insulin
Dependent Diabetes Mellitus) trial, studied individuals with insulin
resistance by treating them with a medication called acarbose
(Precose). Acarbose works in the intestines to slow the absorption of
sugars, and this effect would reduce the need for insulin after meals.
The study found that acarbose reduced the development of diabetes by
Other medications in a class of drugs called thiazolidinediones,
e.g., pioglitazone (Actos), rosiglitazone (Avandia), also increase
sensitivity to insulin. At this time, however, these medications are
not routinely used, in part because of liver toxicity that requires
monitoring of blood liver tests.
One study, the TRIPOD (Troglitazone in Prevention of Diabetes) study,
treated patients with gestational diabetes, a precursor of insulin
resistance and diabetes, with troglitazone (Rezulin), however, because
of severe toxic liver effects; troglitazone has been taken off the
market and is no longer available. Among the women treated with
troglitazone, diabetes was prevented in 25%.?
?Acarbose, which is sold in Europe under the name Glucobay?, is now
sold in the United States with the brand name Precose?. It is
manufactured by Bayer Corporation, Pharmaceutical Division, of West
Acarbose is in a class of pharmaceuticals called alpha-glucosidase
inhibitors, and works in the intestine, slowing down the digestion of
carbohydrates, and lengthening the time it takes for carbohydrates to
convert to glucose, thereby facilitating better blood glucose control.
It mainly influences the level of blood sugar after eating.?
?Acarbose works by slowing the action of certain chemicals that
break down food to release glucose (sugar) into your blood. Slowing
food digestion helps keep blood glucose from rising very high after
?PRECOSE ®, as monotherapy, is indicated as an adjunct to diet to
lower blood glucose in patients with type 2 diabetes mellitus whose
hyperglycemia cannot be managed on diet alone. PRECOSE ® may also be
used in combination with a sulfonylurea when diet plus either PRECOSE
® or a sulfonylurea do not result in adequate glycemic control. Also,
PRECOSE ® may be used in combination with insulin or metformin. The
effect of PRECOSE ® to enhance glycemic control is additive to that of
sulfonylureas, insulin, or metformin when used in combination,
presumably because its mechanism of action is different.?
?What is Avandia used for?
Avandia, in addition to diet and exercise, improves blood sugar
control in adults with type 2 (non-insulin-dependent) diabetes.
Avandia can be used alone or in combination with a sulfonylurea,
metformin, or insulin. Avandia can also be used in addition to a
sulfonylurea plus metformin when diet, exercise, and both agents are
not enough to control blood sugar.?
?Pharmacological studies in animal models indicate that
rosiglitazone improves sensitivity to insulin in muscle and adipose
tissue and inhibits hepatic gluconeogenesis. Rosiglitazone maleate is
not chemically or functionally related to the sulfonylureas, the
biguanides, or the alpha-glucosidase inhibitors.?
?ACTOS is indicated as an adjunct to diet and exercise to improve
glycemic control in patients with type 2 diabetes
(non-insulin-dependent diabetes mellitus, NIDDM). ACTOS is indicated
for monotherapy. ACTOS is also indicated for use in combination with a
sulfonylurea, metformin, or insulin when diet and exercise plus the
single agent does not result in adequate glycemic control.?
?nsulin: ACTOS in combination with insulin may be initiated at 15 mg
or 30 mg once daily. The current insulin dose can be continued upon
initiation of ACTOS therapy. In patients receiving ACTOS and insulin,
the insulin dose can be decreased by 10% to 25% if the patient reports
hypoglycemia or if plasma glucose concentrations decrease to less than
100 mg/dL. Further adjustments should be individualized based on
Resistin (Still under investigation) and Leptin
?Scientists have discovered a hormone that may explain the link
between diabetes and obesity - a tantalizing finding that could
someday lead to new treatments for the disease.
The hormone, dubbed resistin, is produced by fat cells and prompts
tissues to resist insulin, the substance the body needs to process
blood sugar, researchers reported in Thursday's issue of the journal
Nature. Diabetics produce too little insulin or cannot use it
"I don't think it's an exaggeration to say this is a blockbuster paper
with potentially major clinical impact,'' said Dr. Allen Spiegel,
director of the National Institute of Diabetes and Digestive and
Kidney Diseases, a division of the National Institutes of Health,
which funded the research.
Obesity is one of the biggest risk factors for Type II, or
adult-onset, diabetes. The adult-onset form of the disease accounts
for more than 90 percent of all cases of diabetes.
The University of Pennsylvania scientists identified resistin in mice
and found genetic evidence that the same hormone exists in humans,
though they have yet to isolate it.
Mice given resistin were not able to process blood sugar as well as
those that were not given the hormone. And mice given a drug that
lowers resistin levels were better able to process blood sugar and use
?Leptin and resistin are two members of a growing family of
adipocytokines. Leptin is thought to regulate body fat, feeding
behaviour, energy balance, fertility and neuroendocrine responses;
whereas resistin antagonizes insulin action, impairs glucose tolerance
and its activity is modulated by PPAR gamma receptors. It was
previously shown that leptin is expressed in the rat hypothalamus and
pituitary. With regards to resistin, we knew that PPAR-gamma receptors
are expressed in the brain and pituitary. We also knew that ablation
of the hypothalamus in mice led to obesity, insulin resistance and
hyperglycemia. Here we go a step further in answering the questions of
whether leptin is developmentally regulated, whether resistin protein
is expressed in the mouse brain and pituitary, and what the role of
the hypothalamus is in resistin expression.?
?Serum resistin levels were 1.2-fold higher in type 2 diabetes and
1.3-fold higher in CHD than in controls (p = 0.01). In addition, CRP
was significantly increased in both T2DM and CHD patients (p = 0.007
and p = 0.002 respectively). The use of regression analysis also
determined that serum resistin correlated with CRP levels (p = 0.04,
The findings from this study further implicate resistin as a
circulating protein associated with T2DM and CHD. In addition this
study also demonstrates an association between resistin and CRP, a
marker of inflammation in type 2 diabetic patients.
?A study from the University of Pennsylvania has identified a new
hormone - called resistin - which causes the body's cells to become
resistant to the effects of insulin.
Insulin resistance is the cause of many cases of type 2, or
adult-onset, diabetes. It appears that this resistin is produced by
the body in response to obesity. Thus, obesity (in certain
individuals) results in elevated levels of resistin, which, in turn,
results in insulin resistance and type 2 diabetes.?
?The initial reports, however, were followed by others from groups
stating that some types of insulin resistant, obese animals do not
have elevated resistin levels. There were also some papers that
demonstrated that TZDs actually increase resistin levels in mice.
These points of contention have never been completely explained away
by either side, but neither have they deterred researchers from
continuing to investigate resistin and its effects on glucose control.
Now, three years after it?s initial discovery, we know more about this
interesting molecule than ever. The overall picture, however, is still
a bit murky.
Several different investigators have pursued studies in mice and rats,
the workhorses of the modern biology lab. In these animals, it appears
clear that adding extra resistin compromises insulin action, as
predicted by the original reports. Short-term administration of
resistin or a related hormone called RELM-beta caused insulin
resistance, with the dominant effect seen on the liver. The liver
plays an important role in the production of glucose and its release
into the bloodstream between meals; insulin suppresses this activity.
When resistin is given as a single injection, insulin is less able to
exert these repressive effects on the liver. Newer studies have
confirmed this with longer periods of resistin treatment, delivered
either by injection or by genetic modification of mice so that they
produce more resistin than they would normally.?
?Leptin is a hormone produced by the fat cells that researchers
have shown to play a role in controlling appetite. Certain people with
severe insulin resistance have little or no leptin.
The purpose of this study is to investigate people whose leptin levels
have been found to be lower than 85 percent of the general population.
Researchers will determine whether insulin levels in these
participants improve when they are treated with genetically engineered
?A newly discovered hormone produced by fat cells may provide a
long-sought explanation for how obesity triggers insulin resistance
and type 2 diabetes, a University of Pennsylvania School of Medicine
team reports in the January 18, 2001, issue of Nature. The discovery
of the hormone, called resistin (resistance to insulin), is also
helping researchers understand how a new class of antidiabetic drugs
promotes insulin sensitivity in people with type 2 diabetes. Insulin
resistance, a disorder in which target tissues--muscle, fat, and liver
cells--fail to use insulin effectively, accompanies and usually
precedes type 2 diabetes. Eighty percent of people with type 2
diabetes are overweight, but the mechanism by which obesity sets the
stage for insulin resistance and diabetes has long puzzled
?The mechanisms by which glucocorticoid therapy promotes obesity and
insulin resistance are incompletely characterized. Modulations of the
metabolically active hormones, tumour necrosis factor alpha (TNF
alpha), ghrelin, leptin and adiponectin are all implicated in the
development of these cardiovascular risk factors. Little is known
about the effects of short-term glucocorticoid treatment on levels of
?Glucocorticoids are common therapy for inflammatory conditions,
but they generate a diverse array of unwanted side effects . Their
mechanisms of action involve the activation of transcription factors
that interact with a battery of responsive genes, stimulating
inflammatory and immuno-regulatory cross-talk . Glucocorticoid
therapy promotes both insulin resistance [3,4] and central obesity
, perpetuating cardiovascular risk.
However, the mechanisms of glucocorticoid-mediated obesity remain
incompletely characterized, and the impact of glucocorticoids on
hormones and cytokines that regulate hunger, satiety and adiposity
remain unclear. Therefore, we sought to determine the acute effects of
glucocorticoid administration on tumor necrosis factor ? alpha (TNF
alpha), ghrelin, leptin, and adiponectin?all hormones and cytokines
thought to play an important role in the regulation of adiposity.?
Estrogen, Progesterone and other hormones
?Transdermal estrogen substitution alone and combined with cyclical
dydrogesterone may ameliorate hyperinsulinemia in a selected
population of postmenopausal women.?
?The data suggest that estrogen use in American Indian postmenopausal
women may relate to deterioration of glucose tolerance. Longer
duration of estrogen use among current users may relate to an
increased risk of type 2 diabetes.?
?Recent research has shown that women with polycystic ovary
syndrome not only have high levels of androgen hormones but also have
high insulin hormone levels. Insulin is produced in higher quantities
to compensate for the body's increased resistance to insulin's
effects. It is likely, although it has not been proven, that excess
insulin is the root of the problem in polycystic ovary syndrome.
Excess insulin can cause the body's ovaries to make extra androgen
hormones. The high insulin levels cause other significant concerns for
women with this disease. They are much more likely to become obese,
and they are at a high risk of developing diabetes, high blood
pressure, cholesterol problems and heart disease.
No one is certain why insulin resistance occurs. It is thought that
polycystic ovary syndrome, like most cases of insulin resistance, is
caused by an inherited gene defect.
In addition to people with a family history, women with recurrent
seizures are more likely to develop polycystic ovary syndrome. This
might happen because repeated seizures affect the brain's hypothalamus
and pituitary gland, which regulate the production of reproductive
?There is extensive experimental evidence that sex steroids and
insulin interact in their actions on tissues. At physiological levels,
testosterone and oestradiol are thought to be involved in maintaining
normal insulin sensitivity. However, outside this `physiological
window' these steroids may promote insulin resistance. Considerable
research has been carried out on polycystic ovarian syndrome, a common
disorder associated with excessive androgen production
and insulin resistance. Hyperinsulinaemia in patients with this
condition is believed to stimulate ovarian androgen production, and
there is also evidence that androgens act directly on peripheral
tissues to promote insulin resistance. There is the potential for a
vicious circle to develop with increasing androgen production and
Page 2 ?Insulin has a wide range of acute metabolic and anabolic
actions. Of the acute metabolic effects, the most important are
stimulation of glucose uptake into peripheral insulin-sensitive
tissues, suppression of hepatic glucose output, stimulation of
glycogen synthesis and an antilipolytic effect on adipose tissue .
In all cases of insulin resistance, there is a subnormal biological
response to a given level of insulin in its target tissues. The term ?
insulin resistance ? is generally assumed to include insulin?s action
on lipid and protein metabolism and glucose uptake, but also
encompasses its myriad of other actions, including those on vascular
tissue and cellular growth . Impairment of each of these actions
contributes to the consequences of insulin resistance for the
?In a dose-response curve for the effects of four different
concentrations of insulin on glucose infusion rate, the insulin
resistance induced by progesterone is characterized by a decreased
responsiveness to insulin. The results suggest that progesterone may
play an important role in inducing insulin resistance in pregnancy.?
?The literature suggests that there may be an association between
hepatitis C and type 2 diabetes mellitus independent of the presence
of cirrhosis, the likely mechanism for which is insulin resistance.
The prevalence of insulin resistance in patients with hepatitis C is
unknown. Furthermore, there are no studies that indicate an increased
prevalence of insulin resistance in patients with hepatitis C compared
to other etiologies of liver disease. The role that hepatitis C may
have in the development of insulin resistance is unclear. The effect
of antiviral therapy for hepatitis C virus on insulin resistance has
not been addressed. The long-term consequence of insulin resistance is
type 2 diabetes mellitus. There is significant morbidity and mortality
from type 2 diabetes mellitus in the general population, and similar
complications would be expected in patients with hepatitis C and
insulin resistance particularly if they develop type 2 diabetes
Our hypothesis: The prevalence of insulin resistance is increased in
patients with chronic hepatitis C compared to chronic hepatitis B.
Secondarily, insulin resistance when present in patients with chronic
hepatitis C improves with successful antiviral therapy.?
Statins (lipid lowering drugs)
There is not much research to be found on statins and insulin
resistance or lowering. The benefit of statins for diabetics seems to
be the anti-inflammatory effect the drugs have in decreasing heart
disease and stroke.
?As outlined in our previously proposal ´Effect of atorvastatin on
insulin signalling and glucose metabolism´ we hypothesized that
statins may, beyond their lipid lowering effects affect positively the
metabolism of glucose.?
Statins also help diabetics, who are prone to heart disease, in
another way: ?The study involved 20,000 volunteers for 5 years showed
that one third of heart attacks and strokes can be avoided by using 40
mg simvastatin. In addition, statin therapy also reduced the risk of
hospitalization for angina, the need for arterial surgery, angioplasty
and amputations. The benefit was seen in patients aged over 75 years
and in patients with diabetes. The benefits were shown to increase for
each additional year of statin therapy.
Diabetics do not generally receive cholesterol-lowering therapy,
although they have a particularly high risk of heart trouble. The
study included nearly 6,000 diabetics and found that a daily dose of
simvastatin 40 mg cut the risk of a first heart attack or stroke by
about a quarter, even in patients with relatively low cholesterol
levels. The drug also, significantly reduced the chances of suffering
a repeat attack to those who already have had one of these events.?
?After eight weeks, as expected, they found that statin therapy
produced a significant reduction in total cholesterol (25%), LDL
cholesterol (32%), and non-high-density lipoprotein levels (42%),
compared with baseline and placebo. Triglycerides and high-density
lipoprotein cholesterol were unchanged.
Dr. Jialal and his team also found marked reductions in the two
pivotal biomarkers of inflammation. Although these markers are usually
elevated in insulin resistance, simvastatin therapy had marked effects
as shown by a 36% decrease in levels of hsCRP (P<0.005) compared with
baseline and placebo, and a 44% decrease in plasma IL-6 (< 0.025), a
molecule, along with tumor necrosis factor (TNF), involved in insulin
resistance and cardiovascular disease.?
?Statins have multiple actions, independent of their classical
effects on lipoproteins. The data about the effects of statins on
insulin resistance is controversial.?
?As a conclusion, the present study indicates that fluvastatin
treatment improves insulin resistance in dyslipidemic patients who do
not have diabetes or impaired fasting glucose. Also, the effect of
fluvastatin on insulin resistance is not associated with the lowering
of triglycerides. The latter finding indicates that the effect of
statins on insulin sensitivity may not be related with the lowering of
triglycerides in dyslipidemic patients.?
Psychological Insulin Resistance
I hope this has helped you! If anything is unclear, please request
an Answer Clarification, and allow me to respond, before you rate this
Statins + effect + insulin
Metformin + insulin
Insulin + saturated fat
Insulin + omega3
Insulin + omega6
Insulin + sodium
Insulin + calorie restriction
Insulin + calorie restriction + humans
Insulin + vitamins
Insulin + minerals
Insulin + estrogen
Insulin resistance + estrogen
Insulin + progesterone
Reducing insulin resistance
omega fatty acids + effect + insulin
insulin resistance + therapy
fatty acids + insulin resistance
impaired glucose tolerance + insulin + fasting