METABOLIC SYNDROME (SYNDROME X)
Metabolic Syndrome (MetS) is not an actual disease. It‘s a cluster of measurements indicating an unhealthy
condition that increases the risk of heart attack, stroke, type 2 diabetes, and other maladies including all-cause
mortality. For example, if you have MetS, you are five times more likely to develop type 2 diabetes and twice
as likely to develop heart disease. Research links MetS to fatty liver disease, polycystic ovaries, breast cancer,
several other cancers, asthma, excess inflammation, sleep problems, depression, Alzheimer‘s disease, and
other ills. The problem is that no one knows which comes first: MetS or the illnesses associated with it. The
―unhealthy‖ body measurements are high blood pressure (greater than 130/85 mm Hg), high fasting blood
sugar (more than 110 mg/dL), low HDL (so-called ―good‖) cholesterol (less than 40 mg/dL for men; less than
50 mg/dL for women), high triglycerides (greater than 150 mg/dL), and overweight (especially increased belly
fat—an ‗apple‘ shape—a waist circumference greater than 40 inches for men and 35 inches for women). If you
have at least three of these risk factors, you‘re considered to have MetS. According to the criteria, 34% of
North Americans now have MetS with numbers increasing for adults, adolescents and children.
MetS used to be called ―Syndrome X‖ and has been around in various forms and definitions for about 80 years.
During recent years, controversy about its definition and significance has emerged. The biggest complaints
are that MetS had too many definitions and there has been a lack of clarity about its role and value in clinical
practice. Though MetS is a lumping together of risk factors that doctors often see together, there‘s no proof
that it‘s a clear-cut illness in itself. Most scientific reports indicate that, as a group of measurements, it is no
better at predicting heart attacks, diabetes, or disease progression any better than adding up its individual
components—the whole is not greater than the sum of its parts. And placing absolute meanings to a group of
specific measurements doesn‘t work because there are myriad individual differences. However, a fixed
definition of MetS has been sought and won. We now have an almost-precisely-defined label (with some
controversy remaining). There‘s no doubt that many risk factors for diabetes and cardiovascular disease are
often found in combination. But nailing down an exact combination is not accurate and not possible.
Many fingers point to overweight and obesity as central to the development of MetS. Yet not all obese people
develop MetS and not all people with MetS are obese. It‘s more likely that there are a number of causes
including lifestyle—particularly diet and exercise—and other environmental factors (including toxic load). A
core issue is lack of good nutrition: during pregnancy, childhood, or adulthood. It‘s known that MetS can be
avoided or successfully overcome with lifestyle modifications. Although genetic variations are blamed for just
about everything these days including MetS, overall risk attributable to any single genetic morphing is minute.
Instead, subtle alterations in how genes are expressed do seem to increase risk. How genes are expressed
relates to how a person lives his/her life. Nutrition and exercise, for example, influence how genes are
expressed. Altered mitochondria (cellular energy factories central to metabolism) have also been implicated in
MetS. Lowered function or dysfunction of mitochondria can result from poor nutrition, toxic overload, lack of
physical activity, and other factors. Risk of MetS is higher if a person is already headed towards type 2
diabetes, has low blood sugar tendencies, trouble losing weight despite dieting, brain fogginess, energy
crashes, phlebitis or other hyperviscosity syndromes, angina or other cardiovascular problems, unexplained
loss of sex drive or impotence. When most of these symptoms occur, insulin signaling pathways may not be
working. Insulin resistance is a major consequence of this disruption. And insulin resistance is a common
thread that runs through the cluster of signs linked to MetS. It‘s the only way that researchers have found to
explain the collection of abnormal measurements that make up the definition of MetS. 1
Insulin resistance is reduced sensitivity in cells (such as muscle and fat cells) to the action of insulin. It‘s really
a dysfunctional response to insulin, the hormone that plays a big role in orchestrating the body‘s use and
storage of nutrients. Insulin is involved in regulating carbohydrates, fats, and protein. Normally, insulin
stimulates production of proteins and molecules involved in the function, repair, and growth of cells. Its primary
job is to regulate levels of blood sugar (glucose). After we eat, glucose levels rise, triggering the secretion of
insulin from the pancreas. Insulin helps to transport glucose from the blood stream into muscle cells and other
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cells where the glucose is used as fuel for producing energy. Insulin also converts glucose into glycogen (the
storage form of glucose placed in the liver and muscle tissue) which is also used for energy production. Insulin
inhibits excess production of glucose by the liver, stimulates production and storage of fats in fat depots and in
the liver, and suppresses the release of excess fat (primarily triglycerides). The more sensitive your cells are
to insulin, the more efficient the transfer of glucose into cells becomes. But if cells become insulin resistant,
the pancreas has to make and secrete higher amounts of insulin in an attempt to accomplish these goals.
Instead of being used to make energy, some glucose is converted into fatty acids and stored as fat in the liver
and throughout the body. Fats, rather than glycogen, accumulate in muscles, for example. When insulin‘s
influence on cells to convert glucose into energy no longer works properly, the individual is tired, always
hungry, usually craving carbohydrates, and often gaining weight.
As insulin and blood sugar levels drop in the hours after a meal, they allow fatty acids to be moved from stored
fat and signal the mitochondria to ‗burn‘ these fatty acids to make energy. The ability to switch easily between
glucose and fat for fuel is a key feature of healthy people. With insulin resistance, these natural responses
break down. The natural system of feedback loops is overwhelmed or degraded; disease is often the result—
―often‖ but not always. Even among healthy people, measurements of insulin-stimulated glucose uptake,
insulin sensitivity, and insulin resistance will vary by 600% to 800%, an enormous range. According to Dr
Gerald Reaven of Stanford University (who did much to convince researchers to take insulin resistance
seriously), a quarter of this variation is due to differences in physical fitness and another quarter due to weight.
Yet the same wide variation is found in obese people—a third of whom are relatively insulin sensitive (not
resistant). When insulin resistance occurs, the liver‘s function is impaired and the kidneys increase pressure
on blood vessels. Although other cells (in addition to the liver and kidneys) can also clear out insulin—muscle,
fat, gastrointestinal, fibroblasts (which make connective tissues), and monocytes and lymphocytes (white blood
cells)—they can‘t handle the overload resulting from a stressed liver. Gradually the tissues become more
insulin resistant. Scientists haven‘t been able to pin down the causes of insulin resistance at a cellular level.
There are too many theories. One theory is that cells become essentially poisoned by fat. A rival idea is that,
as fat cells increase in size accumulating fat, they release inflammatory molecules that cause insulin resistance
and damage elsewhere. So far, no one can say either of these ‗fat‘ concepts causes insulin resistance.
Sherry A Rogers, MD, offers other verifiable causes. One is consumption of trans fatty acids found in many
processed and fried foods—from commercial salad dressings and baked goods to French fries and fried
chicken. Another is chemicals that leach from plastics (plasticizers or phthalates) such as food and drink
containers which skew our biochemistry and are stored in fat cells. Plasticizers affect peroxisomes, functional
structures within cells that moderate sugars, cholesterol, fatty acids, and triglycerides as well as participate in
energy and healing chemistry. When peroxisomes are poisoned and polluted with plastic chemicals, they no
longer function normally. Plasticizers damage the cell‘s insulin receptors so that insulin is incapable of getting
glucose inside the cell. Once phthalates are in the body, they compromise the ability to make enough DHA
(docosatetraenoic acid)—an omega-3 fat—which can help correct the insulin resistance. Other long chain fatty
acids become abnormal and are also prevented from helping the healing process. Every one of us now has
plasticizers in us, even newborn babies. Dr Rogers is also convinced that nutritional deficiencies are one of
the primary causes of MetS and that every person with MetS has such deficiencies.
There is evidence that excess alcohol consumption suppresses the use of fat for energy, elevates insulin and
free fatty acid concentrations, and increases amounts of substances, such as lactate, that influence glucose
production in the liver. Large amounts of alcohol increase insulin concentration, blood pressure, and glucose
and fat production in the liver. Processing and excreting the alcohol induces nutrient loss that may contribute to
MetS. Smoking appears to be another contributor to MetS. It reduces insulin sensitivity, increases insulin
resistance, elevates triglyceride levels and lowers HDL (so-called ―good) cholesterol concentration. Leading a
sedentary life is another MetS donator. Regular physical activity promotes glucose uptake through increased
activity of glucose transporters and enhances insulin sensitivity. Inadequate sleep also plays a role in MetS.
Data indicate that ―disordered carbohydrate metabolism‖ is linked to insulin resistance. Refined sugars and
other refined carbohydrates can lead to big blood sugar highs and lows. When you eat or drink refined sugar
(especially sucrose, dextrose, fructose, and high fructose corn syrup), your blood sugar spikes much higher
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than when you eat sugar as part of a whole food (such as fruit, whole grains, sugar cane, raw honey). Nearly
everyone‘s pancreas reacts to refined carbs by making a huge amount of insulin to help clean the excess
sugar from the blood stream. As the years go by, the pancreas is required to make more and more insulin to
keep blood sugar levels under control. Eventually cells become increasingly resistant to the insulin. In addition,
the liver responds by producing more LDL cholesterol to deal with damage, the kidneys retain excess sodium
and/or the adrenal glands secrete too much epinephrine in response to the stress (upping blood pressure),
more fats are produced (usually belly fat). High fructose corn syrup is especially culpable for insulin resistance
since it‘s not handled like other sugars and places a lot of stress on the liver.
Low intakes of many nutrients—leading to deficiencies—are common in people who develop MetS. Various
nutrients improve insulin sensitivity including chromium, vitamin C, copper, iron, vanadium, zinc, carotenes,
and others. Since premature breakdown of fats is increased in people with insulin resistance, deficits of fatsoluble vitamins (A, D, E, and K) often occur. How food is cooked can affect insulin sensitivity. High-heattreated foods (grilled, fried, roasted) and industrial foods that are highly cooked (such as corn flakes, coffee,
dry cookies, well-baked bread with browned crust) produce far more AGEs (advanced glycation end products)
than foods cooked at lower temperatures (steamed, low-temperature baking) or foods eaten raw or nearly raw.
AGEs are formed during cooking by a reaction between sugar molecules and protein or amine-containing fat
molecules. AGEs may change protein structures and contribute to insulin resistance as well as cardiovascular
disease, diabetic complications, fibromyalgia, chronic inflammation, and more. AGEs may cause glucose in the
blood to react with hemoglobin, forming hemoglobin A1c, a marker used in diagnosing diabetes. 2
Food and dietary patterns figure predominantly in both cause and cure of MetS. To prevent or overcome
MetS, it‘s crucial to remove most or all refined carbohydrates from the diet. This means refined sugars, artificial
sweeteners, refined flours, refined grains (white rice, etc.) and all nonfoods made with them—in other words, a
big part of the usual Western diet. Sodas and other highly-sweetened beverages are linked to the prevalence
of MetS. Refined, highly-processed nonfoods contain little or no valuable nutrients. Plus many nutrients must
be recruited from body stores to processes such nonfoods. Over time, inadequate intake and depletion of
nutrients makes the body unable to function properly, culminating in illness or disease. The burden that
nonfoods put on the body contributes to suboptimal nutrient levels found in people with MetS. Some studies
indicate that more protein and less carbohydrate in the diet results in lower fasting insulin levels. But they often
don‘t differentiate between the types of carbohydrates consumed—whether refined or unrefined. When this
distinction is made, it becomes obvious that refined carbs are the disruptors, not natural, unrefined real-food
carbohydrates. It‘s also essential to eliminate trans fats (partially hydrogenated oils), refined vegetable oils (in
many items like mayonnaise, salad dressing, cooking oils, and more), and foods fried in vegetable oils.
Foods high in fiber and complex carbohydrates are beneficial. Coincidently, these foods are also rich in
needed nutrients. They include fruit, vegetables, whole grains, nuts, seeds, and beans, all shown to protect
against and improve MetS. Fermentation of nondigestible carbohydrates (primarily certain fibers) increases
tissue glucose uptake and increases insulin sensitivity. Natural protein-containing foods are beneficial (beef,
lamb, pork, poultry—preferably pasture-fed and free-range—fish, eggs, raw milk products, nuts, seeds). The
body breaks proteins down into amino acids or peptides (groups of amino acids), some of which are stored in
the liver for the manufacture of glucagon which allows for the release of glycogen (the storage form of
glucose)—the body‘s backup system when glucose levels start to fall after a meal. No protein means no
glycogen and no backup glucose which triggers intense cravings for sugars or other carbs as the body signals
for more glucose. Natural fats help satiety, are usually easy to digest, and are burned for fuel quickly and
efficiently. Natural fats tend to speed up metabolism in general while slowing the digestion of sugars. Keep in
mind that we are each unique, so how much protein, fats, and carbohydrates each of us needs may differ.
There is some evidence that whole fat dairy products may decrease insulin resistance, help lower excess
weight, and reduce risk of developing type 2 diabetes. One reason is trans-palmitoleic acid, a type of fat found
in whole fat dairy products. Although saturated fats and fats in general have been accused of contributing to
MetS, researchers admit that there are still questions about the importance of the quantity of individual fats as
well as mechanisms underlying their effects. In other words, they don‘t know that any natural fats contribute to
MetS and, even if they did, it‘s not known how it would happen. ―Overall,‖ says a report from PubMed, ―there is
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a lack of data.‖ We do know there is widespread use of refined, altered vegetable oils; they stress the liver and
contribute to a mucked-up metabolism. Trans fats are often not distinguished in studies from natural saturated
fats, so saturated fats are unfairly accused of metabolic disturbances. Trans fats cause elevations in LDL (socalled ―bad‖) cholesterol, lower insulin resistance, and contribute to type 2 diabetes and cardiovascular
disease. People with elevated insulin usually have high trans fats in their bodies. They are also low in omega-3
fatty acids. High triglycerides (usually found in MetS) are a marker of excess refined carbohydrate—not fat—
intake. However, people with MetS may develop elevated triglycerides from eating fats if they have
compromised liver function. In this case, the liver has fatty degeneration and is inflamed (indications of injury)
so fats cannot be properly broken down and processed. Scientists cannot categorically blame fats in general
for causing MetS. They can blame ―fat quality.‖ Although saturated fats are often accused, studies, such as
one in the UK, do ―not support the hypothesis that‖ replacing saturated fats with monounsaturated fats or
carbohydrates ―has a favorable effect‖ on insulin sensitivity. People differ in response to various diets used in
studies that contain various fats. Researchers cannot honestly pin the blame on any one type of natural fat.
Epidemiological studies show that MetS is related to a poor diet low in micronutrients. Diets that stress mostly
natural real foods and downplay refined, over-processed nonfoods all appear to help prevent and overcome
MetS. These include Mediterranean-type diets (vegetables, fruit, whole grains, fish, nuts, olive oil), Nordic diets
(high-fiber plant foods, fruits, berries, vegetables, whole grains, unrefined oils, nuts, fish, low-fat milk products),
Spanish Mediterranean diets (green vegetables, salads, fish, moderate red wine, virgin olive oil, fish, beans),
traditional diets (such as a beans-and-unrefined rice pattern or a seafood, coconut product, fruit, and vegetable
pattern), or a ―healthy‖ diet (high in fruit, cruciferous and green leafy vegetables, other vegetables, legumes,
poultry, whole grains). All these and other helpful diets stress real, un-messed-with whole foods and are low in
or devoid of refined, over-processed, altered nonfoods. Any diet consisting of real foods with plenty of fiber,
some natural fats, plenty of vegetables, some protein, and minimal or no refined carbohydrates successfully
―treats‖ MetS. It‘s the ―overall nutritional quality‖ of the diet that prevents and alleviates MetS. The more
nutrient-dense foods consumed and the less low- or non-nutrient foods consumed, the better the outcome.
Mounting evidence points to the importance of a ―personalized nutrition‖ approach—diet tailored to the
individual. Some people are more efficient at burning fat, others are more efficient at burning carbohydrates,
for instance. Since genetic tendencies are influenced by lifestyle, getting the right balance of nutrients and
pytochemicals that interact with genes will affect metabolic pathways. For example, certain phytochemicals
have been found to influence genes to burn fuel more efficiently. Real food supplies the variety and balance
needed for selective absorption of an individual‘s needed nutrients. 3
A number of studies have indicated that eating foods low on the glycemic index (GI) work better than a
conventional, low-calorie, low-fat diet. Many foods high on the GI are refined carbohydrates, so eliminating
such nonfoods can only be beneficial. Yet some nonfoods are low on the GI due to their content of fat which
makes them slower in spiking blood sugar levels. That‘s why some studies looked further. One study, for
example, found that total refined sugar intake—rather than foods high on the GI or glycemic load—was linked
to higher body fat, lower insulin sensitivity, and lower insulin secretion. The so-called glycemic load doesn‘t
help metabolic risk markers. Even studies that connect low GI foods with better outcomes admit that blood
sugar response to different carbohydrate foods varies substantially. Results of studies using the GI are highly
variable and unreliable. The debate continues about the GI‘s relationship to MetS. 4
Specific nutrients studied and found to be beneficial in preventing or alleviating MetS include:
Alpha-lipoic acid, a coenzyme, improves blood glucose control and insulin resistance, and aids production of
ATP (adenosine triphosphate, cellular energy currency). It helps regenerate vitamins E and C, and glutathione.
Omega-3 fatty acids improve insulin action, insulin resistance, and blood fat profiles. People with higher ALA
(alpha-linolenic acid, a parent omega-3) have a lower incidence of MetS. Fish oils reduce risk of MetS.
Amino acids. Arginine promotes blood vessel health and may enhance insulin secretion and action. Lcarnitine aids in improving insulin levels. Proteins in whey improve fasting blood fats and insulin levels.
Chromium improves blood glucose control and insulin action. There is a link between chromium status and
insulin resistance. Chromium benefits blood sugar levels, blood fats, and insulin resistance.
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Calcium-rich diets plus exercise may lower risk for MetS.
Magnesium reduces blood pressure and improves blood sugar regulation, insulin resistance, and insulin
action. People with MetS tend to have a low ratio of magnesium to calcium in their cells.
Zinc deficiency (and deficits of chromium, manganese, vanadium, selenium) contributes to MetS development.
Zinc is required to convert B6 into its active form, omega-3 EPA into DHA, and carotenes into vitamin A.
Selenium intake reduces an early marker of MetS manifestations.
Vanadium helps improve blood sugar control, increase insulin-receptor sensitivity, and improve insulin action.
It can reduce high glucose levels, hemoglobin(1c), triglycerides, total cholesterol and LDL cholesterol.
Coenzyme Q10 improves blood glucose control, improves insulin action, reduces elevated blood pressure,
and improves blood fat profiles.
Vitamin C complex promotes blood vessel health, reduces elevated blood pressure, improves blood sugar
control, and improves insulin action. It can reduce fasting blood glucose, triglycerides, LDL cholesterol, serum
insulin, and glycated hemoglobin (hbA(1c)).
Vitamin E complex promotes blood vessel health, improves insulin action, and improves insulin sensitivity.
Nutrients called antioxidants—including vitamins A and C and E, bioflavonoids, selenium, zinc, ellagic acid,
etc.—are misused as separated or synthetic compounds; ―single high-dose antioxidants are best avoided.‖
Carotenes (convert into vitamin A), vitamin E, and other fat-soluble vitamins are often deficient when insulin
resistance exists. Carotenes (beta-, alpha-, lycopene, and total carotenoids) may help protect against MetS.
Vitamin D deficiency increases risk for insulin resistance, higher plasma glucose levels and development of
MetS along with its related metabolic derangements. Adequate vitamin D is linked to substantially lower risk.
Vitamin K1 (phylloquinone) intake may play a beneficial role in glucose balance.
B vitamins are needed for proper metabolism of fats, carbohydrates, and proteins. Folate (food form of folic
acid) and vitamin B12 can improve insulin resistance and blood vessel dysfunction.
Phosphatidyl choline (as in lecithin) supports proper function of insulin receptors in cells. Choline and betaine
must be balanced; too much choline with inadequate betaine can cause an imbalance that may contribute to
MetS components. Whole foods do not cause such an imbalance. Inositol also improves insulin resistance.
Quercitin, a bioflavonoid found in fruits and vegetables, helps to inhibit an enzyme that converts blood sugar
to sorbitol, enhances normal insulin secretion, and protects pancreatic cells from injury. 5
All the above nutrients—and all other needed nutrients—are best obtained from whole foods and whole food
supplements. Taking isolated or manufactured chemical imitations does not have the same beneficial effects.
Iron overload, for example, from non-food sources of iron (used in many supplements and processed foods)
has been linked to increased risk of MetS. Or taking large amounts of isolated glucosamine sulfate (to relieve
arthritis) may spur development of insulin resistance and elevated insulin levels. Organically-raised foods
have a much higher nutrient value than do non-organic foods. The work of detoxifying various environmental
chemicals to which we are exposed or may eat in non-organic and processed foods uses up a lot of nutrients.
Herbs that may improve aspects of MetS include:
Gymnema sylvestre helps to improve blood sugar control. It has even been used with blood-sugar-lowering
drugs or insulin for treating people who already have diabetes, causing additional reductions in glucose levels
and glycosylated hemoglobin. Gymnema is effective in lowering total cholesterol, LDL, and triglycerides.
Fenugreek seeds lower cholesterol and triglycerides and have anti-diabetic effects.
Holy basil helps to reduce elevated blood sugar levels.
American Ginseng may prevent sharp rises in blood sugar after eating even refined sugars.
Cinnamon mimics insulin and prevents some damage caused by insulin resistance and high blood sugar. It
helps in the regulating cholesterol. Using ½ teaspoon a day may be fine, but more should be avoided since
people sensitive to coumarin, a compound in cinnamon, can develop liver damage.
Hibiscus helps reduce blood sugar and triglycerides and increase HDL cholesterol.
Maitake mushroom has a weak insulin-sensitizing effect. 6
Anyone diagnosed with MetS or who shows signs attached to it can do much to overcome or prevent it. A diet
of real, organic whole foods, avoidance of refined carbohydrates and other over-processed nonfoods, some
real food supplements, regular physical activity, moderate consumption of alcohol, and avoidance of smoking
can reap amazing rewards including healthy weight loss if needed. Supplements to consider include:
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Just Before Two Meals: After Two Meals:
1 Cataplex GTF – chew or break in mouth 1 Chlorophyll Complex
2 Cataplex C – chew or break in mouth 1 Tuna Omega-3 Chewable – chew
1 Pancreatrophin PMG – chew or break in mouth 1 Cellular Vitality
1 Betafood – chew or break in mouth Before One Meal:
1 Gymnema (MediHerb) 2 tablespoons Whey Pro Complete as part of a shake
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By Judith A. DeCava, LNC, CNC
© 2011, Judith A. DeCava