Diabetes is a chronic disorder marked by increased blood sugar (glucose). Complications often develop
including heart disease (such as heart failure), vascular diseases (including hypertension, heart attack, stroke),
poor circulation (causing problems such as foot ulcers), eye damage (retinopathy that can lead to blindness),
kidney disease (progressing to kidney failure), bone fractures, arthritis, various types of cancer, increased
inflammation without resolution, poor healing, dental disease, loss of cognitive function, neuropathy (nerve
damage) and depression. Type 1 (‘juvenile’ or ‘insulin-dependent’) diabetes occurs when the pancreas does
not produce enough insulin. Type 2 diabetes (T2D) occurs when the body produces insulin but it doesn’t work
well—it is unable to process glucose appropriately or lower glucose levels effectively due to insulin resistance.
T2D used to be referred to as ‘adult-onset’ diabetes but it is becoming more common in children and teenagers
as well as adults of all ages. It now accounts for 90% to 95% of all diabetes. Glucose, the end product of
carbohydrate digestion, is needed by cells for energy and growth. Insulin helps glucose (and some fats and
proteins) enter cells for either oxidation (burning) or storage (of excess glucose as glycogen in the liver). With
insulin resistance, glucose can’t properly enter cells. Instead of the cells using glucose as fuel, it builds up in
the bloodstream, leading to hyperglycemia (high blood sugar). For a while, the pancreatic beta-cells pump out
more insulin to compensate for the added demand so blood sugar levels stay under control. But eventually the
pancreas can’t keep up and the body tips over into diabetes. As insulin output falls, blood sugar climbs. 1 T2D
is now defined as an epidemic. The number of North Americans afflicted is now more than double what it was
in 1991. At the beginning of 2011, there were approximately 25.8 million children and adults in the US (8.3% of
the population) with diabetes. Another 25% of the population has pre-diabetes. However, the definition of T2D
has changed over the years. For example, in the 1970s a fasting blood sugar over 140 resulted in a diagnosis;
in 1997 it was decided that a fasting blood sugar over 126 was diabetes. That ‘little’ alteration converted over
1.6 million people into diabetics. Medical treatment guidelines have also changed strikingly since the 1980s. 2
TESTS. Glycated hemoglobin (HbA1c), a measure of long-term average blood sugar, was previously used
only to monitor glucose control, but is now used to diagnose diabetes. A level of 6.5% or higher is thought to
indicate diabetes. However, one sample does not tell the whole story; interferences occur that can cause a
deceptive result. Also, “the optimum HbA1c seems to vary between patients.” A glucose tolerance test is
usually used and/or random glucose, fasting glucose, and 2-hour glucose concentrations after an oral glucose
(a refined sugar) challenge. Some people who don’t have diabetes react with a blood sugar spike. A 2012
study found that screening people at risk didn’t reduce all-cause, cardiovascular, or diabetes-related mortality
within 10 years. So “benefits of screening might be smaller than expected...” The recommended systolic blood
pressure ceiling of 130 mm Hg was recently raised to 140 mm Hg due to an analysis showing that intensive
blood pressure control (with drugs) did not decrease deaths or heart attacks and only slightly lowered risk of
stroke. 3
In the beginning stages of diabetes, many people have no symptoms or mild symptoms that aren’t
suspected of being diabetes. Symptoms may include: increased thirst, increased hunger, increased urination
(especially at night), sores that don’t heal, fatigue, unaccounted-for weight loss, blurred vision. Although T2D
was thought to involve genetic components, it is becoming clear that, if genes are involved, it is epigenetic
modifications—factors that turn genes on or off—that create the tendency. Epigenetic influences are primarily
environmental including diet, activity levels, chemical exposures, medications, etc. 3
CAUSES. There are many risk factors including poor diet, mother’s diet, a sedentary lifestyle, impaired glucose
tolerance, family history of diabetes, high blood pressure, and others. But the leading cause of T2D is excess
weight or obesity—being overfed but undernourished, over-agitated but underactive. 4 Approximately 80% of
people with T2D are overweight or obese. Eating too much (often due to inadequate nutritional value of the
foods—really, nonfoods) results in more fat storage as subcutaneous fat (beneath the skin) and visceral fat (in
and around organs and tissues such as the liver, heart, muscles, digestive tract. Notably, “excess visceral fat
and insulin resistance, but not general adiposity [excess fat], were independently associated” with pre-diabetes
and T2D. Fat tissue is distributed differently than it is in people without diabetes. Excess stored fat may block
2
an insulin-signaled glucose transporter that normally ferries blood sugar into the cells. 5 Excess liver fat can be
an even better predictor of metabolic dysfunction than visceral fat. It may explain why even a modest drop in
weight can lower fasting blood sugar levels with no change in muscle fat. With some weight loss, the liver
responds better to whatever insulin is made, sometimes enough to control glucose metabolism. The liver is
one of the most metabolically active organs in the body. Among its many functions are bile production (to
emulsify fats), conversion of monosaccharides to glucose, storage of glucose until its energy is needed,
deamination of excess amino acids for use in energy production, detoxification, synthesis of lipoproteins and
cholesterol for transport of fat to tissues, and conversion of fatty acids to ketones or acetyl groups for use as
energy sources. The liver may play a larger role in blood sugar metabolism than the pancreas. 6
Numerous toxins can play a role in causing or worsening T2D such as: inorganic arsenic, persistent organic
pollutants (such as pesticides that accumulate in the environment), bisphenol A and phthalates (from plastics),
dioxins, fresh-water fish contaminated with DDE (major breakdown product of DDT), and a number of organophosphate pesticides. 7 Avoiding toxic exposures and periodic detoxification programs may help. Various drugs
can increase T2D risk including antidepressants, ADHD medications and statins. Some drugs can worsen
diabetes by interfering with insulin or blood sugar levels, including: diuretics, over-the-counter decongestants,
steroids (cortisone, prednisone) and beta-blockers. Others can alter effects of diabetes medications.
8
MEDICAL TREATMENT. Gastric bypass surgery for the obese may lower blood sugar and eliminate the need
for diabetes drugs. But nutrient deficiencies and other complications can develop. There are many antidiabetes
drugs. Some stimulate the pancreas to produce more insulin. Others work on the liver to decrease the amount
of sugar released into the blood. Some are “insulin sensitizers” that attempt to make cells more sensitive to
available insulin. Starch-blocking drugs slow carbohydrate digestion. The popular Metformin lowers blood fat
levels and attempts to prevent the body from producing more sugar. Insulin lowers blood sugar though this
does not address the underlying cause of T2D. Actually, none of the drugs approach underlying causes; they
don’t cure diabetes and have many side effects. There is no evidence that the drugs currently available reduce
risks of long-term complications such as heart disease, stroke, peripheral vascular disease, kidney disease,
retinopathy, or others. Some actually increase risks, including thiazolidinediones (Avandia, Avandaryl, Duetact
or Actos) which increase heart attack rate 43% and increase heart failure risk. Some drugs raise fracture,
anemia and macular edema risks. Most drugs are associated with a greater risk of death from any cause. All
(except Metformin) can contribute to more weight gain and further increases in insulin resistance; one of the
worst is insulin. Metformin can cause vitamin B12 deficiency. Other drugs lead to deficiencies such as folate or
CoQ10. Some drugs increase risk of pancreatitis and cancers such as bladder or pancreatic cancer. Only
about 40% of patients reach target blood sugar levels with standard therapies; many remain uncontrolled or
progress to inadequate control over time. Most people take 2 or 3 diabetes drugs. A new drug type (Invokana)
poses serious risks (falls, dehydration, cardiovascular events, dizziness, renal impairment) that outweigh its
limited benefits. 9 Tight control of blood pressure and cholesterol with drugs increases risk of death. Aggressive
blood-sugar lowering produces only minor benefits and may cause serious drops in blood sugar that can harm
the brain, cardiovascular system, increase risk of death, and more. The intensity of medical treatment needed
“almost certainly varies between individuals;” blood sugar and other targets should be individualized. “Good
glucose control is a potentially life-saving intervention,” says Edwin AM Gale, MD, “but it remains to be
determined what we should use, when, and how vigorously we should use it, and for how long.” 10
LIFESTYLE. Lifestyle is the foremost and often only cause of T2D. Studies show that intensive lifestyle
intervention is very effective in preventing T2D and improving the health of people with diabetes. Early
diabetes can be overcome. Because T2D “is largely rooted in reversible social and lifestyle factors, a medical
approach alone is unlikely to be the solution.” Sadly, in “this respect, medicine might be winning the battle of
glucose control, but is losing the war against diabetes.” Dr Osama Hamdy, MD, PhD, a medical director in
Boston, stated: “We’ve been treating diabetes for 40 years by adding more and more medications, with no big
improvements. But if you act early, keep the weight off, and maintain a healthy lifestyle, you can put this
disease in remission forever.” Research supports “the idea that significant improvements in health may be
attained through lifestyle adjustments.” 11 A healthful diet and exercise have been shown to beat drugs for
improving fitness, glycemic control, insulin sensitivity, blood fats and cardiovascular risk factors. Exercise
quickly lowers blood sugar. When muscles are exercising, glucose and other nutrients can enter muscle cells
3
even in the absence of insulin. Both aerobic and resistance (weight training) exercises reduce HbA1c, improve
insulin resistance and glycemic control, increase muscle mass, decrease artery-wall thickening and reduce
adiposity. Poor sleep patterns or sleep deprivation can impair glucose metabolism and lower control of blood
sugar levels; improving sleep patterns improves long-term outcomes. 12 Diet, exercise and improved sleep are
all important for significant weight loss which improves glycemic control, insulin sensitivity and cardiovascular
risk factors and lessens or eliminates the need for drugs to lower blood sugar, blood pressure and blood fats. 13
DIET. T2D is associated with modern processed-foods; it is rarely seen in cultures relying on a more traditional
diet and way of life. Eating whole natural foods (predominantly organic and non-GMO) to optimize nutrient
status can have profound effects. The quality and source of foods influence all biological systems involved in
insulin resistance and T2D.
14 Avoid: refined sugars like sucrose, corn syrup, high-fructose corn syrup; soda
and other refined and highly-processed items including white rice, white bread, processed meats, refined salt,
and the like. Artificial sweeteners disturb areas of the brain that control appetite and satiety and cause other
imbalances. Include: plenty of fresh vegetables and fruit (restricting fruit does not improve glycemic control),
legumes (lower glucose and insulin), whole grains, nuts and seeds (help glucose control, reduce HbA1c and
LDL cholesterol), and dairy products (certified raw milk products, yogurt and aged cheeses are best; whey
reduces post-meal blood sugar spikes). There is a direct link between fiber—soluble and insoluble—and the
glycemic response to specific foods. Foods containing fiber are vegetables, fruits, whole grains and legumes;
fiber supplements such as inulin or psyllium are also helpful. The recommended amount of fiber is 25 to 35
grams per day; few Americans consume that much. Many traditional cultures ate 3 to 5 times as much.
15
There is a huge difference between natural, whole nutrient-dense foods and refined, over-processed, bogus,
chemicalized nonfoods. The latter are often loaded with added refined or artificial sweeteners and other refined
carbohydrates, contain various artificial ingredients, are low in nutrients, low in fiber, usually digested quickly
so fewer calories are burned, often contain altered or refined or fake fats, and tend to be addictive (leading to
overconsumption). The American Diabetes Association recently updated its nutrition guidelines for diabetics.
Rather than a one-size-fits-all diet, the new recommendations favor individualized plans that take into account
a person’s lifestyle and metabolic needs. Previously a diabetic diet dictated how many grams of carbohydrates,
protein and fats that should be consumed each day based on the person’s weight. It is now conceded that
there is no ideal amount of these nutrients for everyone and each person should have a dietary strategy that is
best suited for him or her. Whole grains, fruits, vegetables, legumes and dairy products provide carbohydrates
that are less likely to produce spikes in blood glucose levels. Foods and beverages that contain added refined
sugars, refined grains, etc. are “more likely to cause fluctuations in blood glucose and they are often ‘empty
calorie’ foods that contribute little or nothing in the way of valuable nutrients.”
16 No news to us.
Protein/Fat/Carbohydrates. Research results regarding high-protein, high-fat or high-carbohydrate diets versus
low-protein, low-fat or low-carbohydrate diets vary. Some studies show that a low-carbohydrate, high-protein
diet improves glycemic control, improves insulin sensitivity, increases plasma glucagon, lowers insulin and
triglycerides. But fiber intake is low. 17 Other studies find that low-carbohydrate Mediterranean-style diets result
in better glycemic control and less need for diabetic drugs than low-fat diets.
18 Some studies show that high
carbohydrate, low protein and moderate or low fat diets improve glycemic control and insulin resistance. Lowfat vegetarian diets (that restrict refined sugars) can lower fasting glucose, weight, blood pressure, HbA1c, total
and LDL cholesterol. Some research indicates that consumption of excess fat impairs insulin receptors. Other
studies report that eating lots of red meat—especially processed meats—increases T2D risk. A low-fat, highfiber diet may promote weight loss without causing unfavorable alterations in blood fats or glycemic control. 19
Natural, unaltered fats (such as fish, nuts, unrefined oils, butter) can reduce blood sugar and insulin levels.
Omega-3 fats are beneficial, no doubt because most people consume excessive omega-6 fats from refined
vegetable oils and commercial meats that contain less omega-3s than pasture-raised meats. Some research
condemns saturated fats; others simply condemn high amounts of fats. There is research showing that either
low-fat diets don’t cause adverse glycemic effects or do cause adverse glycemic effects. Mary G Enig, PhD,
explains that, in most studies, the actual amount of saturated or polyunsaturated or trans fats in diets is not
measured. What occurs to people who eat a diet high in natural saturated fats compared to those eating a lot
of refined vegetable oils is not explored. “Saturated fats have no effect when appropriate comparisons are
made.” T2D was unheard of a hundred years ago when people’s diets were rich in saturated fats. When people
eat less saturated fat, they end up eating more detrimental trans-fats. Trans fats are being eliminated from
4
processed foods but are often replaced by just-as-bad contrived fats.
20 The amount of carbohydrates, protein
and fat needed vary with the individual. “The nutrient composition of the diet should be individualized…” 21
Acidosis and intolerances. Russell M Jaffe, MD, PhD, shows that, when people with T2D eat foods that provide
insufficient minerals to buffer metabolic acids, cellular alkaline reserves are gradually depleted. Deficits of
buffering minerals (magnesium, potassium, zinc, and others) result in intracellular metabolic acidosis that
causes reduced cellular energy production and impaired toxin removal. Intolerances can develop to just about
any food, chemical or contaminant, causing immediate or delayed reactions. When the body is imbalanced,
distressed, suffering a large toxic load or deficient in needed nutrients, it cannot respond healthfully or properly
to substances. A Health Studies Collegium study evaluated sensitivities to environmental chemicals, foods and
food additives in diabetics. By avoiding reactant items and developing an individualized natural, nutrient-rich,
repair-stimulating diet, participants experienced significant benefits such as decreased insulin and HbA1c.
Control subjects receiving only American Diabetes Association guidelines had much less benefit. Reducing
toxic load, immune load, neurohormonal distress and gastrointestinal irritants plus providing sufficient nutrients
and foods for detoxification and healing processes improve diabetic control. Increased intestinal permeability
(leaky gut) can occur from insults or injuries (from processed nonfoods, drugs, toxins), maldigestion and repair
deficits. Avoiding reactant foods is the first step to reduce leaky gut; providing foods and nutrients to support
repair and healing is next.
22 Dr Patrick Kingsley finds that diabetics “inadvertently eat certain foods on a fairly
regular basis that cause their blood sugar to go up too high.” These foods are identified and eliminated from
the diet. A three-week elimination diet, then reintroduction (one food at a time) identifies such items. When
reintroducing a food, a blood sugar measurement should be taken first thing in the morning; then the food
should be consumed for breakfast followed by another blood sugar measurement an hour later. Do not test a
food if the blood sugar is already high before breakfast. William Philpott MD treats diabetics by identifying
foods that individually raise blood sugar levels, then supplying needed nutrients and digestive support. 23
GLYCEMIC INDEX. Some doctors recommend eating only foods rated low on the glycemic index (GI). Others
question the GI validity. Some endorse using the glycemic load (GL) instead. The GI only indicates how fast a
single food turns into blood sugar. It doesn’t take into account how much of the food is eaten or that foods are
rarely eaten alone; eating some protein and/or fat with a carbohydrate greatly lowers its GI effect. The GL is a
calculation of the GI multiplied by the amount of carbohydrate in a serving and divided by 100; it takes into
account the GI, the amount of carbohydrate, and how both impact blood sugar. For example, both white bread
and carrots have high GI numbers. But the GL of 2 slices of white bread is more than 5 times higher than the
GL of ½ cup of carrots. 24 Some nutrient-rich foods are rated as high-GI while some nutrient-poor foods are
rated as low-GI. For instance, sugared chocolate has a lower GI than oatmeal. White potatoes are high on the
GI, yet eating other vegetables and a protein with them slows digestion and lowers the GI. Also, the effect of a
food varies from person to person. “Measurements of GI and GL can vary depending on who’s doing the
testing, and studies have shown that the actual effects of foods on blood sugar vary by individuals.” One study
compared glycemic effects of 50 grams of white bread on healthy adults. The average GI was 78 for the first
test, 60 for the second and 75 for the third. Values varied 17.8% between individuals and 42.8% within
individual scores from one test to another. 25 In 2008, researchers compiled a new set of GI guidelines. Some
of their conclusions oppose other research. For example, they rated whole wheat foods high and refined pasta
low, the opposite of earlier GI versions. Many studies show that people who eat whole grains are less likely to
develop T2D.
22 So the “wise approach…is for patients to know their glucose response to eating certain meals.
Self-monitoring of blood glucose postprandially [after meals] may become more about understanding the
patient’s response to food than monitoring the disease.” This is testing for individual intolerances. There is little
agreement about the role of the GI in managing diabetes and whether it influences the risk of diabetes. 26
SPECIFIC NUTRIENTS. Numerous studies have found alterations in micronutrient status of people with T2D.
There is confusion concerning specific requirements since studies are contradictory depending on the people
studied. Confusion is not surprising since people are not viewed in accordance with biochemical and metabolic
individuality. If supplements are used, they are often isolated or synthetic ‘nutrients’ which also confuse since
such separated/contrived compounds don’t provide the interacting, integrated, multi-nutrient complexes of real
foods. For a specific complication, a more pharmacological approach using single nutrients may be needed for
a limited time; whole foods are superior sustenance. Nutrients consistently found to be involved in T2D include:
5
Nutrient: Supports, improves or helps:
Chromium 27 Weight reduction, insulin sensitivity, glucose metabolism, HbA1c, lipid variables,
cardiovascular function. Adding biotin improves function. Deficiency common.
Magnesium 28 Nerve/ muscle pain, hypertension, cardiovascular disease, kidney disease, retinopathy,
insulin resistance, carbohydrate metabolism, enzymatic reactions. Deficiency common.
Calcium 29 Insulin sensitivity, T2D risk; vitamin D optimizes glucose metabolism effect.
Selenium 30 Cardiomyopathy, cardiovascular disease, neuropathy, glucose metabolism. Tends to be
deficient. Large isolated doses can cause variations in blood sugar levels.
Potassium 31 Insulin resistance, peripheral insulin levels. Depletion common. Avoid large doses.
Vanadium 32 Blood sugar and HbA1c levels without hypoglycemia, frequent urination, thirst, fatigue,
sugar cravings. Mimics insulin. Food sources best.
Zinc 33 Organ damage, albumin excretion (re: kidney), cardiovascular disease, HbA1c. Needed
to convert B6 to active form, P5P. Component of insulin. Deficiency common.
Copper 33 Superoxide dismutase activity, glucose tolerance, lipid peroxidation, HbA1c, insulin level.
Manganese 34 Mitochondria membranes, function. Hyperglycemic tissue damage. Often deficient.
Vitamin A 35 Insulin release from pancreas, retinopathy, kidney problems, neuropathy, slowness to
heal, excess inflammation. Large synthetic doses can inhibit insulin release.
Carotenoids 35 Glucose metabolism, retinopathy. Enzymes to convert into vitamin A may be
deficient in diabetic pancreas.
Vitamin E 36 Glucose control, insulin action, cell membranes, tissue damage, HbA1c, blood vessel
integrity, neuropathy. Isolated d-alpha tocopherol depletes gamma tocopherol (HbA1c).
Thiamine (B1) 37 Damage to nerves, blood vessels, eyes, kidneys. Blood vessel dilation, cardiovascular
disease, carbohydrate breakdown, glucose metabolism enzymes. Deficiency common.
Riboflavin (B2) 38 Glutathione regeneration for detoxification of reactive oxygen species.
Niacinamide (B3) 39 Production of glucose tolerance factor.
Pyridoxal-5-phosphate Amino acid, fat and carbohydrate metabolism. Inhibits linkage of glucose molecules
(B6) 40 to proteins including albumin. Often deficient.
Folate 40 With B12 and B6, lowers elevated homocysteine which can be caused by Metformin.
B12
40 With folate and B6, lowers elevated homocysteine. Neuropathy symptoms, foot ulcers,
kidney disease. Often deficient. Metformin depletes B12.
Biotin 41 Cofactor for glucokinase re: intracellular glucose metabolism, triglycerides.
Inositol 42 Glycemic control by mediating insulin action. Adds to chromium’s effects.
Vitamin C 43 Blood vessel integrity, kidney function, lymphocyte levels. Ascorbic acid alone may
increase cardiovascular risks. Flavonoids: insulin resistance, inflammatory biomarkers.
Vitamin D 44 Blood vessel and nerve function, inflammation and repair.
Amino acids 45 Leucine: insulin secretion, protein synthesis, glycemic control. Glutamine: hormones
Involved in meal-related insulin secretion. Creatine: glycemic control. L-carnitine: insulin
sensitivity, cellular glucose uptake, nerve conduction and regeneration, glycation.
Omega-3 fatty acids Insulin resistance, homocysteine levels, inflammation, depression risk, blood sugar
46 levels, HbA1C, blood-vessel-lining function, blood flow, triglycerides, cholesterol.
CLA 46 (Conjugated linoleic acid). Blood sugar levels. In meats and dairy products.
GLA 46
(Gamma linolenic acid). An omega-6. Glycemic control.
CoQ10 47
(Coenzyme Q-10). Often low. Glycemic control, neuropathy, blood vessel function.
ALA 48 Convert glucose into ATP. Insulin sensitivity, glucose tolerance, post-meal and fasting
(Alpha-lipoic acid) glucose, glutathione levels, HbA1c, cardiovascular & kidney complications, neuropathy.
Gut bacteria 49 Often imbalanced; composition tends to be different in diabetics.
Among the many herbs found to assist blood sugar control, insulin production or release, HbA1c levels, insulin
resistance, triglyceride and cholesterol levels are: Gymnema (if taken with anti-diabetic drugs, glucose levels
may drop significantly), cinnamon (most studied form is cassia; avoid huge doses; ¼ to ½ teaspoon per day
okay), mate tea, berberine (isolated from rhizome Huanglian or goldthread), ginger, fenugreek, curcumin
(extracted from turmeric), Bitter Melon, ginseng (also helps cardiovascular risks). Billberry and ginkgo aid
retinopathy, blood flow, blood vessel function, kidney disease. In addition to helping to lower fasting glucose,
HgA1c, cholesterol & triglycerides, silymarin, (milk thistle extract), lowers liver SGOT and SGPT elevations.
50
6
Supplemental support for the person at risk for T2D can vary, but a foundational schedule may include:
Just Before Two Meals: After Two Meals:
1 Hepatrophin PMG (chew), liver support 1 Cod Liver Oil, omega 3s, vitamins A and D
2 Cataplex B (chew), B vitamins 1 Betafood (chew), ALA, aid nitric acid production
1 Cataplex G (chew), B vitamins 1 Cellular Vitality, CoQ10, B vitamins
1 Cataplex GTF (chew), chromium, pancreas support 1 SP GreenFood, carotenes, ALA, Mg, K, etc.
1 Cataplex C (chew), vitamin C complex 1 Wheat Germ Oil, vitamin E complex
Twice per day: 1 Gymnema (Medi-Herb)
________________________________________________________________________________________
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