Reposted from Life Extensionhttp://www.lef.org/magazine/mag2012/feb2012_Doctors-Overlook-Leading-Cause-Premature-Death_01.htm
By William Faloon
The problem is that physicians are failing to determine how low blood glucose needs to be to protect against dreaded diabetic complications.
In a series of published studies, the definition of what constitutes diabetes, (or said differently, a person with high blood sugar) is about to be turned upside down.
This is not a trivial matter. The term "diabetic complications" encompasses the most common diseases of aging, ranging from kidney failure1-3 and blindness,4-6 to heart disease,7-12 stroke,13,14 neuropathy,15,16 and even cancer.17-22 This means that most degenerative disease can be traced back to undiagnosed glucose control problems, which we assert will soon become the new definition of diabetes.
High blood sugar appears to be the leading killer today, yet the medical mainstream is not properly diagnosing or treating it. The tragic result is an epidemic of diabetic complications that cripple and kill millions of Americans because simple steps are not being taken to suppress after-meal glucose spikes.
As you are about to learn, it is not just elevated fasting glucose that creates diabetic complications. Excess after-meal glucose surges have turned into a silent diabetes plague, thus mandating new steps be taken to protect against what may be the leading cause of premature death.
Fasting Glucose Is a Delayed Marker of DiabetesWhen people take blood tests to measure glucose levels, they are asked to fast for 8 to 12 hours. Doctors ask for this 8-12 hour fast because they want a consistent baseline to measure glucose and lipids in comparison with the general population.
There is one problem with this. A person who suffers from dangerously high blood sugar several hours following a typical meal may artificially drop their fasting glucose to a safe range after fasting 8 or more hours. A person’s ability to clear their blood of excess glucose 8-12 hours after eating may persist for decades, thus masking what may be a dangerous postprandial (after-meal) spike in glucose.
Even tests that measure long-term glycemic control like hemoglobin A1c may not adequately detect these post-meal glucose surges.
This means that many of us spend a part of our day in an acute diabetic state. The lethal impact of these multi-hour glucose surges is just now being understood. As you will read, diabetic complications can develop years or even decades before full-blown type 2 diabetes is diagnosed.
Consequences of Post-meal Glucose Surge
Glucose levels naturally rise in your blood after a high-carbohydrate meal and if you are healthy, glucose will quickly drop back to pre-meal ranges. If glucose rises too much and stays elevated too long, however, a tremendous amount of tissue damage is inflicted.23-27
Diabetics have sharply higher rates of heart attacks compared to non-diabetics.28-30 Yet even in many not considered diabetic, heart attack rates are 40% higher when fasting glucose levels are above 85 mg/dL.31 In a study where after-meal glucose spikes were impeded, heart attacks rates dropped an astounding 91%.32 Even when someone suffers a heart attack, the amount of damage to the heart muscle is significantly reduced when steps are taken ahead of time to reduce post-meal glucose surges.32-36The Honolulu Heart Program found that the risk of coronary artery disease correlated with glucose levels measured one hour after a 50-gram oral glucose load. The incidence of coronary artery disease was twice as high in patients with postprandial glucose levels between 157 and 189 mg/dL compared to those with levels under 144 mg/dL.37 Another study showed the incidence of sudden death was doubled with postprandial glucose levels of 225 mg/dL or higher.38The Whitehall Study of British male civil servants showed that blood glucose levels of 96 mg/dL or higher two hours after a meal were associated with a two-fold increase in mortality from coronary artery disease.39Another British study, the Islington Diabetes Survey, reported that the incidence of major coronary artery disease was 17% in subjects with impaired glucose tolerance, typically defined as 2-hour postprandial glucose levels of 140-199 mg/dL, compared with 9% in subjects with normal glucose tolerance.40 The Oslo Study indicated that risk of fatal stroke in diabetic patients increased by 13% for each 18 mg/dL elevation in postprandial glucose.41
These studies consistently show sharply higher vascular disease in those with higher postprandial (after-meal) glucose spikes.
Diabetic Complications Seen in Non-diabetics
A study showed that many non-diabetics whose glucose elevates to 140 mg/dL or higher after an oral glucose tolerance test suffered the same type of neuropathy as seen in full-blown diabetics. These patients’ fasting glucose and hemoglobin A1c levels were not high, but if their blood glucose levels remained above 140 mg/dL two hours after ingesting 75 grams of pure glucose (a glucose tolerance test), there was a sudden and significant increase in incidence of diabetic neuropathy signs and symptoms.44
Another study found that 56% of neuropathy patients had glucose tolerance levels that fell in the pre-diabetic range, and these individuals suffered damage to their small nerve fibers.45 It has been anecdotally reported that neuropathic pain in the feet of patients worsens when glucose levels exceed 140 mg/dL and diminish when glucose is dropped below this range.44,46
Retinopathy occurs when high blood sugar damages tiny blood vessels in the retina of the eye. It is one of the most feared diabetic complications as it can lead to blindness. The American Diabetes Association thought that retinopathy did not occur until a glucose tolerance test showed glucose levels well over 200 mg/dL after two hours. However, in a large population study, one out of every twelve people with pre-diabetes showed signs of retinopathic changes occurring in their eyes. This study classified pre-diabetes as fasting glucose between 100-125 mg/dL or two-hour glucose tolerance readings between 150-199 mg/dL. These findings show that post-meal glucose spikes over 150 mg/dL are associated with tiny blood vessel changes that lead to diabetic retinopathy.4
Diabetics have higher rates of cancer that have been attributed to higher blood sugar and insulin levels.47-49 When glucose is elevated, the pancreas secretes excess insulin in an attempt to normalize it. Higher insulin levels are believed to stimulate cancer cell proliferation. A study that tracked 10,000 people for 10 years showed substantial increase in cancer in those with fasting glucose over 110 mg/dL or two-hour postprandial glucose levels over 160 mg/dL.50
Excess glucose also increases triglyceride levels, another vascular risk factor.51 Certain drugs like metformin that lower glucose and insulin also reduce artery-clogging triglycerides.52,53
These and other studies demonstrate that those who are unable to control their glucose peaks are prone to suffer diabetic complications. All of this confirms what Life Extension® previously published about the urgent need to protect against after-meal surges of glucose, insulin, and triglycerides.
Clearly, the body does not like to be inundated with after-meal glucose spikes, yet too many Americans suffer from excess postprandial glucose throughout most of the day, and their doctors are not paying attention to the lethal risks this poses.
Not only do glucose spikes acutely damage tissues, but they unfavorably alter gene expression in a way that may accelerate aging processes.54,55 This is one reason why calorie restriction has yielded such robust extensions in life span, along with sharply lower risks of degenerative diseases. Fortunately, there are several proven ways to curb after-meal glucose spikes that do not require severe calorie restriction.
High Glucose Destroys Insulin-producing Cells
Beta cells secrete insulin in response to increases in blood glucose. Unfortunately, beta cells are quite sensitive to even slight increases in blood sugar. There is evidence of beta cell dysfunction when glucose levels stay over 100 mg/dL for more than a few hours.58
When analyzing this data further, scientists found that even small incremental increases in glucose over a two-hour period result in detectable beta cell failure. This study showed that more beta cells fail as a person’s blood sugar rose even within the so-called "normal range."58
Another study showed that beta cells start to die off when fasting glucose is over 110 mg/dL—a level that many doctors tell their patients not to worry about.59 This study indicates that people are killing off their vital insulin-producing beta cells by allowing glucose to spike too high after meals. Once enough beta cells have died, people become insulin-dependent diabetics with markedly shortened life spans. As we now know, when someone has fasting glucose over 110, it means they usually spend several hours after meals with sharply higher glucose levels.
Laboratory studies show that prolonged exposure to high sugar levels destroys beta cells. When these beta cells are removed from high-sugar mediums, they can recover, but only if they were removed before a certain amount of time had passed.60,61
A huge portion of the population spends most of their day with glucose levels above those shown to injure or kill insulin-secreting beta cells. This explains how high blood sugar is in itself a direct cause of the destruction of beta cells needed for insulin production. It used to be thought that beta cells "burned out" because they were forced to overproduce insulin to suppress high blood sugar levels. We now know that high blood sugar itself is killing vital beta cells.
Said differently, many type 2 diabetes cases are not caused because of insufficient insulin production. Instead, high blood sugar destroys beta cells, thus causing chronically elevated blood sugar (because of insufficient insulin secretion) that is eventually diagnosed as type 2 diabetes. The obvious solution is to keep after-meal glucose levels suppressed so beta cells don’t die!
A New Definition of DiabetesDiabetes should be re-defined as "a disease in which a person has acute blood sugar spikes and/or chronically elevated blood sugar levels high enough to increase disease risk."
The definition could be elaborated to include anyone with fasting glucose above 85 mg/dL and/or a 75-gram oral glucose tolerance test load that shows a rise from fasting glucose greater than 40 mg/dL after two hours. What this means is that if a person’s fasting glucose is 80 mg/dL, and their postprandial level is higher than 120 mg/dL two hours after a glucose tolerance test, they have less-than-optimal glycemic control that should be treated.
The upper-limit number for after-meal glucose (120 mg/dL) in the preceding paragraph reflects ranges sought in people who practice calorie restriction. Others may argue that glucose-suppressing treatment should not be initiated until glucose readings are over 140 mg/dL two hours after an oral glucose challenge.23 This higher upper limit after-meal glucose level (140 mg/dL) is more practical for most aging humans to strive for.
It is advantageous for all aging individuals to strive for fasting glucose levels below 86 mg/dL, which may not be feasible in everyone, as some of us are predisposed to higher glucose levels despite aggressive interventions.
In any case, aging humans should view every meal (especially those high in carbohydrates) as a direct threat to their health and longevity. Proven methods should thus be implemented prior to all large meals to blunt postprandial glucose surges. This includes inhibiting amylase62-67 and glucosidase68,69 enzymes to impede absorption of glucose into the bloodstream, along with special fibers70-72 that delay emptying of food into the small intestine where rapid absorption of glucose from carbohydrate foods occurs.
Nutrients, hormones, and drugs (already used by many Life Extension members) improve insulin sensitivity, which facilitates more efficient removal of glucose from the blood.73-81
Despite impeding glucose absorption and improving cellular glucose utilization, too many health-conscious members are not adequately controlling their blood glucose levels.
The good news is that a standardized green coffee bean extract has demonstrated robust after-meal reductions in glucose spikes and functions via novel mechanisms not previously available.82,83
Why Do Aging People Have Too Much Glucose?We know that overconsumption of calories (especially refined carbohydrates) will acutely spike blood glucose and can eventually result in chronically elevated fasting glucose, which is how diabetes is defined today.
Yet as people age, and pay closer attention to their diets, they still often suffer after-meal glucose surges that result in their bloodstreams being bloated with too much glucose for too many hours. This is caused by a variety of factors, including reduced insulin sensitivity that disables the ability of muscle cells to remove surplus glucose from blood for conversion to energy.
There are other reasons, however, why certain individuals have not been able to reduce their glucose to safe ranges.
The Hidden Causes of Glucose OverloadA lesser-known cause of glucose overload is that glucose stored in the body’s tissues (primarily the liver) is inappropriately released into the bloodstream. This pathological release of glucose occurs even though there is plenty of sugar in the blood from a meal that was just eaten.
In those with healthy metabolisms, the liver stores glucose (as glycogen) and only releases enough to maintain a constant blood sugar level to protect against hypoglycemic events. This is called glycogenolysis.84 In healthy individuals, glycogenolysis is suppressed by 90% in the liver after a meal to protect against blood glucose overload.85,86
As people age and their blood sugar rises, this delicate balance destabilizes. High postprandial blood sugar stimulates an enzyme called glucose-6-phosphatase, which in turn prompts the excess release of stored glucose from tissues, even though there is already abundant glucose in the blood.
People with high blood sugar levels lose control over normal glucose tissue release. Instead of turning it off in response to glucose flooding into their bloodstream from their last meal, they release too much. This contributes to the deadly after-meal glucose spikes that cause diabetic complications even among non-diabetics.
The glucose-6-phosphatase enzyme has another dark side. It facilitates the creation of glucose from other substrates (amino acids, fatty acids, or lactate) in the body. This creation of new glucose is called gluconeogenesis.87 The significance of this process is that it explains how the body can break down any food (protein, fat or carbohydrate) into glucose. Gluconeogenesis is what causes some people to have high blood sugar even though they follow a "low-carb" diet.
Elevated glucose-6-phosphatase prompts the release and creation of new glucose into the blood, whether or not you consume any carbohydrate calories. This twin phenomenon of glycogenolysis (release of stored glucose) and gluconeogenesis (creation of new glucose) explains why so many aging people suffer high blood sugar levels.
For some people, even if they follow reduced-calorie diets, their bodies may still create too much glucose internally due to excess glucose-6-phosphatase.
To understand why excess glucose-6-phosphatase is so deadly, aging people barely have the capacity to safely metabolize the calories they ingest throughout the day. As the body creates and releases too much glucose in the presence of excess glucose-6-phosphatase, each additional calorie can add to glucose spikes. So when a meal is consumed, glucose flows into the bloodstream. This in turn causes total blood glucose levels to skyrocket not just from the ingested carbohydrates, but also through the twin processes of gluconeogenesis and glycogenolysis. Blood sugar levels can then remain elevated for most of the day.
Suppression of glucose-6-phosphatase is thus a critical missing link to blunting after-meal (postprandial) glucose surges that are an underlying cause of so many horrific (diabetic) complications.
Green Coffee Bean Extract Suppresses Glucose-6-Phosphatase
Further research has suggested the compound responsible for this beneficial action on glucose metabolism is chlorogenic acid that is found abundantly in raw coffee beans.
What chlorogenic acid does is inhibit the enzyme glucose-6-phosphatase, which reduces the release and creation of excess glucose in the body.89,90 This unique dual property of chlorogenic acid provides a powerful new weapon in our quest to attain optimal fasting and postprandial glucose levels.
In a clinical trial of 56 subjects, 100 grams of glucose was given as an oral glucose challenge test. Study subjects were given escalating doses of standardized green coffee bean extract to measure its ability to reduce the postprandial glucose surge. At a dose of 400 mg of green coffee bean extract, there was a remarkable 32% reduction in the postprandial glucose surge.82 This translates into someone who normally suffers a dangerous postprandial blood glucose surge of 160 mg/dL reducing it to a safe 109 mg/dL.
An article in this month’s issue describes the multi-faceted benefits of green coffee bean extract standardized for chlorogenic acid. If all it did was suppress after-meal glucose spikes, it would be well worth considering for anyone who has not been able to achieve optimal glucose control. Like so many other natural polyphenols, chlorogenic acid has demonstrated a wide range of additional protective properties.91-95
Mitigating the Oxidative Flame-throwerA common complaint amongst newly-diagnosed diabetics is why so many complications develop so quickly. What they fail to understand is their delicate tissues may have been under assault from after-meal glucose surges for decades before full-blown type 2 diabetes was diagnosed.
In the presence of excess glucose, tissues of the body undergo a hyper-oxidation effect analogous to being torched with a military flame-thrower.
While antioxidants can suppress some of the oxidative flame, it is critical to block the underlying catalysts, which are the high blood sugar levels so many aging individuals suffer after every heavy meal.
Scientific studies substantiate that acute damage occurs during after-meal glucose spikes, yet mainstream medicine continues to ignore this deadly phenomenon. On page 80 of this issue is an article about nutrients, hormones, and drugs that can help safely suppress fasting and postprandial glucose levels.
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Last year we introduced PQQ (pyrroloquinoline quinone) to induce the creation of new mitochondria in aging cells.96 PQQ became an overnight blockbuster as Life Extension members were astutely aware of the critical importance that healthy mitochondria play in forestalling aging processes. Mitochondrial insufficiency, in fact, is involved in the promotion of type 2 diabetes via its debilitating effects on cellular glucose utilization.97,98
In this month’s issue, you’ll discover a missing link that causes aging people to suffer acute post-meal glucose surges that trigger common age-related disorders. The good news is that most of you have been taking steps to shield your bloodstream against these acute glucose spikes. With the introduction of low-cost green coffee bean extract, aging humans can exert greater control over their blood glucose levels than ever before.
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