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HEALTH NEWS
Insulin, Leptin, and Blood Sugar – Why Diabetic Medication Fails
August 20, 2012
Type 2 diabetes is a difficult metabolic problem. It is a national embarrassment that so many of our young people are becoming type 2 diabetic. It is a national disgrace that millions of type 2 diabetic patients are being injured with commonly used diabetic medications that are known to make their metabolic situation worse.
An overwhelming body of science demonstrates that insulin resistance leads to obesity and vice versa. Once this problem sets in, a person is on a path of ever worsening metabolic control as diabetes related issues, cholesterol problems, and heart disease risk factors pile up. If nothing is done, very poor health, and early death are certain.
The Big Pharma blood sugar remedies, however, turn out to be really bad for health – they actually complicate rather than improve the patient's health. Even when the drugs aren't directly damaging in a major way, they fail to address the actual reasons for diabetes and typically have the net result of making the factors that cause diabetes worse. I know that may seem hard to believe, but it is true, and I will explain it shortly.
On December 17, 2008 the New England Journal of Medicine1 put the nail in the coffin on another dismal year for the theory of drugs to treat disease, reporting that aggressive use of blood sugar lowering medication to prevent heart disease was a complete failure. Its not that lowering blood sugar in this patient population didn't do anything; it made the patients heavier and more hypoglycemic. This newer study followed equally dismal results from the ACCORD trial (Action to Control Cardiovascular Risk in Diabetes), which earlier in 2008 found a 22 percent increased rate of death in diabetic patients who were aggressively treated with medications.
Some of the newer diabetes medications like Avandia are quite deadly, and likely to injure in multiple ways (such as doubling the risk for bone fractures). Scientists at the FDA were so concerned this drug would cause heart failure that they wanted a black box warning on it from the start. However, Von Eschenbach and his band of FDA management goons forced FDA scientists to not warn anyone! As Avandia treated bodies starting showing up on the doorsteps of morgues around the country, Congress started asking questions. Eventually scientists reported a 43 percent increase in the risk for heart failure from Avandia; however, the FDA had this data from the start and didn't tell anyone. The FDA allowed Avandia sales to reach $3.2 billion per year – while killing and injuring a lot of patients. Even when the high profile type 2 diabetic Tim Russert keeled over dead from a heart attack, nobody in the media seemed interested to know if he was taking Avandia.
At the same time that the FDA was helping to create a market for deadly Avandia sales, they sent out 24 warning letters to small dietary supplement companies telling them that their promotion of various products to lower blood sugar, correct insulin resistance, or improve diabetes is against the law. Against whose law? Certainly not the First Amendment.
The FDA and Big Pharma get away with this nonsense because they set the standard for drug effectiveness on a surrogate endpoint or biomarker, in this case the blood sugar level. Their logic is that if blood sugar levels are better, then health must be better. This means that any drug that takes a toxic sledgehammer to blood sugar levels, knocking them down, is just fine in the eyes of the FDA even though the drug leaves a trail of damage around the body – even killing the person!
On a lesser scale, but using similar logic, doctors think that any medication that helps lower blood sugar is doing the patient a favor. Never do they ask the most obvious question: If you are lowering blood sugar with a drug where is the sugar going? The answer is: most often to stored fat. Or the sugar is simply forced into cells and kills them because the cells can't use the sugar.
What is a diabetes patient to do? And how does anyone whose blood sugar is beginning to rise get the problem under control? Answering these questions requires that you understand something about the subject, as it is rather obvious most doctors, even those who treat diabetes patients as their primary business, don't have adequate practical knowledge to fix the great majority of people coming to them for help.
First off, your blood is not a very sweet beverage. Normal fasting blood sugar is slightly less than one teaspoon of sugar in your five or so quarts of blood. What happens when you drink a sugar sweetened Coke that contains 10 teaspoons of sugar?
When you eat any food, even fat, your insulin level will rise. Higher amounts of refined carbohydrates or simple sugars will raise your insulin faster and in higher amounts. The greater the fiber content of your diet, the slower insulin is raised and the more controlled the process. When you eat a large meal, regardless of the type of calories, it causes a large surge in insulin that is difficult to manage.
Insulin is a taxicab for calories. Its goal is to take blood sugar, as its passenger, to various locations in your body that want it. It helps if you are active, as some of the sugar is more likely to be wanted by cells in your body, including your many muscle cells.
Blood sugar is fuel, like gasoline is to a car. Your brain must have a regular supply or your head conks out. Thus, following a meal your insulin taxi's are busy transporting sugar through your circulation and out to your cells, hoping to find cells that need some sugar.
In a healthy person, insulin drops off a whopping 60 percent of the sugar at your liver, which acts as a warehouse, converting the blood sugar to glycogen for storage.
Insulin is released by your pancreas in two phases. The first phase is from insulin that is already made and stored in your pancreas, which is just waiting for some food to come along. This is your first wave of taxis coming to pick up the first set of blood sugar passengers. The release of this insulin triggers your pancreas' beta cells to start making more insulin to deal with the rest of the meal.
As you are eating, some of the insulin transports blood sugar to your white adipose tissue or stored fat. The blood sugar is taken up by fat cells, activating their metabolism, in turn producing the hormone leptin. Leptin now enters your blood and begins traveling up to your brain. The more you eat, the more insulin you make, and the more leptin you make.
When leptin levels get high enough, meaning you have eaten enough, then leptin permeates into your brain and tells your subconscious brain you are full. At the same time, the higher levels of leptin also tell your pancreas that you are full, which turns off the beta cell production of insulin, as no more taxis are needed.
If you ate the right amount of food for your physical activity level, then blood sugar always has some place healthy to go; insulin rises and falls in a controlled manner, as does leptin.
When insulin has too many blood sugar passengers, and cells don't need any sugar, then insulin stimulates the production of triglycerides, which can become stored fat. This is how you gain weight. Unfortunately, as triglycerides elevate in your blood they get in the way of leptin getting into your brain. This keeps you eating more than you need to because you don't yet have a full signal, a problem called leptin resistance. This encourages even further insulin driven triglyceride formation, making it more likely you will gain weight.
If you stop eating too much and start exercising more, then this simple case issue can improve and will often bounce back to normal function, thus the basic idea of eating less and exercising more to lose weight.
If you continually eat too much and gain weight, then cells get tired of seeing insulin taxis driving up. In fact, they shutter their windows and lock their doors; insulin becomes persona non grata. The reason for this rejection of insulin is rather simple. If the cells take in blood sugar when they can't use it, because they already have enough, then the extra sugar will caramelize and kill the cell. Rejecting insulin is a self defensive measure. This is the mechanism behind basic insulin resistance at the cellular level.
If this problem goes on, blood sugar levels continue to rise, insulin resistance gets worse, leptin resistance gets worse, cholesterol levels go up, blood pressure goes up, triglyceride levels go up, and inflammation really starts heating up. Eventually, this leads to type 2 diabetes, along with many risk factors for heart disease, and then heart and kidney disease lock into place.
The problem for any kind of blood sugar medication is that it only addresses one of many mechanisms that aren't working right, while creating its own side effect complications. At best, it is a temporary solution with a narrow scope of benefit - and does not address the true source of the problem.
Furthermore, when more drugs are added in an effort to more comprehensively address the multiple aspects of the problem, then side effects really pile up in a hurry and injure the patient. This means the risk of multiple drug treatment far outweighs the benefits, even though one or two drugs can't get the job done.
More often, the medication either forces sugar into cells – killing or injuring them or it transfers the sugar into fat, making leptin problems worse that in turn make insulin problems almost impossible to solve. The shortcoming of these medications is openly acknowledged in the scientific literature2, yet this is what passes for standard medical care. It is a disgrace.
The absolute worst possible dietary pattern of eating for a type 2 diabetic IS THE STANDARD DIET ADVICE GIVEN BY DIETICIANS AND DOCTORS ACROSS THIS COUNTRY FOR ALMOST ALL TYPE 2 DIABETIC PATIENTS, which helps lock in a national epidemic of type 2 diabetes. They routinely tell individuals to snack in order to maintain their blood sugar levels and to “stoke” their metabolism with fuel.
In normal health, when you haven't eaten for three hours, insulin levels return to a baseline. Now your pancreas makes a different hormone called glucagon. This hormone tells your liver to release the sugar (glycogen) it has stored to sustain your blood sugar levels, and as it does this it turns on your liver's fat burning system. Thus, under the influence of glucagon your liver simultaneously uses sugar and fat to sustain your blood sugar – a true fat burning time that helps clear up stagnating levels of triglycerides in your blood.
If you snack on anything surpassing 30 calories you will raise insulin, which automatically turns off glucagon, causes fat burning to stop, and blunts the use of sugar that has been stored in your liver. However, since you haven't used the stored sugar in your liver, then insulin can't put more sugar back in your liver as it normally would, meaning it will readily turn blood sugar into fat (even if you snacked on something with no fat).
You are supposed to get a snack between meals, but it is supposed to come from your liver, not from eating.
The worst things for leptin and insulin are eating between meals, eating large meals, eating low fiber, eating highly refined sugar or refined carbohydrates, not eating enough quality protein, and not exercising.
If you eat anything after dinner you make matters even worse, because now you reduce the optimal access into your stored fat during sleep, a prime opportunity to burn fat.
When this system is abused and weight is gained, then fat begins to accumulate in excess in your liver. The fat clogs your liver's metabolism, and reduces the ability of sugar to store in your liver following a meal. This is liver insulin resistance caused by fatty buildup. This means that you are much more likely to become hypoglycemic or have low blood sugar between meals, because you don't have enough sugar in your warehouse to use for blood sugar between meals.
This same fatty liver problem also gets in the way of how glucagon would burn fat between meals, causing glucagon to synthesize sugar in an inappropriate and out-of-control manner, making blood sugar go high even though you haven't eaten. This is why diabetics wake up with very high fasting blood sugar levels. These are complicated metabolic problems that are more difficult to fix than simple case insulin resistance.
Furthermore, your pancreas starts to tune out leptin, meaning that leptin resistance occurs at the level of beta cells and the beta cells aren't getting the leptin message to stop making insulin in a timely manner. This causes extra insulin to be made, which excessively lowers blood sugar by turning sugar to fat, while simultaneously inducing hypoglycemia or low blood sugar symptoms. This makes a person want to eat again two to three hours after the previous meal, in turn making the whole problem worse.
It's about this time, with metabolism clogged and broken, that a young overweight person goes to the doctor and finds out he or she is type 2 diabetic.
If the problem continues, then inflammation begins to damage the insulin secreting beta cells. Not only are these beta cells now leptin resistant, causing them to overproduce insulin and get tired out, but they are also getting damaged, and their numbers are declining – meaning now they can't make insulin either. This sends a person down a path of a mixture of type 1 and type 2 diabetes3 - with an autoimmune4 component sometimes thrown in for good measure, a problem that is seen progressively more often in today's older type 2 diabetics.
If you thought that was hard to understand, then realize that the previous description was the rather simple explanation of the problem; it's worth reading over again until you understand it. The metabolic problems of a diabetic patient are actually far more complex. To prevent yourself from becoming diabetic or to get over the problem, it is very important to understand even more information.
As your fat cells expand and cram into each other, a highly inflammatory state occurs within your white adipose tissue5. These inflammatory signals6 aggravate and lock in the various problems discussed in previous sections. Another hormone made in fat, adiponectin, is a major player in this equation.
In health, leptin and adiponectin elevate in harmony, side by side. When leptin resistance occurs, which is common anytime someone starts gaining weight, then adiponectin levels begin to fall. The fall in adiponectin is caused by the inflammation in white adipose tissue. Interestingly, adiponectin is a primary anti-inflammatory hormone within white adipose tissue. Thus, the inflammation of progressive weight gain eventually overwhelms adiponectin, at which point serious problems really set in.
Once adiponectin levels fall too much7, then inflammation in fat cells really ramps up. The greater the weight gain and leptin resistance, the farther adiponectin levels fall. When adiponectin levels fall your liver's ability to process sugar and insulin dramatically worsen. Plus, your muscles8 become resistant to insulin – speeding the onset of type 2 diabetes.
And that's not all – your brain becomes insulin resistant9, which is actually caused by the leptin resistance10. This problem is now found to lock in all problems of insulin resistance around your body. A great deal of research indicates that the failure of insulin and leptin to register properly in your brain, along with falling adiponectin levels, creates a highly inflammatory state of affairs that is the prime cause of worsening blood sugar regulation and eventual type 2 diabetes.
Diabetic medication does not address these issues, and often makes them worse over time – even if blood sugar numbers appear better for a period of time. Treating blood sugar numbers is not treating the cause of anything. It's like saying the cause of a house fire is because the fire department didn't show up fast enough – so now let's put a fire hydrant in everyone's house so we can put out fires faster. That is an accurate analogy of how the pharma-trained medical profession manages the type 2 diabetic population in our country. Even worse, their monopoly and inept care is sanctioned by the FDA and FTC as law; both act as police force bullies to stamp out any competing interests.
There is no quick fix for type 2 diabetes, or even fasting blood sugar levels that are on the rise. To be healthy, your fasting blood sugar should never be above 90. However, real health is determined by achieving this number because your body is working properly.
No vitamin, mineral, or miracle pill can automatically prevent or treat diabetes. What you are trying to do is create a nutritional environment that supports your body to work normally.
Individuals with simple case insulin and leptin resistance, who cut back on junk food, exercise more, make appropriate dietary adjustments, and use some basic dietary supplement support can typically bring these smaller problems in line relatively quickly.
When problems are more serious they are complicated by the fact that the liver, pancreas, white adipose tissue, circulatory system, and subconscious brain have been irritated and even damaged by inflammatory compounds. This fact alone takes time to heal – it is not a simple nutritional deficiency – it is more like a badly sprained ankle.
Additionally, the liver, muscles, and circulation are clogged with accumulating fat. This is like trying to cook a meal in a filthy kitchen, it is going to be challenging. This problem will only gradually improve as weight is lost, it never improves until the weight is lost, and it will always get worse if weight is gained.
The solution is to create a pattern of health, rooted in a good diet and exercise, wherein these more advanced problems can begin to correct themselves. Type 2 diabetes is completely reversible for almost everyone – if only diabetics knew what to do.
Type 2 diabetes is at epidemic levels in America, reaching down to teenagers and young adults in startling numbers. This problem signifies that key regulatory systems have lost their natural balance – meaning that homeostasis has been compromised. Unfortunately, this locks in a path to poor quality health, the early onset of many serious diseases, and early death. The medical profession, relying on pharmaceutical drugs, has not been able to solve this problem and actually makes it worse on a routine basis.
To make progress an overall program of lifestyle improvement must be undertaken on a consistent basis. There are no shortcuts. There is little margin for error. Weight must be lost in a gradual and consistent way. Weight gain during any “treatment” means the “treatment” is an utter failure. A healthy program requires making dietary adjustments that have been explained in this article. Consistent exercise is mandatory, the more the better. Dietary supplements can be plugged into an overall program to help the program of recovery go easier – and in some cases may be the key to getting the program on track or keeping it from getting derailed. There are many options. Type 2 diabetes can be prevented and in many people it can be completely reversed.
An overwhelming body of science demonstrates that insulin resistance leads to obesity and vice versa. Once this problem sets in, a person is on a path of ever worsening metabolic control as diabetes related issues, cholesterol problems, and heart disease risk factors pile up. If nothing is done, very poor health, and early death are certain.
The Big Pharma blood sugar remedies, however, turn out to be really bad for health – they actually complicate rather than improve the patient's health. Even when the drugs aren't directly damaging in a major way, they fail to address the actual reasons for diabetes and typically have the net result of making the factors that cause diabetes worse. I know that may seem hard to believe, but it is true, and I will explain it shortly.
On December 17, 2008 the New England Journal of Medicine1 put the nail in the coffin on another dismal year for the theory of drugs to treat disease, reporting that aggressive use of blood sugar lowering medication to prevent heart disease was a complete failure. Its not that lowering blood sugar in this patient population didn't do anything; it made the patients heavier and more hypoglycemic. This newer study followed equally dismal results from the ACCORD trial (Action to Control Cardiovascular Risk in Diabetes), which earlier in 2008 found a 22 percent increased rate of death in diabetic patients who were aggressively treated with medications.
Some of the newer diabetes medications like Avandia are quite deadly, and likely to injure in multiple ways (such as doubling the risk for bone fractures). Scientists at the FDA were so concerned this drug would cause heart failure that they wanted a black box warning on it from the start. However, Von Eschenbach and his band of FDA management goons forced FDA scientists to not warn anyone! As Avandia treated bodies starting showing up on the doorsteps of morgues around the country, Congress started asking questions. Eventually scientists reported a 43 percent increase in the risk for heart failure from Avandia; however, the FDA had this data from the start and didn't tell anyone. The FDA allowed Avandia sales to reach $3.2 billion per year – while killing and injuring a lot of patients. Even when the high profile type 2 diabetic Tim Russert keeled over dead from a heart attack, nobody in the media seemed interested to know if he was taking Avandia.
At the same time that the FDA was helping to create a market for deadly Avandia sales, they sent out 24 warning letters to small dietary supplement companies telling them that their promotion of various products to lower blood sugar, correct insulin resistance, or improve diabetes is against the law. Against whose law? Certainly not the First Amendment.
The Blood Sugar Con Job
The FDA and Big Pharma get away with this nonsense because they set the standard for drug effectiveness on a surrogate endpoint or biomarker, in this case the blood sugar level. Their logic is that if blood sugar levels are better, then health must be better. This means that any drug that takes a toxic sledgehammer to blood sugar levels, knocking them down, is just fine in the eyes of the FDA even though the drug leaves a trail of damage around the body – even killing the person!
On a lesser scale, but using similar logic, doctors think that any medication that helps lower blood sugar is doing the patient a favor. Never do they ask the most obvious question: If you are lowering blood sugar with a drug where is the sugar going? The answer is: most often to stored fat. Or the sugar is simply forced into cells and kills them because the cells can't use the sugar.
What is a diabetes patient to do? And how does anyone whose blood sugar is beginning to rise get the problem under control? Answering these questions requires that you understand something about the subject, as it is rather obvious most doctors, even those who treat diabetes patients as their primary business, don't have adequate practical knowledge to fix the great majority of people coming to them for help.
Blood Sugar 101
First off, your blood is not a very sweet beverage. Normal fasting blood sugar is slightly less than one teaspoon of sugar in your five or so quarts of blood. What happens when you drink a sugar sweetened Coke that contains 10 teaspoons of sugar?
When you eat any food, even fat, your insulin level will rise. Higher amounts of refined carbohydrates or simple sugars will raise your insulin faster and in higher amounts. The greater the fiber content of your diet, the slower insulin is raised and the more controlled the process. When you eat a large meal, regardless of the type of calories, it causes a large surge in insulin that is difficult to manage.
Insulin is a taxicab for calories. Its goal is to take blood sugar, as its passenger, to various locations in your body that want it. It helps if you are active, as some of the sugar is more likely to be wanted by cells in your body, including your many muscle cells.
Blood sugar is fuel, like gasoline is to a car. Your brain must have a regular supply or your head conks out. Thus, following a meal your insulin taxi's are busy transporting sugar through your circulation and out to your cells, hoping to find cells that need some sugar.
In a healthy person, insulin drops off a whopping 60 percent of the sugar at your liver, which acts as a warehouse, converting the blood sugar to glycogen for storage.
Insulin is released by your pancreas in two phases. The first phase is from insulin that is already made and stored in your pancreas, which is just waiting for some food to come along. This is your first wave of taxis coming to pick up the first set of blood sugar passengers. The release of this insulin triggers your pancreas' beta cells to start making more insulin to deal with the rest of the meal.
As you are eating, some of the insulin transports blood sugar to your white adipose tissue or stored fat. The blood sugar is taken up by fat cells, activating their metabolism, in turn producing the hormone leptin. Leptin now enters your blood and begins traveling up to your brain. The more you eat, the more insulin you make, and the more leptin you make.
When leptin levels get high enough, meaning you have eaten enough, then leptin permeates into your brain and tells your subconscious brain you are full. At the same time, the higher levels of leptin also tell your pancreas that you are full, which turns off the beta cell production of insulin, as no more taxis are needed.
If you ate the right amount of food for your physical activity level, then blood sugar always has some place healthy to go; insulin rises and falls in a controlled manner, as does leptin.
When insulin has too many blood sugar passengers, and cells don't need any sugar, then insulin stimulates the production of triglycerides, which can become stored fat. This is how you gain weight. Unfortunately, as triglycerides elevate in your blood they get in the way of leptin getting into your brain. This keeps you eating more than you need to because you don't yet have a full signal, a problem called leptin resistance. This encourages even further insulin driven triglyceride formation, making it more likely you will gain weight.
If you stop eating too much and start exercising more, then this simple case issue can improve and will often bounce back to normal function, thus the basic idea of eating less and exercising more to lose weight.
If you continually eat too much and gain weight, then cells get tired of seeing insulin taxis driving up. In fact, they shutter their windows and lock their doors; insulin becomes persona non grata. The reason for this rejection of insulin is rather simple. If the cells take in blood sugar when they can't use it, because they already have enough, then the extra sugar will caramelize and kill the cell. Rejecting insulin is a self defensive measure. This is the mechanism behind basic insulin resistance at the cellular level.
If this problem goes on, blood sugar levels continue to rise, insulin resistance gets worse, leptin resistance gets worse, cholesterol levels go up, blood pressure goes up, triglyceride levels go up, and inflammation really starts heating up. Eventually, this leads to type 2 diabetes, along with many risk factors for heart disease, and then heart and kidney disease lock into place.
The problem for any kind of blood sugar medication is that it only addresses one of many mechanisms that aren't working right, while creating its own side effect complications. At best, it is a temporary solution with a narrow scope of benefit - and does not address the true source of the problem.
Furthermore, when more drugs are added in an effort to more comprehensively address the multiple aspects of the problem, then side effects really pile up in a hurry and injure the patient. This means the risk of multiple drug treatment far outweighs the benefits, even though one or two drugs can't get the job done.
More often, the medication either forces sugar into cells – killing or injuring them or it transfers the sugar into fat, making leptin problems worse that in turn make insulin problems almost impossible to solve. The shortcoming of these medications is openly acknowledged in the scientific literature2, yet this is what passes for standard medical care. It is a disgrace.
Basic Diet Adjustments for Insulin Improvement
The absolute worst possible dietary pattern of eating for a type 2 diabetic IS THE STANDARD DIET ADVICE GIVEN BY DIETICIANS AND DOCTORS ACROSS THIS COUNTRY FOR ALMOST ALL TYPE 2 DIABETIC PATIENTS, which helps lock in a national epidemic of type 2 diabetes. They routinely tell individuals to snack in order to maintain their blood sugar levels and to “stoke” their metabolism with fuel.
In normal health, when you haven't eaten for three hours, insulin levels return to a baseline. Now your pancreas makes a different hormone called glucagon. This hormone tells your liver to release the sugar (glycogen) it has stored to sustain your blood sugar levels, and as it does this it turns on your liver's fat burning system. Thus, under the influence of glucagon your liver simultaneously uses sugar and fat to sustain your blood sugar – a true fat burning time that helps clear up stagnating levels of triglycerides in your blood.
If you snack on anything surpassing 30 calories you will raise insulin, which automatically turns off glucagon, causes fat burning to stop, and blunts the use of sugar that has been stored in your liver. However, since you haven't used the stored sugar in your liver, then insulin can't put more sugar back in your liver as it normally would, meaning it will readily turn blood sugar into fat (even if you snacked on something with no fat).
You are supposed to get a snack between meals, but it is supposed to come from your liver, not from eating.
The worst things for leptin and insulin are eating between meals, eating large meals, eating low fiber, eating highly refined sugar or refined carbohydrates, not eating enough quality protein, and not exercising.
If you eat anything after dinner you make matters even worse, because now you reduce the optimal access into your stored fat during sleep, a prime opportunity to burn fat.
When this system is abused and weight is gained, then fat begins to accumulate in excess in your liver. The fat clogs your liver's metabolism, and reduces the ability of sugar to store in your liver following a meal. This is liver insulin resistance caused by fatty buildup. This means that you are much more likely to become hypoglycemic or have low blood sugar between meals, because you don't have enough sugar in your warehouse to use for blood sugar between meals.
This same fatty liver problem also gets in the way of how glucagon would burn fat between meals, causing glucagon to synthesize sugar in an inappropriate and out-of-control manner, making blood sugar go high even though you haven't eaten. This is why diabetics wake up with very high fasting blood sugar levels. These are complicated metabolic problems that are more difficult to fix than simple case insulin resistance.
Furthermore, your pancreas starts to tune out leptin, meaning that leptin resistance occurs at the level of beta cells and the beta cells aren't getting the leptin message to stop making insulin in a timely manner. This causes extra insulin to be made, which excessively lowers blood sugar by turning sugar to fat, while simultaneously inducing hypoglycemia or low blood sugar symptoms. This makes a person want to eat again two to three hours after the previous meal, in turn making the whole problem worse.
It's about this time, with metabolism clogged and broken, that a young overweight person goes to the doctor and finds out he or she is type 2 diabetic.
If the problem continues, then inflammation begins to damage the insulin secreting beta cells. Not only are these beta cells now leptin resistant, causing them to overproduce insulin and get tired out, but they are also getting damaged, and their numbers are declining – meaning now they can't make insulin either. This sends a person down a path of a mixture of type 1 and type 2 diabetes3 - with an autoimmune4 component sometimes thrown in for good measure, a problem that is seen progressively more often in today's older type 2 diabetics.
The Complexity of Insulin and Leptin Problems
If you thought that was hard to understand, then realize that the previous description was the rather simple explanation of the problem; it's worth reading over again until you understand it. The metabolic problems of a diabetic patient are actually far more complex. To prevent yourself from becoming diabetic or to get over the problem, it is very important to understand even more information.
As your fat cells expand and cram into each other, a highly inflammatory state occurs within your white adipose tissue5. These inflammatory signals6 aggravate and lock in the various problems discussed in previous sections. Another hormone made in fat, adiponectin, is a major player in this equation.
In health, leptin and adiponectin elevate in harmony, side by side. When leptin resistance occurs, which is common anytime someone starts gaining weight, then adiponectin levels begin to fall. The fall in adiponectin is caused by the inflammation in white adipose tissue. Interestingly, adiponectin is a primary anti-inflammatory hormone within white adipose tissue. Thus, the inflammation of progressive weight gain eventually overwhelms adiponectin, at which point serious problems really set in.
Once adiponectin levels fall too much7, then inflammation in fat cells really ramps up. The greater the weight gain and leptin resistance, the farther adiponectin levels fall. When adiponectin levels fall your liver's ability to process sugar and insulin dramatically worsen. Plus, your muscles8 become resistant to insulin – speeding the onset of type 2 diabetes.
And that's not all – your brain becomes insulin resistant9, which is actually caused by the leptin resistance10. This problem is now found to lock in all problems of insulin resistance around your body. A great deal of research indicates that the failure of insulin and leptin to register properly in your brain, along with falling adiponectin levels, creates a highly inflammatory state of affairs that is the prime cause of worsening blood sugar regulation and eventual type 2 diabetes.
Diabetic medication does not address these issues, and often makes them worse over time – even if blood sugar numbers appear better for a period of time. Treating blood sugar numbers is not treating the cause of anything. It's like saying the cause of a house fire is because the fire department didn't show up fast enough – so now let's put a fire hydrant in everyone's house so we can put out fires faster. That is an accurate analogy of how the pharma-trained medical profession manages the type 2 diabetic population in our country. Even worse, their monopoly and inept care is sanctioned by the FDA and FTC as law; both act as police force bullies to stamp out any competing interests.
How to Solve the Diabetes Problem
There is no quick fix for type 2 diabetes, or even fasting blood sugar levels that are on the rise. To be healthy, your fasting blood sugar should never be above 90. However, real health is determined by achieving this number because your body is working properly.
No vitamin, mineral, or miracle pill can automatically prevent or treat diabetes. What you are trying to do is create a nutritional environment that supports your body to work normally.
Individuals with simple case insulin and leptin resistance, who cut back on junk food, exercise more, make appropriate dietary adjustments, and use some basic dietary supplement support can typically bring these smaller problems in line relatively quickly.
When problems are more serious they are complicated by the fact that the liver, pancreas, white adipose tissue, circulatory system, and subconscious brain have been irritated and even damaged by inflammatory compounds. This fact alone takes time to heal – it is not a simple nutritional deficiency – it is more like a badly sprained ankle.
Additionally, the liver, muscles, and circulation are clogged with accumulating fat. This is like trying to cook a meal in a filthy kitchen, it is going to be challenging. This problem will only gradually improve as weight is lost, it never improves until the weight is lost, and it will always get worse if weight is gained.
The solution is to create a pattern of health, rooted in a good diet and exercise, wherein these more advanced problems can begin to correct themselves. Type 2 diabetes is completely reversible for almost everyone – if only diabetics knew what to do.
Summary
Type 2 diabetes is at epidemic levels in America, reaching down to teenagers and young adults in startling numbers. This problem signifies that key regulatory systems have lost their natural balance – meaning that homeostasis has been compromised. Unfortunately, this locks in a path to poor quality health, the early onset of many serious diseases, and early death. The medical profession, relying on pharmaceutical drugs, has not been able to solve this problem and actually makes it worse on a routine basis.
To make progress an overall program of lifestyle improvement must be undertaken on a consistent basis. There are no shortcuts. There is little margin for error. Weight must be lost in a gradual and consistent way. Weight gain during any “treatment” means the “treatment” is an utter failure. A healthy program requires making dietary adjustments that have been explained in this article. Consistent exercise is mandatory, the more the better. Dietary supplements can be plugged into an overall program to help the program of recovery go easier – and in some cases may be the key to getting the program on track or keeping it from getting derailed. There are many options. Type 2 diabetes can be prevented and in many people it can be completely reversed.
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