Post by kewlkat on Nov 29, 2013 5:46:44 GMT -6
I've been reading Dr Eades "review" of the subject book and decided to post some bits here for discussion since our goals in NK are to reduce insulin to burn the fat.
Emphasis is mine -
If we ask how the fat gets into the fat cells, we will discover that all the pathways of fat storage were worked out years ago and are so uncontroversial that they’re described in detail in every biochemistry and physiology textbook currently in use. It’s well known that the metabolic hormone insulin stimulates an enzyme on the surface of the fat cell that moves the fat into the cell.
So if insulin moves fat into the fat cells, it would seem that a lot of insulin would move a lot of fat into the fat cells. And indeed it does. Given this, the rational person trying to figure out the previous step in our progression would ask What causes a lot of insulin? Or the rational person, should he/she have been steeped for a lifetime in the marinade of ‘fat is bad’ might ask, What about fat? If there is a lot of fat in the blood as a result of fat in the diet, wouldn’t that fat get into the fat cell? If so, then doesn’t dietary fat lead to fat?
A good question, but the answer is no. Type I diabetics can have a lot of fat in their diets and in their blood, but if they have no insulin, they can’t store that fat. In fact, most pre-diagnosis type I diabetics lose enormous amounts of weight despite eating ravenously because without insulin they can’t store the fat. So dietary fat itself – even large amounts of it – won’t find its way into the fat cell without the help of insulin.
Here are some more snippets -
When you hack through the thicket of all the biochemical pathways involved in the metabolic process, you find that insulin is the primary force involved in the storage of nutrients. Insulin is the body’s storage hormone: it puts fat in the fat cells, protein into muscle cells and glucose into it’s storage form, glycogen.
If we have a lot of insulin, the insulin dominant-pathways (the storage pathways) hold sway, and fat is partitioned away in the fat cells; if insulin is low, then the glucagon-dominant pathways (the energy-release pathways) take over and start moving fat out of the fat cells, so it can be consumed by the body as fuel. This is how it is supposed to work. We eat. Insulin comes out and stores away the energy. We go for a while without eating, insulin goes down and glucagon comes out to retrieve our stored fat so we’ll have a continuous energy supply.
Problems arise when this system goes off the rails, which most commonly happens when people develop insulin resistance, a problem of disordered insulin signaling. Insulin talks, but the cells don’t listen. So insulin keeps talking louder until the cells finally get the message. In other words, the pancreas keeps producing insulin and the blood levels continue to rise until the cells finally get the message. But it’s a message that has taken a lot of insulin force to deliver.
If all the different types of cells developed resistance to insulin at the same rate, we wouldn’t have as much of a problem. But they don’t. Different cells develop insulin resistance at different rates. Typically the first cells to become insulin resistant are the liver cells. The liver cells are continuously producing sugar and dumping it into the blood. Insulin shuts this process down. If the insulin level drops to zero, as it does in type I diabetes, the liver dumps a huge load of sugar in the blood causing all the blood sugar problems associated with this disease. Under normal circumstances, just a little insulin stops the liver cells in their tracks. But if these cells are resistant to insulin, much more is required to get them the message to turn off the sugar spigot.
In most people, the fat cells develop insulin resistance later, which creates the problem. If insulin levels are high to control the liver’s sugar factory output, then these elevated insulin levels are sending a strong message to the non-insulin-resistant fat cells. The message is take this fat and store it. High insulin not only drives fat into the fat cells, it prevents it from getting out. Fat is packed into the fat cells and kept there.
Between meals when insulin levels would normally fall, allowing the liberation of fat to feed all the body’s tissues, insulin remains high in an effort to keep the liver in check. Fat can’t get out of the fat cells, and the tissues begin to starve. Even though there is plenty of stored fat, the body can’t get to it because elevated insulin is preventing its release.
I've not read the subject book, but based on this review I think I'm gonna see if my library has it. Here is the link to the review if you want to read the entire article.
Emphasis is mine -
If we ask how the fat gets into the fat cells, we will discover that all the pathways of fat storage were worked out years ago and are so uncontroversial that they’re described in detail in every biochemistry and physiology textbook currently in use. It’s well known that the metabolic hormone insulin stimulates an enzyme on the surface of the fat cell that moves the fat into the cell.
So if insulin moves fat into the fat cells, it would seem that a lot of insulin would move a lot of fat into the fat cells. And indeed it does. Given this, the rational person trying to figure out the previous step in our progression would ask What causes a lot of insulin? Or the rational person, should he/she have been steeped for a lifetime in the marinade of ‘fat is bad’ might ask, What about fat? If there is a lot of fat in the blood as a result of fat in the diet, wouldn’t that fat get into the fat cell? If so, then doesn’t dietary fat lead to fat?
A good question, but the answer is no. Type I diabetics can have a lot of fat in their diets and in their blood, but if they have no insulin, they can’t store that fat. In fact, most pre-diagnosis type I diabetics lose enormous amounts of weight despite eating ravenously because without insulin they can’t store the fat. So dietary fat itself – even large amounts of it – won’t find its way into the fat cell without the help of insulin.
Here are some more snippets -
When you hack through the thicket of all the biochemical pathways involved in the metabolic process, you find that insulin is the primary force involved in the storage of nutrients. Insulin is the body’s storage hormone: it puts fat in the fat cells, protein into muscle cells and glucose into it’s storage form, glycogen.
If we have a lot of insulin, the insulin dominant-pathways (the storage pathways) hold sway, and fat is partitioned away in the fat cells; if insulin is low, then the glucagon-dominant pathways (the energy-release pathways) take over and start moving fat out of the fat cells, so it can be consumed by the body as fuel. This is how it is supposed to work. We eat. Insulin comes out and stores away the energy. We go for a while without eating, insulin goes down and glucagon comes out to retrieve our stored fat so we’ll have a continuous energy supply.
Problems arise when this system goes off the rails, which most commonly happens when people develop insulin resistance, a problem of disordered insulin signaling. Insulin talks, but the cells don’t listen. So insulin keeps talking louder until the cells finally get the message. In other words, the pancreas keeps producing insulin and the blood levels continue to rise until the cells finally get the message. But it’s a message that has taken a lot of insulin force to deliver.
If all the different types of cells developed resistance to insulin at the same rate, we wouldn’t have as much of a problem. But they don’t. Different cells develop insulin resistance at different rates. Typically the first cells to become insulin resistant are the liver cells. The liver cells are continuously producing sugar and dumping it into the blood. Insulin shuts this process down. If the insulin level drops to zero, as it does in type I diabetes, the liver dumps a huge load of sugar in the blood causing all the blood sugar problems associated with this disease. Under normal circumstances, just a little insulin stops the liver cells in their tracks. But if these cells are resistant to insulin, much more is required to get them the message to turn off the sugar spigot.
In most people, the fat cells develop insulin resistance later, which creates the problem. If insulin levels are high to control the liver’s sugar factory output, then these elevated insulin levels are sending a strong message to the non-insulin-resistant fat cells. The message is take this fat and store it. High insulin not only drives fat into the fat cells, it prevents it from getting out. Fat is packed into the fat cells and kept there.
Between meals when insulin levels would normally fall, allowing the liberation of fat to feed all the body’s tissues, insulin remains high in an effort to keep the liver in check. Fat can’t get out of the fat cells, and the tissues begin to starve. Even though there is plenty of stored fat, the body can’t get to it because elevated insulin is preventing its release.
I've not read the subject book, but based on this review I think I'm gonna see if my library has it. Here is the link to the review if you want to read the entire article.
.