Free will is largely an illusion; our behavior results because it is the only possible option. Choice, or the illusion of choice, is just a delusion our brain makes up to explain reality... kinda how we made up god to explain life.
WHat results in behavior, is the way our brain is wired (genetics/experience), influenced by the sum of our experiences to that point (our knowledge, learning). The only way to change behavior is to affect either the way it's wired (drugs) OR what it has learned (education).
Being a "bum" doesn't cause alcoholism, it results form alcoholism. Being a "gluttonous fat sloth" doesn't cause obesity, it results form obesity. The psychological traits of some obese people (addiction to junk food, not dealing with problems in life, over eating, lack of activity)... these are affected by hidden, but no less real changes in the brain and metabolism.
Sometimes, recognizing your own power is all you need, but rarely is a change that simple... and one thing is consistently shown that stigmatizing and berating these people (whether they are alcoholics or obese) tends to just make them more stressed, overwhelmed, therefore unable to make any permanent change in their lifestyle.
Hi,
What you must understand is that insulin resistance (the primary underlying pathological change resulting in type 2 diabetes) does not occur in an egalitarian fashion. Muscle cells lose their ability to absorb and metabolize glucose before fat cells... possibly due to the greater energy needs of muscle cells.
So when someone says "fat cells become too good at extracting glucose from the blood and storing it", what they mean is that insulin resistance changes how food is metabolized, so that foods that yeild a lot of glucose are preferentially stored as fat, as opposed to burned in the muscle for energy. This creates a paradoxical condition of obesity, while the individual still expresses signs and symptoms of starvation observed in type 1 diabetes (type 1 diabetes, due to insulin deficit, is classic starvation with emaciation; type 2 diabetes, which is caused by a cellular-level defect in glucose metabolism, results in paradoxical obesity with starvation of tissues).
The polydipsia, polyphagia, and polyuria are all signs of starvation and hyperglycemia... and all diabetics express them, because diabetes automatically implies cellular starvation (to be diabetic means glucose is not being metabolized for energy, which results in starvation; body fat need not be liberated, as just the *smallest* amount of fat-cell insulin sensitivity with insulin production will prevent ketoacidosis).
Or to put this another way... imagine a body, with a LOT of insulin receptors on fat cells, but the insulin receptors on liver, and muscle cells were sluffed off and dulled. A normal body has an appropriate balance of insulin receptors, on fat, on muscle, on the liver.
This insulin-receptor damaged person eats a bagel.
The polysaccharides in the bagel are broken apart, and glucose rapidly enters the blood. Insulin rises, a lot, because they have less insulin receptors therefore have a really difficult time clearing out blood glucose. Insulin causes hypoglycemia in a dose-dependent relationship, therefore compensatory hyperinsulinemia results to try to keep homeostasis of blood sugar. Blood sugar is elevated, but starts to decrease a few hours after the meal.
What do you think will happen to this person's level of energy and weight?
Remember, the ratio of insulin receptors are unbalanced. Most of them are on the fat cells, less of them are on the muscle.
Also, I should introduce an additional concept: High insulin suppresses fat burning very strongly. Considering the insuiln resistant (less receptor) person needs to make a great deal of insulin to mobilize blood sugar, and because suppressing the liberation of fat from fat cells requires less insulin than does mobilizing blood sugar into the cell in insulin resistance, this creates an imbalance in fat storing vs fat burning. Due to hyperinsulinemia, all carbohydrate they eat is stored as fat preferentially, meanwhile all subsequent body fat tends to be retained in the cell. Ironically the type 2 diabetic usually can burn fatty acids for energy much more effectively than glucose, because fatty acids require very little insulin to mobilize into muscle cells.
Summary:As a result of insulin resistance, people store carbohydrate as fat vs burning it off as energy, producing a paradoxical state of appearing obese yet actually being emaciated and starved at the cellular level (and the health of an insulin resistant person, underneath this "fat coat", is very similar to a starved food deprived person: they have no immune system to speak of, no ability to repair tissues, etc).
Due to compensatory hyperinsulinemia, fat is kept in fat cells vs being liberated at a disproportionate rate. The insulin sensitivity of fat cells is reasonably well preserved, so when fat cells see extremely high insulin, they respond logically: store food, don't release fat. The rest of the body is dead and dumb to insulin, and it wastes away, while adipose grows. This results in the hallmark signs of diabetes (the three P's previously mentioned). These individuals eat and eat and eat, and only become more lethargic and obese from it.
Make sense?
This is the best summary of taubes book I've ever read.
Taubes book is definitely something a person who struggles with weight or their health ought to read... and please read it with an open mind or else you do yourself a great disservice.
(This is the same as my previous post, except formated with HTML...Sorry didn't realize this forum didn't auto-format).
Though the risk of certain cardiovascular diseases and incidents increase with cholesterol, it is not true that a lower cholesterol protects against all forms of cardiovascular problems, injury, or even death.
What is a "heart attack"? It's when a clot, lodges in the lumen of a cornary vessel, usually stenosised because of atherosclerotic plaques.
Without this clot, there is no heart attack.
One thing you might understand if you had basic medical education, is that the ability for the blood to clot, is strongly influenced by inflammation. That is to say, when the body is in a pro-inflammatory state, the body shifts to increased blood clotting. Asprin, for example, works by inhibiting the synthesis of arachidonic acid into certain proinflammatory chemicals. In doing so, it reduces the cardinal signs of inflammation (like swelling and pain), while also thinning the blood.
With me so far? Okay.
Insulin levels correlate with both inflammation (positive) and cholesterol (positive).
Insulin is increased on a high carbohydrate diet, especially a high carbohydrate/high calorie diet.
What does this mean? If you eat a diet high in carbohydrates, you make more insulin. If you make more insulin, your body is more inflammatory, and if your body is more inflammatory, you are at a greater risk for blood clots, and blood clots cause heart attacks and strokes. You also probably have a high cholesterol, since the influence of insulin on inflammation, also promotes cholesterol synthesis and fat storage. The cholesterol is not causing the atherosclerosis (more on that later), and the cholesterol certainly isn't causing the clots that lead to vascular accidents/MIs. The cholesterol is a marker for metabolism, and it is the metabolism doing all of these things. Statin drugs work not by reducing cholesterol, but by reducing inflammation, simialr to your handy 2 dollar bottle of asprin.
Cholesterol is a material that the body uses to repair cell membranes and tissues. Without cholesterol, we would be dead. It's a key component of brain cells, and hormones. Atherosclerosis tends to occur in those populations who sustain a high amount of tissue damage; the elderly, smokers, people who eat sh*tty diets high in carbs (thus hyperinsulinemic), so on. An increase in cholesterol, tends to occur any time the body sees an increased need for tissue synthesis and repair. For example, cholesterol (as well as clotting ability) will increase during pregnancy (for obvious reasons, increased blood clotting and cholesterol levels are a boon for pregnant woman and child and were selected). Cholesterol causes atherosclerosis, like white blood cells cause infections. The problem is the primary insult which is promoting inflammation and tissue damage (example, smoking: hypoxia and an increase breakdown of tissues with inefficient repair).
Those things which decrease cholesterol, tend to be those things which also decrease insulin OR inflammation depending on where the intervention is targeting (and remember, anything that reduces insulin usually reduces inflammation too).
Is any of this making sense to you?
Cholesterol, while being a marker for certain metabolic derrangements (thus diseases) is ultimately passive. Therefore, drugs / interventions which target cholesterol specifically are misguided. Those things which lower cholesterol also tend to reduce inflammation and insulin, and it is likely this way they are theraputic.
...and, since cholesterol is only a marker for certain metabolic derrangements, and these are not absolutely conclusive with the TOTAL cholesterol or even the LDL cholesterol, a "lower is better" attitude is not justified.
Oh, and, it's also not true that less cholesterol/inflammation is better. Just as a highly inflammatory state with very high insulin
Though the risk of certain cardiovascular diseases and incidents increase with cholesterol, it is not true that a lower cholesterol protects against all forms of cardiovascular problems, injury, or even death.
What is a "heart attack"? It's when a clot, lodges in the lumen of a cornary vessel, usually stenosised because of atherosclerotic plaques.
Without this clot, there is no heart attack.
One thing you might understand if you had basic medical education, is that the ability for the blood to clot, is strongly influenced by inflammation. That is to say, when the body is in a pro-inflammatory state, the body shifts to increased blood clotting. Asprin, for example, works by inhibiting the synthesis of arachidonic acid into certain proinflammatory chemicals. In doing so, it reduces the cardinal signs of inflammation (like swelling and pain), while also thinning the blood.
With me so far? Okay.
Insulin levels correlate with both inflammation (positive) and cholesterol (positive).
Insulin is increased on a high carbohydrate diet, especially a high carbohydrate/high calorie diet.
What does this mean? If you eat a diet high in carbohydrates, you make more insulin. If you make more insulin, your body is more inflammatory, and if your body is more inflammatory, you are at a greater risk for blood clots, and blood clots cause heart attacks and strokes. You also probably have a high cholesterol, since the influence of insulin on inflammation, also promotes cholesterol synthesis and fat storage. The cholesterol is not causing the atherosclerosis (more on that later), and the cholesterol certainly isn't causing the clots that lead to vascular accidents/MIs. The cholesterol is a marker for metabolism, and it is the metabolism doing all of these things. Statin drugs work not by reducing cholesterol, but by reducing inflammation, simialr to your handy 2 dollar bottle of asprin.
Cholesterol is a material that the body uses to repair cell membranes and tissues. Without cholesterol, we would be dead. It's a key component of brain cells, and hormones. Atherosclerosis tends to occur in those populations who sustain a high amount of tissue damage; the elderly, smokers, people who eat sh*tty diets high in carbs (thus hyperinsulinemic), so on. An increase in cholesterol, tends to occur any time the body sees an increased need for tissue synthesis and repair. For example, cholesterol (as well as clotting ability) will increase during pregnancy (for obvious reasons, increased blood clotting and cholesterol levels are a boon for pregnant woman and child and were selected). Cholesterol causes atherosclerosis, like white blood cells cause infections. The problem is the primary insult which is promoting inflammation and tissue damage (example, smoking: hypoxia and an increase breakdown of tissues with inefficient repair).
Those things which decrease cholesterol, tend to be those things which also decrease insulin OR inflammation depending on where the intervention is targeting (and remember, anything that reduces insulin usually reduces inflammation too).
Is any of this making sense to you?
Cholesterol, while being a marker for certain metabolic derrangements (thus diseases) is ultimately passive. Therefore, drugs / interventions which target cholesterol specifically are misguided. Those things which lower cholesterol also tend to reduce inflammation and insulin, and it is likely this way they are theraputic....and, since cholesterol is only a marker for certain metabolic derrangements, and these are not absolutely conclusive with the TOTAL cholesterol or even the LDL cholesterol, a "lower is better" attitude is not justified.
Oh, and, it's also not true that less cholesterol/inflammation is better. Just as a highly inflammatory state with very high insulin tends to cause atherosclerosis and fatal clots... it's also true that starvation, very low cals, thus low levels of insulin and inflammation promote an insufficient inflammatory response which promotes increase risk for death from accidental
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Free will is largely an illusion; our behavior results because it is the only possible option. Choice, or the illusion of choice, is just a delusion our brain makes up to explain reality... kinda how we made up god to explain life.
WHat results in behavior, is the way our brain is wired (genetics/experience), influenced by the sum of our experiences to that point (our knowledge, learning). The only way to change behavior is to affect either the way it's wired (drugs) OR what it has learned (education).
Being a "bum" doesn't cause alcoholism, it results form alcoholism. Being a "gluttonous fat sloth" doesn't cause obesity, it results form obesity. The psychological traits of some obese people (addiction to junk food, not dealing with problems in life, over eating, lack of activity)... these are affected by hidden, but no less real changes in the brain and metabolism.
Sometimes, recognizing your own power is all you need, but rarely is a change that simple... and one thing is consistently shown that stigmatizing and berating these people (whether they are alcoholics or obese) tends to just make them more stressed, overwhelmed, therefore unable to make any permanent change in their lifestyle.
Hi, What you must understand is that insulin resistance (the primary underlying pathological change resulting in type 2 diabetes) does not occur in an egalitarian fashion. Muscle cells lose their ability to absorb and metabolize glucose before fat cells... possibly due to the greater energy needs of muscle cells.
So when someone says "fat cells become too good at extracting glucose from the blood and storing it", what they mean is that insulin resistance changes how food is metabolized, so that foods that yeild a lot of glucose are preferentially stored as fat, as opposed to burned in the muscle for energy. This creates a paradoxical condition of obesity, while the individual still expresses signs and symptoms of starvation observed in type 1 diabetes (type 1 diabetes, due to insulin deficit, is classic starvation with emaciation; type 2 diabetes, which is caused by a cellular-level defect in glucose metabolism, results in paradoxical obesity with starvation of tissues). The polydipsia, polyphagia, and polyuria are all signs of starvation and hyperglycemia... and all diabetics express them, because diabetes automatically implies cellular starvation (to be diabetic means glucose is not being metabolized for energy, which results in starvation; body fat need not be liberated, as just the *smallest* amount of fat-cell insulin sensitivity with insulin production will prevent ketoacidosis).
Or to put this another way... imagine a body, with a LOT of insulin receptors on fat cells, but the insulin receptors on liver, and muscle cells were sluffed off and dulled. A normal body has an appropriate balance of insulin receptors, on fat, on muscle, on the liver. This insulin-receptor damaged person eats a bagel. The polysaccharides in the bagel are broken apart, and glucose rapidly enters the blood. Insulin rises, a lot, because they have less insulin receptors therefore have a really difficult time clearing out blood glucose. Insulin causes hypoglycemia in a dose-dependent relationship, therefore compensatory hyperinsulinemia results to try to keep homeostasis of blood sugar. Blood sugar is elevated, but starts to decrease a few hours after the meal.
What do you think will happen to this person's level of energy and weight?
Remember, the ratio of insulin receptors are unbalanced. Most of them are on the fat cells, less of them are on the muscle.
Also, I should introduce an additional concept: High insulin suppresses fat burning very strongly. Considering the insuiln resistant (less receptor) person needs to make a great deal of insulin to mobilize blood sugar, and because suppressing the liberation of fat from fat cells requires less insulin than does mobilizing blood sugar into the cell in insulin resistance, this creates an imbalance in fat storing vs fat burning. Due to hyperinsulinemia, all carbohydrate they eat is stored as fat preferentially, meanwhile all subsequent body fat tends to be retained in the cell.
Ironically the type 2 diabetic usually can burn fatty acids for energy much more effectively than glucose, because fatty acids require very little insulin to mobilize into muscle cells.
Summary:As a result of insulin resistance, people store carbohydrate as fat vs burning it off as energy, producing a paradoxical state of appearing obese yet actually being emaciated and starved at the cellular level (and the health of an insulin resistant person, underneath this "fat coat", is very similar to a starved food deprived person: they have no immune system to speak of, no ability to repair tissues, etc).
Due to compensatory hyperinsulinemia, fat is kept in fat cells vs being liberated at a disproportionate rate. The insulin sensitivity of fat cells is reasonably well preserved, so when fat cells see extremely high insulin, they respond logically: store food, don't release fat. The rest of the body is dead and dumb to insulin, and it wastes away, while adipose grows. This results in the hallmark signs of diabetes (the three P's previously mentioned). These individuals eat and eat and eat, and only become more lethargic and obese from it.
Make sense?
This is the best summary of taubes book I've ever read. Taubes book is definitely something a person who struggles with weight or their health ought to read... and please read it with an open mind or else you do yourself a great disservice.
(This is the same as my previous post, except formated with HTML...Sorry didn't realize this forum didn't auto-format).
...and, since cholesterol is only a marker for certain metabolic derrangements, and these are not absolutely conclusive with the TOTAL cholesterol or even the LDL cholesterol, a "lower is better" attitude is not justified.
Though the risk of certain cardiovascular diseases and incidents increase with cholesterol, it is not true that a lower cholesterol protects against all forms of cardiovascular problems, injury, or even death.
What is a "heart attack"? It's when a clot, lodges in the lumen of a cornary vessel, usually stenosised because of atherosclerotic plaques. Without this clot, there is no heart attack.
One thing you might understand if you had basic medical education, is that the ability for the blood to clot, is strongly influenced by inflammation. That is to say, when the body is in a pro-inflammatory state, the body shifts to increased blood clotting. Asprin, for example, works by inhibiting the synthesis of arachidonic acid into certain proinflammatory chemicals. In doing so, it reduces the cardinal signs of inflammation (like swelling and pain), while also thinning the blood.
With me so far? Okay.
Insulin levels correlate with both inflammation (positive) and cholesterol (positive). Insulin is increased on a high carbohydrate diet, especially a high carbohydrate/high calorie diet.
What does this mean? If you eat a diet high in carbohydrates, you make more insulin. If you make more insulin, your body is more inflammatory, and if your body is more inflammatory, you are at a greater risk for blood clots, and blood clots cause heart attacks and strokes. You also probably have a high cholesterol, since the influence of insulin on inflammation, also promotes cholesterol synthesis and fat storage. The cholesterol is not causing the atherosclerosis (more on that later), and the cholesterol certainly isn't causing the clots that lead to vascular accidents/MIs. The cholesterol is a marker for metabolism, and it is the metabolism doing all of these things. Statin drugs work not by reducing cholesterol, but by reducing inflammation, simialr to your handy 2 dollar bottle of asprin.
Cholesterol is a material that the body uses to repair cell membranes and tissues. Without cholesterol, we would be dead. It's a key component of brain cells, and hormones. Atherosclerosis tends to occur in those populations who sustain a high amount of tissue damage; the elderly, smokers, people who eat sh*tty diets high in carbs (thus hyperinsulinemic), so on. An increase in cholesterol, tends to occur any time the body sees an increased need for tissue synthesis and repair. For example, cholesterol (as well as clotting ability) will increase during pregnancy (for obvious reasons, increased blood clotting and cholesterol levels are a boon for pregnant woman and child and were selected). Cholesterol causes atherosclerosis, like white blood cells cause infections. The problem is the primary insult which is promoting inflammation and tissue damage (example, smoking: hypoxia and an increase breakdown of tissues with inefficient repair).
Those things which decrease cholesterol, tend to be those things which also decrease insulin OR inflammation depending on where the intervention is targeting (and remember, anything that reduces insulin usually reduces inflammation too).
Is any of this making sense to you?
Cholesterol, while being a marker for certain metabolic derrangements (thus diseases) is ultimately passive. Therefore, drugs / interventions which target cholesterol specifically are misguided. Those things which lower cholesterol also tend to reduce inflammation and insulin, and it is likely this way they are theraputic.
Oh, and, it's also not true that less cholesterol/inflammation is better. Just as a highly inflammatory state with very high insulin
Though the risk of certain cardiovascular diseases and incidents increase with cholesterol, it is not true that a lower cholesterol protects against all forms of cardiovascular problems, injury, or even death. What is a "heart attack"? It's when a clot, lodges in the lumen of a cornary vessel, usually stenosised because of atherosclerotic plaques. Without this clot, there is no heart attack. One thing you might understand if you had basic medical education, is that the ability for the blood to clot, is strongly influenced by inflammation. That is to say, when the body is in a pro-inflammatory state, the body shifts to increased blood clotting. Asprin, for example, works by inhibiting the synthesis of arachidonic acid into certain proinflammatory chemicals. In doing so, it reduces the cardinal signs of inflammation (like swelling and pain), while also thinning the blood. With me so far? Okay. Insulin levels correlate with both inflammation (positive) and cholesterol (positive). Insulin is increased on a high carbohydrate diet, especially a high carbohydrate/high calorie diet. What does this mean? If you eat a diet high in carbohydrates, you make more insulin. If you make more insulin, your body is more inflammatory, and if your body is more inflammatory, you are at a greater risk for blood clots, and blood clots cause heart attacks and strokes. You also probably have a high cholesterol, since the influence of insulin on inflammation, also promotes cholesterol synthesis and fat storage. The cholesterol is not causing the atherosclerosis (more on that later), and the cholesterol certainly isn't causing the clots that lead to vascular accidents/MIs. The cholesterol is a marker for metabolism, and it is the metabolism doing all of these things. Statin drugs work not by reducing cholesterol, but by reducing inflammation, simialr to your handy 2 dollar bottle of asprin. Cholesterol is a material that the body uses to repair cell membranes and tissues. Without cholesterol, we would be dead. It's a key component of brain cells, and hormones. Atherosclerosis tends to occur in those populations who sustain a high amount of tissue damage; the elderly, smokers, people who eat sh*tty diets high in carbs (thus hyperinsulinemic), so on. An increase in cholesterol, tends to occur any time the body sees an increased need for tissue synthesis and repair. For example, cholesterol (as well as clotting ability) will increase during pregnancy (for obvious reasons, increased blood clotting and cholesterol levels are a boon for pregnant woman and child and were selected). Cholesterol causes atherosclerosis, like white blood cells cause infections. The problem is the primary insult which is promoting inflammation and tissue damage (example, smoking: hypoxia and an increase breakdown of tissues with inefficient repair). Those things which decrease cholesterol, tend to be those things which also decrease insulin OR inflammation depending on where the intervention is targeting (and remember, anything that reduces insulin usually reduces inflammation too). Is any of this making sense to you? Cholesterol, while being a marker for certain metabolic derrangements (thus diseases) is ultimately passive. Therefore, drugs / interventions which target cholesterol specifically are misguided. Those things which lower cholesterol also tend to reduce inflammation and insulin, and it is likely this way they are theraputic. ...and, since cholesterol is only a marker for certain metabolic derrangements, and these are not absolutely conclusive with the TOTAL cholesterol or even the LDL cholesterol, a "lower is better" attitude is not justified.
Oh, and, it's also not true that less cholesterol/inflammation is better. Just as a highly inflammatory state with very high insulin tends to cause atherosclerosis and fatal clots... it's also true that starvation, very low cals, thus low levels of insulin and inflammation promote an insufficient inflammatory response which promotes increase risk for death from accidental