I am an endocrinologist. I see and treat persons with hormonal disorders that can often be diagnosed with measurement of hormones in the peripheral bloodstream. I have long told patients that psychiatric disorders have a biologic basis, but cannot be assessed with a simple measurement of substances that show up in the systemic circulation.
I would be skeptical that events (ie measurable substances) beyond the CNS Blood-Brain barrier would show up with sufficient sensitivity and specificity to diagnose a condition that takes psychiatric specialists to assess. I think the most promising means of assessing CNS neurochemistry may be specialized imaging studies like PET scanning of metabolic activity of different regions of the brain. Psychiatry is where endocrinology was 50 years ago. Until we improve means of measuring the biologic basis of psychiatric disorders, I would be hesitant to make ER-based decisions on management based upon a peripheral blood test result.
Micro-cancers may spontaneously occur (and perhaps regress) frequently; no one really knows. However, most cancers presumably started as micro-cancers.
I fear this test will pick-up "cancers" of questionable significance. What impact will such a test have on healthcare costs, if a battery of additional diagnostic tests are used to work-up a "positive" screening test?
I, for one, appreciate the opinion of the NYT staff writers; I don't always agree with them, but they are generally knowledgeable and critical of important issues. Their views are filtered by professional editors that try to afford some balance and accountability. In addition, NYT occasionally have Op-Ed pieces from political figures.
Blogs may or may not have those qualities on a consistent basis.
All type 2 diabetics have some insulin deficiency, even if it is only relative deficiency.
Semantics. Some diabetics have extremely high insulin levels, albeit not high enough to overcome their insulin resistance.
They all have impaired beta cell function.
Not true. In many cases of insulin resistance, the beta cells are taxed to overproduce insulin in order to attain glycemic control. The beta cells work quite well, early on. The impairment is thought to arise from either beta cell overload (after months-years of excess taxation), amyloid deposition, or glucose toxicity. Other mechanisms may also be responsible.
Insulin resistance alone doesn't cause diabetes...
Not true for some (but not all) cases. NIH has identified several individuals with specific mutations in the insulin receptor which lead to severe insulin resistance and diabetes mellitus. Persons with Maturity Onset Diabetes of the Young (MODY) have insulin resistance from mutations in certain gene transcription factors that mediate some of the downstream actions of insulin. An extreme example is genetic knockout mice that lack the insulin receptor die of diabetic ketoacidosis within hours of birth. A whole array of other knockout mice have been produced that lack some key mediator(s) of insulin action, producing insulin resistance. Some, however, never become diabetic or even hyperglycemic. Insulin resistance is thought to be one of the hallmarks of type II diabetes mellitus, perhaps in concert with other diabetes genes that may trigger other mechanisms of diabetes, including glucose toxicity and beta cell overload. However, some lean type II diabetics may have little, if any insulin resistance at all, and are biochemically similar to a type I diabetic, albeit, without the autoimmune insulitis.
Loss of beta cells occurs at different times in different type II diabetics. Some patients with profound insulin resistance and diabetes due to insulin resistance can become normoglycemic with weight loss (such as gastric bypass), but it is highly dependent on the individual and when the weight loss occurs.
My only point was that type II diabetes mellitus is not one single disease, but is a collection of subtypes with polygenic causes, all with a common endpoint, hyperglycemia. For some individuals, treating the insulin resistance will be effective, but for others, it will not be. Determining all the biochemical causes of type II diabetes mellitus through genomic medicine should elucidate the best way(s) to treat various subtypes of type II diabetes
I can't speak for to the immediate parent, but based on my previous experience, persons with Type I have far more knowledge about diabetes in general than those without any diabetes, whether Type I or Type II is being considered.
Diabetics may respond differently to different types of foods, whether it is protein, carbohydrates, or fat. Insulin release is triggered by glucose (which is rapidly converted from a variety of other carbohydrates), and some amino acids (the substrates that compose proteins). Fat won't acutely trigger insulin release, but can if glucose production occurs in the liver.
The comments on Atkins do not apply to Type I, but as far as Type II diabetes is concerned, there is little biochemical evidence that there is any rational basis for subscribing to this hypothesis. It might work for some persons, but it often does nothing for many persons. No long term studies have demonstrated that this is an effective dietary therapy. Some persons might benefit for reasons that are still unclear, but many do not, and you never read about those folks.
As for how the other comments rebut the original parent, here are the explicit differences:
Fat consumption has nothing whatsoever to do with diabetes.
Yes, for many, but not all, individuals, excess fat calories lead to weight gain, and insulin resistance. No prospective trial has been conducted to address this question.
You could eat bacon 3 meals a day and not have high glucose levels. (Your blood pressure and cholesterol levels might not be so terrific...)
Some persons do get elevated glucose levels. Paradoxically, some persons do not necessarily have elevated cholesterol or BP, but why that happens to some persons is unclear.
Type 2 diabetes is one of two things: 1. You are not producing insulin fast enough to process large amounts of glucose in the blood.
Or 2. Your body is not absorbing the insulin fast enough to do so.
Basically, this is true, but there are many shades of grey between the amount that is contributed by these 2 causes.
In either case, when you eat foods that are quickly turned to sugar in the blood (any foods which are high in starch or sugar, including white bread and potato products, and especially sugary foods like Pepsi) your blood's glucose level goes way up, because your body can't process it. This causes all kinds of problems. Fatty foods do neccesarilly raise your blood sugar levels. You may be confused because obesity (fat tissue, not fat consumption) slows insulin absorbtion, and is a contribuiting factor to Type 2 diabetes.
The above statements are generally true, except that the "processing" of glucose is dependent upon glucose uptake by tissues. The issue about elevated glucose levels is variable in different individuals, as commented above. The final sentence would be more correct if it read that obesity contributes to insulin resistance, which means that individuals may become resistant to insulin, but "insulin absorption" is not affected.
Final disclaimer: Atkins (and South Beach, etc) is controversial. I think the jury will be out for several months-years. These ideas are not new, but have not been rigorously tested by formal scientific investigation (there are about a half-dozen well-designed published studies to date). It might help some persons, but may not work for other persons. Extrapolating the benefits of one dietary therapy for a polygenic disorder would be premature at this point.
This is incorrect. Type II diabetes is not a single disease, but rather a collection of phenotypes/genotypes that result in a common endpoint: hyperglycemia (elevated blood glucose).
Unlike Type I (also known as Juvenile-Onset) diabetes, Type II diabetes is most certainly a "polygenic" disorder, characterized by some individuals who have insulin resistance, some with relative insulin deficiency, and many who have both.
Obesity contributes to insulin resistance through multiple mechanisms. Although eating "fat" may not raise your blood glucose level acutely, it will probably cause other metabolic derangements that could be equally detrimental.
Some diabetologists feel that hyperglycemia may be a rather late endpoint of insulin deficiency/resistance, and that other complications may be inflammatory in nature, not necessarily due to glucose directly. Whether this is borne out by ongoing research remains to be seen.
Also, insulin is not "absorbed", it acts on a cell-surface membrance receptor, and stimulates the uptake of glucose and free fatty acids. Fat tissue releases numerous cytokines that modulate the action of insulin and other metabolic hormones.
Slashdot Mirror
I am an endocrinologist. I see and treat persons with hormonal disorders that can often be diagnosed with measurement of hormones in the peripheral bloodstream. I have long told patients that psychiatric disorders have a biologic basis, but cannot be assessed with a simple measurement of substances that show up in the systemic circulation. I would be skeptical that events (ie measurable substances) beyond the CNS Blood-Brain barrier would show up with sufficient sensitivity and specificity to diagnose a condition that takes psychiatric specialists to assess. I think the most promising means of assessing CNS neurochemistry may be specialized imaging studies like PET scanning of metabolic activity of different regions of the brain. Psychiatry is where endocrinology was 50 years ago. Until we improve means of measuring the biologic basis of psychiatric disorders, I would be hesitant to make ER-based decisions on management based upon a peripheral blood test result.
Micro-cancers may spontaneously occur (and perhaps regress) frequently; no one really knows. However, most cancers presumably started as micro-cancers. I fear this test will pick-up "cancers" of questionable significance. What impact will such a test have on healthcare costs, if a battery of additional diagnostic tests are used to work-up a "positive" screening test?
I, for one, appreciate the opinion of the NYT staff writers; I don't always agree with them, but they are generally knowledgeable and critical of important issues. Their views are filtered by professional editors that try to afford some balance and accountability. In addition, NYT occasionally have Op-Ed pieces from political figures. Blogs may or may not have those qualities on a consistent basis.
Lord Farquaad is supposedly Eisner: http://www.shrek.com/igallery/large_images/800x600 /Farquaad_800.jpg
All type 2 diabetics have some insulin deficiency, even if it is only relative deficiency.
Semantics. Some diabetics have extremely high insulin levels, albeit not high enough to overcome their insulin resistance.
They all have impaired beta cell function.
Not true. In many cases of insulin resistance, the beta cells are taxed to overproduce insulin in order to attain glycemic control. The beta cells work quite well, early on. The impairment is thought to arise from either beta cell overload (after months-years of excess taxation), amyloid deposition, or glucose toxicity. Other mechanisms may also be responsible.
Insulin resistance alone doesn't cause diabetes...
Not true for some (but not all) cases. NIH has identified several individuals with specific mutations in the insulin receptor which lead to severe insulin resistance and diabetes mellitus. Persons with Maturity Onset Diabetes of the Young (MODY) have insulin resistance from mutations in certain gene transcription factors that mediate some of the downstream actions of insulin. An extreme example is genetic knockout mice that lack the insulin receptor die of diabetic ketoacidosis within hours of birth. A whole array of other knockout mice have been produced that lack some key mediator(s) of insulin action, producing insulin resistance. Some, however, never become diabetic or even hyperglycemic. Insulin resistance is thought to be one of the hallmarks of type II diabetes mellitus, perhaps in concert with other diabetes genes that may trigger other mechanisms of diabetes, including glucose toxicity and beta cell overload. However, some lean type II diabetics may have little, if any insulin resistance at all, and are biochemically similar to a type I diabetic, albeit, without the autoimmune insulitis.
Loss of beta cells occurs at different times in different type II diabetics. Some patients with profound insulin resistance and diabetes due to insulin resistance can become normoglycemic with weight loss (such as gastric bypass), but it is highly dependent on the individual and when the weight loss occurs.
My only point was that type II diabetes mellitus is not one single disease, but is a collection of subtypes with polygenic causes, all with a common endpoint, hyperglycemia. For some individuals, treating the insulin resistance will be effective, but for others, it will not be. Determining all the biochemical causes of type II diabetes mellitus through genomic medicine should elucidate the best way(s) to treat various subtypes of type II diabetes
I can't speak for to the immediate parent, but based on my previous experience, persons with Type I have far more knowledge about diabetes in general than those without any diabetes, whether Type I or Type II is being considered. Diabetics may respond differently to different types of foods, whether it is protein, carbohydrates, or fat. Insulin release is triggered by glucose (which is rapidly converted from a variety of other carbohydrates), and some amino acids (the substrates that compose proteins). Fat won't acutely trigger insulin release, but can if glucose production occurs in the liver. The comments on Atkins do not apply to Type I, but as far as Type II diabetes is concerned, there is little biochemical evidence that there is any rational basis for subscribing to this hypothesis. It might work for some persons, but it often does nothing for many persons. No long term studies have demonstrated that this is an effective dietary therapy. Some persons might benefit for reasons that are still unclear, but many do not, and you never read about those folks. As for how the other comments rebut the original parent, here are the explicit differences: Fat consumption has nothing whatsoever to do with diabetes. Yes, for many, but not all, individuals, excess fat calories lead to weight gain, and insulin resistance. No prospective trial has been conducted to address this question. You could eat bacon 3 meals a day and not have high glucose levels. (Your blood pressure and cholesterol levels might not be so terrific...) Some persons do get elevated glucose levels. Paradoxically, some persons do not necessarily have elevated cholesterol or BP, but why that happens to some persons is unclear. Type 2 diabetes is one of two things: 1. You are not producing insulin fast enough to process large amounts of glucose in the blood. Or 2. Your body is not absorbing the insulin fast enough to do so. Basically, this is true, but there are many shades of grey between the amount that is contributed by these 2 causes. In either case, when you eat foods that are quickly turned to sugar in the blood (any foods which are high in starch or sugar, including white bread and potato products, and especially sugary foods like Pepsi) your blood's glucose level goes way up, because your body can't process it. This causes all kinds of problems. Fatty foods do neccesarilly raise your blood sugar levels. You may be confused because obesity (fat tissue, not fat consumption) slows insulin absorbtion, and is a contribuiting factor to Type 2 diabetes. The above statements are generally true, except that the "processing" of glucose is dependent upon glucose uptake by tissues. The issue about elevated glucose levels is variable in different individuals, as commented above. The final sentence would be more correct if it read that obesity contributes to insulin resistance, which means that individuals may become resistant to insulin, but "insulin absorption" is not affected. Final disclaimer: Atkins (and South Beach, etc) is controversial. I think the jury will be out for several months-years. These ideas are not new, but have not been rigorously tested by formal scientific investigation (there are about a half-dozen well-designed published studies to date). It might help some persons, but may not work for other persons. Extrapolating the benefits of one dietary therapy for a polygenic disorder would be premature at this point.
This is incorrect. Type II diabetes is not a single disease, but rather a collection of phenotypes/genotypes that result in a common endpoint: hyperglycemia (elevated blood glucose).
Unlike Type I (also known as Juvenile-Onset) diabetes, Type II diabetes is most certainly a "polygenic" disorder, characterized by some individuals who have insulin resistance, some with relative insulin deficiency, and many who have both.
Obesity contributes to insulin resistance through multiple mechanisms. Although eating "fat" may not raise your blood glucose level acutely, it will probably cause other metabolic derangements that could be equally detrimental.
Some diabetologists feel that hyperglycemia may be a rather late endpoint of insulin deficiency/resistance, and that other complications may be inflammatory in nature, not necessarily due to glucose directly. Whether this is borne out by ongoing research remains to be seen.
Also, insulin is not "absorbed", it acts on a cell-surface membrance receptor, and stimulates the uptake of glucose and free fatty acids. Fat tissue releases numerous cytokines that modulate the action of insulin and other metabolic hormones.