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Or eating a lot of saturated fat? http://nutritionfacts.org/video/what-causes-diabetes/ http://nutritionfacts.org/video/what-causes-diabetes/

deleted 11y ago
[deleted]
Mz 11y ago
My view is strongly influenced by the fact that I have "atypical cystic fibrosis." Cystic Fibrosis predisposes people to CFRD (Cystic Fibrosis Related Diabetes). My understanding is that this form of diabetes is neither Type 1 nor Type 2. CF is a genetic disorder. With CF, your immune system does not work right and you are basically chronically infected with some infection or other. I have a relatively mild form of it, which helped create a situation where I was diagnosed late in life. I finally got diagnosed due to my health deteriorating drastically and I spent a year at death's door. With finally getting a diagnosis, I was empowered to get myself a great deal healthier. I have fewer blood sugar issues than I used to have. I did nothing to specifically address that issue. I was primarily trying to erradicate the antibiotic resistant infections that were threatening to kill me. People with CF misprocess fats and most of them are seriously underweight. To my mind, this suggests that fat is probably not the real culprit with diabetes. I have become very picky about the types of fats I eat. Butter and coconut oil are fats that are very beneficial to my condition. I sometimes get pain under control by spreading a half a stick of butter on a roll and eating that (or did so at one time -- it has been a while as my condition is more stable). Butter and coconut oil are high in saturated fats. My blood sugar is a great deal more stable than it used to be. (Yes, I know that is "anecdotal." If you want to dismiss it, please come up with a stronger criticism than that. Thanks.)
- hga 11y ago
  Putting my biologist hat on, I don't want to dismiss it, consider it to be interesting, but would have to look a lot more closely to get a guess if your observations are useful in this context. CF is a regulatory derangement, so I don't know what all else it might be doing and how much it might be relevant to normal type humans. That said, no one's come up with any vaguely useful citations linking saturated fats to diabetes, and this doesn't help the case for that.
  - Mz 11y ago
    Putting my biologist hat on, I don't want to dismiss it, consider it to be interesting, Thank you. I would be happy to discuss it with you further. I do not know what you mean by CF is a regulatory derangement. It is caused by a defect in a specific cell channel that manages traffic of specific molecules into and out of the cell. I have paid enormous attention to that and kind of ignored the hand-wavy and apparently incorrect mental models popular in the medical literature. For example, the official explanation on the CF Foundation website is that people with CF are drowning in an excess of mucus. I found one study that says we produce too little mucus, not too much. This fits with my firsthand experience, it more logically fits with the fact that mucus is a protective coating that helps keep out germs and it fits with the extremely well known and well established fact that women with CF suffer vaginal dryness that often seriously interferes with their sex lives. I think we cough up phlegm, not mucus -- ie infection -- and if you improve mucus production, you reduce infection and see less phlegm. I have seen that hypothesis work effectively for me and my oldest son who has the same diagnosis I have. I have explained it to one woman with CF who was out of time and dying and tracked me down after I left all CF lists and took down my health site. She is gradually getting healthier. So that is a very long way of saying that a) I have no idea what you mean by that phrase and b) the odds are high that you and I have completely different mental models for what is going on with CF.
    - hga 11y ago
      Let me state that I haven't studied CF specifically at all, I'm going from what I just read in Wikipedia and my general biology education. It is caused by a defect in a specific cell channel that manages traffic of specific molecules into and out of the cell. Per Wikipedia: "It is caused by the presence of mutations in both copies of the gene for the protein cystic fibrosis transmembrane conductance regulator (CFTR)." Per the article on CFTR: Cystic fibrosis transmembrane conductance regulator (CFTR) is a membrane protein and chloride channel in vertebrates that is encoded by the CFTR gene. CFTR is an ABC transporter-class ion channel that codes for a protein that conducts chloride and thiocyanate ions across epithelial cell membranes. More detail: CFTR functions as an ATP-gated anion channel, increasing the conductance for certain anions (e.g. Cl−) to flow down their electrochemical gradient. ATP-driven conformational changes in CFTR open and close a gate to allow transmembrane flow of anions down their electrochemical gradient. This in contrast to other ABC proteins, in which ATP-driven conformational changes fuel uphill substrate transport across cellular membranes. Essentially, CFTR is an ion channel that evolved as a 'broken' ABC transporter that leaks when in open conformation. The CFTR is found in the epithelial cells of many organs including the lung, liver, pancreas, digestive tract, reproductive tract, and skin. Normally, the protein moves chloride and thiocyanate ions (with a negative charge) out of an epithelial cell to the covering mucus. Positively charged sodium ions follow passively, increasing the total electrolyte concentration in the mucus, resulting in the movement of water out of cell by osmosis. So, based on ATP getting to it, it allows movement (passive transport) of a set of ions and H2O in and out of cells. I assume there's some regulatory function that mediates the opening and closing of it; the CF mutations interfere with its function one way or another (e.g. one class is thought to result in the CFTR degrading quickly, don't know if it functions normally while in place). So while we're mostly focused on the consequences of these ions and water not getting out of the cell and deranging the production of proper mucus, it could also result in metabolic derangement inside these cells. Per https://www.cff.org/Living-with-CF/Cystic-Fibrosis-Related-Diabetes/ https://www.cff.org/Living-with-CF/Cystic-Fibrosis-Related-D... there's a Type 1 style due to direct pancreas damage interfering with production of insulin, but also a Type 2 style interfering with insulin response. The latter is the sort of thing I'm getting at, I'd want to understand how it works before extrapolating from CF populations to the general one. As the article says, "Unlike people with type 1 or type 2 diabetes, people with CFRD need the same high-calorie CF diet they would normally eat in order to gain weight and build muscle. A healthy diet means eating a variety of foods that are high in protein, fat and salt. The only difference is that people with CFRD need to track or count the foods that affect their blood sugar levels the most." So your eating plenty of fat without apparent harm might or might not be significant for the general population and "normal" Type 2 Diabetes (and I don't know if there's only one form/cause of it).

deleted 11y ago

[deleted]

Mz 11y ago

My view is strongly influenced by the fact that I have "atypical cystic fibrosis." Cystic Fibrosis predisposes people to CFRD (Cystic Fibrosis Related Diabetes). My understanding is that this form of diabetes is neither Type 1 nor Type 2. CF is a genetic disorder. With CF, your immune system does not work right and you are basically chronically infected with some infection or other. I have a relatively mild form of it, which helped create a situation where I was diagnosed late in life. I finally got diagnosed due to my health deteriorating drastically and I spent a year at death's door. With finally getting a diagnosis, I was empowered to get myself a great deal healthier. I have fewer blood sugar issues than I used to have. I did nothing to specifically address that issue. I was primarily trying to erradicate the antibiotic resistant infections that were threatening to kill me. People with CF misprocess fats and most of them are seriously underweight. To my mind, this suggests that fat is probably not the real culprit with diabetes. I have become very picky about the types of fats I eat. Butter and coconut oil are fats that are very beneficial to my condition. I sometimes get pain under control by spreading a half a stick of butter on a roll and eating that (or did so at one time -- it has been a while as my condition is more stable). Butter and coconut oil are high in saturated fats. My blood sugar is a great deal more stable than it used to be. (Yes, I know that is "anecdotal." If you want to dismiss it, please come up with a stronger criticism than that. Thanks.)

hga 11y ago
Putting my biologist hat on, I don't want to dismiss it, consider it to be interesting, but would have to look a lot more closely to get a guess if your observations are useful in this context. CF is a regulatory derangement, so I don't know what all else it might be doing and how much it might be relevant to normal type humans. That said, no one's come up with any vaguely useful citations linking saturated fats to diabetes, and this doesn't help the case for that.
- Mz 11y ago
  Putting my biologist hat on, I don't want to dismiss it, consider it to be interesting, Thank you. I would be happy to discuss it with you further. I do not know what you mean by CF is a regulatory derangement. It is caused by a defect in a specific cell channel that manages traffic of specific molecules into and out of the cell. I have paid enormous attention to that and kind of ignored the hand-wavy and apparently incorrect mental models popular in the medical literature. For example, the official explanation on the CF Foundation website is that people with CF are drowning in an excess of mucus. I found one study that says we produce too little mucus, not too much. This fits with my firsthand experience, it more logically fits with the fact that mucus is a protective coating that helps keep out germs and it fits with the extremely well known and well established fact that women with CF suffer vaginal dryness that often seriously interferes with their sex lives. I think we cough up phlegm, not mucus -- ie infection -- and if you improve mucus production, you reduce infection and see less phlegm. I have seen that hypothesis work effectively for me and my oldest son who has the same diagnosis I have. I have explained it to one woman with CF who was out of time and dying and tracked me down after I left all CF lists and took down my health site. She is gradually getting healthier. So that is a very long way of saying that a) I have no idea what you mean by that phrase and b) the odds are high that you and I have completely different mental models for what is going on with CF.
  - hga 11y ago
    Let me state that I haven't studied CF specifically at all, I'm going from what I just read in Wikipedia and my general biology education. It is caused by a defect in a specific cell channel that manages traffic of specific molecules into and out of the cell. Per Wikipedia: "It is caused by the presence of mutations in both copies of the gene for the protein cystic fibrosis transmembrane conductance regulator (CFTR)." Per the article on CFTR: Cystic fibrosis transmembrane conductance regulator (CFTR) is a membrane protein and chloride channel in vertebrates that is encoded by the CFTR gene. CFTR is an ABC transporter-class ion channel that codes for a protein that conducts chloride and thiocyanate ions across epithelial cell membranes. More detail: CFTR functions as an ATP-gated anion channel, increasing the conductance for certain anions (e.g. Cl−) to flow down their electrochemical gradient. ATP-driven conformational changes in CFTR open and close a gate to allow transmembrane flow of anions down their electrochemical gradient. This in contrast to other ABC proteins, in which ATP-driven conformational changes fuel uphill substrate transport across cellular membranes. Essentially, CFTR is an ion channel that evolved as a 'broken' ABC transporter that leaks when in open conformation. The CFTR is found in the epithelial cells of many organs including the lung, liver, pancreas, digestive tract, reproductive tract, and skin. Normally, the protein moves chloride and thiocyanate ions (with a negative charge) out of an epithelial cell to the covering mucus. Positively charged sodium ions follow passively, increasing the total electrolyte concentration in the mucus, resulting in the movement of water out of cell by osmosis. So, based on ATP getting to it, it allows movement (passive transport) of a set of ions and H2O in and out of cells. I assume there's some regulatory function that mediates the opening and closing of it; the CF mutations interfere with its function one way or another (e.g. one class is thought to result in the CFTR degrading quickly, don't know if it functions normally while in place). So while we're mostly focused on the consequences of these ions and water not getting out of the cell and deranging the production of proper mucus, it could also result in metabolic derangement inside these cells. Per https://www.cff.org/Living-with-CF/Cystic-Fibrosis-Related-Diabetes/ https://www.cff.org/Living-with-CF/Cystic-Fibrosis-Related-D... there's a Type 1 style due to direct pancreas damage interfering with production of insulin, but also a Type 2 style interfering with insulin response. The latter is the sort of thing I'm getting at, I'd want to understand how it works before extrapolating from CF populations to the general one. As the article says, "Unlike people with type 1 or type 2 diabetes, people with CFRD need the same high-calorie CF diet they would normally eat in order to gain weight and build muscle. A healthy diet means eating a variety of foods that are high in protein, fat and salt. The only difference is that people with CFRD need to track or count the foods that affect their blood sugar levels the most." So your eating plenty of fat without apparent harm might or might not be significant for the general population and "normal" Type 2 Diabetes (and I don't know if there's only one form/cause of it).