Then it's not relevant to the OP either! I for one found what @noblehead said to be very helpful even though I'm not one of the elite T1s of this forum. If eating fat with carbs increases insulin resistance because of increased trigs even temporarily then it's very relevant to me in my fight to lose weight.Right, but you are not an insulin dependent diabetic. You have functioning beta cells, so the discussion isn't really relevant to you.
well thought so, do you know you can edit what you already has written but the edit beneath you column in which yo did write the messageSorry. I meant fats and proteins not carbs.
All I know is eating fat does not raise my blood sugar..as I no longer eat any of the items on his menu I guess I shouldn't comment any further.
I don't normally consider Mendoza as a primary source of info, but in this case he seems to be referring to research that was published last year that seemed to indicate that Type 1's suffer Insulin Resistance as described in the article. Normally IR is condidered to be a mainly T2 thing, and T1's were not generally prone to IR. But this research was on a group of T1's and gives a reasonable hypothesis to explain the pizza effect.This Mendosa article explains what happens once the carbs have stopped effecting bg levels:
So what about after the carbohydrates are finished doing their thing? That’s when the fat itself begins to exert its effects. The process goes something like this:
This is what causes the gradual, delayed blood glucose rise after consumption of large amounts of fat. The response seems to be “dose-dependent” – the more fat you consume, the more insulin resistant the liver becomes, and the more glucose it produces. The type of fat also appears to play a role. Saturated fats (the type found in dairy and animal products) seem to cause more insulin resistance than monounsaturated and polyunsaturated fats (the type found in vegetable products).
- You eat a high-fat meal or snack (this is the fun part).
- In a few hours, the fat begins to digest; this continues for several hours.
- The level of fat in the bloodstream (triglycerides) rises.
- High triglycerides in the bloodstream cause the liver to become resistant to insulin.
- When the liver is insulin resistant, it produces and secretes more glucose than usual.
- The blood glucose rises steadily as the liver’s glucose output goes up.
http://www.mendosa.com/The-Fat-of-the-Matter-How-Dietary-Fat-Effects-Blood-Glucose.htm
I think there is a basic difference in how IR presents for T1 and T2. In T1 it seems to be mainly the liver that is affected, but in T2 it seems to be muscles that stop using the glucose. Thus T2 meds like Gliclazide work by forcing the pancreas to push out extra insulin that forces the glucose into the cells. Unfortunaltely for T2, this actually forces storage more than burning off in muscles, so T2 tend to expand widthways and put on weight.I have only looked at the first article and quote from it:-
For many years scientists thought that fat was a metabolically inert substance. Fat on the body was considered dead weight, just extra blubber people carted around. Well it turns out that fat has been masquerading as the quiet shy guy in the back row, all the while packing a considerable metabolic punch.
A high fat meal can increase the amount of free fatty acids (FFAs) in the blood. Both repeatedly elevated levels of FFAs as found in chronic intake of high fat (especially high saturated fat) meals and obesity are associated with both skeletal muscle and liver insulin resistance.
This is surely very relevant to T2s. The main symptom of T2 is insulin resistance. OK most of us don't inject insulin, our body supplies the extra insulin for us automatically. That's a bad thing, we aren't able to regulate it like T1s, and anything we can do to stop excess insulin entering our bloodstreams has to be good . I intend to use this info to help my exercise be more effective for me. At present exercise normally puts up my BGs, maybe if I can time it right I can find the optimum time to exercise after each type of meal.
It's relevant to all types but especially RH. We all have problems with the levels of insulin our bodies produce whether that's none, too little or way too much.
I think the answer to that depends on what you do with the triglycerides. If you are converting them to free fatty acids for energy use, then I suspect that it is less of an issue. If you are not using them as energy sources, then I can believe that this would be true.but if we rather fat diabetic type 2 people do leak from our excess fat storage triglycerides out in our blood all day, or eat high or higher fat all days do we then contribute to insuline resistance in that way ? and thereby getting it harder to get into remision ?
I think the answer to that depends on what you do with the triglycerides. If you are converting them to free fatty acids for energy use, then I suspect that it is less of an issue. If you are not using them as energy sources, then I can believe that this would be true.
If you consider that the classic ketogenic diet is not high protein precisely to induce the lipid burning state, it is highly likely that very high proteins will be the cause.thanks yes you are maybe right, it seems I lost weight more rapidly when not doing higher fat diet and very high proteins , but maybe it is because of normal weight stalling after longer time weightloss instead... just wondering
hope it is not due to self-induced insuline resistance...
If you consider that the classic ketogenic diet is not high protein precisely to induce the lipid burning state, it is highly likely that very high proteins will be the cause.
From my experience, excess FFAs seem to be taken out by the gall bladder and excreted via the bile duct. The HF that I think you are referring to here is meant to be part of a ketogenic diet, and so the FFAs are supposed to be burnt off and turned into ketones unstead of using glucose for energy. the large amount od FFAs in the Mendoza article are probably packaged into chylomicrons and VLDL so are not actually free radicals unless the package is damaged during transit (sdLDL). Certainly experimental reports show that higher fat leads to these effects and the blood takes on a milky hue. In this form the body is doing exactly as it should, and it is not (so far) been shown to be dangerous. The liver only releases trigs from storage when glucose levels fall, i.e. ketogenic or starvation or fasting state, and it also needs an absence of insulin to do this..but if we rather fat diabetic type 2 people do leak from our excess fat storage triglycerides out in our blood all day, or eat high or higher fat all days do we then contribute to insuline resistance in that way ? and thereby getting it harder to get into remision ?
Not sure about Type 1 but as a Type 2 I have made great improvements with cutting carbs and increasing fat (60% of diet a day). I just now have to watch that I don't over indulge on protein as my doctor informs me that an excessive amount of protein above what the body needs can be turned into sugar which is no good for me at least.All I know is eating fat does not raise my blood sugar..as I no longer eat any of the items on his menu I guess I shouldn't comment any further.
From my experience, excess FFAs seem to be taken out by the gall bladder and excreted via the bile duct. The HF that I think you are referring to here is meant to be part of a ketogenic diet, and so the FFAs are supposed to be burnt off and turned into ketones unstead of using glucose for energy. the large amount od FFAs in the Mendoza article are probably packaged into chylomicrons and VLDL so are not actually free radicals unless the package is damaged during transit (sdLDL). Certainly experimental reports show that higher fat leads to these effects and the blood takes on a milky hue. In this form the body is doing exactly as it should, and it is not (so far) been shown to be dangerous. The liver only releases trigs from storage when glucose levels fall, i.e. ketogenic or starvation or fasting state, and it also needs an absence of insulin to do this..
Although we do not know exactly what causes IR, a ketogenic diet does show success in helping remission to happen, so if used properly, it should not increase IR as a long term effect. In fact, evidence has shown recently that increased fat intake actually improves the lipid panel for many if part of a low carb diet, The jury is still out on high fats with high carb diet.
Not sure about Type 1 but as a Type 2 I have made great improvements with cutting carbs and increasing fat (60% of diet a day). I just now have to watch that I don't over indulge on protein as my doctor informs me that an excessive amount of protein above what the body needs can be turned into sugar which is no good for me at least.
I'll blame my lazy muscles then huh? Is that why I can walk 10 -14 miles at a decent speed and hurt like hell and not lose any weight whilst increasing my BG level then?I think there is a basic difference in how IR presents for T1 and T2. In T1 it seems to be mainly the liver that is affected, but in T2 it seems to be muscles that stop using the glucose. Thus T2 meds like Gliclazide work by forcing the pancreas to push out extra insulin that forces the glucose into the cells. Unfortunaltely for T2, this actually forces storage more than burning off in muscles, so T2 tend to expand widthways and put on weight.
What worked for me was only eating within a 10 hour window (between 10am and 8pm as I don't mind missing breakfast). I also alternated between a cooked brunch and light dinner or beef broth/soup brunch and cooked dinner). I guess you have to go with what works and when your body gets used to one thing - surprise it and switch to something else.yes thats also the reason why I have started lowering my proteins and hightening my fats but I seem to have a hard time loosing weight since that change even on a 1000 calorie diet and very hard training weekly like at least 12 hours a week....
What worked for me was only eating within a 10 hour window (between 10am and 8pm as I don't mind missing breakfast). I also alternated between a cooked brunch and light dinner or beef broth/soup brunch and cooked dinner). I guess you have to go with what works and when your body gets used to one thing - surprise it and switch to something else.
I read the first one until here...
"First, Fettuccine Alfredo, garlic bread and tiramisu are, for the most part, a mixture of carbohydrate and fat. But it’s the fat in the meal that is contributing to the elevated readings."
What utter cobblers.. the carb causes the elevated readings... the fat delays the spike and maybe slows it down.
Take your blood before and after a bulletproof coffee or fat bomb and you'll see minimal changes.
Try it after garlic bread and pasta...
I will let another answer this:I'll blame my lazy muscles then huh? Is that why I can walk 10 -14 miles at a decent speed and hurt like hell and not lose any weight whilst increasing my BG level then?
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