I understand this but then given that some T2 end up on Insulin why not allow them to take long acting as lets face it if you were stable for many years then your pancreas might not give up and complications would also be kept to a minimum.
My levels reside around 4.5 - 6 and 7 - 8 30 mins to 1 hr after meals - When my fasting goes closer to 7 on average I will consider surgery or Insulin or a GLP4 Inhibitor. I think pushing the pancreas to make more is the wrong approach and after all its my body and my life. My doctor probably wont live with the complications I have form this disease and as such is not qualified to tell me what I feel is best.
One wonders what the relative survival rates of diet controlled and insulin controlled diabetics are?
Lowering blood sugars is good provided you don't increase insulin in the body to toxic levels.
There is a blog by Jason Fung on insulin and heart disease. ... https://intensivedietarymanagement.com/not-treat-diabetes-t2d-38/
With type 2 diabetes there are twin risks of excess glucose and excess insulin in the system. It appears that Metformin reduces the risk of CVD, but taking insulin has no benefits of reduced CVD, despite lowering blood sugars more. This is probably because too much insulin is toxic causes inflammation and increases the risk of heart disease and cancer. Insulin also causes weight gain, which is a problem with 80% of type 2 diabetics who are already overweight or obese.
Lowering blood sugars is good provided you don't increase insulin in the body to toxic levels.
There is a follow-up blog by Jason Fung from the one quoted earlier ... https://intensivedietarymanagement.com/medications-actually-work-type-2-diabetes-t2d-40/That really depends on whether or not the T2 person has sufficient insulin themselves. Diagnostic tests should really be done before changing treatment. Those of us that don't produce insulin we need have no choice. I'm sure my insulin to carb ratio is higher than most type 1's would be because of insulin resistance I already have. I've worked out I need an average of 5 units of bolus per 10g of carb.
A daft question, I expect but here goes. How can they diagnose T2 on the basis of HbA1c if this test is just an indication ?
Shouldn't there be a definitive test given after the HbA1c for everyone with higher readings than normal as per course?
@Bluetit1802Didn't you realise .... one size fits all ..... as per usual.
@Bluetit1802
Ah, so. But... Yeah, I forgot about the £/time/common sense versus NHS practise. Oh, silly me.
Seriously?.. from my reading of the site I would say that is exactly what most of us do.. I do for sure..I know many here dont condone taking healthcare into their own hands
Seriously?.. from my reading of the site I would say that is exactly what most of us do.. I do for sure..
But in answer to your main point .. if you can get rid of insulin resistance by changing what you eat so your pancreas can repair itself you won't need exogenous insulin. By taking exogenous insulin you won't do this so from my reading it would be counterproductive.
There is a follow-up blog by Jason Fung from the one quoted earlier ... https://intensivedietarymanagement.com/medications-actually-work-type-2-diabetes-t2d-40/
Basically, what he is saying is that Type 2 diabetes is a problem where there is too much sugar in the body (not just the blood), Drugs like sulphonylureas and insulin lower blood sugars, but don't remove these sugars from the body. Hence they tend to increase weight as the excess glucose is stored as fat by insulin. This then causes long-term health problems such as heart, liver and kidney disease. Drugs which help eliminate this excess sugar have significant benefits to life expectancy.
However, the simplest way to get rid of this excess sugar is to reduce the amount of carbs we eat and to burn off the excess sugar (fat) by intermittent fasting. Lowering blood sugars will lessen the likelihood of diabetic complications such as blindness and neuropathy. However, most type 2 diabetics die of heart disease and the just lowering blood sugars does not reduce the likelihood of heart disease, but reducing the amount of accumulated stored sugar in the body (e.g. liver fat) does significantly increase life expectancy.
When one considers initiation of insulin therapy in a type 2 diabetic patient with the intention to preserve β-cell function, the level of evidence supporting this decision is relatively high.
For the subgroup of patients with severe symptomatic hyperglycemia, there is strong evidence, in addition to guideline recommendations (American Diabetes Association/ European Association for the Study of Diabetes, International Diabetes Federation, American Association of Clinical Endocrinologists, Canadian, and National Institute for Health and Care Excellence [12–16]), to support initiation of short-term insulin therapy. Insulin therapy is an effective way to reverse short-term glucotoxicity and lipotoxicity and shows evidence of midterm β-cell preservation. Short-term insulin treatment is safe, with low incidence of hypoglycemia (23–25) and less concern for weight gain. However, the best method for insulin treatment in such cases—basal insulin, premix insulin analogs, MDII, or CSII—and the length of insulin therapy should be further studied.
FINDINGS:
More patients achieved target glycaemic control in the insulin groups (97.1% [133 of 137] in CSII and 95.2% [118 of 124] in MDI) in less time (4.0 days [SD 2.5] in CSII and 5.6 days [SD 3.8] in MDI) than those treated with oral hypoglycaemic agents (83.5% [101 of 121] and 9.3 days [SD 5.3]). Remission rates after 1 year were significantly higher in the insulin groups (51.1% in CSII and 44.9% in MDI) than in the oral hypoglycaemic agents group (26.7%; p=0.0012). beta-cell function represented by HOMA B and acute insulin response improved significantly after intensive interventions. The increase in acute insulin response was sustained in the insulin groups but significantly declined in the oral hypoglycaemic agents group at 1 year in all patients in the remission group.
Several clinical and experimental studies have clearly shown that even minimally preserved beta cell function is metabolically beneficial. This leads to lower HbA1C levels, lower insulin dosage and lesser metabolic decompensation after insulin withdrawal.
Oh. So that explains how none obese sufferers can be interferred with IR too.
So why all the emphasis on it being internal and external fat which causes IR?
My specialist believes IR improves on fat/BMI weight loss. Muscle and fat. I guess.
Weight loss specialist (surgeons and dieticians) believe the same.
Well, for me.
All I did was eat low carb to get excellent bgs with the correct amount of injected insulin.Having fat on the liver reduces how much glucose the liver can take up, external fat is a predictor of this. Losing the fat from the Liver improves insulin resistance.
It is very hard for anyone with insulin resistance to lose weight without breaking the cycle of insulin resistance hence if someone loses weight then IR is very likely to have improved. The actions you have to take to lose weight are the same as the actions to break the cycle of IR.
Increased muscle mass improves IR, but most people lose more in fat then they gain in muscle, hence once again losing weight is a good predictor of outcome when you study a large group of people.
Insulin resistance effect different parts of the body in different ways, I expect there will be some Nobel prizes given out when someone works out all the details........
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