Jump to content

Recommended Posts

Posted

So, when you said that there was a 20 minute delay between the insulin reaching the blood (by injection or release from the pancreas) and it having an effect, you were wrong.

 

I accept that the normal natural process for control is a whole lot better but if you are diabetic then it's not an option.

 

"4% to 6% of all type 1 diabetic deaths are due to hypoglycemia. So the side-effects of the treatment are today actually killing more people every year than the disease itself, "

Seems like a non sequiteur to me.

If only 5% of the deaths are due to too little sugar i.e. too much insulin; then the other 95% are due to some manifestation of the disease.

 

Last time I checked 5% wasn't more people than 95%

Posted

The 20-minute delay arises from injecting insulin subcutaneously, not when it is released from the pancreas. A subcutaneous bolus of insulin has to find its way slowly from the injection site to the arterial distribution, which causes delay. Also, insulin produced in the pancreas is normally metabolized on a first pass through the portal circulation, which allows it to be utilized much quicker than if it gradually feeds into the body for metabolism from a subcutaneous injection. A further problem with the dissonance in timing between injected and naturally produced insulin is that insulin is naturally emitted by the pancreatic beta cells in millions of microdoses per day, with each beta cell acting as a sensor for the amount it should produce. This continuous output of insulin means that the lag time for insulin to be effective is smoothed out by constant dosings. But when a patient injects insulin in four or five boluses a day, there is going to be a significant lag between the bolus and the amount of insulin required. Since it has proved impossible to develop an implantable, closed-loop insulin pump after more than 40 years of development efforts, the present 'insulin pumps' have no artificial pancreas or 'brain' to sense glucose and put out a constant stream of insulin microdoses to meet the slightest change in insulin requirements as a normal pancreas would. Instead, the present generation of pumps rely on the patient testing capillary blood glucose (itself an inaccurate measure of the total insulin required in the body) and then making an educated guess on what present levels of insulin resistance at the cell walls and what the current vectors pushing the insulin requirements up or down require as a dose.

 

The inaccuracy of dosing is made even worse by the new genetically engineered insulins developed in the early 1980s, which left out elements of the natural molecule as 'irrelevant to blood sugar control,' but which turned out to be vital in breaking the hypoglycemic action of insulin to permit smoother dosing with less dangerous drops in blood sugar levels. Other types of insulin have other problems, since they all have different periods of peaking and maximum duration of action, which of course do not correspond to the constantly fluctuating insulin requirements of the human body, where variations in the process of digestion, changing thyroid and adrenal hormone levels, and changing insulin resistance all cause considerable variation in the demand for insulin througout the day.

 

With respect to the death rates from hypoglycemia in diabetics, these definitely exceed the deaths from the disease in the developed world, since the disease can in almost all cases be diagnosed and treated in time before lethal hyperglycemia sets in. Your criticism seems to assume that since 4% to 6% of type 1 diabetics die from hypoglycemia caused by the drug which treats diabetes, that number cannot exceed the number of patients who do die from diabetes, which you assume must be 96% to 94%, or the rest of the patients. But many diabetics in the insulin era do not die from diabetes or its complications at all, and of those who do, their deaths are usually officially counted as resulting from complications of the disease, such as heart disease, renal failure, stroke, septicemia secondary to gangrene, athero- or arterosclerosis, etc. Most official causes of death classify these factors as the actual cause of death, not the diabetes which may have contributed ot them in ways that are difficult to quantify.

Posted

So a "diabetic death" isn't related to diabetes.

Sorry, misunderstanding there on my part.

 

You seem to be arguing against yourself.

 

Lots of deaths that arise from diabetes are not recorded as such but are lost in, for example, the deaths from heart disease.

You can't say if that's more or less than 5% because, as you say, they are not recorded.

Yet you claim that they are less than 5% (which are definitely due to diabetes - but also to "overtreatment").

Posted

The $60,000 question in diabetology now is how much all those deaths from what used to be called 'complications' of diabetes are caused by diabetes per se or just by a disposition to those other conditions and their associated deaths resulting from yet another genetic disease, X, which is typically inherited along with the complex cluster of genes that goes into predisposing someone to develop diabetes. There have actually been reports of patients presenting with the full-blown syndrome of 'diabetic' vascular and neurological damage but who have a normal response to a glucose tolerance test and so are not even pre-diabetic, which strongly indicates that these complications may be an independent condition linked with a higher than normal statistical frequency to diabetes. The fact that some patients with very poor glucose control never develop diabetic complications while others with very good control quickly die of them again suggests that we are dealing with the inheritance of a parallel disease.

 

Now you could pose the metaphysical objection that if this other genetic predisposition to the vascular and neurological changes associated with diabetes is usually linked to diabetes, then perhaps it should be regarded as part of diabetes itself. Or you could look at the fact that some diabetics have it while others don't, and that it is rarely inherited independently of diabetes, as indicating that it should be regarded as an autonomous condition. I think it makes more sense to adopt the latter approach.

 

So when we look at the mortality data, whether we call the high rate of deaths from heart disease, stroke, renal failure, gangrene, etc. as 'deaths from diabetes' or 'deaths from another disease that is often inherited along with diabetes' depends on what your reading of the science suggests to your ontological inclinations. Even if you want to argue that those deaths are influenced by diabetes, the question then becomes, to what extent? since many people die of these conditions even if they don't have diabetes, so the diabetes may have been a 30% contributor to a 70% disposition to cardiac death from the more usual causes, such as overweight, hyperlipidemia, too much salt in the diet, etc. Even if autopsies were performed on all people who died with diabetes, there would still be room to argue about how important all the component factors were in any disease causing death.

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now
×
×
  • Create New...

Important Information

We have placed cookies on your device to help make this website better. You can adjust your cookie settings, otherwise we'll assume you're okay to continue.