June 25, 2006

Big Pharma's Guinea Pigs & Nazi Doctor-Type Ethics

Read any drug study involving a new diabetes drug and you'll notice that the subjects invariably start out with A1cs between 8 and 10%.

For anyone reading this who isn't diabetic, the A1c is a blood test that is used to assess long-term blood sugar control. Normal values are under 5%. The American Association of Clinical Endocrinologists' guidelines recommends that A1cs be kept under 6.5%, the leve at which dangerous complications become more likely.)

Drug companies trying to prove the efficacy of new drugs love the patient with a 10% A1c because those are the ones likely to show the most response to a drug. It's much better to be able to say, "Our drug dropped the average patient's A1c by a full 1%" than to say, "Our drug dropped the average a1c by .1%," which is what happens when you give a diabetes oral drug to a patient whose blood sugar is already under the level associated with diabetic retinopathy.

Even worse, when you look at the results of these drug tests, you also will see, just as invariably, that the drug only dropped the person with that 8-10% a1c by an average of 1%. So while the drop looks good, percentage wise, at the end of the year of study, the subjects were still running blood sugars well over the level where they are almost guaranteed to experience nerve damage, amputation, blindness and/or heart attack death.

And this is where the ethical problem arises that has me fuming.

If there were no way of lowering the typical diabetic's blood sugar below that damaging level, one could say, well, that is how it is. But this is far from the case. We have a drug that can lower the A1c to the safe levels in almost any diabetic--one that has been thoroughly tested and used in one form or another for almost 90 years: Insulin. But in these drug approval studies, NONE of the people with type 2 diabetes who are running those dangerous blood sugar levels are taking insulin.

So it seems to me that the patients in these drug studies who start out with that 8- 10%a1c should not be screwing around with experimental drugs. They should be put on carefully tailored insulin regimens until they have brought their A1cs down to the safe level below 6.5%. Then, once they are no longer walking time bombs, doctors can sign them up for new and experimental drugs that might lower their A1cs a tiny bit more.

You may hear doctors say that they can't get their Type 2 patients on insulin down to those levels, but if you probe further, you'll always find that the reason is that these same doctors are instructing their patients to eat a "healthy low fat diet" where each meal contains enough carbohydrates to overwhelm the generic insulin doses they've prescribed. Or you may find that they are only prescribing a basal insulin, like Lantus, which has no effect on the carbohydrates eaten at meals.

When doctors (or diabetes educators) take the time to learn how each individual's body responds to a set dose of insulin and design meal plans that work with sliding insulin doses, insulin, will bring blood sugar into the safe range of 6.5% or less. When doctors and nutritionists combine insulin used with moderate carb restriction (less than 25 grams per meal, for example) insulin can often bring blood sugar into the NORMAL range.

So if doctors were being ethical, i.e. working in the best interests of the patients, no study of any new and possibly ineffective drug should ever start with a population of diabetics whose blood sugar is at a level that even the ultra-conservative American Diabetes Association agrees causes severe complications. And those with responsibility for managing health care should make it clear that drug company operatives who draft patients into drug studies where their blood sugar from start to finish is allowed to remain in the danger zone are operating in an ethical zone only one step removed from Nazi doctors.

As Hippocrates said, "First Do No Harm!"


Scott said...

You are wrong on several counts. Technically speaking, insulin, human growth hormone (known generically as somatropin) and many other biotechnology medicines cannot be considered drugs; they are synthetic versions of actual human hormones, proteins, enzymes or antibodies. These are usually made by splicing genes into fast-growing organisms such as bacteria or yeast using recombinant DNA technology, which then multiply to produce vast quantities of the desired medicine. Because they are derived from living cells, as opposed to smaller, chemical molecules derived from chemical processes, determining bioequivalency is not the same as it is for chemical drugs.

The second point you fail to understand is that type 2 diabetes is caused by the cells in the body's failure to respond properly to insulin (making it a completely different disease than type 1 diabetes, which is an autoimmune condition caused when the body's immune system mistakenly attacks and destroys the insulin producing beta cells). If the cells do not respond correctly to that hormone, giving more of the hormone can do more harm than good because excessive insulin (which does not apply to most type 1 patients) has been proven to cause inflammation of various cells and body's vessels, increasing the risk for heart attack, stroke, edema and other health problems. In fact, most patients with type 2 diabetes suffer from what is known as "hyperinsulinemia" or too much insulin in the bloodstream. Eventually, insulin resistance will cause the beta cells to die of exhaustion, but a simple c-peptide test can determine how much endogenous insulin production is happening.

As a type 1 (immune-mediated) diabetes patient, I find your lack of knowledge on this topic embarrassing as well as offensive.

Paul said...


I think your understanding of type 2 diabetes is incorrect. The jury is very much out of whether or not type 2 diabetes is caused by insulin resistance or beta cell failure.

The concensus seems to be that by the stage that diabetes is diagnosed beta cell failure has occurred and inuslin production is insufficient to overcome insulin resistance where it is present. It should be noted that not all type tow diabetics "suffer" from inuslin resistance.

Standard treatment regimes tend to treat bith the insulin resistance and the inadequate inuslin production. Initially this is through stimulating additional insulin production. If this fails, asit tends to over time, inusin is prescribed.

In many respects insulin works well for type 2 diabetics. It rests the surviving beta cells, and the pancreas retains the ability to turn off its own supply of insulin once normal BG levels have been achieved, thus recuding the chances of hypoglycemia.

I would not underplay the [roblems associated with high levels of circulating inuslin, which can be present in some type 2 diabetics.

Additionally, another feature of type 2 diabetes is the absence of phase 1 insulin secretion.This results in elevated Post Prandial BG levels, and inappropriate hepatic production of glucose which further elevates already high BG levels. Injected insulin can counter both problems.

Your view of type 2 diabeties is far too simplistic. If you were correct all research would be focused on inuslin resistance and patients wouldn't be prescribed with OHA's and insulin, as the majority are.

You have ignored the fact that 80 percent of people with IR aren't dibetic and many never will be.