5 reasons to think twice before taking diabetes drugs

Australia is facing an avalanche of newly-diagnosed type 2 diabetes cases, brought on by our increasingly toxic food environment and burgeoning obesity epidemic.

Depending on the severity of their condition at diagnosis, newly-diagnosed diabetics may either be given a trial of dietary management (which usually fails, because the standard dietary recommendations made to diabetics are laughably inadequate), but the growing trend is to start them on diabetes medication immediately.

There’s no denying that diabetes is a dangerous condition that requires urgent treatment. Diabetes damages the eyes, potentially leading to blindness; the kidneys, often resulting in kidney failure; the nerves, frequently resulting in gangrene and limb amputation; and the arteries, worsening atherosclerosis and therefore increasing the risk of heart disease and stroke.

In fact, being diabetic raises the risk of dying from ischaemic heart disease (i.e. death due to clogged arteries) by a factor of 3.3 in women, and nearly 2 in men, after adjusting statistically for age, blood pressure, cholesterol, body mass index, and cigarette smoking (1).

But all classes of diabetes medication carry serious risks, and dubious benefits:

#1. Thiazolidinediones (one of the newest diabetes drugs to hit the market) such as Actos and Avandia, lower blood glucose but raise death rates in diabetics.

These drugs (also known as glitazones) were greeted with much enthusiasm by doctors, who were frustrated by the phenomenon of ‘secondary failure’ that dogs the older diabetes drugs: they are initially quite effective at lowering blood glucose, but their effectiveness wanes over time.

Avandia was released onto the market in 1999, despite pre-licensing trials demonstrating an 80% higher risk of ischaemic cardiovascular events (e.g. acute heart attack) in people taking Avandia compared to those taking older diabetes drugs (2).

Reports of heart problems including congestive heart failure began surfacing soon after its commercial release, and concerns about an increased risk of heart attack and cardiovascular death mounted over subsequent years (2). These concerns were dismissed by the drug’s manufacturer, Glaxo SmithKline (GSK), despite their own (initially unpublished) researched having unearthed a significantly increased risk of ischaemic events in patients taking Avandia (2).

A meta-analysis published in 2007 found a 43% higher risk of heart attack in patients taking Avandia compared to controls, and a 64% greater risk of death from cardiovascular causes (3). GSK still denies that the drug increases the risk of cardiovascular disease, despite having paid out as much as US$4670 million by July 2011 in out-of-court settlements, with a fund of US$6.4 billion set aside for anticipated future claims (4).

(Read this for a detailed and gripping account of the sordid saga of Avandia. John Le Carre couldn’t make stuff like this up!)

The other thiazolidinedione drug available in Australia, Actos, also raises the risk of congestive heart failure, as well as bone fractures, and possibly bladder cancer (5).

#2. Sulfonylureas such as Diamicron MR and Minidiab cause weight gain (which exacerbates diabetes) and have high failure rates.

This class of drugs works by stimulating the pancreas to produce more insulin. In contrast to type 1 diabetes, in which the pancreas no longer produces enough insulin due to autoimmune attack on the insulin-secreting cells, in type 2 diabetes the pancreas initially overproduces insulin, often for 5-10 years before diagnosis. This excess insulin secretion is the body’s attempt to overcome insulin resistance – the failure of insulin receptors to respond normally to the hormone.

Think of it this way: the receptors have gone deaf to the hormone, so the pancreas turns up the volume. Eventually, the insulin-secreting cells start to ‘burn out’ and the pancreas can no longer pump out so much insulin. The person’s insulin production may still be somewhat higher than a nondiabetic, but the ‘deaf’ receptors don’t respond sufficiently to the reduced volume.

At this point, symptoms of hyperglycaemia (high blood sugar level) such as excessive thirst and urination, headaches. blurred vision, difficulty concentrating and extreme fatigue, start to occur.

Drugs that force the already overworked pancreas to secrete more insulin only hasten this burning-out process (6), as well as causing weight gain which worsens the insulin resistance. This is why secondary failure (described in point #1 above) occurs at such a high rate with sulphonylurea treatment. The United Kingdom Prospective Diabetes Study, for example, found a secondary failure rate of 50% in both normal and overweight patients after 3 years of sulfonylurea treatment, escalating to 76% after 9 years of treatment (7).

#3. Metformin (sold as Glucophage) frequently causes intolerable side effects, and loses effectiveness over time.

Metformin does not cause weight gain or hypoglycaemia as do sulfonylureas, and is the preferred drug for obese diabetics. However, many patients cannot tolerate its side effects, which include nausea, diarrhoea and abdominal pain; changes in taste; muscle pain; flu-like symptoms such as muscle pain, fever, chills, and weakness; heart palpitations; and rarely, potentially life-threatening lactic acidosis.

Metformin also reduces absorption of vitamin B12 and can cause impaired kidney and liver function, occasionally leading to liver or kidney failure.

56% of obese diabetic patients taking metformin experience secondary failure by 3 years of treatment, rising to 87% after 9 years (7).

#4. Insulin therapy causes more weight gain than any other diabetic medication.

Insulin-containing treatment regimens for type 2 diabetes cause significantly more weight gain than regimens using only oral medication (8). As with all the other diabetes medications, secondary failure rates are high: 53% after 3 years, and 72% after 9 years (7).

#5. Intensive drug treatment of type 2 diabetics to maintain ‘ideal’ blood glucose (‘tight control’) causes a higher death rate.

3 large studies, all published in 2008, demonstrated the failure of intensive drug treatment of diabetes to reduce diabetic complications or prolong the diabetic’s life. The ACCORD (Action to Control Cardiovascular Risk in Diabetes) trial was terminated early because it found that, despite patients in the tight control group achieving lower (i.e. more favourable) glucose readings, more of them died.

This is what Dr John McDougall has termed ‘dying sooner with good-looking numbers’ (9).

In fact, despite achieving a significantly lower glycated haemoglobin level (a marker of average blood glucose level of 2-3 months), the intensive therapy group had a 22% higher death rate and a much higher risk of gaining over 10 kg after starting treatment. There was no clinically significant reduction in cardiovascular events (10).

The ADVANCE (Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation) trial found no clinically significant improvement with intensive therapy, but an 80% higher risk of hypoglycaemia (which can cause diabetic coma if untreated) (11); while the VADT (Veterans Affairs Diabetes Trial) found no reduction in diabetic complications or death rate with intensive therapy, but a nearly three times higher risk of sudden death (12).

In my opinion, the attempt to make diabetics’ blood glucose and glycated haemoglobin look ‘normal’ by forcing them down with drugs, while ignoring the primary causes of the disease, is the height (or should that be the depth?) of foolishness. Elevated blood glucose is the symptom of the disease, not its cause.

My own experience in caring for people with type 2 diabetes, as well as that of many doctors such as John McDougall and Joel Fuhrman, indicates that the majority of type 2 diabetics can completely reverse their condition, and achieve normal blood glucose, glycated haemoglobin and other biomarkers, without medication, by making comprehensive dietary changes and adopting a well-planned exercise program.

The standard dietary advice for diabetics is abysmally ineffective; only 9% of diabetics are in the target range for fasting blood glucose 9 years after diagnosis when following the ‘low-fat, high-carbohydrate, high-fiber diet’ prescribed by dietitians (7).

Dietary change that consists of tinkering at the edges of the SAD (Standard Australian Diet) will not reverse type 2 diabetes or save the lives of those who suffer from it. A diabetes-reversal diet must be high in micronutrients including the antioxidants required to combat oxidative stress (which is rampant in diabetics due to their hyperglycaemia, and which is a major contributor to diabetic complications); rich in resistant starches; contain no added oils but sufficient fats from nuts and seeds; and be low in high glycaemic index carbohydrates.

If this diet is adopted when a diabetic is first diagnosed, the disease is stopped in its tracks. But even diabetics who have experienced secondary failure of treatment and ended up on insulin can usually be restored to full health, with normal biomarkers. For those already on medication, it’s important to have the cooperation of a doctor who can monitor blood glucose and HbA1c and taper medication dosages as your body recovers its insulin sensitivity.

The bottom line: if you have diabetes, you need to be on an integrated program that addresses all the factors that caused the condition in the first place, and therefore lowers your risk of diabetic complications – not a drug that tries to push your blood glucose down, while increasing your risk of dying!

Are you diabetic or pre-diabetic? Do you have a family history of diabetes? Would you like expert guidance in constructing and adopting the ultimate diabetes prevention and reversal diet?

Apply for a Roadmap to Optimal Health Consultation to discover how I can help you.

Watch Dennis’ remarkable story of reversal of type 2 diabetes (and 2 other chronic conditions):