Simple test reveals How Your Body Causes Cancer to Grow Faster — And How You Can Stop It

Many years ago, this newsletter showed you how drugs can actually fuel cancer and cause it to grow. But now there is evidence that drugs are not the only fuel that feeds cancer. Your body actually creates a fuel that is far more dangerous than drugs. In fact, the amount of this fuel your body creates determines how fast your cancer will grow.

And while this sounds terrible, there is some great news to go along with it. Because your body creates this fuel, and because we already know why your body creates it, we now have a lot more power over cancer than ever before.

In fact, if you already have cancer, we can now determine how aggressive that cancer will be. But, more importantly, we can put a clamp on cancers feeding tube. That means you can stop feeding your cancer and let it go hungry.

On the other hand, if you do not have cancer, we now have a pretty good idea of how to predict your cancer risk. And we also have the ability to prevent it from ever growing in the first place.

All of this means you and you alone can control your major risk of invasive cancer. Not your doctor. Not your pharmacist. Just you!

The fuel Ive referred to is insulin. You might remember that Ive repeatedly referred to insulin as the hormone of aging and death. With this report, you will understand much more of that statement.

Insulin, as you know, is the hormone that controls your blood glucose (sugar). Your pancreas makes more insulin when you ingest carbohydrates, especially simple or refined carbs. Your body knows that too much sugar is bad for your circulation, eyes, kidneys, and just about every part of your body. When blood sugar is too high, can reduce the blood flow to your capillaries (smallest blood vessels). You do not want that. So your control mechanism is insulin.

But too much insulin carries its own problems. Insulin converts the excess carbs into fat for storage. It stuffs the fat into your arteries, increases your abdominal fat, and raises your cholesterol, uric acid, lipids and blood pressure. This results in what is now called metabolic syndrome.

Now, how does insulin relate to cancer? Jan Hammarsten, MD, PhD, a urological surgeon in a Swedish hospital, has the answer. Hes been at the forefront of research into the connection of insulin and prostate cancer. While most of his research is on prostate cancer, it applies to most, if not all, other cancers.

Dr. Hammarsten says there is no evidence that insulin actually causes cancer. However, several medical studies report that insulin is a stimulus for prostate cancer (and other cancers) to grow and become more aggressive. And now Dr. Hammarsten’s team has made the definitive connection. In a study conducted between 1995 and 2003, they studied 320 patients with biopsy-proven prostate cancer. They also measured the size of the prostate with ultrasound. And they did lab tests for insulin and all the parameters of the metabolic syndrome of high insulin (cholesterol, triglycerides, and uric acid).

His team found that insulin caused disease to become more aggressive. In fact, the men who died had a faster rate of benign prostate tissue growth, and they had more aggressive scores on their cancer biopsy samples.

But perhaps their most important finding was that blood levels of insulin (as measured after an eight-hour fast) were directly associated with lethal clinical prostate cancer. This confirmed that your fasting plasma insulin is linked to your ability to survive prostate cancer. The higher your scores, the more aggressive the cancer, and the less likely you will survive.

What all this means is that fasting insulin levels can predict not only how aggressive your cancer is going to grow, but also what your prognosis is. And this measurement is more accurate than the stage of the cancer or your PSA level. So, in my book, the fasting insulin level is now your most important marker for your ultimate risk of dying from the disease. That is the bad news.

Now for the good news. These findings suggest that even if you already have cancer, you can still change your risk. All you have to do is reduce the amount of insulin your body produces.

But does it work? Indeed, it does! Low-fat guru Dr. Dean Ornish found that cancer markers in men on his plant-based program actually decreased over a year. But men on the control diet (the standard American diet) saw their tumors march on.

So what should you do? In light of this news, I now think most everyone should change their diet to a low-fat, low-refined-carb diet. That is the only way to keep your cancer risk low. Its the diet Ive followed for years and my risk is very low.

Beyond that, ask your doctor for a fasting insulin test at least once a year. Its the best way to determine how fertile your body is for cancer. Your fasting insulin level should be less than 5 mU/L according to the lab. But the closer to zero you can get, the better. The last time I checked my fasting insulin, it was not detectable. That is because I eat almost no sugar or refined carbs. If you do not have a sugar (carb) demand on your pancreas, it will not have to make insulin.

You may have to go to an integrative physician to get the test done. And even some of them may resist. One of my colleagues was disciplined 10 years ago by a state board for daring to order the test. The negligent board was only 15 years behind the eight ball. But please persist. And if he tells you that your level is in the reference range, remember that many who are sick or at risk are within that range. Ask for the specific number. You now know how to interpret it. The closer to zero, the better.

By the way, you do not have to be heavy to have high insulin levels. Many people are able to keep relatively trim due to exercise and other factors, while their insulin is higher than it should be. Unless your diet is pristine, the lab test makes sense.

Ref: Hyperinsulinaemia: a Prospective Risk Factor for Lethal Clinical Prostate Cancer, Eur J Cancer, 2005 December;41(18):2887-95; Epub

2005, October 20. 44412 (5/2006); Ornish, D. et al. J. Urol. 2005; 174(3):1065-9.