By Bonnie Jenkins, Advanced Natural Wellness

For years, I’ve been talking about the dangers of insulin resistance. It’s an important issue, especially since one in four Americans has been diagnosed with the condition. But insulin resistance doesn’t just affect adults.

Thanks to chips and sodas in schools, a glut of fast food joints and video games, this problem affects a whopping 52 percent of teens – setting them up for a lifelong battle to be healthy.

So what is insulin resistance, anyway? Simply put, insulin resistance occurs when the body can’t respond to and use the insulin it produces. As a result, higher levels of insulin are needed in order for it to have any effect.

As a result, this insidious condition is a known harbinger of type 2 diabetes and a key component of metabolic syndrome. But, new evidence reveals that insulin resistance may foretell an additional danger. Recent research has uncovered a disturbing link between this reluctance of the body to recognize insulin and the development of cancer, particularly of the colon, breast, endometrium and pancreas.

Insulin Resistance Explained

The role of insulin, a hormone secreted in response to the ingestion of carbohydrates, is to shuttle glucose out of the blood and into cells where it is needed to produce energy. The more carbohydrates you eat, the more insulin the body releases to process it. In insulin resistance, however, some cells become desensitized to the action of insulin. This inaction only serves to stimulate the pancreas to secrete ever-larger amounts of the hormone in an all-out effort to get glucose into cells. This excessive response leads to too much insulin in the blood, a condition called hyperinsulinemia.

Who’s most likely to develop insulin resistance?

Anyone over the age of 40, especially if they are overweight with a body mass index over 25; men with a waist more than 40 inches or women with a waist more than 35 inches; those with a family history of Type 2 diabetes, high blood pressure or arteriosclerosis; those who have high blood pressure, high blood triglycerides, low HDL cholesterol or arteriosclerosis; minorities (Latino, African American, etc.); or women with a history of gestational diabetes or polycystic ovarian disease.

The Cancer Connection

So what’s the cancer connection?

In addition to regulating blood glucose, insulin has other functions, one of which is to act as a growth hormone for cells.

When nutrients are plentiful after a meal, insulin helps cells use the nutrients to grow. Insulin also stimulates the release of other more potent growth hormones, such as insulin-like growth factor-1 (IGF-1), and may make cells more receptive to this and other growth factors.

Unfortunately, mounting evidence suggests that cancer cells feed off these growth hormones just like healthy cells do. An excess of insulin can cause them to grow uncontrollably and to resist programmed cell death – nature’s way of halting the cancer process.

Being overweight or obese is now a widely recognized risk factor for cancer – and insulin resistance is increasingly cited as a major player in all this. How? Weight gain aggravates insulin resistance, which in turn raises hormone levels known to feed the growth and development of cancer cells. This cascade of events may explain, in part, why obesity is second only to cigarette smoking as a preventable cause of cancer.

The Big Four

While this chain of events could potentially contribute to any type of cancer, four types – colon, breast, endometrial and pancreatic cancer – appear to have a stronger link to insulin resistance than other forms of cancer.

Research suggests the colon is most susceptible to the negative effects of the hyperinsulinemia that accompanies diabetes. In fact, diabetes increases the risk of developing colon cancer by 30 to 40 percent. Diabetes and colon cancer share many of the same risk factors, including being overweight (particularly abdominal obesity, a known trigger of insulin resistance), being physically inactive, and eating a diet low in fiber and high in calories, saturated fat and sugar.

Most studies tend to show an association between colon cancer and high levels of circulating insulin, as well as high levels of C-peptide (a marker for hyperinsulinemia and inflammation). Other studies have linked IGF-1 levels to an increase in colon cancer risk as well. And some research suggests these connections may hold up even in those who aren’t overweight. One analysis of the Harvard Nurses’ Health Study compared 182 people with colon cancer to 350 healthy people and found that hyperinsulinemia was associated with a greater risk of colon cancer no matter what the subjects weighed. That led the study’s authors to conclude that elevated insulin and growth hormone levels are likely driven not just by excess weight, but also by a sedentary lifestyle and the typical American diet high in refined sugars and unhealthy fats, while low in nutrient-rich, high-fiber foods.

What about breast cancer? Obesity has long been linked to an increased risk of breast cancer which has been attributed mainly to increased exposure of breast tissue to excess estrogen produced by body fat. But recent research suggests insulin resistance may also play a role.

Researchers from the Shanghai Breast Cancer Study compared 1,459 women with breast cancer to 1,556 healthy women and found that those with breast cancer were less active and had a higher body mass index (particularly abdominal obesity). They also had significantly higher blood levels of insulin-like growth factors and C-peptides, all factors linked to insulin resistance.

Another large study of Asian women, the Shanghai Endometrial Cancer Study, compared 832 women with endometrial cancer to 846 healthy women. The researchers found that long-term exercise lowered endometrial cancer risk by 30 to 40 percent. The reason? People with higher activity levels have lower levels of insulin, growth factors and sex hormones (like estrogen).

Finally, a growing body of research supports a link between insulin resistance and pancreatic cancer, a particularly deadly disease with few controllable risk factors.

One study – the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study – of more than 29,000 male smokers in Finland found that men with the highest fasting insulin levels were twice as likely to develop pancreatic cancer as men with the lowest levels. Another recent analysis of 144 people with pancreatic cancer – gleaned from four large Harvard trials – found that low levels of a protein that inhibits IGF-1 activity significantly predicted an increased risk of pancreatic cancer, suggesting that insulin resistance plays a role in its development.

One Last Thing …

Fortunately there are three things you can do, starting today, to lower your odds of insulin resistance. And, while we should all follow this advice, it’s especially crucial if you are genetically wired for the condition.

–Lose weight. I know, it’s easier said than done, but moderating your portion sizes is a smart place to start. And keeping a diary of what you eat and when.

–Establish a regular exercise routine. Physical activity is known to be a major modifier of insulin resistance. Just walking 45 minutes four to five times per week will improve insulin resistance and your overall health.

–Eat a healthy whole foods diet. Research suggests that insulin resistance may be fueled by a diet high in sugar, saturated fat and trans fats. Reverse this trend by eating more fruits, vegetables, whole grains and fish – and less animal fat and processed carbohydrates. The monounsaturated fats in olive and canola oils, nuts, seeds and avocados also improve insulin sensitivity, so include them regularly as well.

The good news is that even small changes in weight and physical activity can improve insulin resistance and lessen its negative health effects.

This Just In …

Experts have long known that diet can affect the genes that trigger cancer. However, they now realize that chemical changes can also alter how genes function without causing any obvious physical changes in the genes.

What this means is that what you eat may be able to “turn on” or “turn off” genes, triggering detrimental or protective effects. For example, depending on what you eat, a tumor-suppressor gene that keeps cell growth in check may be silenced, allowing cancer cells to grow unimpeded. Such environmental exposures may explain why identical twins with identical DNA can have very different disease risks.

One of the most provocative findings to date comes from Duke University in a study using a special breed of mouse with an on/off switch near the gene that determines predisposition to obesity, diabetes and cancer. By supplementing the diets of pregnant mice with certain nutrients, the researchers essentially “turned off” the gene in the offspring that made them susceptible to those diseases. The $64,000 question, then, is whether you can switch your own genes on or off with the right diet.

Though it’s too early to say what role diet might play in the genes that govern disease, it’s probably a key player. Future studies should give us a better picture – and I’ll keep you posted. But for now, it’s a good bet that eating a healthy diet packed with fresh fruits and veggies, whole grains, nuts and legumes can positively impact those critical genetic switches.

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References:

Gao J, Xiang YB, Xu WH, et al. “A case-control study on genetic polymorphism of CYP17 MspA(1)I and its association with endometrial cancer risk” Zhonghua Zhong Liu Za Zhi. 2007;29:266-269.

Lee JM, Okumura MJ, Davis MM, et al. “Prevalence and determinants of insulin resistance among U.S. adolescents: a population-based study.” Diabetes Care. 2006; 29:2427-2432.

Shin A, Cai Q, Shu X, et al. “Genetic polymorphisms in the matrix metalloproteinase 12 gene (MMP12) and breast cancer risk and survival: the Shanghai Breast Cancer Study.” Breast Cancer Research 2005; 7:R506-R512.

Stolzenberg-Solomon RZ, Pietinen P, Taylor PR, et al. “A prospective study of medical conditions, anthropometry, physical activity, and pancreatic cancer in male smokers (Finland).” Cancer Causes and Controls. 2002;13:417-426.

Wei EK, Ma J, Pollak MN, et al. “A prospective study of C-peptide, insulin-like growth factor-I, insulin-like growth factor binding protein-1, and the risk of colorectal cancer in women.” Cancer Epidemiological Biomarkers and Prevention. 2005; 14: 850-855.

Xue A, Scarlett CJ, Jackson CJ, et al. “Prognostic Significance of Growth Factors and the Urokinase-Type Plasminogen Activator System in Pancreatic Ductal Adenocarcinoma.” Pancreas. 2008;36:160-167.