A recently published study based on data from the Womans Health Initiative (WHI) sheds light on a question many of us have wondered about: Is the higher incidence of cancer among people with Type 2 caused by higher insulin levels (or, perhaps injected insulin) or something else?
The study was conducted by a team at The Albert Einstein College of Medicine, which some of you may remember is where Dr. Bernstein earned his M.D.. It has through the years done several low carb studies, too.
The study is summarized here:
Science Daily: High Blood Sugar Levels in Older Women Linked to Colorectal Cancer
The actual abstract is found here:
A longitudinal study of serum insulin and glucose levels in relation to colorectal cancer risk among postmenopausal women. G C Kabat et al. British Journal of Cancer , (29 November 2011) | doi:10.1038/bjc.2011.512
From the abstract we learn that in a group of 4902 middle aged women who were tracked for 12 years, about 1.6 percent developed colorectal cancer. They had had their fasting blood sugar and fasting insulin measured at the beginning of the study and occasionally through the study. This study found that women whose fasting blood sugar was over 99.5 mg/dl (5.53 mmol/L) at the beginning of the study had a greater risk of developing colorectal cancer than those with blood sugars under 89.5 mg/dl (4.98 mmol/L). The relationship held true for subsequent blood tests too.
However--and this is what is interesting about this study--there was no relationship between these women's fasting insulin levels or the calculated HOMA values (which are believed to measure insulin resistance) and their risk of getting this cancer.
So this data would suggest that it is the high blood sugars, not the high insulin which promotes the cancer.
Before you panic because your fasting blood sugar is over 99.5 mg/dl (as is the case with many of us thanks to dawn phenomenon) remind yourself of this: from what we can see in other contexts, it isn't actually mildly elevated fasting blood sugars that damage our bodies. We see the correlation between fasting sugars and complications in studies because in people eating high carbohydrate diets, mildly elevated fasting blood sugars almost always go hand in hand with significantly elevated post meal sugars. Especially in women, who may be diabetic by glucose tolerance test for up to a decade before they would be diagnosed using a fasting glucose test. (You can see the data backing this up HERE.)
So a woman with a fasting sugar of 105 mg/dl, for example, when she eats her morning bagel with jelly, along with a sweetened latte, may easily reach a blood sugar that approaches 200 mg/dl even if it resolves fairly quickly due to a near-healthy second phase insulin release. But if diabetic you should wake up with a blood sugar of 105 mg/dl and eat an egg and bacon for your breakfast with no carbs, you may easily end up with a blood sugar of 95 an hour later, which suggests you would have a similar health outcome to a completely non-diabetic woman with a fasting blood sugar of 89 mg/dl who ends up at 95 mg/dl an hour after eating her breakfast.
It's also worth noting that the statistical measure the study calculated was "risk" not incidence--and that risk is a statistical artifact that magnifies numbers to provide a more dramatic impact. The actual increase in incididence due to elevated blood sugar was likely around 5 cases per thousand or .5%.
But on the positive side, the fact that even after using magifying statistical techniques like "risk" the researchers couldn't find the expected connection between fasting insulin levels, HOMA, and cancer gives us one more, intriguing, piece of data to answer the quesion, "Do people with diabetes get cancer because of high insulin levels (injected or natural) or because of high blood sugars?" Here at least, it looks like the answer is, as is the case with all the other diabetic complications, "It's the blood sugars, stupid!"
This is very good news because our insulin levels are very hard to control and insulin resistance may be genetic and not something we can lower. Even many devout low carbers with Type 2 continue to be insulin resistant no matter what they weigh (based on how much insulin they have to inject to lower their blood sugars.) But insulin resistant or not, we can control our blood sugars--often most effectively with insulin--and if the conclusion of this study is reinforced by findings in other studies, we may be able to relax about the potential impact on cancer of our injecting insulin to control those blood sugars.
One last note: If you have had years of exposure to higher than normal blood sugars, you might be interested in knowing that Metformin has been shown to suppress the growth of existing early colorectal growths in people without diabetes. Read about that HERE.
Though researchers often state that metformin inhibits cancer due to its effect on lowering insulin, this is just a guess. The belief that it is high insulin levels that cause a greater incidence of cancer among people with diabetes is far from proven and that theory is exactly the belief this study debunks.
In fact, there is evidence emerging that metformin's anti-cancer properties are independent of its effect on insulin and have to do with its ability to suppress TORC1, a cell growth factor. (For example, see THIS STUDY.)
NOTE: Since posting this I have reviewed the full text of the study and see nothing to change the conclusions discussed here. It looks very well conducted, involved people from various well-respected public health departments in universities and medical schools, and gives no hint of corporate meddling.
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