THE AGING BRAIN, PART 2
Diabetes and Alzheimer’s disease: Understanding the sticky connection
In the 1950s, two molecular biologists, James Watson and Francis Crick, took a huge step forward in helping us understand the structure of DNA, the genetic material passed on from parents to children that’s used as a blueprint for our bodies to develop and function.
Back then, the prevailing belief was that there wasn’t much role for the environment in how genes functioned. Essentially, we were the way our DNA programmed us to be.
It wasn’t until the late 1990s, when the Human Genome Project had mapped most of the 6 billion “letters” of our DNA that we began to appreciate that the environment interacts with DNA on a moment to moment basis to change the way genes express themselves.
In fact, it’s these environmental factors “above the genes” – or epigenetics – that are key to understanding many of the chronic diseases plaguing us.
The outside world impacts genes more than we ever thought possible
We’re learning, for instance, that meditation can turn off 500 different genes related to stress – in other words, meditating doesn’t just make you feel calmer, it actually beneficially affects how your genes function.
We’ve even learned that epigenetic changes in one generation can be passed on to the next, just like genes themselves. For instance, researchers studying people who grew up during the Irish Potato Famine found that their offspring, born years after the famine had ended, were smaller than average – as if the children’s genes remembered their parents’ experience decades before. The genes affecting growth didn’t change but the environment altered how these genes behaved, long after the famine itself had passed.
Bottom line: the environment’s effect on our genes may be just as important as the genes themselves.
Our unhealthy love affair with sugar
Type 2 diabetes for example is a condition highly dependent on epigenetic factors, most notably the prevalence of too many calories in our diets derived from fat and especially sugar, that ends up in our blood. It’s no secret that North Americans have a love affair with high fructose corn syrup and other sugars. That’s led many of us to become overweight, develop diabetes and suffer the many negative effects of it, including cardiovascular and kidney disease, damage to the retina and the epidemic of men’s erectile dysfunction.
HbA1c or Hemoglobin A1 is a lab test that measures the average level of sugar in our blood over the previous three months. An important behavior of sugar is its tendency to stick itself to proteins rendering them less functional. HbA1c is a convenient measure of the amount of hemoglobin in our red blood cells that have a sugar molecule attached. If your HbA1c level is 6.5% or higher, you have diabetes. If it’s between 5.7 and 6.4% you have pre-diabetes.
What’s become clearer recently is the direct diabetes/Alzheimer’s disease connection – the fact that people with diabetes have a three- to four-fold higher risk of developing dementia during their lifetime. And for those with pre-diabetes, the chance of getting Alzheimer’s is two to three times greater.
But that’s just the tip of the iceberg.
The truth about blood sugar levels and Alzheimer’s
For years, doctors have told patients that if their HbA1c level was below 5.7%, they had nothing to worry about. It turns out though that even at this “safe” level, your risk of getting Alzheimer’s disease is nearly twice that of someone with the healthiest HbA1C level of 4%. In other words, there are millions of us whose average blood sugar level is low enough that we may thankfully never develop diabetes, but it’s still high enough that we may end up with Alzheimer’s.
What’s the connection between the two diseases? While the mechanism is still not fully understood, it appears that too much sugar in our system causes the formation of so-called advanced glycemic end-products (AGEs). AGEs are known to be a significant contributor to aging, and by preventing proteins and enzymes from doing their work, lead to damage of cells’ energy source – mitochondria. Mitochondria are the tiny battery packs necessary for brain and muscle cells to function. As mitochondria degrade, so too do neurons in the brain and this leads to memory decline and eventually Alzheimer’s.
The right lifestyle can help mitigate risks
The good news for people like Janet, who we met in my last post, THE AGING BRAIN, PART 1, is that even if genetic factors made her particularly prone to developing Alzheimer’s disease, a considerable amount of that risk could be countered with lifestyle and behavior changes. Things like:
1) A diet low in processed, high carbohydrate and particularly high fructose foods, which helps lower HbA1C levels.
2) Exercise, which also lowers HbA1C levels,
3) Stress management with meditation, which can stimulate growth of new brain cells and enhanced brain networking.
4) Certain supplements with anti-inflammatory and anti-oxidant effects – these may mitigate mitochondrial injury.
5) Smoking cessation – this is essential.
And the even better news, whether or not we are at risk for Alzheimer’s, is that all of us can benefit from lifestyle changes that improve brain function – more on that later.
In Part 3 of our look at the aging brain, I’ll discuss the role of our genes in the development of Alzheimer’s disease and how genomic testing can help spot dementia risk early.