Flash back to your moment with those hunters and gatherers. Their brains are not too different from yours. Both have evolved to seek out foods high in fat and sugar. After all, it’s a survival mechanism. The problem is that your hunting efforts end quickly because you live in the age of plenty, and you’re more likely to find processed fats and sugars. Your cave man counterparts are likely to spend a long time searching, only to come across fat from animals and natural sugar from plants and berries if the season is right (and those plants and berries are far less sugary than what you picture when you think of fruit). So while your brain might operate similarly, your sources of nutrition are anything but. In fact, take a look at the following graphic, which depicts the main differences between our diet and that of our forebears. And what, exactly, does this difference in dietary habits have to do with how well we age and whether or not we suffer from a neurological disorder or disease?
The studies describing Alzheimer’s as a third type of diabetes began to emerge in 2005, but the link between poor diet—notably a high-carb one—and Alzheimer’s has only more recently been brought into sharper focus with newer research showing how this can happen.
These studies are both convincingly horrifying and empowering at the same time. To think we can prevent Alzheimer’s just by changing the food we eat is, well, eye-opening. This has many implications for preventing not just Alzheimer’s disease but all other brain disorders, as you’ll discover in the upcoming chapters. But first, a brief lesson on what diabetes and the brain have in common. The moniker “type 3 diabetes” sounds a little confusing at first, but all the types of diabetes share one feature in common: a bad relationship with insulin, one of the body’s most important substances for cellular metabolism.
Evolutionarily, our bodies have designed a brilliant way to turn the fuel from food into energy for our cells to use. For almost the entire existence of our species, glucose—the body’s major source of energy for most cells—has been scarce. This pushed us to develop ways to store glucose and convert other things into it. The body can manufacture glucose from fat or protein if necessary through a process called gluconeogenesis. But this requires more energy than the conversion of starches and sugar into glucose, which is a more straightforward reaction.
The process by which our cells accept and utilize glucose is an elaborate one. The cells don’t just suck up glucose passing by them in the bloodstream. This vital sugar molecule has to be allowed into the cell by insulin, which is a hormone produced by the pancreas. Its job is to ferry glucose from the bloodstream into muscle, fat, and liver cells. Once there, it can be used as fuel. Normal, healthy cells have a high sensitivity to insulin. But when cells are constantly exposed to high levels of insulin as a result of a persistent intake of glucose (much of which is caused by an overconsumption of hyper-processed foods filled with refined sugars that spike insulin levels beyond a healthy limit), our cells adapt by reducing the number of receptors on their surfaces to respond to insulin. In other words, our cells desensitize themselves to insulin as if they are revolting against its deluge. This causes insulin resistance, which allows the cells to ignore the insulin and fail to retrieve glucose from the blood. The pancreas then responds by pumping out more insulin. So higher levels of insulin become needed for sugar to go into the cells. This creates a cyclical problem that eventually culminates in type 2 diabetes. By definition, people with diabetes have high blood sugar because their body cannot transport sugar into cells, where it can be safely stored for energy. And this sugar in the blood presents many problems—too many to mention. Like a poisonous venom, the toxic sugar inflicts a lot of damage, leading to blindness, infections, nerve damage, heart disease, and, yes, Alzheimer’s and even death. Throughout this chain of events, inflammation runs rampant in the body.
I should also point out that insulin can be viewed as an accomplice to the events that unfold when blood sugar cannot be managed well. Unfortunately, insulin doesn’t just escort glucose into our cells. It’s also an anabolic hormone, meaning it stimulates growth, promotes fat formation and retention, and encourages inflammation. When insulin levels are high, other hormones can be affected adversely, either increased or decreased due to insulin’s domineering presence. This, in turn, plunges the body further into unhealthy patterns of chaos that cripple its ability to recover its normal metabolism.
Genetics are certainly involved in whether or not a person becomes diabetic, and genetics can also determine at what point the body’s diabetes switch gets turned on, once its cells can no longer tolerate the high blood sugar. For the record, type 1 diabetes is a separate disease thought to be an autoimmune disorder—accounting for only 5 percent of all cases. People with type 1 diabetes make little or no insulin because their immune system attacks and destroys the cells in the pancreas that produce insulin, so daily injections of this important hormone are needed to keep blood sugars balanced. Unlike type 2, which is usually diagnosed in adults after their bodies have been abused by too much glucose over time, type 1 diabetes is typically diagnosed in children and adolescents. And unlike type 2, which is reversible through diet and lifestyle changes, there is no cure for type 1 yet, though It can be managed relatively well through drugs and diet. That said, it’s important to keep in mind that even though genes strongly influence the risk of developing type 1 diabetes, the environment can play a role, too. It has long been known that type 1 results from both genetic and environmental influences, but the rising incidence over the last several decades has led some researchers to conclude that environmental factors could be more instrumental in the development of type 1 than previously thought.
What we’re beginning to understand is that at the root of “type 3 diabetes” is the phenomenon in which neurons in the brain become unable to respond to insulin, which is essential for basic tasks, including memory and learning. We also think that insulin resistance, as it relates to Alzheimer’s disease, may spark the formation of those infamous plaques that are present in diseased brains. These plaques are the buildup of an odd protein that essentially hijacks the brain and takes the place of normal brain cells. Some researchers believe that insulin deficiency is central to the cognitive decline of Alzheimer’s disease—brain cells can’t get their insulin because they are resistant to it! And the fact that we can associate insulin resistance with brain disease is why talk of “type 3 diabetes” is starting to circulate among researchers. It’s all the more telling to note that obese people are at a much greater risk of impaired brain function, and that those with diabetes are at least twice as likely to develop Alzheimer’s disease. And those with pre-diabetes or metabolic syndrome—a cluster of biochemical abnormalities associated with the development of type 2 diabetes as well as cardiovascular disease—have an increased risk of pre-dementia or mild cognitive impairment (MCI), which often progresses to full-blown Alzheimer’s disease.
This statement is not meant to imply that diabetes directly and always causes Alzheimer’s disease, only that they share the same origin. They both often spring from overconsuming foods that force the body to develop biological pathways leading to dysfunction and, further down the road, illness. While it’s true that one person with diabetes and another person with dementia may look and act differently, they have a lot more in common than we previously thought. And what I find really interesting (and which I mentioned earlier) is that newer studies are showing that people with high blood sugar—whether or not they have diabetes—have a higher rate of cognitive decline than those with normal blood sugar. This was true in one particularly disturbing longitudinal study from 2018 following more than 5,000 people over 10 years. Their rate of cognitive decline—regardless of whether or not they were diabetic—hinged on blood sugar levels. The higher the blood sugar, the faster the decline—even in the nondiabetics.
In the last 20 years, we’ve witnessed a parallel rise in the number of type 2 diabetes cases and the number of people who are considered obese. Now, however, we’re starting to see a pattern among those with dementia, too, as the rate of Alzheimer’s disease increases in sync with type 2 diabetes. I don’t think this is an arbitrary observation. It’s a reality we all have to face as we shoulder the weight of soaring health care costs and an aging population. New estimates indicate that Alzheimer’s will more than triple in prevalence and likely affect 16 million Americans by 2050, a crippling number for our health care system and one that will dwarf our obesity epidemic. There were an estimated 50 million people worldwide living with dementia in 2017, and this number will almost double every 20 years, reaching 75 million in 2030 and 131.5 million in 2050. Today, someone in the United States develops Alzheimer’s dementia every 66 seconds. By midcentury, someone in the United States will develop the disease every 33 seconds (remember, someone in the world develops dementia every 3 seconds). The prevalence of type 2 diabetes, which accounts for 90 to 95 percent of all diabetes cases in the United States, has tripled in the past 40 years, and millions of people go undetected and untreated for a long time. By anyone’s definition, this is absolutely an epidemic. No wonder the U.S. government is anxiously looking to researchers to improve the prognosis and avert a catastrophe. According to the Centers for Disease Control and Prevention (CDC), more than 30 million people have diabetes, which amounts to nearly 10 percent of the U.S. population; other reports have calculated that the percentage among adults is more like 12 to 14 percent, depending on the criteria used. An estimated 7.2 million adults, 18 years or older, are undiagnosed (23.8 percent of people with diabetes).
Excerpted from Grain Brain (revised edition) Copyright © 2018 by David Perlmutter, M.D., and Kristin Loberg. Used with permission of Little, Brown and Company, New York. All rights reserved.