Deterioration and loss of the microscopic connections between brain cells (referred to as synapses) underlies the memory loss and other mental dysfunction seen in Alzheimer disease. The culprit behind all of this damage and destruction is believed to be soluble beta amyloid fibrils. They bind to specific sites on nerve cell membranes (the outer coatings of the nerve cells) in the region of synaptic connections. In so doing, they trigger the production of inflammation and subsequent damage to the tiny nerve cell connections. As they are lost, the nerve cells become functionally disconnected and can't perform the computer-like computations that are the basis for every thought we have.

This information is not particularly new. However, the observation that a protective mechanism exists that can shield nerve cells from the beta amyloid toxins is. The exciting thing about this finding is that it can prevent the deleterious changes from happening before symptoms develop! The savior in all of this drama is the hormone insulin. It so happens that insulin in the brain prevents the binding of beta amyloid fibrils to the receptors they must interact with to cause damage to the synaptic connections.

The proposed mechanism behind the insulin protective effect is not one of insulin interfering with the binding of beta amyloid to its receptors, but the actual down-regulation, or reduction , in the number of beta amyloid binding sites on the nerve cell membranes. To cause this reduction in beta amyloid binding sites, insulin must first bind to insulin receptors on the same nerve cell and produce an insulin signal within the nerve cell. The end result of this complex process is the loss of beta amyloid binding sites in the synaptic region. Without the binding sites, beta amyloid is almost helpless.

The novel finding that insulin mitigates synaptic vulnerability suggests that mechanisms that enhance brain insulin signaling, which declines with aging and diabetes, could potentially slow the onset or development of Alzheimer disease. In brain cells grown in tissue culture (like growing bacteria in a Petrie dish), this observation was confirmed in two separate ways -- by directly adding insulin to nerve cells, and by adding a drug that improves insulin sensitivity (meaning when the insulin that was normally present binds to its receptor of the nerve cells, the response is enhanced). Both interventions improved insulin signaling and decreased inflammation and loss of synapses.

While these studies were done in tissue culture, there are other ways to enhance brain insulin signaling, which include calorie and carbohydrate restriction. These interventions were studied in mice who were placed on low calorie/low carb diets. The lead author in this study was Dr. Giulio Maria Pasinetti. Based on his findings, he noted, "Both clinical and epidemiological evidence suggest that modification of lifestyle factors such as nutrition may prove crucial to Alzheimer's disease management. This research, however, is the first to show a connection between nutrition and Alzheimer's disease neuropathy by defining mechanistic pathways in the brain and scrutinizing biochemical functions."

When we are young and are eating a healthy diet, there are minimal fluctuations in the level of blood glucose. This is not very exciting because blood glucose doesn't get too high or too low. But that's exactly how things should work. However, as we get older the body is not as efficient at regulating and controlling blood glucose. As a result, the swings get bigger -- too high at some times and too low at others. What we eat can have the same effect. A sugary meal or snack can send blood glucose sky rocketing minutes after the meal ... and then plummeting down below normal an hour later. As a matter of fact, this is a fairly common occurrence today and is easily observed at work. Look around at your coworkers an hour or so after lunch. What do you see? Most of them are ready for a nap. They are sluggish and inefficient. This is what happens when glucose levels fall. Why? Because the brain burns glucose and when it's main fuel supply is not available, it suffers. Mental brownouts occur, energy levels fall and mental torpor is the result. Clearly, these dramatic glucose fluctuations are not good for the brain. This is what I call the Roller Coaster Effect.

Most of us think immediately about diabetes when a doctor mentions blood sugar problems. Now it appears that memory loss and Alzheimer disease might  be just around the corner. This is due to the Roller Coaster Effect. We have just discussed why so many of us feel sleepy and just not very sharp after lunch. Let's look at a more extreme example of the same thing. We all know people who were diagnosed with childhood diabetes (Type 1 diabetes, or "insulin-dependent" diabetes) because they are always checking their glucose level and injecting themselves with insulin shots throughout the day. One of the major complications this group of individuals experience is low blood glucose -- or hypoglycemia. When this occurs they can feel jittery, light-headed or even sleepy. If the condition goes uncorrected, and the blood sugar becomes quite low, they think more slowly and may even become comatose. This is related to low blood glucose and the resultant lack of an energy supply for the brain. It causes power outages and loss of mental function. These periods of low glucose represent the dips in the roller coaster ride.

Brain researchers have recently discovered a link between brain health and high blood glucose levels. At first, this may seem counterintuitive because with high glucose levels one would think that the brain would be happy. However, such appears not to be the case. Over the past couple of years, researchers have starting connecting the link between elevated blood sugar and and elevated risk for Alzheimer disease. That is now a well-known fact. More recently, a study presented by Swedish scientists showed that simply experiencing higher than normal blood sugar levels may be enough to potentially lead to Alzheimer disease.

The number of individuals this affects is not trivial. More than 40 million Americans fall into this category. They are in the "pre-diabetic" group. It is well known that obesity is a risk factor for memory loss and more serious conditions. Now we can add to this the Roller Coaster Effect -- that is, poor control of blood sugar.

What concerns many public health officials about these recent findings is that Alzheimer disease is expected to increase fourfold in the next four decades as baby boomers live longer. Now, in addition to living longer, we have a huge pool of aging Americans with increasingly more abnormal blood glucose control, another potent risk factor for these afflictions. It now appears that aging and poor glucose control are going to dramatically magnify the numbers of Americans developing Alzheimer disease. As a result, many researchers are worried that Alzheimer's will swamp health care systems worldwide.

More recently, investigators at Columbia University found that even modest swings in blood sugar levels can lead to memory loss severe enough to affect everyday function. These sugar fluctuations can be subtle enough not to even be considered a disease state!

One of the major processing regions for memory function is called the hippocampus. Subjects with abnormal blood glucose levels were found to have decreased hippocampal volumes compared to subjects with normal blood glucose levels.

To make matters worse, other researchers have noted an association with poor blood glucose control and the buildup in the brain of sticky clumps of protein that lead to the development of senile plaques -- the hallmarks of Alzheimer disease.

How can blood sugar be controlled? Eating properly and  exercising! The same recommendations that insure a healthy body. So get started now and avoid the Roller Coaster Effect!