Is there a cure for America’s scariest disease, now affecting more than 6 million citizens? The government frowns on their methods, but functional and anti-aging doctors think they are getting close to the answer.
WORDS J.P. Faber
There was a time when the scariest diagnosis you could hear from a doctor began with the letter “C.” Now the name of fear begins with the letter “A”, and it stands for Alzheimer’s.
Of all the things we fear about growing older, few top the fear of dementia. It’s the vision that we, too, could become that elderly relative we all know, the one who has lost his or her memory, the one who can no longer recognize beloved relatives, the one with that lifeless stare. At least with cancer there is the hope of a cure. Alzheimer’s still has no cure, at least not officially.
Among anti-aging medical researchers, finding a cure for Alzheimer’s is the Holy Grail. It is a disease specifically associated with aging—and therefore at the heart of anti-aging medicine’s mission to promote the early detection, prevention, treatment and/or reversal of aging-related disorders. It’s also at the heart of a raging debate between the old-line medical establishment and the leading-edge doctors practicing in clinical settings.
Here’s the heart of the debate: The established medical institutions, like the National Institutes of Health, say there’s nothing proven that you can do to prevent, delay or reverse Alzheimer’s. Meanwhile, anti-aging doctors on the frontline who are trying to do just that are reporting at least limited success, especially when it comes to preventing the disease. Some are even reporting success with reversing the most severe symptoms of the disease, something that mainstream institutions refuse to acknowledge, at least officially.
“The research that we are relying upon comes straight from Harvard Medical School led by the Kennedy Chair of Neurology, Dr. Rudolph Tanzi,” says Thomas Lewis, Ph.D., CEO of The Boston Brain Clinical Institute, a company that has developed methods to detect, monitor, and treat Alzheimer’s Disease and dementias and also trains physicians to do the same. “But even though he is a leading neurologist, the mainstream neurologists will be very, very slow to accept this thesis and will require years of clinical studies.”
What is widely accepted is the discovery of the infamous ‘amyloid’ protein, which is the hallmark of the disease, and forms in the brains of Alzheimer’s patients, sort of like plaque in the arteries. This biological ‘marker’ was a major first step in predicting the disease, since the protein develops in a patient’s brain prior to their exhibiting the symptoms of the disease.
What Dr. Tanzi contends is that this Alzheimer’s disease indicator may not be the villain, as all the rest of medicine believes, and in fact may be part of the immune system’s response to protect the brain. The question is, protect it from what? In his 2010 paper, Dr. Tanzi indicated that the amyloid may be protective against infection and thus, inflammation. While this assertion is disruptive and controversial, it is exactly what Dr. Alois Alzheimer’s suggested, a century ago, as the cause of the disease named after him.
STEP ONE: PREDICTING THE DISEASE
The idea that Alzheimer’s can be predicted way ahead of time was finally acknowledged by the medical establishment this year. In April, the Alzheimer’s Association and the National Institute on Aging (NIA) issued their first new guidelines for diagnosing Alzheimer’s disease in 27 years.
The main thrust of the new guidelines revolves around the one big concept that you can see Alzheimer’s coming. Part one of the report concludes that everyone who gets Alzheimer’s goes through a preliminary stage of what’s called Mild Cognitive Impairment (MCI), where people experience a mild but noticeable decline in memory, reasoning and visual perception. That prequel seems kind of obvious, but still worth noting. The number two conclusion was much bigger: Years before you can detect any loss of memory or cognitive abilities there are certain biological ‘markers’ that can predict the disease.
This is just what the frontline doctors have been saying for years: You can predict Alzheimer’s, perhaps even decades ahead of time, from changes in the brain. What is interesting is how many ways there are to see it coming.
“This is what we’ve been saying, that Alzheimer’s is a disease that starts 20 years earlier,” says Dr. Eric Braverman, the best-selling author of A Younger You, whose PATH Medical Institute in New York City specializes in maintaining and restoring a more youthful brain. “Our tests give us 80 percent predictability of all dementia, and we expect to save people…”
Dr. Braverman’s clinic uses what’s called a PT300 brain scan, which measures brain speed. Standard brain reaction time to stimuli is 320 milliseconds for a 20-year-old, says Uma Damle, PATH’s research manager, a speed that slows down approximately 10 milliseconds each decade. When it goes slower than 340 milliseconds, you are witnessing the beginning of cognitive decline; when it gets worse you are seeing the beginning stages of dementia.
The Boston Brain Clinical Institute, meanwhile, uses a protein model of prediction based on the research of Dr. Tanzi. What they have learned is that the presence of the amyloid protein that Dr. Tanzi discovered in the brains of Alzheimer’s patients can be detected years before in the eye and through blood testing, using a much-less-expensive approach. “With a basic slit-lamp microscope, which all optometrists have in their office, they can see the protein [in the eye], which usually forms as a (cortical or supranuclear) cataract,” says Lewis. Using this model, they can predict the disease “a good ten years ahead of time,” he says. “And the blood work sometimes allows us to elucidate a physiological root-cause.”
Another model for prediction relates to the brain’s ability to metabolize glucose—in other words, its ability to process and use sugar. Current research shows that the areas in the brain where the deadly Alzheimer’s amyloid protein appears are the very same areas of the brain that were unable to get enough energy to function properly.
“Studies show that in groups of people who are at risk for Alzheimer’s, but have not yet shown the symptoms, there are signs of glucose metabolism problems in the same area where the [amyloid] plaque appears,” says Larry McCleary, MD, a pediatric neurosurgeon and author of The Brain Trust Program and Feed You Brain, Lose Your Belly. “I refer to it as a kind of brain starvation.”
Interestingly, this inability of brain cells to absorb sugar is very similar to the insulin resistance that causes diabetes—interesting because diabetics are at high risk for Alzheimer’s and several groups now classify the disease as Type III diabetes.
STEP TWO: DEFINING THE DISEASE
With so many ways to predict Alzheimer’s, the next big question is simple: Just what is Alzheimer’s?
According to the national Alzheimer’s Association, “Alzheimer’s is a type of dementia that causes problems with memory, thinking and behavior.” It occurs most frequently in older people (the majority of victims are 65 and older) and gets progressively worse over time. Eventually the victim looses memory, language, decision-making ability and judgment, as well as their basic personality.
The official causes of the disease are plaques (amyloid proteins) and tangles that damage and kill nerve cells. These may be just biological markers for the disease; anti-aging doctors believe the disease is caused by a host of interrelated factors, including bacteria in the body that cause inflammation of the neural tissue. In that sense, most see it as part of the same syndrome that leads to cardiovascular diseases, which is one reason why there is a close link between the two.
Alzheimer’s is the most common form of senile dementia, accounting for half or more of all cases, but not the only cause. The fact that there are many other forms of dementia, and that memory loss can occur for other reasons, is one of the difficulties in dealing with the disease. “Alzheimer’s is just a 1906 term used by a Russian scientist who found tangles in the brain,” says Dr. Braverman. “There are dozens of types of dementia, and Alzheimer’s is used interchangeably [as a name for them.]” You can also have what is known as ‘pseudo dementia,’ where the loss of mental functions occurs for other reasons and can be reversed fairly easily.
If the patient has Alzheimer’s, then the real work to manage the disease begins.
STEP THREE: PREVENTING AND CURING ALZHEIMER’S
Most mainstream treatments for Alzheimer’s involve drugs that mask the symptoms. That is a far cry from the treatment plans and preventative programs being implemented by anti-aging doctors who are fighting to prevent, halt or reverse the disease.
Richard S. Isaacson, MD, a Harvard-trained neurologist and associate professor of clinical neurology at the University of Miami’s McKnight Brain Institute, has treated hundreds of patients with a 10-step prevention plan and a 20-step treatment plan.
“You can stabilize or improve mild Alzheimer’s disease, though there is no cure yet,” he says. “I have several [ongoing] vaccine trials that reverse it for a couple of years, but there is no complete reversal.”
Dr. Isaacson says there is far more hope in the area of prevention. “For patients who are at risk, there is scientific evidence that you can delay the onset of Alzheimer’s. You have to take a comprehensive approach, with all sorts of interventions, invoking the biologic process of synergy. But it puts brakes on it… The goal is to delay the onset of full-blown Alzheimer’s, to stay actively engaged in life.”
Dr. Isaacson agrees with Dr. McCleary: Insulin resistance is a big part of what causes the disease, and that inflammation—something which results from too much sugar in the blood stream, thanks to insulin resistance—plays a significant role as well. Dr. Clement Trempe, CMO of The Boston Brain Clinical Institute, also agrees with the assertion of the connection between insulin resistance, inflammation and Alzheimer’s. For that reason, Dr. Isaacson’s prevention program involves keeping patients away from what are called ‘high glycemic’ foods that are loaded with quick-release sugar. He goes as far as to recommend ‘mild periods of starvation,’ which is a dramatic way of saying that if you go without eating for 12 to 14 hours at a time (overnight, for instance) your brain cells use your own fat for power and avoid the inflammatory damage of glucose, i.e. sugar.
The idea that Alzheimer’s is a complex disease with multiple causes that requires a complex response is one of the tenants of anti-aging clinics working to prevent or reverse the disease. “We see it as a systemic disease versus an isolated disease of the brain,” says Lewis. “And this concurs with Dr. Alzheimer’s original assertions.” In order to treat it, then, requires a complete regimen of diet, nutritional supplements, exercise and immune system health. If the causes for inflammation can be reversed, says Lewis, then the disease can be delayed, avoided or even brought under control.
“We are seeing everything from slowing the progression [of Alzheimer’s] to some degree of cognitive improvement,” says Lewis. “The current dogma is that the course of the disease is a progressive downward slope, and there is nothing we can do for the degradation of [brain tissue], but we can change the course of the disease from less deep, to flat, and in some cases, to improve or reverse the decline.”
What has given doctors the greatest hope is the discovery, in recent years, that the brain is capable of generating new brain cells, a process called neurogenesis.
“If you arrest the inflammatory cause of the disease, the brain can recover,” says Lewis. “There is the question of how much damage has already been done and how serious the damage is, but if you remove the disease, the patient can rebuild brain tissues and brain cells.”
Dr. Richard Smayda, one of Braverman’s colleagues at PATH, reports considerable success with reversing Alzheimer’s symptoms with just that approach—improving and rebuilding brain function.
“We maximize blood flow [to the brain] with aspirin, certain herbs and certain nutrients,” says Dr. Smayda. “The brain is the most sensitive [organ] to lack of oxygen, to lack of glucose and to lack of blood flow. We want to maximize these things and the natural neurotransmitters in the brain.”
Dr. Smayda reports substantial success with bringing patients back from dementia of all stripes using a comprehensive approach. “If you can repair everything that was knocking them out of the game, you can repair them to the level of nuero-replacement,” he says. “They can return from dementia and can live a normal life.”
PREVENTION AS THE BEST CURE
Whether patients can completely return to their former selves, versus recovering to the point of functioning in the world again, is a question still to be answered. Clearly the best path is to prevent the onset of the disease.
This is where doctors in the field again diverge significantly from the medical establishment. Anti-aging doctors are convinced that through a combination of diet, nutrients, supplements, physical exercise and mental gymnastics, an individual can delay or avoid the onset of Alzheimer’s. Their programs include the same basics that most anti-aging doctors recommend for avoiding age-related diseases in general: A diet rich in fruits and vegetables, micro-nutrient supplements to he
lp fight cellular damage, regular cardiovascular and resistance exercise and so on—with additional mental and social engagement to keep the brain in top form.
The authorities still aren’t convinced that any of this has been scientifically proven. In the very same month that NIA officials announced their new guidelines, a National Institutes of Health (NIH) panel issued a report that there was not enough solid evidence supporting the concept that diet, supplements, exercise or social engagement could modify the onset of Alzheimer’s disease. Instead, what they concluded was that factors which seemed to increase the risk Alzheimer’s—diabetes, smoking, depression—and factors which seemed to decrease the risk of Alzheimer’s—Mediterranean diet, social engagement, physical and mental activities—were merely “associated” with increasing or decreasing the risk.
“These associations are examples of the classic chicken or the egg quandary. Are people able to stay mentally sharp over time because they are physically active and socially engaged, or are they simply more likely to stay physically active and socially engaged because they are mentally sharp?” asks Dr. Martha L. Daviglus, a professor of preventive medicine at Northwestern University who chaired the NIH panel. “An association only tells us that these things are related, not that one causes the other.”
The NIH conclusions were based on a review of all the existing studies about Alzheimer’s prevention and/or cure. What the panel saw, says Dr. Daviglus, were lots of studies that contradicted each other, or that were sloppy, or that were conducted for other reasons. The famous Framingham Heart Study, for
example, which has been testing 5,209 people in the town of Framingham, Mass., since 1948 (now looking at their kids and grandkids), is cited as evidence that certain lifestyle habits can reduce the risk of Alzheimer’s. People who took fish oil supplements, an anti-inflammatory, had fewer cases of Alzheimer’s, for example. But that bit of data needs to be studied with higher scientific standards, says Dr. Daviglus.
Anti-aging proponents of a lifestyle cure disagree.
“The Framingham study showed that the risk of Alzheimer’s is 50 percent less in those with higher-than-average levels of fish oil in their blood. I’d say taking fish oil is a treatment,” says Lewis. “Alzheimer’s is an inflammatory disease, and if you have a method to determine the cause and treat it to reduce inflammation, that’s a treatment.”
Lewis, along with other members of the anti-aging community, feels that the NIH—like the big pharmaceutical companies—wants to find a single pill that will cure Alzheimer’s. That approach, they say, misses the point.
“Alzheimer’s is a process that develops over 25 years,” says Lewis. “We are not looking to develop a drug [as a solution], but to treat a complex disease with multiple causes that leads to the degeneration of neurons. You need a comprehensive approach.”
Says Dr. Daviglus: “The one thing we know for sure is that age is a risk factor for Alzheimer’s. That has been shown in every study. Now, with people living longer, they will have a higher risk of Alzheimer’s. We have to have answers very, very soon… Whoever solves this will have made a great contribution to science.”
