Alternative Protocol Could Prevent, Reverse Alzheimer’s Disease

Alternative Protocol Prevent Reverse Alzheimers

Alzheimer’s disease is on the rise and has become one of the more alarming public health issues. But what if, by using a holistic approach to treating this disease, there was a way to prevent and reverse the onset of Alzheimer’s?

Researchers have studied the disease for over a century, and while they’ve come to understand the mechanisms that lead to Alzheimer’s, there haven’t been significant breakthroughs in finding a viable treatment to prevent patients’ decline into dementia and death. Dr. Ilene Naomi Rusk is a behavioral neuroscientist and co-director of the healthy brain program in Boulder, CO, who has focused her life’s work on the disease.

Dr. Rusk is one of many doctors who now ascribe to the protocols of Dr. Dale Bredesen, which shows that a personalized, holistic approach to Alzheimer’s can not only prevent the disease but even reverse its onset in early phases. But when she began her work, they were looking for one single cure. 

“I started in this field in the ‘80s looking at single-targeted strategies for dementia thinking that there would be a silver bullet because that’s the way we thought — receptors, specificity, working with a targeted approach to one brain chemical, for example, acetylcholine would be the answer,” Dr. Rusk said. “It turns out, it isn’t the answer, so there’s a background. All of this new and exciting work in dementia is because we have a foundation of what doesn’t work. If you spoke to any neurologist, any neuropsychologist, any physician they would say ‘No, we don’t really have anything that’s disease-modifying for Alzheimer’s disease, and nothing that slows progression.’ It certainly lends credence to a new approach, and the new approach to me emerged in 2016 when I read a paper by Dr. Bredesen.”

In a proof-of-concept trial, Dr. Bredesen looked at 25 patients suffering from Alzheimer’s disease and evaluated their cognitive ability before and after they followed protocols that focused on a number of lifestyle and environmental factors believed to contribute to Alzheimer’s.

“So some of those root causes are nutritional imbalances; difficulties with gut health; toxins in food, air, and water; things like mold (and) air pollution; the effects of combined prescription medication, polypharmacy for example. I’d say there are external mediated factors too, root causes and modifiable contributors like how much we exercise, I said the food we eat, but the nutrition we derive from the food we eat as well. Remember that Alzheimer’s disease particularly seeds itself very early, so the amyloid and tau begin to create problems up to 20+ years prior to the actual clinical symptoms of the disease,” Dr. Rusk said.

Interestingly, dr. Bredesen found that a large contributor to Alzheimer’s was a lack of neuroplasticity, or the brain’s ability to grow new neural pathways. Neuroplasticity has been found to be boosted by activities that challenge the brain, particularly those that fall outside our daily habits and routines.

“Neuroplasticity requires a challenge, what I like to call a disorienting dilemma for the nervous system, which means stress — which means good stress. Good stress provides healthy neuroplastic change, bad stress provides negative neuroplastic change,” Dr. Rusk said.

In addition to a lack of activity supporting neuroplasticity, improper sleep has also been found to be a major factor in the onset of Alzheimer’s — so much so, that some studies have found a 20-30% increased risk in the development of Alzheimer’s and dementia in patients who don’t get sufficient rest.

“I think sleep is one of the most modifiable and important contributors. What happens at night, what we take to sleep with us, whether we’re stressed, whether we have sleep apnea — so if we’re losing oxygen at night and we’re a little bit hypoxic, we’re a little bit low on oxygen, that can really affect our brain health,” Dr. Rusk said. “Sleep is a huge contributor to cognitive decline and then to later dementia. Actually, a recent study has shown that sleep patterns in mid-life, so earlier in life prior to people getting dementia, contribute to later dementia risk. So basically if you’re getting, I think it’s less than seven hours of sleep, in your 50s or 60s it can contribute to later cognitive decline and dementia; you’re 30 percent more likely to get dementia later in life.” 

As more research considers this personalized, multi-factor approach that assesses the various root causes of dementia, practitioners like Dr. Rusk says she believes we will be able to drastically reduce the number of new Alzheimer’s sufferers, with Dr. Bredesen going so far as to say we may someday eliminate it altogether.

Telomerase May Be The Secret to Anti-Aging

dna strand helix concept dna research crispr

Dr. Bruce Lipton invites us to consider this: “contained within our bodies is what so many have studied, sought after, and dreamed about—the fountain of youth.”

What he’s talking about are telomeres; sections of DNA found at the end of each chromosome that can offer us insight into how we can “create a long-lived biology,” filled with wellness and meaning.

Telomeres And The Genetics of Aging

The science of genetics was formed in large part because of the human need to grapple with a limited lifespan. Central to this discussion is the role telomeres play in understanding the genetic coding of our aging. Telomeres have two essential functions:

  • To allow DNA to be replicated without losing genetic information 
  • To prevent the double helix of DNA from unraveling

The process of DNA replication involves a shortening of our chromosomes from their original version, reducing the length of the original DNA molecule. This process invariably leads to aging, depression, and disease.

The role of the telomere is to extend that replication time by adding a piece of DNA at the end of the strand that doesn’t code for anything and acts as a mechanism to prevent the degradation, or unwinding, of the double helix structure. 

Lipton uses the analogy of shoelaces to bring the concept of telomeres to life. At the end of shoelaces are little plastic caps known as “aglets,” which make the process of lacing shoes simple and fluid, while holding the strands of the shoelace material together. And the same concept can be applied to the telomeres at the ends of our chromosomes.

While the role telomeres play in retaining the integrity of a DNA strand is important, Lipton stresses they have an even more important function—telomeres form an extension of the DNA that allows for replication without affecting the gene programs, allowing for an extended amount of divisions before running out; the implication of this on our longevity is profound.

For many years, it was believed the lifespan of an organism was directly proportional to how many times a cell can divide before losing the telomere extensions and cutting into the DNA program. 

Leonard Hayflick, a scientist in the 1960s calculated that a human could live approximately 90 years before telomeres were lost. However, in 1984, research scientist Elizabeth Blackburn made a truly life-changing and life-extending revelation with the discovery of the enzyme telomerase, which extends telomere length. Her discovery made an exciting impact on our understanding of the human lifespan. 

But as interesting as Dr. Blackburn’s discovery was, the enzyme’s ability to be activated or inhibited is dependent upon a number of external factors. The inhibition of telomerase can be caused by improper nutrition, childhood abuse and neglect, domestic violence, post-traumatic stress disorder (PTSD), as well as a lack of self-love, love from others, and life purpose—factors that can all have a negative impact on our lifespan.

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