The gene ApoE has one job in the human body. It determines how the body transports lipids. It’s known as the fat bucket.
There are 3 types, or alleles, of ApoE; 2, 3, and 4, and each one of us has two copies; one inherited from our mother, and one from our father. ApoE 3/3 is the most common, comprising approximately 64% of the population. 2/2 is the rarest, at around 1%.*
Close to 65% of Alzheimer’s patients have at least one ApoE 4 allele. Those with two ApoE 4 alleles, the third rarest combination, have a 94% chance of developing Alzheimer’s or similar dementia.**
How this seemingly innocuous “fat bucket” gene contributes to the development of Alzheimer’s is WAY above my pay grade, though I have come to understand, at least on a very esoteric level, how it works. I’m not going to delve into it here, though. I don’t like these posts to go too far over 2000 words.
The ApoE 4 gene plays a huge part in two of the three subtypes of Alzheimer’s, and it is these two types against which the most success has been found using the protocols we’re to begin soon.
Jacquelynn is an ApoE 2/3, or as they now say, “ApoE 4 negative”. While this means a statistically much lower likelihood of developing Alzheimer’s, here we are. How? Because hers is the third type.
Type one is inflammation-related. The second is keyed to a loss or lack of certain synapse-supportive hormones or biological compounds. Both of these types result in the growth of A-beta, or amyloid-beta, a plaque which blocks synaptic communication and eventually strangles the nerve.
Type three is toxic. Birthed by any or many of the toxins in our environments, in the horrible substances that western society calls “food”, and even created by our own bodies…
In February of 2016, I rushed Jacquelynn to the hospital with an obvious kidney stone. We’ve both had them before, and the symptoms were unmistakable. While the pain meds were taking effect, the urologist came in to discuss her C-T scan results; several stones in both, and a 10mm stone lodged in the ureter of her left kidney. The tube was completely blocked, and immediate surgery was imperative to insert a stent, allowing the infection to drain, after which the stone could be removed.
Then the conversation got interesting. Though blocked, the left kidney was but barely functional and, worse yet, approximately 1/4 the size of its mate. It was shriveled, misshapen, and dying.
Some background: it was mid-2015 when I began noticing something was wrong. Nothing severe, but things like general confusion, a drastic decline in her handwriting and decrease in her interest in reading., and an occasional difficulty finding the right words (more alarming from a woman with one of the largest vocabularies I’d ever encountered). Where she would normally spend time at her computer reviewing job opportunities, I would often find her staring at a blank screen.
Her general health had been pretty poor as well, with colds, ear infections, strep, and repeated urinary tract infections. Worst, she had shone occasional symptoms of depression.
I first began to get truly concerned in the fall of 2015, when we first visited her new primary care physician. Claiming an inability to see it clearly (her glasses were old, and she was having difficulty manipulating her contacts so had temporarily given up trying), she asked me to fill out her paperwork. She had difficulty remembering both her birth date and her social security number, as well. The capper for me was watching her try to sign the form. I almost cried there and then.
The best guess at the time of the C.T. scan in February was that the kidney had been essentially destroyed by the stones inside it. Probably over the past several months or so. Clearly, this dovetails perfectly with the visible and noticeable cognitive decline.
The toxins that remain unfiltered by an injured/failing kidney are extremely neurotoxic. This is why a patient in kidney failure (trust me, I’ve seen it plenty) shows symptoms of extreme aphasia and are almost universally tested for stroke. When I rushed her to the ER on Valentine’s Day of 2017, Jacquelynn could have passed for a late-stage-seven dementia patient. Totally disoriented, unable to express herself, no bladder control, and little ability to follow simple instructions such as “squeeze my hand”. The last straw for rushing her to the hospital was the inability to grasp a spoon when I tried to get her to eat a little yogurt. Every time she reached for it and missed, she winced and “ow!”, as if missing had caused her physical pain.
There are many tests yet to be run when we get to Savannah, but the toxic overload of the gradual destruction and death of her kidney at the very least contributed significantly to the development and eventual diagnosis of Alzheimer’s dementia, and, typical of the toxic type, it has progressed much more rapidly than in the other types, and in a much less “organized” fashion.
Success treating toxic, type 3 Alzheimer’s has increased significantly, as long as the patient isn’t too far gone when treatment begins. I won’t lie and pretend as though that fear hasn’t crossed my mind, but living in fear only serves to paralyze one from action. I believe in our success. I believe I was led to this path, both to save my Jacquelynn, and also to tell you and everyone else about this process, to show the world, every step along the way, the path to a cure for Alzheimer’s disease
* **Statistics and figures quoted from “The Perfect Gene Diet”, by Pamela McDonald, NP, Integrative Medicine Nurse Practitioner