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Posted July 2, 2018: by Bill Sardi
In 1993, in what was called “the most important finding that’s ever been made in the study of Alzheimer’s disease,” investigators reported a variation of the APOE gene, a protein that transports cholesterol throughout the human body, drastically increases risk for this memory-robbing brain disease. The APOE gene provides instructions for making a protein called apolipoprotein E. APOE regulates the clearance of beta amyloid brain plaque, which is a common hallmark of age-related brain disease. Carriers of the APOE e4 gene in their brain cells are at such an increased risk for memory loss that it is called “the forgetting gene.” Carry two copies of this gene and the risk is worrisome. Look at the risk chart below:
|
GENE |
% Risk |
Age of Onset |
|
No APOE e4 |
20% |
84 years |
|
APOE e4 gene (1-copy) |
47% |
76 years |
|
APOE e4 gene (2-copies) |
91% |
68 years |
Carriers of APOE-ε4 have a faster rate of decline in memory between ages 43 and 69, when compared to non-carriers. APOE-ε4 is associated with a subtly faster rate of memory decline from midlife to early old age.
Even in non-demented older adults, a carrier of APOE e4 gene is predictive of a higher rate of memory decline between 79 and 87 years of age.
Now, for the first time in a lab dish researchers have “edited out” APOE e4 gene that dramatically increases the risk for Alzheimer’s disease and converted it into a less harmful (null effect) gene (APOE e3). The prospect of gene editing or using small molecules among carriers of this high-risk gene is now a possibility for millions of adults who are at greater risk to develop Alzheimer’s memory loss.
The gene editing breakthrough was announced in the journal Natural Medicine in April of 2018. A new technology called CRISPR that allows genetic material to be added, removed or altered is one such technology.
But wait! Before such new technologies are given the green light, maybe society should understand the pitfalls and the cost and any alternatives.
According to the National Institute on Aging about 25% of people carry a copy of the APOE e4 cholesterol carrier gene that dramatically increases the risk for Alzheimer’s disease. However, some people with APOE e4 gene never develop Alzheimer’s disease, so there are unexplained factors. And if you make it beyond age 80 without developing Alzheimer’s, you’re no longer at elevated risk, even being an APOE e4 carrier. Yet an estimated 75 million Americans have a single copy of the APOE e4 gene that modern medicine chooses not to ignore.
23andMe has received approval for its health risk gene test kit and among other genes, determines whether a person carries one or two copies of the APOE e4, which, as previously stated, is the strongest genetic risk factor for Alzheimer’s disease. The cost of the test is ~$100-160.
To find all of the human carriers of the APOE e4 gene in their brain cells, obviously millions of adults would need to be screened. Only 1 in 4 people tested would be APOE e4 positive. The cost to screen for this risk factor in the population at large would be over 100 billion dollars.
Then presume a gene editing technology like CRISPR or some other small molecule technology would repair the APOE e4 gene or convert it to APOE e3, which neutralizes risk. Let’s say such a technology would cost just $2500. That is a very low price. If modern medicine attempts to treat just 1 in 10 APOE e4 subjects, or 7.5 million adults @$2500, that would run up a bill of $18.7 billion for treatment. Treat all 75 million Americans with APOE e4 and it would cost $187.5 billion! That is more than three times the total cost to provide healthcare to retirees in America annually under the Medicare program, which of course, would be absurd.
Adults who mothers and fathers developed Alzheimer’s disease are likely the most fearful of this brain disease and most likely to opt for the APOE e4 gene test.
A news report says: “When a former nurse learned that she carried two copies of a gene called ApoE4, she was reported to have “lost hope and direction,” and her “days were filled with fear, anxiety and sadness.” It meant that as she got older, she would likely develop Alzheimer’s disease, as her father had done before her.” But there are those who really don’t want to know they will lose their memory and become feeble as they age. According to a New York Times report, those who bury their heads and don’t want to know include James Watson, a co-discoverer of the DNA double helix. He deliberately decided to redact his ApoE4 sequence.
There is considerable evidence that APOE e4 gene carriers either have low levels of DHA-omega-3 fish oil in their diet or that DHA-omega-3 is degraded or metabolized among APOE e4 subjects.
Scientific studies show that APOE e4 carriers transport less DHA-omega 3 oil to the brain than carriers of APOE e3 carriers. Therefore, it’s possible APOE e4 carriers simply need more DHA-rich fish oil to compensate for their genetic makeup. Metabolism of DHA-omega 3 is disrupted in APOE e4 carriers, which may result in cognitive (thinking) impairment.
A study concludes: “In E4 carriers, supplementation with DHA as early as possible might help to prevent the onset of Alzheimer’s disease and could halt the progression of, and reverse some of the neurological and behavioral consequences of their higher vulnerability to omega-3 deficiency.”
In animals, DHA supplementation prevented cognitive decline in lab animals. Indeed, higher levels of EPA-DHA omega-3 oil have been shown to reduce the risk for memory loss in humans.
Recently researchers suggest APOE e4 carriers institute high-dose DHA supplementation “before the onset of Alzheimer’s disease dementia” and describe this as a “promising approach to decrease the incidence of Alzheimer’s disease.”
In laboratory animals the combination of DHA-omega-3 oil and the red wine molecule resveratrol (a copper chelator) limits inflammation in the brain and reduces APOE gene activity. Resveratrol, a copper binder, facilitates the disposal (efflux) of beta amyloid plaque in the brain.
There are obvious environmental and dietary factors that prevail over APOE e4 as it is more common in the general population residing in Northern Europe (61%) than in the Mediterranean regions of France and Italy or in Asia (40%). This suggests there may be natural gene editing factors on the diet, such as DHA-omega-3.
Only recently has it been reported that vitamin C and E supplement users experience a 40% reduction in risk for Alzheimer’s disease.
More recently a study conducted in Japan among females with the APOE e4 gene found a 90% reduced risk for mental decline that was associated with the highest blood levels of vitamin C; a 81% reduced risk was found for highest levels of vitamin E.
Among individuals with two copies of the APOE e4 gene, higher vitamin D levels are associated with better memory.
Causation of Alzheimer’s disease memory loss may be elusive due to many contributing factors. But a major underlying cause of brain disease originates in the age-related accumulation of metals in the brain.
Higher iron levels in the brain and lower zinc levels are commonly found in Alzheimer’s disease. Zinc helps to control iron.
APOE e4 is linked with higher iron levels in spinal fluid. Higher cerebrospinal iron (ferritin) levels predict conversion from mild mental impairment to Alzheimer’s memory loss. In a study conducted over two decades ago, the use of an iron-chelating (key-lay-ting) drug halved mental decline.
Blood letting to remove excess iron and iron-binding molecules like IP6 rice bran would be safe ways to reduce excess iron in the brain and blood circulation.
Zinc via its competition with iron also reduces accumulation of beta amyloid plaque in the brain.
Unbound copper in the brain distinguishes mild brain impairment from healthy individuals. For each unit of copper (micromole/liter) increment there is a 24% increased in the probability of mild thinking impairment. APOE e4 and unbound copper explain the beginnings of Alzheimer’s disease.
Given that red blood cells harbor most of the iron in the body as bound to hemoglobin, researchers hypothesize that blood letting (phlebotomy) would be useful in prevention and treatment of Alzheimer’s disease.
APOE e4 conversion therapy (APOE e4 to APOE e3) does not always delay or prevent the onset of Alzheimer’s brain disease. Nor does APOE e4 therapy address the cause of the disease, believed to be accumulation of unbound metals in the brain with advancing age. The news media, enthralled with high technology, has given undeserved attention to gene editing techniques that are simply unaffordable and waste limited financial resources. Metal chelation and blood letting address a primary driver of Alzheimer’s disease and DHA-omega-3 fish oil supplementation addresses a deficiency induced by the APOE e4 and may even convert APOE e4 to APOE e3. Vitamin supplementation appears to be very effective at reducing risk and progression of Alzheimer’s disease. These are cost effective approaches to APOE e4 associated memory loss. #### ©2018 Bill Sardi, Knowledge of Health, Inc.
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