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Alzheimer's Disease (AD)

Let's walk through this.

Alzheimer's is connected to beta-amyloid plaques in the brain.

What Happens to the Brain in Alzheimer's Disease?

Amyloid Plaques
The beta-amyloid protein involved in Alzheimer’s comes in several different molecular forms that collect between neurons. It is formed from the breakdown of a larger protein, called amyloid precursor protein. One form, beta-amyloid 42, is thought to be especially toxic. In the Alzheimer’s brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function. Research is ongoing to better understand how, and at what stage of the disease, the various forms of beta-amyloid influence Alzheimer’s.

And...β-amyloid Peptides and Amyloid Plaques in Alzheimer’s Disease

Many lines of evidence support that β-amyloid (Aβ) peptides play an important role in Alzheimer’s disease (AD), the most common cause of dementia. But despite much effort the molecular mechanisms of how Aβ contributes to AD remain unclear. While Aβ is generated from its precursor protein throughout life, the peptide is best known as the main component of amyloid plaques, the neuropathological hallmark of AD. 

Is there any researched association between increased Poison/"Vitamin A" content (carotenoids and retinol in this study) of the brain areas associated with Alzheimer's?  Yes.

Objective: To measure the major carotenoids, tocopherols, and retinol in frontal and occipital regions of human brain.

Design:  Ten samples of brain tissue from frontal lobe cortex and occipital cortex of five cadavers were examined.

Results: At least 16 carotenoids, 3 tocopherols, and retinol were present in human brain. Major carotenoids were identified as lutein, zeaxanthin, anhydrolutein, α- cryptoxanthin, ß- cryptoxanthin, α-carotene, cis- and trans-ß-carotene, and cis- and trans-lycopene. Xanthophylls (oxygenated carotenoids) accounted for 66-77% of total carotenoids in all brain regions examined.

Conclusions: The frontal cortex, generally vulnerable in Alzheimer’s disease, had higher concentrations of all analytes than the occipital cortex which is generally unaffected.

Greater concentrations of all things Poison/"Vitamin A" in the frontal cortex associated with Alzheimer's.  Now, let's dive right in. Poison/"Vitamin A" has been shown to increase beta-amyloid plaque production in nerve cell lines, among other things!

Retinol (Vitamin A) Increases α-Synuclein, β-Amyloid Peptide, Tau Phosphorylation and RAGE Content in Human SH-SY5Y Neuronal Cell Line.

Retinoids (vitamin A and derivatives) are recognized as essential factors for central nervous system (CNS) development. Retinol (vitamin A) also was postulated to be a major antioxidant component of diet as it modulates reactive species (RS) production and oxidative stress in biological systems. Oxidative stress plays a major role either in pathogenesis or development of neurodegenerative diseases, or even in both. Here we investigate the role of retinol supplementation to human neuron-derived SH-SY5Y cells over RS production and biochemical markers associated to neurodegenerative diseases expressed at neuronal level in Parkinson's disease and Alzheimer's disease: α-synuclein, β-amyloid peptide, tau phosphorylation and RAGE. Retinol treatment (24 h) impaired cell viability and increased intracellular RS production at the highest concentrations (7 up to 20 µM). Antioxidant co-treatment (Trolox 100 µM) rescued cell viability and inhibited RS production. Furthermore, retinol (10 µM) increased the levels of α-synuclein, tau phosphorylation at Ser396, β-amyloid peptide and RAGE. Co-treatment with antioxidant Trolox inhibited the increased in RAGE, but not the effect of retinol on α-synuclein, tau phosphorylation and β-amyloid peptide accumulation. These data indicate that increased availability of retinol to neurons at levels above the cellular physiological concentrations may induce deleterious effects through diverse mechanisms, which include oxidative stress but also include RS-independent modulation of proteins associated to progression of neuronal cell death during the course of neurodegenerative diseases.

I want to make the above crystal clear.

Excess Poison/"Vitamin A" made EVERY SINGLE MARKER OF NEURODEGENERATION they measured--which are related to Parkinson's and Alzheimer's--WORSE!!!  It "impaired cell viability" (viability being the ability to survive or live successfully).  That's really bad.

A quick summary of the other neuroDEGENERATIVE markers that Poison/"Vitamin A" INCREASED in the nerve cell lines:

  • Increased RS (Reactive Species, aka Reactive Oxygen Species, aka ROS). "A type of unstable molecule that contains oxygen and that easily reacts with other molecules in a cell. A build up of reactive oxygen species in cells may cause damage to DNA, RNA, and proteins, and may cause cell death. Reactive oxygen species are free radicals. Also called oxygen radical."
  • Increased alpha-synuclein. "Substantial genetic, neuropathological, and biochemical evidence implicates the presynaptic neuronal protein α-synuclein in Parkinson's disease and related Lewy body disorders."
  • Tau phosphorylation. "In particular, aberrant tau phosphorylation is acknowledged to be a key disease process, influencing tau structure, distribution, and function in neurons. [...] Here we review the evidence showing that tau phosphorylation plays a key role in neurodegenerative tauopathies."
  • RAGE (Receptor for Advanced Glycation Endproducts).  "Extensive evidence has implicated RAGE as a critical player in regulating inflammation, as well as oxidative and cellular stress in a variety of organ niches and disease settings, including the CNS during neurodegeneration []."

It looks to me like retinol is a perfectly designed compound to slowly destroy the brain.

Taking a tangent for a second.  I want to cover the subject of aluminum in Alzheimer's.  Is aluminum toxicity likely related to Alzheimer's?  Yes, I believe so.  I also believe that the FOUNDATION of Alzheimer's is Poison/"Vitamin A".  It should be noted that aluminum is used as an adjuvant in vaccines (with its safety greatly in question, see link), and that Poison/"Vitamin A" has also been studied for its potential use as a (vaccine) adjuvant, so there is that relation.  In the next study, cells that were differentiated using retinoic acid (Poison/"Vitamin A") that were then exposed to aluminum, formed more tau proteins (see above) even at very low concentrations of aluminum!

Effects of aluminum on tau proteins in human neuroblastoma cells.

The presence of the trivalent metallic cations, aluminum and boron, in the culture medium of differentiated human LAN-5 neuroblastoma cells results in increased amounts of specific isomers of microtubule-associated tau proteins. The cells were differentiated to a neuronal phenotype by the addition of retinoic acid. Six-day exposures of the differentiated cells to a 1-mM dose of aluminum or boron yielded increases in tau protein immunoreactivity to the monoclonal antibodies Tau-1 and Alz-50. Significant increases in immunoreactivity were seen at treatment levels of aluminum down to 100 microM. The increases in tau proteins were independent from increases in levels of total cell protein. Control cultures treated with the divalent cations zinc and iron showed no increases in levels of tau proteins.

To understand what was going on up there, the nerve cells were first bathed in a foundation of Poison/"Vitamin A", then exposed to aluminum (down to very low doses), and it was observed that they formed more tau proteins and also had more immunoreactivity.  Let's take a second to go into "immunoreactivity":

  • Immunoreactivity is a measure of the immune reaction caused by an antigen.
  • Antigens are a toxin or other foreign substance which induces an immune response in the body, especially the production of antibodies.
  • Both aluminum AND Poison/"Vitamin A" have been studies as ADJUVANTS.  I consider both of them ANTIGENS, in the toxin aspect mentioned just above.

[SIDE NOTE for those that noticed boron in the above.  I believe boron is generally helpful and that many are deficient.  In my programs, we "test, don't guess, then address" boron levels through hair mineral analysis.  I personally take boron regularly to the level that my hair mineral analysis suggests.  I do believe the people out there doing massive drug-level doses of boron, typically through drinking Borax solutions, may be causing themselves problems.  The study above shows one potential example of excessive boron potentially causing neurological toxicity.  My approach stays with nutritional-level doses of boron, NEVER with drug-like, aka supraphysiological, aka "orthomolecular" doses trying to FORCE the body to do something.]

What does all this in combination mean?

What is an Adjuvant?

What role does the Adjuvant play in Antibody Development?
Directly immunizing most antigens will lead to a poor immune response and rapid removal of the antigen from the body. To prevent this, the antigen is first combined with an adjuvant, which is a material that helps stimulate and enhance the immune response against the antigen through the creation of a depot effect. By forming a stable emulsion between the antigen and adjuvant, a sustained presentation of the antigen to the immune system is permitted and removal of the antigen from the body is delayed."

So what they're saying is that cells that were first exposed to retinoic acid (toxin-antigen-adjuvant), then to aluminum (toxin-antigen-adjuvant), had a significantly higher immune reaction!  Should we be surprised at that, with what we know about them now?

Note the "depot effect" mentioned above.  A depot is a body area (the BRAIN is one of these) in which a substance can be accumulated, deposited, or stored.  Maybe you've heard of aluminum depots/deposits in the areas of the brain related to Alzheimer's?  Let me show you.

Aluminium in brain tissue in familial Alzheimer's disease.

One such environmental factor is human exposure to aluminium and aluminium has been shown to be present in brain tissue in sporadic Alzheimer's disease. We have made the first ever measurements of aluminium in brain tissue from 12 donors diagnosed with familial Alzheimer's disease. The concentrations of aluminium were extremely high, for example, there were values in excess of 10μg/g tissue dry wt. in 5 of the 12 individuals. Overall, the concentrations were higher than all previous measurements of brain aluminium except cases of known aluminium-induced encephalopathy.

I believe that aluminum is a problem that is layered on top of the Poison/"Vitamin A" foundation.

Let's come back around to that first retinol paper we had started working on.  When they gave Trolox, it helped improve several of the problems the retinol caused.  What is Trolox?

"Trolox is a water-soluble analog of vitamin E sold by Hoffman-LaRoche."

Hoffman-LaRoche.  The largest manufacturer of Vitamin A products in the world.  Curious, right?  It is important to note that the Trolox did NOT undo ALL the damage the retinol caused though!

I have written another huge article about how Vitamin E is extremely protective against Poison/"Vitamin A" toxicity.  This is all fitting together nicely already.

Next, the researchers in this study were quite confused when they found that the enzyme pathway that makes retinoic acid--the most damaging of all the forms of Poison/"Vitamin A"--was 1.5-2X HIGHER in Alzheimer's brain tissue samples!

Retinoic acid synthesis in normal and alzheimer diseased brain and human neural cells

In these studies, extracts of autopsy tissues recovered from histopathologically confirmed control and Alzheimer diseased brains were tested for their ability to synthesize retinoic acid. Retinaldehyde dehydrogenase (RLDH), the enzyme that forms retinoic acid from retinaldehyde, was present in hippocampus, frontal cortex, and parietal cortex. The RLDH activity of hippocampus and partietal cortex from Alzheimer diseased brains was 1.5- to 2-fold higher (p<0.05) compared to the controls.
These studies establish the presence of retinoids and RLDH activity in human brain tissues, and indicate that retinoic acid synthesis is modulated in some regions of Alzheimer diseased brain.

The following is a great research review paper covering the MANY research-demonstrated neurotoxic effects of retinoids (Poison/"Vitamin A"), I'm going to include the parts of it that relate to Alzheimer's, beta-amyloid plaques, and the other markers of neurodegeneration mentioned above:

The neurotoxic effects of vitamin A and retinoids

An introduction:

Even though vitamin A and its derivatives are essential during both development and maintenance of central nervous system activity, there is a considerable body of evidences showing that vitamin A concentrations exceeding that which is required for normal function of cells lead to deleterious effects including disruption of the redox environment, mitochondrial dysfunction, and induction of cell death, as discussed below (Napoli 1999Myhre et al. 2003Lane and Bailey 2005).

What is the "concentrations exceeding that which is required for normal function of cells", exactly?  What I can tell you is that no one knows, and the number seems to be shrinking more and more as real science on the topic comes out.  I believe the amount NEEDED by cells, assuming a diet adequate in fats, proteins, and other micronutrients, is ZERO.  I have other posts that go into this.

Increases oxidative stress, increases reactive (oxygen) species, decreased viability, loss of viability:

All-trans-retinoic acid, a retinoid originated from retinol, is able to induce oxidative stress in cultured Sertoli cells (Conte da Frota et al. 2006), but not in PC12 cell line (Gelain and Moreira 2008), which is derived from pheochromocytoma of rat adrenal medulla (which is, in turn, originated from the neural crest) and produces dopamine and norepinephrine. In PC12 cell line treated with retinol, increased rates of reactive oxygen species production through a real-time 2′,7′-dichlorohydrofluorescein diacetate (DCFH-DA) assay designed for live cells were observed (Wang and Joseph 1999). Also, decreased viability was reported in PC12 cells treated with retinol. DCFH-DA serves as a probe to detection of hydrogen peroxide, hydroxyl, and peroxyl radicals (LeBel et al. 1992). Then, retinol, but not all-trans retinoic acid may alter redox environment of such catecholamine producing cells, possibly leading to loss of viability by a mechanism that may be associated to its ability to act as a pro-oxidant. 

Common clinical doses of retinyl palmitate caused multiple "disturbances" in rat brains:

Actually, it was reported that vitamin A supplementation (in the form of retinol palmitate) at doses commonly utilized clinically (1,000 to 9,000 IU/ for 3, 7, or 28 days) induced some redox disturbances in the nigrostriatal axis of adult male rats. Increased lipid peroxidation, protein carbonylation, and oxidation of protein thiol groups were observed in the substantia nigra and striatum of vitamin A-treated rats (De Oliveira et al. 2007a, 2008). 

Poison/"Vitamin A" increases susceptibility of mitochondria to later chemical insults (ie. reduced the resilience of the mitochondria to resist damage of multiple types):

Interestingly, it was reported that in vivo retinol palmitate supplementation increased in vitro susceptibility of mitochondrial to different challenges. Mitochondria were isolated from substantia nigra, striatum, frontal cortex, and hippocampus and challenged with H2O2, β-amyloid peptide1-40, and CaCl2and it was observed an increased impact of each challenge on mitochondria that were isolated from retinol palmitate-treated rats (De Oliveira et al. 2012ab). It suggests that prior vitamin A supplementation may increase vulnerability of mitochondria to posterior chemical insult that affect mitochondrial electron transfer chain activity, for example, as demonstrated. Thus, excessive intake of vitamin A may, at least in part, facilitate neuronal abnormalities (including both redox and bioenergetics states) that may appear from other pathological event, as for instance increased rates of β-amyloid peptides production in the case of Alzheimer disease.

Increased alpha-synuclein:

Sub acute vitamin A supplementation also increased both 3-nitrotyrosine (total and mitochondrial) and α-synuclein contents in the rat substantia nigra and striatum (De Oliveira et al. 2012a).

Beta-amyloid plaque and tumor necrosis factor-alpha (TNF-alpha) formation:

More recently, De Oliveira et al. (2012a)demonstrated that vitamin A supplementation at 500 to 2,500 IU/ mitochondrial dysfunction and increased β-amyloid1-40 peptide and tumor necrosis factor-alpha (TNF-α) contents in substantia nigra and striatum of adult rats.


In another study, it was observed that vitamin A daily administrated to rats is able to increase receptor for advanced glycation endproducts (RAGE) immunocontent in rat cerebral cortex (De Oliveira et al. 2009e). This receptor is implicated in the amplification of oxidative stress by a neuroinflammation-related mechanism (Brownlee 2000Schmidt et al. 2001Bierhaus et al. 2005). Moreover, RAGE may play a crucial role in the onset and progression of Alzheimer's disease, as previously postulated (Sato et al. 2006). In fact, RAGE mediates the transport of β-amyloid peptides from blood to brain across the blood-brain barrier (Deane et al. 2003) and possibly plays a crucial role in the onset of Alzheimer's disease in diabetic patients. Additionally, sustained RAGE activation may trigger cell death and tissue dysfunction (Bierhaus et al. 2005). More investigations are needed to better address the role of vitamin A on inducing RAGE activation in brain.

Here's a graphic from that paper that shows all the nasty changes in the brain and nervous system from "excess Vitamin A":


Figure 1 - A summary of possible effects elicited by vitamin A (either retinol or retinol palmitate) on the mammalian central nervous system. It has been demonstrated that vitamin A supplementation (in the form of retinol palmitate or retinol) is able to induce an increase in the immunocontent of RAGE, which mediates neuroinflammation in some experimental models. Additionally, such supplementation may lead to altered redox environment parameters, which has been evidenced as oxidative and nitrosative stress. Moreover, vitamin A supplementation induces mitochondrial dysfunction in vitro and in vivo. Increased levels of O2-• may affect the function of several enzymes, including catalase (CAT) and Mn-superoxide dismutase (Mn-SOD, the mitochondrial isoform of SOD). Furthermore, O2-• may be a consequence of impaired electron transfer chain due to vitamin A-dependent electron leakage from that complex system. Vitamin A, which is liposoluble, may interact with mitochondrial membranes disrupting the normal flow of electrons between mitochondrial complexes, which in turn may favor abnormal electron flux. Alternatively, increased activity of this system may be due to an augmentation in the need for adenosine triphosphate (ATP) in acute phases of intoxication with vitamin A. Both Mn-SOD and monoamine oxidase (MAO) enzyme activities may lead to increased hydrogen peroxide (H2O2) production, which may diffuse from mitochondria to other organelles. Increased levels of oxidative and nitrosative stress markers may induce α-synuclein aggregation, which may interact negatively with mitochondria (please see text for details). General cell dysfunction and cell death may result if vitamin A concentration remains elevated. Other effects may be induced by vitamin A and/or retinoids on neuronal cells. This figure represents just a summary of some of them. 

The next study is important, as it shows an association between higher blood Poison/"Vitamin A" (both carotenoids AND retinol) with a higher risk of Alzheimer's!

Circulating antioxidants and Alzheimer disease prevention: a Mendelian randomization study

In order to infer whether long-term circulating antioxidant exposure plays a role in AD etiology, we tested the hypothesis that AD risk would be lower in individuals with lifelong, genetically predicted increases in concentrations of 4 circulating antioxidants that are modifiable by diet.

The bolded part above shows that these scientists had a plan going in. They really wanted to show that more antioxidants = less Alzheimer's.  They presented what they found in that vein as best as they could (trying to minimize the unwanted results that showed up).

Our findings suggest that higher exposure to ascorbate, β-carotene, retinol, or urate does not lower the risk of AD.

It "does not lower the risk of AD".  What if it actually raised it?  Keep reading.

SNPs instrumenting β-carotene are in beta-carotene oxygenase 1 (BCO1/alias BCMO1), which encodes the enzyme carotenoid 15,15′-monooxygenase, responsible for catalyzing the cleavage of carotenoids into retinal in the small intestine (). Rare loss-of-function mutations in this gene can produce hypercarotenemia, because excess carotenoids are not removed from circulation (as required for hepatic storage in the form of vitamin A) ().

This is really important for other reasons.  If carotenoids can't be broken down, then they accumulate.  Regardless of what you've heard elsewhere, carotenoids are toxic by themselves, and are the ROOT of all food-sourced Poison/"Vitamin A" problems everywhere.

The SNP used to instrument retinol is located near retinol binding protein 4 (RBP4), encoding retinol-binding protein 4, the major carrier that facilitates the transport of retinol from liver stores to peripheral tissues. Deleterious mutations in RBP4 produce nominal circulating retinol () and may lead to vitamin A–related disorders, such as retinitis pigmentosa ().

A lack of RBP relative to retinol levels means more damage from Poison/"Vitamin A", PARTICULARLY TO THE EYES (xerophthalmia, night blindness, retinitis pigmentosa) spite of significantly lower circulating Poison/"Vitamin A".  It's really THAT toxic if it is free to run around.

Ensuing Wald estimators for these 3 traits were then scaled to be expressing AD risk as ORs [Odds Ratios, a measure of association between an exposure and an outcome] with CIs [Confidence Interval] according to 10% relative increases in concentrations of β-carotene and retinol.

Only a 10% relative increase in beta-carotene or retinol.  That's not much.

Higher predicted exposure to circulating β-carotene was associated with marginally elevated AD risk—although the OR was similar to results for other antioxidants, it was estimated with more precision.

More exposure to beta-carotene was associated with elevated AD risk!  Boy, that's not what everyone else likes to spew!

The most prominent exceptions were inverse associations of β-carotene with triglycerides [higher beta-carotene goes with lower triglycerides], and retinol with smoking initiation, and possible associations of retinol with higher BMI [higher retinol goes with being fatter] and urate with higher triglycerides (however, no association would survive Bonferroni correction for multiple testing).

Re-stating the most important things from above:

  • higher retinol went with higher BMI (being fatter)
  • higher urate went with higher triglycerides

Another study showed that higher urate (uric acid) levels go with higher retinol levels.  Do you see how this all lines up?

All estimates of effects of antioxidant exposure on AD risk were close to null, with ORs for retinol, β-carotene, and urate >1, implying that higher exposure confers slightly more risk of AD (if any difference at all), rather than neuroprotection.

So they're saying that any ORs over 1, implying higher exposure to that "antioxidant" is associated with a higher risk of AD, and is NOT protective.  What were the ORs, you ask?

Beta-Carotene, Odds Ratio = 1.02

Retinol, Odds Ratio = 1.05

Urate, Odds Ratio = 1.03

Higher beta-carotene was associated with higher risk for AD.

Higher retinol was associated with higher risk for AD.

Higher urate (which goes with higher retinol levels, see previous link above) was associated with higher risk for AD.

In conclusion, this evidence casts doubt on the role of several circulating antioxidants in AD prevention and suggests caution toward planning RCTs to test the effect of related nutritional supplements or urate-elevating therapeutics on AD risk.

I'd say it does a lot more than just "casts doubt".

There are lots out there THEORIZING that Poison/"Vitamin A" retinoids would be good for treating Alzheimer's though!  That is, except for those pesky safety issues!

Not a single study actually showing results on AD patients, just a bunch of talk about "how great it SHOULD work". Wait, I found a study.

Bexarotene in the next study is a retinoid (Poison/"Vitamin A") that was designed/intended to be used for CHEMOTHERAPY.  I don't know about you, but I don't associate the words "chemotherapy" and "healthy" in any way, shape, or form.

Bexarotene cannot reduce amyloid beta plaques through inhibition of production of amyloid beta peptides: in silico and in vitro study.

This result has been also confirmed by our in vitro experiment implying that bexarotene cannot clear amyloid plaques through inhibition of Aβ [amyloid-beta plaque] production.

Whoops, well that didn't work!  At all.

If the folks with Alzheimer's actually had Poison/"Vitamin A" toxicity when the studies started, and then they gave them retinoids of any type, I can tell you how it will go.  Badly.  VERY badly.  Maybe that's why I can't find any published human studies after 7 years?  There are no coincidences.

Next is an example of why I refer to myself as the "Nutrition Detective".  I'm going to show you the clues in this article about a mysteriously high occurrence of Alzheimer's (and Amytrophic Lateral Sclerosis, aka ALS, aka Lou Gehrig's Disease -like symptoms) in a specific area of Guam.  The scientist described in this article is looking in the right place, but at the WRONG compound.

Could This Radical New Approach to Alzheimer’s Lead to a Breakthrough?

Big Pharma has spent billions and gotten nowhere. Here's what we could learn from a new theory.

Spoiler:  Their new theory is wrong and will go nowhere too.  It's a red herring (something, especially a clue, that is or is intended to be misleading or distracting).

Our unusual tale begins with ethnobotany: the study of the way indigenous people use plants in their customs and diet.

Yes, plants are at the root of this problem.

Cox’s interest in neuro­degeneration began when he set out to solve a puzzle that had bedeviled researchers for decades: Why did an extraordinary number of the Chamorro people of Guam develop an odd hybrid of ALS and Alzheimer’s symptoms? Cox’s answer: They had been poisoning themselves every time they indulged in their greatest culinary delight, a bat boiled in milk—eyeballs, wings, and all.

So they are poisoning themselves with a traditional food, you say?

They're eating every part of a type of bat (aka flying fox), you say?

Note that means that they are eating all of the ORGANS, including the LIVER.  The organs, particularly the liver, are the highest sources of Poison/"Vitamin A".

Boiling it in milk, you say?

I consider dairy products to be a nearly "perfect storm" of Poison/"Vitamin A" and its additional negatively synergistic cofactors (high calcium content, Vitamin D content, and casein content being the biggest ones).

So we have the setup for a Poison/"Vitamin A" problem.  The next question is, what do these bats eat?  Is it particularly high in anything related to Poison/"Vitamin A"?

Cox approached the mystery through the lens of ethno­botany—examining the Chamorro not in the clinic, but in their culture. “And we discover that the flying fox is the most important item in their whole diet,” he said. “They identify themselves as the hunters of flying foxes. One village elder told me, ‘You don’t get this. I would not sell one of those for any price. If I had one, I would lock the door, bolt the windows, cook it, and eat it, and people would be trying to break in to get some.’ ”

Cox believed that this culinary predilection might explain lytico-bodig. One clue was that only older generations of the Chamorro got ill. They had hunted the native bats into extinction. Young Chamorro, who hadn’t grown up feasting on those flying foxes, weren’t getting sick. A second clue was that the Guam bats lived on cycad seeds.   If, as Cox believed, BMAA (or another noxious substance) accumulated and magnified over time in bat fat, then every bowl of flying fox stew was toxic.

Poison/"Vitamin A" is fat-soluble.  As I've shown above, it is capable on its own of causing every single marker known associated with the neurodegenerative changes associated with Alzheimer's.

The next question becomes, are cycad seeds high in carotenoids?

Seed coat carotenoids of the cycad genera Dioon, Encephelartos, Macrozamia and Zamia: Evolutionary significance

Lycopene is the principal pigment of Zamia while Encephelartos, Dioon and Macrozamia coats contain a mixture of the unsubstituted, mono-and di-hydroxy-β-carotenes.

Limited data on ripe seed coat carotenoids indicated a simple mixture of classic carotenoids occurring in the chromoplasts of seeds of some cycads (Bouchez et al., 1970; Baumann and Yokoyama, 1976; Whatley, 1985).

I'd say that if there are multiple entire studies examining the carotenoid content of cycads, there's probably a lot there to investigate.

It must always be remember that ALL forms of Poison/"Vitamin A" in the world are due to carotenoids, which animals and humans either consume directly via plant foods (including algaes, as discussed in the article elsewhere) and then convert to retinol themselves, or they eat retinol by eating other animals (particularly the liver).

So, let's summarize the clues in this sad mystery in Guam:

  • Cycad seeds are full of carotenoids, aka the root source of all Poison/"Vitamin A".
  • These bats feed on cycad seeds almost exclusively.
  • The suspected "toxin" in these bats is thought to be fat-soluble and accumulates in their tissues.  These are all characteristic qualities of Poison/"Vitamin A".
  • Carotenoids and retinoids (each beta-carotene molecule that is cleaved by animals can turn into two retinol molecules, and carotenoids in the skin can be converted into retinyl esters and re-released into the circulation to be stored in the liver) would accumulate in all parts of these bats.
  • Eating the entire bat, which is done, would maximize Poison/"Vitamin A" intake by consuming all the organs (liver) and all the skin (where carotenoids particularly accumulate).
  • Boiling the bats in milk, which is done, would not only add the "perfect storm" of Poison/"Vitamin A" problems that are inherent in all would also contribute fat, which is utterly NECESSARY for the carotenoids to be absorbed from these bats.
  • The obvious sign that the root of this problem is from consuming these bats is shown in the fact that the younger generations are not getting Alzheimer's like the older generations...because these bats have been hunted to extinction.  The root source of the poisoning (cycad seeds -> bats -> humans -> Alzheimer's) has been eliminated.

That was fun, and it didn't take billions of dollars, did it?!?!

This next part is more connections, but you'll have to look deeper for them, as they are not obvious without some background.

The first thing you must know about is the "Duration Paradox" of Poison/"Vitamin A".  This is the observed phenomenon that any disease/condition/issue that Poison/"Vitamin A" seems to help in the beginning stages, will eventually be completely DESTROYED by Poison/"Vitamin A".  It's why many in vitro ("petri dish") studies look promising short-term, and then end up later causing or aggravating the very problems they were trying to fix in vivo (in real people) long-term.

This is what will eventually happen with the Yarumal people in Colombia, who will be Guinea pigs for new Poison/"Vitamin A" related drugs, I'm sure.

Colombian villagers worry over 'Yarumal curse'

Yarumal, a Colombian village perched in the Andes Mountains, has a high incidence of a genetic mutation that predisposes its population to Alzheimer’s — a bleak heritage that scientists now hope could help lead to a treatment to prevent the disease.
Inherited from the village’s European ancestors, the “paisa” genetic mutation — named for the residents of the Colombian province of Antioquia — causes a devastating form of early-onset Alzheimer’s.

A single parent can hand down the mutation, located on the 14th chromosome.

Those who have it have a 50 per cent chance of developing Alzheimer’s, sometimes by age 40.
The trials are part of a US$100 million (RM350 million) project financed by the National Institutes of Health and Banner Research Institute in the United States, as well as Swiss pharmaceutical group Roche.

Let's first understand just how important Vitamin A is to Roche, the gigantic pharmaceutical company:

Roche Vitamin Plant, Taishan, Shanghai

Roche Holding opened this plant for the manufacture of vitamin A as part of its joint venture (JV) with the Shanghai Number Six Pharmaceutical Factory. The JV was formed in 1995 and Roche took a 70% stake.
The vitamin plant commenced production in October 1999, slightly after the expected deadline. The plant is the largest vitamin A plant in China and was built at a cost of $25m.

Wow.  In 1999 dollars (that's 20 years ago!), the factory cost $25 MILLION to build.  Imagine that in today's dollars.  All to make a plant that makes ONE vitamin!

Why China?  Well, if you read my other post on Poison/"Vitamin A" and the Gates Foundation, and then you realize the population that China has, you might start putting 2+2 together.

So these researchers are studying a gene called Presenilin-1 (PS1 aka E280A).  Is it connected to Poison/"Vitamin A" at all?  All the following studies are looking at Presenilin and utilize retinoic acid in the process:

In all those in vitro ("petri dish" type) studies above, they are using retinoic acid (the most damaging form of Poison/"Vitamin A") to induce differentiation (the process by which a less specialized cell becomes a more specialized cell type).  One must remember the Duration Paradox rule I mentioned above.  If things look good in the petri dish short-term, they will be disastrous in humans long-term.  You don't have to believe me, that's just the way it is.

What are we seeing these days in people's brains as they age?  What's that? Alzheimer's is happening EARLIER in life to people (link below is from the Alzheimer's Association), almost as if they are being poisoned earlier in life than they used to be?  Interesting coincidence:

What is Alzheimer's? - Younger/Early Onset

Who gets early-onset Alzheimer's?
Many people with early onset are in their 40s and 50s. They have families, careers or are even caregivers themselves when Alzheimer's disease strikes. In the United States, it is estimated that approximately 200,000 people have early onset.

Once you understand the EPIDEMIC of chronic insidious Vitamin A toxicity, and how glyphosate/Roundup has contributed, and you see that all things related to it are getting WORSE and not better, then it all makes sense.  Everything, that is, except how all the scientists, doctors, politicians, billionaires, and so many others let it get this far!

So, in summary:

  • Higher concentrations of carotenoids and retinol in the brain areas associated with Alzheimer's.
  • Nerve cells cultures showed an increase in every degenerative marker measured after exposure to Poison/"Vitamin A".
  • Various forms of Poison/"Vitamin A" have been shown to be neurotoxic in nearly every single way that scientists know how to assess it.
  • Alzheimer's is happening earlier and earlier in people, suggesting that the main cause has NOT been addressed at all, and that the cause of the problem is actually worsening.
  • A large human study suggests that increased exposure to beta-carotene AND retinol over the long-term increases one's risk of Alzheimer's Disease.
  • Researchers theorize that retinoids could be used to treat Alzheimer's, YET one study on a retinoid in neuronal cell cultures showed that it did NOT reduce beta-amyloid plaques at all.  It didn't work!
  • It was mentioned in 2012 that studies on the use of retinoids in human Alzheimer's were already in process.  As far as I have seen, there have been NO successful treatment papers published. The ASSumption then must be that it DIDN'T WORK, and the studies were simply buried.
  • The Presinilin-1 gene expression in the Yarumal people of Colombia probably suggests that they have impaired Poison/"Vitamin A" metabolism or are more sensitive to the damaging effects of Poison/"Vitamin A" in the brain.  This means that they show the neurodegenerative changes in greater numbers and earlier than others without the gene.

If you like your brain, you should NOT like Poison/"Vitamin A".

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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