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Anti-malarial drugs block Poison/"Vitamin A" metabolism, cause mental toxicity

Let's walk through this.

First, has Poison/"Vitamin A" been shown to cause neurological (brain and nervous system) disorders, from both natural and synthetic sources?  Yes.

The neurotoxic effects of vitamin A and retinoids

In spite of this, there is a growing body of evidences showing that vitamin A doses exceeding the nutritional requirements may lead to negative consequences, including bioenergetics state dysfunction, redox impairment, altered cellular signaling, and cell death or proliferation, depending on the cell type. Neurotoxicity has long been demonstrated as a possible side effect of inadvertent consumption, or even under medical recommendation of vitamin A and retinoids at moderate to high doses.
Disturbances related to nervous functions also appear on the list of side effects resulting from excessive vitamin A intake, as for instance confusion, irritability, anxiety, depression, and suicide ideation (Snodgrass 1992). However, such central effects are more commonly observed after chronic vitamin A exposition.On the other hand, acute behavioral impairment was reported in individuals that experienced high vitamin A concentrations due to consumption of bear liver. Such altered behavior was called "polar hysteria" and was compared to schizophrenia (Rodahl and Moore 1943Restak 1972).

From the above, we know now that polar bear liver, a fully natural source of Poison/"Vitamin A", can cause all sorts of mental issues, all the way up to schizophrenia and suicidal ideation!  It could be assumed that lower levels of toxicity would then be capable of causing lower-level symptoms, such as the irritability, anxiety, and depression mentioned.

Accutane, a concentrated form of retinoic acid (the absolute worst form of it), has also been shown to drastically increase depression and suicide risk.

So what we see is that when the Poison/"Vitamin A" levels rise too high in the system, then we can see mental symptoms ranging all the way from depression to schizophrenia to suicide.

I'm going to tell you that elevated Poison/"Vitamin A" can come about from one of two ways.  One way, the obvious one, is too much coming in (diet, supplements, skincare, etc.).  The other one, that is even MORE problematic, is when the liver loses its ability to break it down (so it builds up, just like if the drain on a tub was blocked).

Now, I'm going to suggest that some anti-malarial drugs that have a large history of causing mental issues--like schizophrenia--likely gain their effectiveness against malaria by raising the Poison/"Vitamin A" in the body, which kills the malaria parasite along with causing Poison/"Vitamin A" toxicity!  Will I provide a trail you can follow to this conclusion?  If you know me at all, of course I will!

In the next study, they presented that retinol (Poison/"Vitamin A") by itself was anti-malarial, particularly at doses that were TOXIC.  They also showed that an anti-malarial drug (chloroquine) worked synergistically with retinol to kill the malaria.

Interactions between Retinol and Some Established Antimalarials in Plasmodium yoelii nigeriensis Infection in Mice

The result of the study showed that retinol increased the antiplasmodial effect of chloroquine...

...several studies suggest that it [Vitamin A] could play a role in potentiating resistance to malaria.  In an in vitro study by Hamzah et al. (2004), direct antiplasmodial effect was confirmed across all stages of parasite development but at actual media retinol concentration that were above the range in normal human serum.

We have also shown in vivo, using malaria models in rodents that retinol possesses some degree of antiplasmodial activity and that toxic doses led to total parasite clearance (Oreagba and Ashorobi, 2006).

Mefloquine use, psychosis, and violence: A retinoid toxicity hypothesis

Mefloquine use has been linked to severe gastrointestinal and neuropsychiatric adverse effects, including cognitive disturbances, anxiety, depression, psychosis, and violence. The adverse effects of the drug are thought to result from the secondary consequences of hepatocellular injury; in fact, mefloquine is known to cause a transient, anicteric chemical hepatitis. However, the mechanism of mefloquine-associated liver damage and the associated neuropsychiatric and behavioral effects of the drug are not well understood. Mefloquine and other 8-amino-quinolines are the only antimalarial drugs that target the liver-stage malaria parasites, which selectively absorb vitamin A from the host. Vitamin A is also stored mainly in the liver, in potentially poisonous concentrations. These observations suggest that both the therapeutic effectiveness of mefloquine and its adverse effects are related to the ability of the 8-aminoquinolines to alter the metabolism of retinoids (vitamin A and its congeners). Several lines of evidence support the hypothesis that mefloquine neurotoxicity and other adverse effects reflect an endogenous form of hypervitaminosis A due to a process involving: mefloquine-induced dehydrogenase inhibition; the accumulation of retinoids in the liver; retinoid-induced hepatocellular damage; the spillage of stored retinoids into the circulation; and the transport of these compounds to the gut and brain in toxic concentrations.

Note that chloroquine, a relative of mefloquine, also has toxic psychosis associated with it:

Prolonged neuropsychiatric effects following management of chloroquine intoxication with psychotropic polypharmacy

With subsequent widespread use of chloroquine, a drug developed as a less toxic replacement for quinacrine 3, similar idiosyncratic cases of intoxication 4-6 were soon reported. More recently, similar intoxicating effects from mefloquine, itself developed as a replacement for chloroquine 7, have become well characterized in the literature 8. Although the naturally occurring quinoline antimalarials have traditionally been considered free of such effects, cases of a related syndrome of intoxication have also occasionally been reported after relatively low doses of quinine 910 and quinidine 1112, suggesting a common intoxicating class effect.

Descriptions of chloroquine intoxication in the literature, commonly characterized as toxic psychosis, are similar to those associated with other quinolines and typically feature insomnia 1314, mania 1516, paranoia and persecutory delusions 17, and auditory and visual hallucinations 18. Symptoms of intoxication may resemble those of brief psychotic disorder but are more likely to include prominent visual hallucinations, anxiety, restlessness, agitation, and derealization 19. Suicidality is not uncommon reported 20, and reports of completed suicide 2122 attest to the potentially life‐threatening nature of such intoxication. Other symptoms of intoxication may include impulsivity, over‐talkativeness with flight of ideas, unprovoked laughing or crying 20, personality change, grandiosity, depersonalization 6, and delusional misidentification 23.

Occasionally, intoxication may also induce a delirium 24 or encephalopathy whose symptoms may include confusion 25, difficulties with concentration 26, memory loss and amnesia 27, and catatonia 28.

Although theories have been proposed to explain quinoline intoxication 2930, the precise pathophysiological basis of these effects remain unclear despite numerous molecular mechanisms having been identified experimentally.

And, in a similar vein to birth control pills--oral contraceptives--that inhibit alcohol dehydrogenase and cause Poison/"Vitamin A" toxicity by reducing the body's ability to get rid of has been shown that chloroquine (CQ) inhibits aldehyde dehydrogenase (ALDH1) and can then also cause toxicity by inhibiting proper detoxification of Poison/"Vitamin A":

Discovery of Novel Targets of Quinoline Drugs in the Human Purine Binding Proteome

Our results show that ALDH1 and QR2 are selective targets of the quinolines and may provide new insights into the mechanism of action of these drugs.
he quinolines were also found to interact with human ALDH1. ALDH1 was efficiently recovered from whole blood using γ-ATP and PQ- and HCQ-Sepharose. However, in vitro assays of ALDH1 in the presence of CQ revealed that CQ was a relatively weak inhibitor of ALDH1 at physiological levels of NAD+. This finding indicates that it is unlikely that ALDH1 is a target for the quinolines unless they accumulate to high levels within tissues. As a result, we hypothesize that ALDH1 is not involved in the antimalarial action of the drugs, but rather it may contribute to the side effects observed. For example, CQ actively accumulates to millimolar concentrations in tissues such as the skin and eye when administered at therapeutic levels (Lindquist, 1973Rynes, 1997). One of the major functions of ALDH1 in the eye is to generate retinoic acid (visual pigment) from retinaldehyde, and the prolonged use of CQ [chloroquine] or HCQ in the treatment of malaria, arthritis, or lupus can result in retinopathy and blindness as a result of the accumulation of retinaldehyde in the retina (Lindquist, 1973Rynes, 1997Van Beek and Piette, 2001).

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