So one treatment I’ve never experimented with is killing of parasites. I’ve just learn protozoa means micro parasites. Now I’ve had problems in my gut previously, mainly jock itch years ago which wouldn’t go away until I supplemented probiotics, and then just supplementing zinc and other supplements to keep it in bay. However I was still getting sore skin in that area if I smoked cigarettes, which was largely helped recently by taking selenium (even though I took every other essential nutrient under the sun). Other things with my gut is if I eat pizza or bread, especially with Tabasco sauce, I will get depressed and even triggered an emotional flashback by it once (something I’ve only been able to trigger with amygdala tickling, and recently, with dopamine precursors), i.e. my brain seems to be gluten sensitive. Regardless with all my stack I take I’ve never focused on killing parasites or micro parasites.
Now there is an interesting article here: Protozoa Could Be Controlling Your Brain
Some protozoa infect the brain of their host, shaping its behavior in ways most suited to the pathogen, even if it leads to the suicide of the host
THE ANCIENT DEBATE surrounding the existence of free will appears unresolvable, a metaphysical question that generates much heat yet little light. Common sense and volumes of psychological and neuroscientific research reveal, however, that we are less free than we think we are. Our genes, our upbringing and our environment influence our behaviors in ways that often escape conscious control. Understanding this influence, the advertisement industry spent approximately half a trillion dollars worldwide in 2010 to shape the buying decisions of consumers. And extreme dictatorships, such as that in North Korea, remain in power through the effective use of insidious and all-pervasive forms of propaganda. Yet nothing approaches the perfidy of the one-celled organism Toxoplasma gondii, one of the most widespread of all parasitic protozoa. It takes over the brain of its host and makes it do things, even actions that will cause it to die, in the service of this nasty hitchhiker. It sounds like a cheesy Hollywood horror flick, except that it is for real.
We know that illness in general can slow us down, incapacitate us and, in the worst case, kill us. Yet this organism is much more specific. Natural selection has given rise to pathogens that infiltrate the nervous system and change that system’s wiring to achieve its ultimate purpose, replication—like a computer virus that reprograms an infected machine.
Such is the case with T. gondii. It sexually reproduces only in the intestines of cats yet can maintain itself indefinitely in any warm-blooded animal. Infected cats shed millions of their oocysts in their feces. Taken up by all kinds of animals, including dogs, rodents and humans, they infect muscle and the brain to escape attacks by the host’s immune system. Hidden away, they remain dormant as cysts, surrounding themselves with a tough cell wall. Yet this quiet stage of infection, called toxoplasmosis, is deceptive. Violating all rules of good hospitality, these invaders make the host’s brain do things counterproductive to its own survival.
Toxoplasmosis has been most thoroughly studied in rats and mice. Both species have a deep-seated, innate fear of cats for obvious reasons. Spray a bit of cat urine into a corner, and the rodent will avoid this location, well, like the plague. In contrast, an infected animal loses its innate fear of cats. By some measures, it even appears to be mildly attracted to the smell of felines. This is an unfortunate turn of events for the rodent, because it is now more likely to be successfully hunted by a cat. On the other hand, this is a great deal for T. gondii. When the cat devours the sick critter and its contaminated brain, T. gondii moves into its final host, where it reproduces, completing its life cycle. Not quite what the romantics have in mind when they write about “the circle of life”!
The behavioral manipulation induced by T. gondii is quite specific. The infected rodent doesn’t look sick; its weight is normal; it moves about normally, possibly a bit more frantically than other mice; it grooms itself; and it interacts routinely with its conspecifics. Think how different this case is from what happens in rabies, another nasty infection. The animal loses its instinctual shyness, aggressively attacking others (the proverbial mad dog), thereby spreading the rabies virus through its bite. But because T. gondii can reproduce only in felines, it wants its host to be eaten by cats, not by just any carnivore. And because cats hunt live prey and do not eat carrion, T. gondii must not immediately kill its temporary host.
Rodents Aren’t Superheroes
How does T. gondii effect its insidious changes in the host? Experiments by Joanne P. Webster of Imperial College London, Robert Sapolsky of Stanford University and others have shown that infected rats or mice do not turn into the murine equivalent of Siegfried, the hero of Wagner’s Ring who knew no fear. No, they still avoid open spaces, remain nocturnal creatures, retain their aversion to the urine of other predators and learn to fear a tone associated with a foot shock. Might the protozoa have stunted their smell? After all, if they cannot smell anything anymore, they would not know how to avoid places smelling of cat urine. But infected mice still avoid food if it smells different—an aversion that arose partly because for centuries humans have been trying to control rodents by poison. The infected mice also respond appropriately to the smell of their littermates.
Clues about how the parasites affect the animal come from several observations. First, the density of cysts in the amygdala is almost double that in other brain structures involved in odor perception. Parts of the amygdala have been linked to anxiety and the sensation of fear. Second, the genome of T. gondii contains two genes related to mammalian genes involved in the regulation of dopamine, the molecule associated with reward and pleasure signals in the brain, including in ours. So perhaps the creepy protozoa makes suicidal activities, such as hanging around places frequented by cats, feel more pleasurable for the infected rodent?
What elevates this vignette about evolution and life in the wild to epic proportions for humanity is that about a tenth of the U.S. population is infected by T. gondii (in some countries, such as France, the infection rate is seven to eight times higher, possibly because of the widespread consumption of uncooked and undercooked meat). Human toxoplasmosis is usually considered to be symptom-free (what doctors refer to as asymptomatic). Exceptions are patients with a weakened immune system and the unborn (hence the need for pregnant women to avoid cleaning cat-litter boxes).
Science has known for a long time that schizophrenic patients are two to three times more likely to carry antibodies to T. gondii than are controls who are not schizophrenic. Furthermore, antipsychotic drugs that block the action of dopamine, such as haloperidol, commonly used in the treatment of schizophrenia, are also effective in combating toxoplasmosis in both rats and people. And some infected adults go on to develop psychotic symptoms similar to schizophrenia. Little is known about the mode or site of action of this pathogen in the human brain. The exact link between T. gondii and psychiatric diseases is tantalizing but remains murky.
Recent claims go so far as to argue for a role of T. gondii in shaping distinct cultural habits, depending on the rate of infection in the population. A prospective study tracking the road safety in Czech recruits during their 18 months of compulsory military draft found a rate of accidents six times higher in affected drivers. Are the young men with toxoplasmosis infection simply slowed down? Or do they drive more aggressively?
In my November 2009 column, I described the discovery by cognitive neuroscientists that the feeling of freely willing an action (called authorship or agency) is a subjective, conscious sensation no different, in principle, from the conscious awareness of seeing the azure blue sky or feeling the sharp pain of a toothache. When I engage in a dangerous pursuit, such as taking the end of the rope on a steep section of a granite wall in Yosemite Valley while climbing, I feel as if “I freely decided” to do so, whatever this might mean in a metaphysical sense. Yet my action is most likely caused by an inexhaustible multiplicity of factors not accessible to my conscious introspection, including, yes, possibly some tiny single-celled parasites lodging in my brain and making me act out their silent commands. The wonder of it all.
So a few things in this article about Toxoplasma gondii interest me:
1. A tenth of the US population has it, so that’s around 33 million people. 1 in 10 according to the CDC.
2. The French population has it 7 to 8 times higher.
3. The cysts are double in the amygdala?
4. Those infected have more care accidents which may be caused by them driving more aggressively.
Regardless, it’s pretty damn widespread, and can effect the brain.
So I’ve just discovered Fenbendazole due to rumours of it curing cancer. There’s even a study of brain cancer being cured or helped by it.
Having such a widespread infection rate, and fenbendazole being quite tolerable and doesn’t build drug resistance in the body, so it’s effective the 90th time as the first time you take it (there’s a study on this somewhere). I’m going to see if I can get my hands on some and dose it everyday at 222mg, as I’ve pretty much tried every supplement out there, maybe this might help fight the root cause?
Here’s an interesting study on the Protozoa and the amygdala: https://dmm.biologis...content/6/2/516
Toxoplasma gondii infection induces dendritic retraction in basolateral amygdala accompanied by reduced corticosterone secretion
Pathological anxiety is thought to reflect a maladaptive state characterized by exaggerated fear. Naturally occurring perturbations that reduce fear can be crucial in the search for new treatments. The protozoan parasite Toxoplasma gondii invades rat brain and removes the fear that rats have of cat odors, a change believed to be parasitic manipulation of host behavior aimed at increasing parasite transmission. It is likely that mechanisms employed by T. gondii can be used as a heuristic tool to understand possible means of fear reduction in clinical settings. Male Long-Evans rats were infected with T. gondii and compared with sham-infected animals 8 weeks after infection. The amount of circulating plasma corticosterone and dendritic arborization of basolateral amygdala principal neurons were quantified. Previous studies have shown that corticosterone, acting within the basolateral amygdala, enhances the fear response to environmental stimuli. Here we show that T. gondii infection causes a dendritic retraction in basolateral amygdala neurons. Such dendritic retraction is accompanied by lower amounts of circulating corticosterone, both at baseline and when induced by an aversive cat odor. The concerted effects of parasitism on two pivotal physiological nodes of the fear response provide an animal model relevant to interactions between stress hormones and amygdalar plasticity.
So here we show it has an effect on amygdala neurons and amygdala plasticity. Now in rats it took away fear, but still it effects the amygdala, and is an extremely widespread Protozoa.
https://www.cell.com...?code=cell-site
“Recent studies have revealed that Toxoplasma alters both excitatory and inhibitory neurotransmission in the central nervous system and that these changes lead to unbalanced synaptic activity and seizures.”
Something else of interest.
https://www.robertsa...oplasmosis.html
”It takes about 6 weeks for toxo to migrate from the gut to the brain. In the brain it forms cysts in multiple locations, but mainly in the amygdala region. The amygdala is the brain's center for fear and anxiety. It is also the brain center for forming predator aversion pathways. Once in the amygdala toxo is able to take dendritic nerve cell endings and cause them to shrivel up.”
https://www.sciencedaily.com/releases/2011/11/111104102125.htm
Brain parasite directly alters brain chemistry
Research shows infection by the brain parasite Toxoplasma gondii, found in 10-20 per cent of the UK's population, directly affects the production of dopamine, a key chemical messenger in the brain.
Findings from the University of Leeds research group are the first to demonstrate that a parasite found in the brain of mammals can affect dopamine levels.
Whilst the work has been carried out with rodents, lead investigator Dr Glenn McConkey of the University's Faculty of Biological Sciences, believes that the findings could ultimately shed new light on treating human neurological disorders that are dopamine-related such as schizophrenia, attention deficit hyperactivity disorder, and Parkinson's disease.
This research may explain how these parasites, remarkably, manipulate rodents' behaviour for their own advantage. Infected mice and rats lose their innate fear of cats, increasing the chances of being caught and eaten, which enables the parasite to return to its main host to complete its life cycle.
In this study, funded by the Stanley Medical Research Institute and Dunhill Medical Trust, the research team found that the parasite causes production and release of many times the normal amount of dopamine in infected brain cells.
Dopamine is a natural chemical which relays messages in the brain controlling aspects of movement, cognition and behaviour. It helps control the brain's reward and pleasure centres and regulates emotional responses such as fear. The presence of a certain kind of dopamine receptor is also associated with sensation-seeking, whereas dopamine deficiency in humans results in Parkinson's disease.
These findings build on earlier studies in which Dr McConkey's group found that the parasite actually encodes the enzyme for producing dopamine in its genome.
"Based on these analyses, it was clear that T. gondii can orchestrate a significant increase in dopamine production in neural cells," says Dr McConkey.
"Humans are accidental hosts to T. gondii and the parasite could end up anywhere in the brain, so human symptoms of toxoplasmosis infection may depend on where parasite ends up. This may explain the observed statistical link between incidences of schizophrenia and toxoplasmosis infection."
Dr McConkey says his next experiments will investigate how the parasite enzyme triggers dopamine production and how this may change behaviour.
Toxoplasmosis, which is transmitted via cat faeces (found on unwashed vegetables) and raw or undercooked infected meat, is relatively common, with 10-20% of the UK population and 22% of the US population estimated to carry the parasite as cysts. Most people with the parasite are healthy, but for those who are immune-suppressed -- and particularly for pregnant women -- there are significant health risks that can occasionally be fatal.
The parasite infects the brain by forming a cyst within its cells and produces an enzyme called tyrosine hydroxylase, which is needed to make dopamine. Dopamine's role in mood, sociability, attention, motivation and sleep patterns are well documented and schizophrenia has long been associated with dopamine, which is the target of all current schizophrenia drugs on the market.
The enzyme tyrosine hydroxylase is a crucial step in making L-DOPA (prescribed as levodopa for Parkinson's Disease), a chemical that is readily converted to the neurotransmitter dopamine.
The US-based Stanley Medical Research Institute, which focuses on mental health conditions and has a particular emphasis on bipolar illnesses. Dunhill Medical Trust supports research on diseases of aging.
Wow. So this article is saying 10-20% of the UK population is infected (relevant to me). Also says 22% of the US population.
Not only that but it may increase dopamine. I’ve noticed in recent years I am dopamine dominant, or at least low serotonin, mainly brain zaps and my OCD, and dopamine precursors send me over the edge with anger and can even trigger an emotional flashback.
I wonder if all this excessive dopamine is the reason my reward system is so screwed up. I.e. suffer from anhedonia, haven’t had an orgasm in 16 years. Maybe I’m dopamine dominant but very desensitised to it.
Time to try and kill some parasites with Fenbendazole whether I may have them or not, and see if anything happens mentally and emotional. Main observation I hope to see improvement in would be any alleviation in my anhedonia, i.e. an increase in pleasure, emotions, and motivation. But first I have to get my hands on the stuff.
