At issue: is household crowding a risk factor for schizophrenia and bipolar disorder?


Schizophr Bull. 1998;24(3):321-4. Torrey EF1, Yolken RH.

Five studies have reported that being born or raised in an urban area is a risk factor for developing psychosis later in life. The authors hypothesize that increased exposure to infectious agents through household crowding might account for this association.

The paper is interesting, but I cannot copy and paste it here. It is available at the link above.
A probable mechanism of how infections can influence the cerebral immune balance could be the activation of the tryptophan catabolism via infectious agents and elevated proinflammatory cytokines.


In summary infectious agents might influence the cerebral neurotransmitter balance via activating on the tryptophan catabolism. The precise mechanism, how an altered metabolism of tryptophan might contribute to the pathogenesis of schizophrenic symptoms and tics is not yet fully understood. On the one hand it could reflect a state of immune activation; or on the other hand it might be possible that kynurenine and its neuroactive metabolites (e.g. quinolinic acid) cause directly a toxic effect in the basal ganglia and the CNS.

From what I can understand, this is very interesting and it might be a clue to link these microbes to autoimmune disease and many "psychological" conditions, since, all autoimmune diseases have elevated proinflammatory cytokines; and many psychological conditions are linked to trytophan and other neurochemicals... and the hypothesis of toxic effect is quite interesting as well...

Thanks Gaby!
Yas said:
From what I can understand, this is very interesting and it might be a clue to link these microbes to autoimmune disease and many "psychological" conditions, since, all autoimmune diseases have elevated proinflammatory cytokines; and many psychological conditions are linked to trytophan and other neurochemicals... and the hypothesis of toxic effect is quite interesting as well...

Yes, very interesting! More clues posted on the Schizophrenia thread:,5155.msg590384.html#msg590384

[A ray of hope bolded in blue]

Gaby said:
Association between Intracellular Infectious Agents and Schizophrenia


Clin Psychopharmacol Neurosci. 2012 Aug; 10(2): 117–123. Mi-Hee Park,1 Young-Joon Kwon,1 Hee-Yeun Jeong,1 Hwa-Young Lee,1 Young Hwangbo,2 Hee-Jung Yoon,3 and Se-Hoon Shimcorresponding author1


In addition, we have also compared the PANSS subscale score between schizophrenic patients with seropositive and seronegative group for T. gondii and C. trachomatis infection. For T. gondii, the seropositive group scored significantly higher score in several negative subscales and one general psychopathology scale, 'disturbance of volition'. Fellerhoff et al.,13) treated patients with schizophrenia and other mental disorders with evidence of infection by using adoptive immunotherapy and antibiotics, but no antipsychotics. The improvement in the status of the patients was mainly related with regain of energy and volition, improvement of social withdrawal, which are main components of negative symptom. Based on these findings, we cautiously suggest the relation between negative symptoms and 'disturbance of volition' with infectious agent. In the case of C. trachomatis infection, the seropositive group scored significantly higher score in one general psychopathology subscale, disorientation. Still, evidence to underpin relation between infectious agents and disorientation is insufficient.

Despite numerous studies performed to reveal relation between infectious agents and schizophrenia, it is still controversial whether infectious agents play a causal role in inducing psychotic symptoms. Proving causality is one of the major limitations of studies about the association of schizophrenia and infections. As schizophrenia is constituted of a number of inhomogeneous symptoms, it seems more probable that infections might just be one of the contributing factors among others.13) In the case of schizophrenia, one possible causality could be that infectious agents do not directly cause psychiatric symptoms, but influence the immune balance via the status of a chronic infection. We assume that these different infections have an impact on the immune system and therefore might contribute to psychiatric symptoms. Several studies have identified the important role of immunological parameters in schizophrenia.23) Recently, it has been demonstrated that proinflammatory cytokines that could enhance the activity of the enzyme, indoleamine 2,3-dioxygenase (IDO) plays an important role in the pathophysiology of schizophrenia. The IDO increases tryptophan degradation into kynurenine and decreases tryptophan availability in the brain to synthesize neurotransmitters.24) Reduced type-1 immune response and Increased type-2 immune response in schizophrenic patients promote the production of the endogenous N-Methyl-D-aspratate (NMDA) receptor antagonist, kynurenic acid. A hypofunction of the glutamatergic cortico-striatal pathway is associated with opening of the thalamic filter, which leads to an uncontrolled flow of sensory information to the cortex and promotes psychotic symptoms.25)

There are some limitations in our study: First, the sample size was rather small and therefore the statistical power might be restricted. Although there were 96 patients with schizophrenia in the study, the number of the seropositive patients for T. gondii (n=21), C. pneumoniae (n=64), C. trachomatis (n=27) were small. Therefore, the results of the clinical symptoms of the seropositive and seronegative schizophrenia need to be further verified, especially through prospective studies. Second, it was not possible to evaluate the rate of sexual activity in patients and controls. This aspect seems to be important, as C. trachomatis is a sexually transmitted disease. There are studies showing that schizophrenic patients suffer from sexual dysfunction and possess less social activity and have therefore an impaired sexual life.26) It also remains possible that schizophrenic patients might show riskier sexual behavior.

In conclusion, the present research found that the prevalence of IgG antibody to T. gondii and C. trachomatis in the patients with schizophrenia was higher than that of the control groups. These findings suggest that the elevated rate of infectious agents within the schizophrenic patients could provoke an immunological disturbance that might influence the cerebral neurotransmitter balance. This study lent further weight to the hypothesis that exposure to T. gondii and C. trachomatis may be the risk factors for schizophrenia. Further studies investigating the association between the infection status and immune parameters are needed.
Those ARE interesting clues, Gaby. I wonder if the neurotransmitters such as serotonin are always low, or it could also be too high (depending on other circumstances). Also, if an infectious agent is what causes the cascade of events that lead to the immune system disturbance and/or neurotransmitter anomalies, then it seems like splitting hairs to say whether the infectious agent is the direct cause or a contributing factor in figuring out effective treatments, I think.
Gaby said:
Infectious Agents are Associated with Psychiatric Diseases


In some psychiatric disorders environmental factors are involved in the pathophysiology of the diseases. Especially in schizophrenia and Gilles de la Tourette’s syndrome (TS) the precise underlying pathophysiology is yet unknown, however epidemiological studies have revealed different environmental factors in the pathogenesis such as winter and spring birth, birth in an urban area and complications during pregnancy.1,2 Moreover it has been suggested that infections might also be involved in the aetiology of some cases of schizophrenia.3 While until now different microbial agents have been proposed as risk factors for schizophrenia, many recent studies have focused on members of the viral family of Herpesviridae,4 Borna virus,5 intracellular bacteria like Chlamydia as well as the protozoan organism Toxoplasma gondii.6,7 Reasons for focusing on these agents include their ability to establish persistent infections within the central nervous system as well as the occurrence of neurological and psychiatric symptoms in individuals infected with these agents.8


The outcome of this study emphasizes on the association between infectious agents and psychiatric diseases (schizophrenia and TS). It highlights the differential distribution of seropositivity to these agents in both patient groups. Future studies with larger sample sizes are needed to investigate the precise role of infectious agents as possible contributing factors to psychiatric diseases.

That puts a totally different perspective on the mind-body connection. Is it emotions that cause diseases or pathogens that cause diseases and some associated emotional states due to their influence on the CNS? Or both occur in some kind of feedback loop?
Pierre said:
That puts a totally different perspective on the mind-body connection? Is it emotions that cause diseases or pathogens that cause diseases and some associated emotional states due to their influence on the CNS?

It could perhaps go both ways.

But I've been thinking along the lines of:
A healthy human being should be able to experience life to its fullest, which would include good emotions, periods of happiness, abundance and relaxation, but also trauma, periods of scarcity and stress.

The view I've had for a while is that our emotions are screwed up as a child and this makes it really difficult in later life to regulate our emotions or survive stress, which then leads to disease.

But really we shouldn't be crippled or made ill by bad emotions. Considering the world we live in, shouldn't we be a bit more resilient than that? And if so, perhaps it is pathogens that are undermining this resilience (i.e. transmarginal inhibition in the latest session).
While doing some quick research about brain cancer and infections, I stumbled upon this interesting short video:

In a nutshell, a patient was diagnosed with brain tumor, it was removed surgically and deemed cancerous. All the pathology criteria of cancerous cells were met. But further analysis were performed on the tumor and it appeared that it was actually a Brucella (a mycoplasma, i.e. membrane-free bacteria) infection.

Now one could wonder how doctors can't distinguish a cancer from an infection. The thing is, it looks exactly the same. As stated in the video, the "mass' was clinically and radiologically indistinguishable from a (cancerous) brain tumor.

Really? So the next logical question is: how many masses were called 'cancer' because they looked exactly like a cancer but actually were infectious masses not labeled so because proper infectious tests were not performed?

Well, I didn't see any mention of pathogen tests conducted on my tumors. A microscope examination of the first 'tumor' cell led to the conclusion it was a grade III brain cancer but was it? How did doctors reach this conclusion?

Actually there are five criteria that characterize cancerous cells. Those criteria apply to any cancer but as you will see each of of them could very well be caused by an infection:

Anaplasia: it means cells dedifferentiate (they're all the same). Could it because they all get same genetic code from the pathogen?

Atypia: it means cells have unusual conformation. Its it because they integrate foreign pathogen genetic sequences?

Neoplasia: meaning uncontrolled cell division. Is it a body reaction in order to encapsulate the infected area or maybe pathogens trigger through host cells mutation their overgrowth in order to increase their hosting environment?

Necrosis: it means cells death. This is a typical effect of infections. Plus, in 'cancerous' tissues, the dead cells are not disposed of by phagocytes because they send the wrong chemical signal. Is this wrong signal caused by the host pathogen?

Hypoxia: meaning increased oxygen/blood supply in the 'cancerous' area. Is it because pathogens need oxygen and stimulate through mutations of the host cells the development of surrounding blood vessels?

Most of the above supposes that the infectious agent literally hijacks the host cells and takes full control including fundamental aspects like differentiation, division, shape, signals sent to macrophages,... This is actually a documented property of pathogen particularly viruses which transfer part of their genetic code of their host cell, hacking the development template of the host and modifying it in all possible ways.

Interestingly, some cancers are already consider as infectious (cervical cancer , some lymphoma) but this is a minority of cancers. what about all the other 'non-infectuous' cancers?

The video above rang a bell because the patients got a brucella infection a few months before her 'cancer'. She took antibiotics then stopped, the cancer appeared soon later. The doctor in the video hypothesizes that the brucella that triggered the first infection re-developed after the end of the treatment and led to the infectious brain mass. I got my first tumor symptoms in September 2008 but in February and March 2008 I had been quite sick. Lasting flue like symptoms that required the use of antibiotics. Five months later the first brain tumor appeared. Is there a link between the two events? Is this the same pathogens that caused the flue then the tumor?

As a positive side note, it seems that mycoplasma don't like the cold.
Pierre said:
Now one could wonder how doctors can't distinguish a cancer from an infection. The thing is, it looks exactly the same.

Good catch, and very intriguing.

These pathogens behave like malignant viruses in more ways than one!
I had a hunch that parasites could be feeding off of neurotransmitter building blocks - in this case tryptophan which is used for serotonine production (and the theory goes that low serotonine causes depression).
Importance of L-tryptophan metabolism in trypanosomiasis.

African trypanosomiasis or sleeping sickness is caused by extracellular trypanosomes. The presence of seric antibodies directed to a tryptophan-like epitope in trypanosome infected patients and animals led us to investigate the roles of tryptophan in trypanosomiasis. These antibodies are directed against a tryptophan-rich conserved sequence inside the major parasite surface glycoprotein. In vitro, a rapid uptake of tryptophan by trypanosomes is measured. Seric tryptophan levels are decreased during trypanosomiasis. This decrease may be linked with an increase in indoleamine 2,3-dioxygenase (IDO) induced by Interferon-gamma. In vivo inhibition of IDO by norharman provokes a dramatic increase in circulating parasite number. All these data show the essential role of tryptophan in parasite growth. Moreover, antibodies against tryptophan, the decreased concentration of the neurotransmitter serotonin in the brain following infection and the tryptophan metabolites (tryptophol) produced by trypanosomes may participate to the pathophysiological mechanisms provoking sleeping sickness.

Expanding it further, dopamine/serotonine (decreased by parasites)
Effect of some parasitic infection on neurotransmitters in the brain of experimentally infected mice before and after treatment.

The effects of some parasitic infection (bilharziasis, toxocariasis and trichinosis) on the brain of experimentally infected mice were investigated. Eighty animals were classified into four groups, group I contained five non infected animals as a control group. The other groups each contained twenty-five mice infected with Schistosoma mansoni (group II), Toxocara canis (group III) and Trichinella spiralis (group IV). Each infected group was divided into two subgroups (a,b). Subgroup (a) left untreated and subgroups (b) treated by praziquantel (in group II) and mebendazole (in group III and IV). Histopathological and immunological examination using peroxidase antiperoxidase (PAP) technique and neurotransmitters estimation (nor-epinephrine, dopamine and serotonine) were carried. In the untreated animals, there were mild histopathological changes and mild antigenic deposition in subgroups (IIa and IIIa) and marked changes in subgroup (IVa). There were significant decrease in dopamine in subgroup (IIIa), not improved after treatment (subgroup IIIb) and significant decrease in nor-epinephrine and serotonine in subgroup (IVa) improved after treatment in subgroup (IVb). The neurotransmitters changes may explain the motor, behavioural and emotional changes that occurred with these parasites.

Opiods (produced by parasites)
Evidence of opiates and opioid neuropeptides and their immune effects in parasitic invertebrates representing three different phyla: Schistosoma mansoni, Theromyzon tessulatum, Trichinella spiralis.

Studies done in our laboratories have demonstrated that the parasitic trematode, Schistosoma mansoni is capable of producing several proopiomelanocortin (POMC) peptides including beta-endorphin, adrenocorticotropin (ACTH), melanocyte stimulating hormone (alphaMSH) and enkephalin as well as morphine. Some of these opioids have been demonstrated to be immunosuppressive and may play an important part in immune evasion by these parasites. The parasitic nematode Trichinella spiralis also produces immune suppressive substances in vitro as well as causes immune suppression in its encysted stage in vivo. We recently have demonstrated the presence of morphine in both infected mice and in the nematode by HPLC and RIA. In a recent study of the leech Theromyzon tessulatum, we demonstrated the presence of proopiomelanocortin (POMC) and its derived peptides, ACTH and alphaMSH, in the immune tissues. The peptide was cloned and extensively purified by HPGPC and reversed-phase HPLC, and then sequenced. The 25.4 kDa protein was purified by gel permeation chromatography, anti-ACTH-affinity column separation followed by reversed-phase HPLC. Its amino acid determination was performed by Edman degradation, enzymatic treatments and electrospray mass spectrometry. The structure of the leech POMC-like precursor and its derived peptides demonstrates considerable amino acid sequence similarity with mammalian POMC. Taken together, these studies demonstrate that opiates and opioid neuropetides are present in invertebrates and their immunoregulatory actions have been conserved during evolution. The role of opiates and opioid peptides in immune and behavior modification of hosts is also discussed.

So the above would make you numb to everything, and put you in a fog.
And if long term could lead to extreme sensitivity to pain (physical/emotional) from constantly elevated opiod levels.

Glutamate (feeding from)
The cause of the predilection of Babesia gibsoni for reticulocytes.

Yamasaki M, Otsuka Y, Yamato O, Tajima M, Maede Y.

Author information: Department of Veterinary Clinical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.


This study was conducted to determine why Babesia gibsoni replicates well in reticulocytes. First, B. gibsoni was cultivated in resealed erythrocyte ghosts loaded with either erythrocyte or reticulocyte lysate, and in reticulocyte ghosts loaded with either erythrocyte or reticulocyte lysate.

The parasites multiplied well in the erythrocyte or reticulocyte ghosts loaded with reticulocyte lysate compared to the other resealed cells loaded with erythrocyte lysate.

Second, the parasites were cultivated in erythrocytes in culture medium supplemented with either erythrocyte or reticulocyte lysate. The parasites multiplied better in reticulocyte lysate-containing cultures than in erythrocyte lysate-containing cultures.

Finally, the parasites were cultivated in erythrocytes in culture medium supplemented with glutamate, aspartate, asparagine, glycine, isoleucine, proline, taurine or GSH, which were present in higher concentrations in reticulocytes than in erythrocytes.

Supplementation of the culture medium with glutamate and GSH resulted in enhancement of the multiplication of the parasites, while the other amino acids did not enhance the multiplication.

These results indicated that the high levels of the multiplication of B. gibsoni in reticulocytes are partly due to the high concentrations of glutamate and GSH in reticulocytes.

GABA (released from parasites)
How T. gondii gets in

T. gondii spreads into humans through contact with infected animal feces or undercooked meat. Questions remain about how the parasite is so successful at evading the immune system and infecting the body, however. Swedish researchers led by Antonio Barragan of Karolinska University Hospital Huddinge in Sweden wanted to find out.

Earlier studies had found that an infection by T. gondii makes a certain type of immune cell go haywire. These cells, called dendritic cells, are spiny little free-floaters that move throughout the body's tissues. When a dendritic cell meets a foreign invader, it engulfs and processes it, carrying the pieces to lymph nodes, which then launch a full immune attack.

When infected by T. gondii, dendritic cells start moving at hyper-speed. Barragan and his colleagues suspected that the parasite might be invading the cells and using them to get around the body like a city bus, but they didn't know how. [Top 10 Most Disgusting & Diabolical Parasites]

Chemical hijacking

By infecting both human and mice dendritic cells with the parasite, the researchers found the cells suddenly produced increased levels of GABA, a neurotransmitter that is important for brain cell function. GABA also makes dendritic cells go, the researchers found — infected cells making more of the chemical began moving in more random directions and did so faster than uninfected dendritic cells.

"For toxoplasma to make cells in the immune defense secrete GABA was as surprising as it was unexpected, and is very clever of the parasite," Barragan said in a statement.

The researchers then infected live mice with T. gondii and treated some of them with compounds that inhibit the release of GABA. They found that in treated mice, parasite levels were 2.8 times lower than untreated mice four days post-infection. Those findings suggest that T. gondii is indeed using the immune system as a free ride around the body.

The findings are published today (Dec. 6) in the open-access journal PLOS Pathogens.
RedFox said:
Glutamate (feeding from)

Then, it might not be a good idea to supplement on high doses of L-glutamine to restore the gut?

Is Glutamine Supplementation Helpful or Harmful?
Glutamine is an amino acid that makes up the majority of our skeletal muscle. There is some controversy over whether oral glutamine supplementation is toxic or helpful to healthy people. In a past article, Dr. Robert Crayhon expressed the view of many natural medicine experts, "After reviewing the literature, I am unconvinced that high-dose oral glutamine supplementation is toxic to neurons in healthy persons."

However, Dr. Russell Blaylock, a board-certified neurosurgeon and author of the highly recommended Excitotoxins: The Taste that Kills wrote in to me with another viewpoint and his response is below [...]

Numerous recent studies as well as Siegel’s Basic Neurochemistry textbook emphatically state that the major source of glutamate is from glutamine in the brain. Normally, when the brain finishes using glutamate for chemical communication between brain cells at the synapse the glutamate is taken up by surrounding glial cells and changed by the enzyme glutamine synthease into glutamine, where it is stored.[...]

The major use for high-dose glutamine would be to repair gastrointestinal injury. In such cases, I would recommend short-term use only. Those with a history of the following conditions should avoid glutamine, even for short-term use:

Neurodegenerative disease
Recent vaccinations
Multiple sclerosis
Other neurological disorders

Gluten vs. Glutamate (glutamic acid) vs. Glutamine

[...] It is “interesting” that some of the new anticonvulsants work by blocking glutamate. This should not be a surprise. The glial cells that control the level of glutamate at the synapse are the targets of numerous pleomorphic bacteria and viruses, some of the latter being embedded in the very DNA. Yes, idiopathic epilepsy runs very consistently though certain breeds of dogs and is one of the myriad of genetic viruses in their DNA (side-by-side with all of the cancer-producing ones). The field of epigenetics is a fascinating one.

[...]There are many factors in the development of this “syndrome” we call epilepsy. One component is clearly a genetic virus. There are other acquired viruses and pleomorphic bacteria that can be involved along with food lectins, malabsorption/malnutrition, free radicals from chemicals/pollutants, vaccines, seasonal variants, fluorescent lights/computer graphics/etc. and more. But when we identify these things and remove them, we can undermine the syndrome and miracles can happen. I no longer put any limitations on what this body can do, only what WE can do for our body.
I've been following this thread from the beginning with extreme interest.

I note that one of the red flags about not doing this protocol is if one has a kidney impairment, then it is not advised to take Doxycycline.

Well I was really disappointed to learn that, because I had intended to start the protocol as soon as the searing hot weather was over - mostly 48-50 degrees C here, daily.

I have a non functioning kidney, in fact is has zero function. My left kidney is the one that keeps me alive.

Is there an alternative to the antibiotic Doxycycline which I could take. I did read somewhere that Doxycycline can be used cautiously by people with kidney impairment, but I don't want to do this unless I can know for sure that it is safe.

Here is the link :-

All the tetracyclines, with the exception of minocycline and doxycycline, are excreted renally. Plasma half- lives are markedly prolonged (up to 100h) in renal impairment and as they are antianabolic there is a concentration- related increase in blood urea, which itself may cause an osmotic diuresis. Doxycycline or minocycline can be used cautiously in patients with renal impairment, but the other tetracyclines are contraindicated. Doxycycline does have some renal clearance but hepatic clearance increases with renal impairment, partly because there is a reduction in binding to plasma proteins and red blood cells (9,11,12).
Very interesting thread - particularly in the light of yesterday's session.

One thing that came to mind was that once the Herxheimer effect hits, it might be a good idea to do a coffee enema to assist the liver in getting rid of the pathogens. However, this would only be a good idea if you're not taking any meds at the same time as you'd then be flushing them out before they get a chance to do their job.

I'm wondering how the mind-body connection comes into play in combination with the parasites as Pierre also mentioned. To me it makes sense if the feedback loop works in a way that a healthy mind changes the living conditions for the parasites and as such it's possible to get some effect from working with the mind alone.

I've suffered from debilitating back pain for ten years and managed to get over 80% of it by the methods described by John Sarno which I've written about in another thread. As a matter of fact I had a 100% recovery whilst in India and when I returned to Denmark about 20% of the pain returned. It's no longer debilitating and I can hold it at bay by daily yoga, breathing and meditation. Maybe the remaining 20% of the symptoms are due to low-grade long term infection?

As Nicklebleu, I'm a bit hesitant to go on such a severe protocol if it isn't necessary. I'll wait and see where the research takes us.
Gaby said:
RedFox said:
Glutamate (feeding from)

Then, it might not be a good idea to supplement on high doses of L-glutamine to restore the gut?

Could be. I think if the infection is eating glutamine it may be one reason the gut can be slow to heal, if it heals at all.

Adding some more pieces to the puzzle:

IRON: Bacterial, Fungal, Viral, Protozoan Infections and infectious Processes

As on other Science Library pages, we do not present a lengthy narrative on each body system affected by infection, but rather will briefly summarize or quote the most relevant take-home points and/or research conclusions from each study. Article titles are linked to abstracts archived at the U.S. National Library of Science. Many articles also have Full free text PDF links. Our Iron Science Library pages include:


Iron availability and infection (1)

In this 2009 review of the literature the author notes that, "To successfully sustain an infection, nearly all bacteria, fungi and protozoa require a continuous supply of host iron." "Mechanisms of microbial iron acquisition are determinants for the kinds of cells, tissues and hosts in which pathogens can flourish." And with respect to human and other "hosts," "As a corollary, hosts possess an array of iron withholding devices whereby they can suppress or abort microbial invasions." "Awareness of environmental and behavioral methods that can prevent iron loading plus development of pharmaceutical agents that can block microbial access to iron may help to reduce our dependence on antibiotics."

Iron loading and disease surveillance (2) Free full paper

This 1999 review and the accompanying full paper describe, "Iron is an oxidant as well as a nutrient for invading microbial and neoplastic cells. Excessive iron in specific tissues and cells (iron loading) promotes development of infection, neoplasia, cardiomyopathy, arthropathy, and various endocrine and possibly neurodegenerative disorders. To contain and detoxify the metal, hosts have evolved an iron withholding defense system, but the system can be compromised by numerous factors. An array of behavioral, medical, and immunologic methods are in place or in development to strengthen iron withholding. Routine screening for iron loading could provide valuable information in epidemiologic, diagnostic, prophylactic, and therapeutic studies of emerging infectious diseases." [Health-e-Iron note: Tables 1 and 2 from this paper appear below]




Iron availability increases the pathogenic potential of Salmonella typhimurium and other enteric pathogens at the intestinal epithelial interface (5) Free full text

Reported in 2012, this research team noted, "Recent trials have questioned the safety of untargeted oral iron supplementation in developing regions. Excess of luminal iron could select for enteric pathogens at the expense of beneficial commensals in the human gut microflora, thereby increasing the incidence of infectious diseases." The researchers observed in this laboratory study that, "Growth of Salmonella typhimurium and other enteric pathogens was increased in response to iron." The researchers concluded, "our data fit with the consensus that oral iron supplementation is not without risk as iron could, in addition to inducing pathogenic overgrowth, also increase the virulence of prevalent enteric pathogens."


Hepatic iron overload is common in chronic hepatitis B and is more severe in patients coinfected with hepatitis D virus (7)

In this 2012 study from Italy the researchers noted, "Hepatic iron overload has been described in chronic hepatitis C as a cofactor affecting fibrosis progression. Data in patients with chronic hepatitis B infection are scarce. We investigated hepatic iron deposits and serum iron indices in 205 consecutive patients with hepatitis B and compensated liver disease. Mean age of the patients was 42.4 ± 12.4 years and 72.5% were males." "Hepatic iron deposits were detected in 35.1% of patients, most of them being minimal (grade I) (59.7%) or mild (grade II) (27.8%). Variables significantly associated with hepatic iron deposits were male gender (P = 0.001), serum ferritin (P = 0.008), GGT (P = 0.05) and alkaline phosphatase (P = 0.05) levels." "A significant correlation between coinfection with HDV and hepatic iron deposits was also found (OR 4.23, 95% CI 1.52-11.82, P = 0.003). When compared to monoinfected cases, HDV positive patients had more elevated GGT (P = 0.03), more advanced fibrosis and more severe iron deposits (P < 0.0001)." "In conclusion, in well-compensated chronic hepatitis B infection, hepatic iron deposits and elevation of serum iron indices are common, especially in male gender and in patients coinfected with HDV. As HBV/HDV liver disease is generally more rapidly progressive than that caused by HBV monoinfection, we speculate that iron overload may be one of the factors contributing to the severity of liver disease."


Enhanced iron availability by protein glycation may explain higher infection rates in diabetics (12)

This 2012 laboratory study done in California reported, "The results, in addition to data in the literature, support the hypothesis that glycation of serum proteins may effectively increase the available free iron pool for bacteria in blood serum and weaken our innate immunity. This phenomenon may be partially responsible for higher infection rates in some diabetics, especially those with poor glycemic control."


One wonders then if iron overload is caused by a pathogen triggering the body to absorb more than it needs (in order for the pathogen to survive/thrive).

Human DNA Shows Traces of 40 Million-Year Battle For Survival Between Primate and Pathogen

(SALT LAKE CITY) – Examination of DNA from 21 primate species – from squirrel monkeys to humans – exposes an evolutionary war against infectious bacteria over iron that circulates in the bloodstream. Supported by experimental evidence, these findings, published in Science on Dec. 12, demonstrate the vital importance of an underappreciated defense mechanism, nutritional immunity.

“We’ve known about nutritional immunity for 40 years,” says Matthew Barber, Ph.D., first author and postdoctoral fellow in human genetics at the University of Utah. “What this study shows us is that over the last 40 million years of primate evolution, this battle for iron between bacteria and primates has been a determining factor in our survival as a species.” The study models an approach for uncovering reservoirs of genetic resistance to bacterial infections, knowledge that could be used to confront antibiotic resistance and emerging diseases.

Following infection, the familiar sneezing, runny nose, and inflammation are all part of the immune system’s attempts to rid the body of hostile invaders. Lesser known is a separate defense against invasive microbes, called nutritional immunity, that quietly takes place under our skin. This defense mechanism starves infectious bacteria by hiding circulating iron, an essential nutrient it needs for survival. The protein that transports iron in the blood, transferrin, tucks the trace metal safely out of reach.

Clever as it sounds, the ploy is not enough to keep invaders at bay. Several bacterial pathogens - including those that cause meningitis, gonorrhea, and sepsis - have developed a weapon, transferrin binding protein (TbpA), that latches onto transferrin and steal its iron. Though scientists have known of the offensive strategy, they failed to realize how pivotal the battle over iron has been in the conflict between host and pathogen.

“Interactions between host and pathogen are transient and temporary,” says senior author Nels Elde, Ph.D., assistant professor of human genetics at the University of Utah. “It took casting a wide net across all of primate genetic diversity to capture the significance.”

Just as details of a struggle can be gleaned from battle scars, Barber and Elde reconstructed this evolutionary conflict by documenting when and where changes in transferrin and TbpA have occurred over millennia. They examined the DNA of transferrin in 21 species from the primate family tree, and of TbpA from dozens of bacterial strains. The majority of accumulated changes in transferrin and TbpA cluster around a single region of contact between the two proteins, highlighting it as a site of evolutionary conflict.

The authors then used these genetic observations as a guide to perform experiments, which showed changes in TbpA enable the protein to grasp hold of transferrin, and that recent changes in transferrin allow it to evade TbpA. An attack and counterattack that has lasted 40 million years, these findings highlight a central role for nutritional immunity in an ongoing clash between primates and bacterial pathogens.

There are still signs of the battle today. Up to 25 percent of people in the world’s populations have a small alteration in the transferrin gene, which prevents recognition by several infectious bacteria, the most recent sign of this long battle. “Up until this study no one had come up with a functional explanation for why this variation occurs at an appreciable frequency in human populations,” says Elde. “We now know that it is a consequence of the pathogens we and our ancestors faced over millions of years.”

Understanding the strategies that underlie natural defense mechanisms, including nutritional immunity, could inform new approaches to combatting antibiotic-resistant bacteria and emerging diseases. “By examining the natural conflicts that have played out for millions of years, we can determine what has worked in the past, and apply them in new situations,” says Elde.

Escape from iron piracy through rapid evolution of transferrin. MF Barber, NC Elde, Science Dec 12, 2014
Almost all forms of life require iron to thrive. Iron plays essential biochemical roles in oxygen binding, ATP synthesis and DNA metabolism. During infection, pathogens need to acquire iron from their human host. If iron availability is high, infections can progress more rapidly. On the other hand, denying iron to invading microbes can slow down the course of disease, and allow immune mechanisms more time to clear the infection. Pathogens can become resistant to antibiotics, and can sometimes mutate to avoid recognition by the immune systems, but they cannot escape the metabolic requirement for iron. By manipulating iron transport we hope to develop a new strategy to combat infections.

The human peptide hepcidin is the master controller of iron metabolism; too little hepcidin leads to iron overload, too much causes anaemia. We are defining how hepcidin is modulated during infections, by testing which aspects of pathogen recognition by the host influence hepcidin synthesis. We then will assess whether deliberately altering hepcidin can control experimental infections of iron-requiring bacterial strains.

We are also studying hepcidin regulation in the context of important infectious diseases, namely HIV, malaria and Hepatitis C virus infection. In each of these three diseases imbalances of iron are known to contribute to disease and mortality. For HIV, we found some years ago that the viral protein Nef targets the host protein HFE, which is dysfunctional in the iron-overloading disorder haemochromatosis. By interacting with HFE, HIV manipulates iron transport in infected cells. We are investigating the causes and consequences of altered iron metabolism and hepcidin levels in the context of HIV/AIDS.

In malaria, after a mosquito bite the Plasmodium parasite infects the liver, then invades red blood cells, before differentiating to form gametocytes which leave the human host in a mosquito blood meal, beginning the cycle again. We are investigating the role of hepcidin and iron in each of these life-stages. We have found that the blood stage of infection, associated with anaemia, causes an increase in hepcidin synthesis. If we can block this induction of hepcidin by the parasite we may be able to alleviate malarial anaemia, which is a major cause of illness worldwide. {is the up-regulation of hepcidin to stop iron absorption more to do with the body attempting to starve the parasite? blocking it would probably be a bad idea then - unless it's the anemia that's killing people}

Finally, hepatitis C virus infection can suppress hepcidin and lead to iron overload.{So pathogens can cause iron overload in order to thrive} Increased iron is an important co-factor for morbidity in the context of HCV. We are investigating the molecular basis for hepcidin suppression by HCV - if we could reverse it, we may prevent iron overload and in so doing make HCV infection less harmful.
RedFox said:
Iron availability and infection (1)

In this 2009 review of the literature the author notes that, "To successfully sustain an infection, nearly all bacteria, fungi and protozoa require a continuous supply of host iron." "Mechanisms of microbial iron acquisition are determinants for the kinds of cells, tissues and hosts in which pathogens can flourish." And with respect to human and other "hosts," "As a corollary, hosts possess an array of iron withholding devices whereby they can suppress or abort microbial invasions." "Awareness of environmental and behavioral methods that can prevent iron loading plus development of pharmaceutical agents that can block microbial access to iron may help to reduce our dependence on antibiotics."


One wonders then if iron overload is caused by a pathogen triggering the body to absorb more than it needs (in order for the pathogen to survive/thrive).

That 's an interesting points that reminds me of this session where iron was mentioned in connection to bloodlines:

session 7 June 1997 said:
Q: So, it is the iron that the Celts need? Well, that brings me to the next question: In all the Celtic folklore when they talk about 'fairies,' which are obviously other density beings very similar to our modern
'Gray alien,' these fairy/slash aliens insist that no iron come near them in any way. It was also said that bringing iron into contact with someone thought to be a 'changeling' would prove whether or not they were because if they were, they would disappear instantly. Also, the instructions for the building of the Temple of Solomon included restrictions on the use of iron in either the preparation of the materials or the putting together of the building itself, even down to the rejection of the use of iron nails in any part. What is the significance of this restriction on the use of iron by these other density beings, whoever they are?
A: Bloodline trails.
Q: Are you saying that... I don't understand... not even well enough to frame another question...
A: You will, my dear, oh will you!
Q: If it was necessary for the Aryans to have iron... okay, maybe the iron is something that interacts...
A: What about iron as an element?
Q: Okay, let's see: Iron - derived from early Celt 'iserno,' via Illyrian 'eisarno' from the IndoEuropean base 'eis,' which means to 'move vigorously; strong, holy.' It is a white, malleable, ductile, metallic hemical element that can be readily magnetized, rusts rapidly in moist or salty air, and is vital to plant and animal life; it is the most common and important of all metals, and its alloys, as steel, are extensively used. Symbol: Fe; atomic weight:55.847; atomic number: 26; specific gravity: 7.86; melting point: 1535 degrees Centigrade; boiling point 3,000 degrees C. The electron shells are thus: ,14,8,2. Iron is an element of blood, hemoglobin, and is easily magnetized... there is some new work about iron and magnetite in the brains of people who are psychic or have 'abduction' experiences... is it the magnetism?
A: Yes....
Q: Is it something that holds one more firmly in 3rd density, and the elimination of it enables one to switch densities... or...A: Tis magnetite that acts as a conduit, and perhaps, just perhaps, allows for transference back and forth at will?!? And what about the legend about the alchemists? Is not the key term there really transformation?!? And has not the "smoke screen" really been delivered so effectively by all the concentration upon the substance?!? And does not this remind one indeed of all the misguided concentration upon substance rather than meaning that one finds so regularly on 3rd density??
Q: I get it! So, it is the magnetite in the body, that collects and holds the charge, and it has absolutely nothing to do with an external substance at all! Is that it?
A: You are getting "warmer."

Knowing that in the last session bloodlines were mentioned again but in the context of susceptibility to pathogens:

session 18 July 2015 said:
Q: (Perceval) The reference to bloodlines becoming parasitically infected, does that refer to certain bloodlines that were particularly targeted for infestation?
A: Yes
Q: (Perceval) As in bloodlines or genetic profiles that were more likely to have an increase in awareness or to be more of a threat to the system?
A: Yes

Added: actually Yas made the same iron / bloodlines / parasites connection in the Session 18 July 2015 thread and provides more extensive quotes of the relevant session.
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