VGCC mechanism explains all the EHS symptoms?

https://vimeo.com/132870272

It may in Martin Pall's mind but it is very obvious that there is a lot he does not know about or even address. If you read his book he does not address Ach at all. He deals with only one aspect in any depth.  This is a catastrophic failure to recognise the obvious. It looks like he is just trying to sell books to me. It is good the he recognises his own weaknesses but it would not be correct to say that with a pollution as all invasive and penetrating that the the only system effected by voltage IE calcium. The effects of EMR are multiple individualised and as varied as the the different pattern of radiations. Pulsed, modulated etc. Most significant he has no "cure" that works. Apart from the obvious, get out of the radiations.

 The real eye opener is "THE ELECTROMAGNETIC MAN"  br Cyril Smith. A must for any one trying to understand where we have come from and how we got here. ISBN 13: 9780460860444
Proff Andrew Goldsworthy  is really the man of now but is old and retired. Definitely needs to be read now. He understands it all.

Rev Environ Health. 2015;30(4):251-71. doi: 10.1515/reveh-2015-0027.
https://www.ncbi.nlm.nih.gov/pubmed/26613326

Reliable disease biomarkers characterizing and identifying electrohypersensitivity and multiple chemical sensitivity as two etiopathogenic aspects of a unique pathological disorder.
Belpomme D, Campagnac C, Irigaray P.

Abstract

Much of the controversy over the causes of electro-hypersensitivity (EHS) and multiple chemical sensitivity (MCS) lies in the absence of both recognized clinical criteria and objective biomarkers for widely accepted diagnosis. Since 2009, we have prospectively investigated, clinically and biologically, 1216 consecutive EHS and/or MCS-self reporting cases, in an attempt to answer both questions. We report here our preliminary data, based on 727 evaluable of 839 enrolled cases: 521 (71.6%) were diagnosed with EHS, 52 (7.2%) with MCS, and 154 (21.2%) with both EHS and MCS. Two out of three patients with EHS and/or MCS were female; mean age (years) was 47. As inflammation appears to be a key process resulting from electromagnetic field (EMF) and/or chemical effects on tissues, and histamine release is potentially a major mediator of inflammation, we systematically measured histamine in the blood of patients. Near 40% had a increase in histaminemia (especially when both conditions were present), indicating a chronic inflammatory response can be detected in these patients. Oxidative stress is part of inflammation and is a key contributor to damage and response. Nitrotyrosin, a marker of both peroxynitrite (ONOO°-) production and opening of the blood-brain barrier (BBB), was increased in 28% the cases. Protein S100B, another marker of BBB opening was increased in 15%. Circulating autoantibodies against O-myelin were detected in 23%, indicating EHS and MCS may be associated with autoimmune response. Confirming animal experiments showing the increase of Hsp27 and/or Hsp70 chaperone proteins under the influence of EMF, we found increased Hsp27 and/or Hsp70 in 33% of the patients. As most patients reported chronic insomnia and fatigue, we determined the 24 h urine 6-hydroxymelatonin sulfate (6-OHMS)/creatinin ratio and found it was decreased (<0.8) in all investigated cases. Finally, considering the self-reported symptoms of EHS and MCS, we serially measured the brain blood flow (BBF) in the temporal lobes of each case with pulsed cerebral ultrasound computed tomosphygmography. Both disorders were associated with hypoperfusion in the capsulothalamic area, suggesting that the inflammatory process involve the limbic system and the thalamus. Our data strongly suggest that EHS and MCS can be objectively characterized and routinely diagnosed by commercially available simple tests. Both disorders appear to involve inflammation-related hyper-histaminemia, oxidative stress, autoimmune response, capsulothalamic hypoperfusion and BBB opening, and a deficit in melatonin metabolic availability; suggesting a risk of chronic neurodegenerative disease. Finally the common co-occurrence of EHS and MCS strongly suggests a common pathological mechanism.

There are also many other induced effects that are not covered in these markers. These are just the most testable ones.  Did not their mums tell them not to play with the electricity?  Some people never listen!

https://www.sciencedirect.com/science/article/pii/S2305050015000305




6.2. Pesticides inhibit acetylcholine esterase

An acetylcholine esterase inhibitor (AChEI) or anti-cholinesterase is a chemical that inhibits the acetylcholine esterase enzyme from breaking down acetylcholine (Figure 1), thereby increasing both the level and duration of action of the neurotransmitter acetylcholine. Existence of reversible, quasi-irreversible and irreversible inhibitors of ACh like chloropyrifos, Malathion has been reported [65]. Increase in acetylcholine inhibits the release of gonadotrophin releasing hormone (GnRH) and that inhibits release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). It results into inhibition of gametogenesis and steroidogenesis [66,67]. So, it is quiet likely that synthesis of testosterone being a steroid hormone may get hampered that could further result in erectile dysfunction. Pesticides like chlorpyrifos and carbofuran inhibit acetylcholine esterase [68,69]. Hence increased acetylcholine suppresses the reproductive functions [53–57].

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Figure 1. Inhibitory action of pesticides on Acetylcholine esterase.
6.3. Oxidative stress

Oxidative stress occurs when cells are exposed to excessive levels of reactive oxygen species (ROS) as a result of an imbalance between pro-oxidants and the protective mechanisms conferred by antioxidants [70]. ROS are formed during regular metabolism due to the univalent reduction of oxygen molecule. Superoxide (O2−) is the most important among the ROS. Organophosphate induces production of ROS and hence causes reproductive tissue damage [71]. Atrazine and imidachloroprid is also responsible for oxidative stress by reducing levels of glutathione [59,60]. Hydrogen peroxide (H2O2), hypochlorous acid (HOCL), and peroxynitrite (OONO−) are other important free radicals implicated in the pathophysiological mechanism of vascular disease. The vascularendothelium is the major source for these free radicals. Besides this, platelets and leukocytes are the other important sources of ROS [72]. Superoxide radicals are generated because of incomplete oxygen reduction in the electron transport system. Membrane bound enzymes, such as nicotinamide adenine dinucleotide hydrogenase–nicotinamide adenine dinucleotide phosphate hydrogenase oxidase, are the major source of superoxide radicals in activated phagocytic cells [73]. It has been reported that up regulation of these enzymes is associated with an increased risk of vascular disease [74,75]. Superoxide dismutase (SOD) is an important enzyme that removes the superoxide radicals from the human body. There are 3 types of SOD isoenzymes: cytosolic Cu Zn-SOD, mitochondrial Mn SOD, and extracellular SOD. Extracellular SOD reportedly plays a critical role in maintaining the redox state of vascular interstitium and thereby prevents the pathophysiological effects of superoxide in the vasculature. Extracellular SOD converts superoxide to H2O2.

The interaction between NO and ROS is one of the important mechanisms implicated in the pathophysiological process of erectile dysfunction [76]. NO interacts with superoxide to form peroxynitrite, which has been reported to play a central role in atherogenesis [72]. The stability of peroxynitrite allows a greater opportunity for it to diffuse through a cell to find a target. The unusual stability of peroxynitrite is due to its being folded into the &-conformation (Figure 2), which cannot directly isomerize to the much more stable form, nitrate [77]. Peroxynitrite reacts with the tyrosyl residue of proteins, which inactivates superoxide dismutase and leads to increased amount of superoxide [78]. This further increases the formation of peroxynitrite and reduces the available NO concentration. Peroxynitrite causes smooth-muscle relaxation and is less potent than NO. The effect of NO and peroxynitrite have been studied on stripped cavernosal tissue from rabbits [79]. They reported that relaxation induced by NO is short lived and immediate in onset compared with that due to peroxynitrite, which is prolonged and slow in onset. Moreover, the tissues returned to original tension immediately with NO, whereas with peroxynitrite, the tissues were unable to recover their original tension. These mechanisms ultimately produce an ineffective relaxation in cavernosal tissue, which produces erectile dysfunction shown in Figure 3.

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Figure 2. Pesticides causing oxidative stress.

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Figure 3. Apoptotic and necrotic action of pesticides.
6.4. Apoptosis and necrosis

The new findings are consistent with the well-known involvement Ca2+ in cell death from oxidative stress. Oxidative stress causes Ca2+ influx into the cytoplasm from the extracellular environment and from the endoplasmic reticulum [80]. Rising Ca2+ concentration in the cytoplasm in turn causes Ca2+ influx into the mitochondria and nuclei. In the mitochondria, Ca2+ accelerates the disruption of normal oxidative metabolism leading to necrotic cell death. In nuclei, Ca2+ modulates gene transcription and nucleases that control apoptosis (programmed cell death that involves fragmentation of DNA). Insecticides and pesticides has been shown to act as reproductive toxicants in male rats and histologically induce severe focal necrosis of the germinal cells in seminiferous tubules associated with tubular atrophy (shown in Figure 3). [81–83] NO interact with peroxide to form peroxynitrile. Peroxynitrite and superoxide have been reported to increase the incidence of apoptosis in the endothelium. This leads to denudation of endothelium and reduction of available NO [77,79]. Currently, the following are considered biomarkers of vascular endothelial dysfunction: insulin resistance, homocysteinemia, lipoprotein (a), endogenous nitric oxide (NO) synthesis inhibitors, vasodilators (nitrites, nitrates, and 6-keto prostaglandin F1a), adhesion molecules (vascular adhesion molecule-1 [VCAM-1], intercellular adhesion molecule-1 [ICAM-1], and P- and E-selectins), and thrombotic hemostatic factors [84]. Since, endothelium is made up of endothelial cells and these cells are responsible for NO production via eNOS. Superoxide is reported to have a direct vasoconstriction effect through mobilization of calcium ions [85]. This can potentially produce ED. According to the literature, the decreased availability of NO is the key pathophysiological process that leads to erectile dysfunction [86].

The relevance of the above is that exposure to NI radiations has the same effect as an acetylcholine esterase inhibitor (AChEI) or anti-cholinesterase.  This means that if your lucky enough not to be exposed to pesticide you are getting the same poisoning effect from NI radiations.

Symptoms of High Acetylcholine

Subdued or depressed mood
Anhedonia (inability to experience pleasure)
Difficulty concentrating
Difficulty with higher-order or complex thought processes
Mental fatigue
Mental confusion
Memory problems
Decreased motivation
Feeling overly sleepy or tired (particularly in the evening), despite adequate sleep and rest
Difficulty understanding or performing tasks
Pessimistic, negative ideation or rumination
Feelings of helplessnes and hopelessnes
ETC ....  many more


Note: There is an inverse, antagonistic relationship between acetycholine (ACh) and serotonin (SE) in the brain. In other words as the quantity of one increases, the quantity of the other decreases. A certain amount of ACh is necessary for normal, optimal brain function. Memory, motivation, higher-order thought processes, sexual desire and activity, and sleep (among other things) depend on ACh. In lower amounts, ACh can act like a stimulant by releasing norepinephrine (NE) and dopamine (DA).  However, those brain chemicals are used up (depleted) in the process; and a deficiency can occur. Too much ACh relative to other brain chemicals such as SE, NE, and DA has an adverse effect on brain function. This is because in larger quantities ACh acts like an inhibitory neurotransmitter, causing increased nervous system inhibition (depression). Important to remember is that, in general, as ACh levels go up in the brain, the levels of the other brain transmitters go down.

In terms of mood, the combination of higher ACh and NE, together with lower SE, produces anxiety, emotional lability, irritability, anger, aggressiveness, negative rumination, impatience, and impulsiveness (among other things). When NE, DA, and SE are low and acetylcholine is high, the result is simply depression. SSRI antidepressants, by increasing serotonin, are able to lower acetylcholine levels, thereby lessening or eliminating the symptoms associated with high acetylcholine. However, the major drawback is that increasing serotonin also leads to a reduction of norepinephrine and dopamine in the brain. Therefore, long-term use of SSRI antidepressants will result in a high serotonin condition, which is actually another type of depression (see separate article on this site about serotonin). So, in spite of all of the publicity and common usage, SSRI antidepressants are really not the best choice (at least, not in the long run) for treating depression. Unless the problem of low NE and DA is also addressed, a high acetylcholine depression, in time, will merely be replaced by a high serotonin depression. This explains why SSRI antidepressants do not help everyone, lose their effectiveness over time, make some people more depressed, or cause intolerable side effects.



http://mindrenewal.us/page13.html

This excess of ACh is induced by exposure to EMRs.   Seem familiar?

Nicotinic antagonist
From Wikipedia, the free encyclopedia

A nicotinic antagonist is a type of anticholinergic drug that inhibits the action of acetylcholine (ACh) at nicotinic acetylcholine receptors. These compounds are mainly used for peripheral muscle paralysis in surgery, the classical agent of this type being tubocurarine,[1] but some centrally acting compounds such as bupropion, mecamylamine, and 18-methoxycoronaridine block nicotinic acetylcholine receptors in the brain and have been proposed for treating nicotine addiction.[medical citation needed]

Would/could these help?   They should counter the effects at the nicotine receptor.   My response was extremely good.

Atropine works on the muscaric receptors apparently.

Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation


http://www.tandfonline.com/doi/full/10.3109/15368378.2015.1043557?src=recsys


ABSTRACT

This review aims to cover experimental data on oxidative effects of low-intensity radiofrequency radiation (RFR) in living cells. Analysis of the currently available peer-reviewed scientific literature reveals molecular effects induced by low-intensity RFR in living cells; this includes significant activation of key pathways generating reactive oxygen species (ROS), activation of peroxidation, oxidative damage of DNA and changes in the activity of antioxidant enzymes. It indicates that among 100 currently available peer-reviewed studies dealing with oxidative effects of low-intensity RFR, in general, 93 confirmed that RFR induces oxidative effects in biological systems. A wide pathogenic potential of the induced ROS and their involvement in cell signaling pathways explains a range of biological/health effects of low-intensity RFR, which include both cancer and non-cancer pathologies. In conclusion, our analysis demonstrates that low-intensity RFR is an expressive oxidative agent for living cells with a high pathogenic potential and that the oxidative stress induced by RFR exposure should be recognized as one of the primary mechanisms of the biological activity of this kind of radiation.

Could Myelin Damage From Radiofrequency Electromagnetic Field Exposure Help Explain the Functional Impairment Electrohypersensitivity? A Review of the Evidence.

http://www.tandfonline.com/doi/abs/10.1080/10937404.2014.923356

Abstract

Myelin provides the electrical insulation for the central and peripheral nervous system and develops rapidly in the first years of life, but continues into mid-life or later. Myelin integrity is vital to healthy nervous system development and functioning. This review outlines the development of myelin through life, and then considers the evidence for an association between myelin integrity and exposure to low-intensity radiofrequency electromagnetic fields (RF-EMFs) typical in the modern world. In RF-EMF peer-reviewed literature examining relevant impacts such as myelin sheath, multiple sclerosis, and other myelin-related diseases, cellular examination was included. There are surprisingly little data available in each area, but considered together a picture begins to emerge in RF-EMF-exposed cases: (1) significant morphological lesions in the myelin sheath of rats; (2) a greater risk of multiple sclerosis in a study subgroup; (3) effects in proteins related to myelin production; and (4) physical symptoms in individuals with functional impairment electrohypersensitivity, many of which are the same as if myelin wereaffected by RF-EMF exposure, giving rise to symptoms of demyelination. In the latter, there are exceptions; headache is common only in electrohypersensitivity, while ataxia is typical of demyelination but infrequently found in the former group. Overall, evidence from in vivo and in vitro and epidemiological studies suggests an association between RF-EMF exposure and either myelin deterioration or a direct impact on neuronal conduction, which may account for many electrohypersensitivity symptoms. The most vulnerable are likely to be those in utero through to at least mid-teen years, as well as ill and elderly individuals.

The implications of non-linear biological oscillations on human electrophysiology for electrohypersensitivity (EHS) and multiple chemical sensitivity (MCS).

https://www.ncbi.nlm.nih.gov/pubmed/26368042

Abstract

The 'informational content' of Earth's electromagnetic signaling is like a set of operating instructions for human life. These environmental cues are dynamic and involve exquisitely low inputs (intensities) of critical frequencies with which all life on Earth evolved. Circadian and other temporal biological rhythms depend on these fluctuating electromagnetic inputs to direct gene expression, cell communication and metabolism, neural development, brainwave activity, neural synchrony, a diversity of immune functions, sleep and wake cycles, behavior and cognition. Oscillation is also a universal phenomenon, and biological systems of the heart, brain and gut are dependent on the cooperative actions of cells that function according to principles of non-linear, coupled biological oscillations for their synchrony. They are dependent on exquisitely timed cues from the environment at vanishingly small levels. Altered 'informational content' of environmental cues can swamp natural electromagnetic cues and result in dysregulation of normal biological rhythms that direct growth, development, metabolism and repair mechanisms. Pulsed electromagnetic fields (PEMF) and radiofrequency radiation (RFR) can have the devastating biological effects of disrupting homeostasis and desynchronizing normal biological rhythms that maintain health. Non-linear, weak field biological oscillations govern body electrophysiology, organize cell and tissue functions and maintain organ systems. Artificial bioelectrical interference can give false information (disruptive signaling) sufficient to affect critical pacemaker cells (of the heart, gut and brain) and desynchronize functions of these important cells that orchestrate function and maintain health. Chronic physiological stress undermines homeostasis whether it is chemically induced or electromagnetically induced (or both exposures are simultaneous contributors). This can eventually break down adaptive biological responses critical to health maintenance; and resilience can be compromised. Electrohypersensitivity can be caused by successive assaults on human bioelectrochemical dynamics from exogenous electromagnetic fields (EMF) and RFR or a single acute exposure. Once sensitized, further exposures are widely reported to cause reactivity to lower and lower intensities of EMF/RFR, at which point thousand-fold lower levels can cause adverse health impacts to the electrosensitive person. Electrohypersensitivity (EHS) can be a precursor to, or linked with, multiple chemical sensitivity (MCS) based on reports of individuals who first develop one condition, then rapidly develop the other. Similarity of chemical biomarkers is seen in both conditions [histamines, markers of oxidative stress, auto-antibodies, heat shock protein (HSP), melatonin markers and leakage of the blood-brain barrier]. Low intensity pulsed microwave activation of voltage-gated calcium channels (VGCCs) is postulated as a mechanism of action for non-thermal health effects.

2.45 GHz radiofrequency fields alter gene expression in cultured human cells.

https://www.ncbi.nlm.nih.gov/pubmed/16107253

Abstract

The biological effect of radiofrequency (RF) fields remains controversial. We address this issue by examining whether RF fields can cause changes in gene expression. We used the pulsed RF fields at a frequency of 2.45 GHz that is commonly used in telecommunication to expose cultured human HL-60 cells. We used the serial analysis of gene expression (SAGE) method to measure the RF effect on gene expression at the genome level. We observed that 221 genes altered their expression after a 2-h exposure. The number of affected genes increased to 759 after a 6-h exposure. Functional classification of the affected genes reveals that apoptosis-related genes were among the upregulated ones and the cell cycle genes among the downregulated ones. We observed no significant increase in the expression of heat shock genes. These results indicate that the RF fields at 2.45 GHz can alter gene expression in cultured human cells through non-thermal mechanism.

Electrohypersensitivity: a functional impairment due to an inaccessible environment.
Johansson O.

https://www.ncbi.nlm.nih.gov/pubmed/16107253

Abstract

In Sweden, electrohypersensitivity is recognized as a functional impairment which implies only the environment as the culprit. The Swedish view provides persons with this impairment a maximal legal protection, it gives them the right to get accessibility measures for free, as well as governmental subsidies and municipality economic support, and to provide them with special Ombudsmen (at the municipality, the EU, and the UN level, respectively), the right and economic means to form disability organizations and allow these to be part of national and international counterparts, all with the simple and single aim to allow persons with the functional impairment electrohypersensitivity to live an equal life in a society based on equality. They are not seen as patients, the do not have an overriding medical diagnosis, but the 'patient' is only the inferior and potentially toxic environment. This does not mean that a subjective symptom of a functionally impaired can not be treated by a physician, as well as get sick-leave from their workplace as well as economic compensation, and already in the year 2000 such symptoms were identified in the Internal Code of Diagnoses, version 10 (ICD-10; R68.8/now W90), and have been since. But the underlying cause still remains only the environment.

I've been anxious and depressed since leaving my job.
I had been on Remeron at a low does for years and decided to increase it and see what happens and all I got were strange dreams and feeling spacy.
I tried natural remedies to varying effect but always woke up very anxious so I decided to go back to the Remeron which really helped me 10 years ago.
Remeron isn't an SSRI so I don't know what effect ot has on what you are describing.
I also had some strange feeling in my eyes, lost focus a couple of times and feel pressure behind them and a lot of brain fog.
I have fibromyalgia but was concerned that it could be MS. My doctor ordered a Ct Scan of my head but I know an MRI would better detect MS. Also concerned about the radiation from the Ct Scan.

Interesting articles, thank you, Plop.

And Steve, I don't know what to tell you, as I have no experience with drugs.
I just know drugs never worked for me, I'm more than 50, the last 20 years I barely touched an aspirine.

I think they cause me the opposite: bring me out of a healthy state, pollute my body, create chronic diseases that get harder to heal after, damage organs, nerves, stomach, gut...

I long gave up on drugs. I prefer homeopathy and energy medicine.
They at least, do not damage me, and I can tune them as I want.

I hope you find someone to help you.

Jinna wrote

https://vimeo.com/132870272

Quoted from:
http://es-forum.com/VGCC-mechanism-explains-all-the-EHS-symptoms-tp4031619.html

Hi Jinna,

My investigations about causal mechanism emphasise the heart, which creates a large magnetic field, detectable at 2meters and the magnetic field envelops the brain.

I believe that the ferromagnetic receptive capacity of mammals is implicated in mechanism to explain eM band sensitivity to Wireless electromagnetic fields.

The neurons of our brains, like those of all mammals and Avian species (birds) has the same ferromagnetic compound.  All mammalian species evidence magnetic sensitivity.  Birds migratory instincts are ferromagnetic.

eM band information (electromagnetic radiation) of the Wireless range interacts with magnetism.  I believe humans suffering from eM sensitivity are mammals in the process of recovering ferromagnetic instinct.

stavros

There's a PS.

the heart bears approximately 50,000 neurons of biology like neurons in the brain.  Although that represents a very small percentage of the number of neurons in the brain, the heart's kickass magnetic field means that a small number of neurons with that size magnetic field are impacted, by ratio, very greatly.

If anyone remembers Sydney Sheldon, Maxwell Smart and an episode "but Max, the mini magnet is more powerful than the maxi magnet" it's a metaphor I offer to kind of emphasise mechanism.  So a Wireless device near this magnetic field with the ferromagnetic compound in such neuronal cells, in the heart, then in the brain, it's not a long shot at all to implicate wireless sensitivity with such a basic biological substrate.

Wireless Lambda (wavelength) being longer than redband eM radiation means that it's energy would be more greatly influenced by magnetic fields of the heart.

Stav

Stavros, yep, certainly it seems that metals in the body play some role in this antenna effect.

And here in Switzerland, there was a research on cell phone towers and bees, somehow proving that many bees loose their ability to come back to the colony if their colony is close to a mast.

I don't remember which university did that (from Lausanne?).

Interesting point about the magnetic field being amplified in the heart. And the brain, I suppose?

------------------------------------


Recently, I 've been reading about fat-soluble toxins.
Heavy metals are fat soluble, so they like to bind to fat cells, nerve cells and joint liquid. All fat-rich.

It seems it's simply a matter of chemistry: they dissolve in fat.

Fatter people tend to be also more relaxed, possibly because they store toxins in their fat cells.
Thinner people are usually more anxious, POSSIBLY because the toxins will go directly to joints (sinovial liquids) AND to brain cells / nerve cells.

It means, more heavy metals there, which could explain the antenna effect....

If the radiation signals still get magnified, well, it's not a good thing, specially when we are loaded with metals...

That's really disturbing about bees.  To lose your homing instinct or to lose your direction home is really disturbing and I'm sure the bee hive mind or nett hive life is affected.

thank you for prompting that about bees.  I'll keep an eye out for that area as well here forwards.

kind regards

http://www.dailymail.co.uk/sciencetech/article-1386124/Why-mobile-phone-ring-make-bees-buzz-Insects-infuriated-handset-signals.html

https://inhabitat.com/its-official-cell-phones-are-killing-bees/

--------------------------
Hey, I found the main scientific article published in English!!:
https://link.springer.com/article/10.1007%2Fs13592-011-0016-x

Honeybees possess magnetite crystals in their fat body cells and they present magnetic remanence (Gould et al. 1978; Keim et al. 2002).

These magnetite structures are active parts of the magnetoreception system in honeybees (Hsu and Li 1994; Hsu et al. 2007).

 Honeybees can be trained to respond to very small changes in the constant local geomagnetic field intensity (Walker and Bitterman 1989a).

"In that study, magnetic anomalies as low as 26 nT (nanoTesla) were responsible for changes in the foraging behavior (of bees).

  Therefore, it remains to be established which minimal level in variations of the local pulsed electromagnetic fields induced by mobile phone handsets and base stations might trigger changes in the bees’ behavior, such as the induction of honeybee worker piping shown here. "

That was in the conclusion part.

There was no study with cell masts, as I thought.

They placed mobile phones and dect stations inside hives to see what happens. Catastrophe.
----------------------

I guess the study with mast towers I heard was another study, that the author mentions here:


"Recently, a study suggested that cell phones and cellphone towers near beehives interfere with honeybee navigation: in one experiment, it was found that when a mobile phone was kept near a beehive it resulted in collapse of the colony in 5 to 10 days, with the worker bees failing to return home, leaving the hives with just queens, eggs and hive-bound immature bees (Sahib Pattazhy 2009).

To minimize harm to the bees, it was decided to limit their continuous exposure to mobile phone communications to a maximum of 20 h in the present study."