Top class magnetic therapy
There is no lack of evidence that geomagnetic storms of solar origin sometimes have a significant impact on the central nervous and, above all, vegetative parameters of humans and animals. Changes in blood pressure [1] , [2] , [3] , heart attack rate [4] , [5] , [6] , [7] , [8] , the frequency of epilepsy attacks [9] , the increase in suicides [ 10] , [11] , strokes [12] , accidents [13] or mood changes (depression and states of aggression) are just a few of the many examples.
The underlying physiological mechanisms are not yet fully understood, which is also related to the frequency of around 2.8 GHz, which is not familiar for PEMF, and also to ultraviolet radiation. In any case, there is a short-term weakening of the earth’s magnetic field, which, however, is only in the range of around 250 nT.
This sounds very low compared to the natural earth’s magnetic field of around 50 µT. On the other hand, magnetic field intensities in the middle nT range are quite comparable with therapeutic PEMF, since intensities in the pT range are already effective in the treatment of central nervous disorders such as multiple sclerosis or Parkinson’s disease [14] , [15] . In any case, there are many indications that geomagnetic storms do not respond directly to the organ systems, but rather to the timing of the pituitary gland and the autonomic nervous system.
A geomagnetic storm is a disturbance of the natural earth’s magnetic field. This is triggered by the “solar wind” or solar eruptions and usually lasts 1 to 2 days. The earth’s magnetic field is abruptly weakened by 50 – a maximum of 650 nT.
In order to adapt to constantly changing conditions and to ensure survival by means of a lightning-fast response, a nervous system has developed in highly developed organisms, including humans, that conducts almost all bodily functions independently of the mind, motivation, desire and intention. It consists of the opponents sympathetic and parasympathetic, whereby the sympathetic in the sense of a fight and flight reaction (“fight or flight” [16] ), for example, increases the blood flow to the muscles, widens the bronchi, increases the heartbeat and blood pressure or increases digestion immobilize.
The parasympathetic, on the other hand, has the task of relaxation, that is, after a challenging situation, “licking the wounds”, gathering strength, sinking into a restful sleep, giving space for digestion and overall serving the hedonistic principle of pleasure and self-actualization , So there is no important organ that is not “unconsciously” influenced by the vegetative or is even controlled directly. We can see this from the fact that all of the body functions necessary for survival, such as breathing, heartbeat and metabolic functions, function without our conscious intervention, although the brain stem is also involved here.
However, the vegetative is not the only actor acting independently of our consciousness. Rather, the actual control center lies in the diencephalon, which programs and controls the vegetativeum as the hypothalamus and which has to produce the homeostasis of vegetative, hormonal and somatic functions.
Since the stress pioneers Walter Cannon [17] , Hans Selye [18] or Paul Rosch [19] at the latest, there has been little doubt that a large part of all chronic (and in some cases also acute) illnesses directly or indirectly with chronic stress or one as a result caused impaired regulatory ability of the autonomic nervous system. Because when the sympathetic nervous system gains the upper hand and becomes independent by setting the smallest key stimuli in the mode of a “constant fire”, its direct signal receivers such as the cardiovascular system, central nervous structures, hormone-forming glands or the inflammatory process are forced into one Continuous operation and a subsequent exhaustion reaction.
Stress is any type of stress that forces the organism to adapt. Although the associated hormonal change is natural and increases performance, this evolutionarily developed protective mechanism is very often exaggerated after the original pattern of action of fight and flight in modern life is mostly only mentally fought out.
If one takes a closer look at the course of a stress reaction, both the limbic systems – sympathetic nerve – adrenal medullary axis (LSNMA) and the hypothalamic-pituitary axis-adrenal axis (HPA) play a key role [20] . If a stress stimulus arrives, an emotional reaction in the form of anger, fear, aspiration, envy, greed etc. arises in the limbic system. The messenger substance glutamate thus produced in turn initiates noradrenaline, which reaches the adrenal medulla and stimulates the synthesis of adrenaline there.
The limbic system, which only mammals possess, is more an electrical functional circuit than a locality that can be found somewhere between the neocortex (cerebral cortex) and the midbrain together with the hippocampus (memory) and the hypothalamus. It is responsible for fear, love, anger, lust, motivation and repression. Laughter and crying also originate here.
Minutes later, the pituitary gland signals the pituitary gland to instruct the adrenal cortex to release increased amounts of cortisol. This is done via the messenger substance ACTH.
Cortisol (the body’s own cortisone) supports the energy supply for the physical changes caused by the sympathetic nervous system or by adrenaline (adrenaline increases vascular tone, blood pressure and heart rate, among other things), for example by increasing the blood sugar level and also providing fatty acids. At the same time, it slows down the microcirculation in order to secure the increase in blood pressure induced by the adrenaline. Although it also ensures short-term well-being, it has an immunosuppressive (“dampening”) and strong anti-inflammatory effect.
While adrenaline and noradrenaline undergo a relatively rapid enzymatic breakdown, the cortisol level can remain at a high level through constant new production. In the hippocampus, a part of the brain that, like the hypothalamus and the pituitary gland, is located in the midbrain or the “limbic system”, there is a measuring system in the form of receptors that constantly inform the hypothalamus about the level of cortisol levels.
If there is constant stress, which is not uncommon in today’s professional life, the cortisol receptors are damaged. The hypothalamus no longer receives any information about the cortisol concentration, ie the natural feedback mechanism is destroyed. Via the hypothalamus and increased sympathetic activation, cortisol production is increasingly rocking – which in turn further damages cortisol receptors [21] .
To make matters worse, the receptor sensitivity decreases with increasing age [22] . This also corresponds to the aging theory of the Russian Dilman, who as early as the 1960s found that a stress response is stronger in older people and lasts longer than in young people [23] , [24] . Who is not familiar with the situation at the supermarket checkout, where older people who, based on their experience, would have to stand calmly over things, are trembling with excitement for their wallets.
Furthermore, a permanently elevated cortisol level is a risk factor for the development of dementia and also has a negative effect on memory formation and memory capacity in healthy people [25] , [26] . Because in addition to the cortisol receptors, the hormone also damages other areas in the hippocampus, the part of the brain that is responsible for learning and memory processes. From animal experiments it is known that low stress hormones slow the memory decline in old age. On the other hand, animals with an excessive cortisol response seem to lose more thought and memory as they get older.
The civilization man in particular is helplessly exposed to the cortisol flood because only through a lot of exercise and physical exertion can an accelerated breakdown of stress hormones occur [27] , [28] , [29] .
Probably because of the activation of pro-inflammatory cytokines, chronic stress contributes to the development of atherosclerosis [30] , [31] , [32] and is therefore an important risk factor for a myocardial infarction [33] and a stroke [34] . Psychological distress is also a suitable predictor or predictor of mortality [35] .
For example, in a cohort study (27 studies) with over 600,000 men and women who reported stress at work, the risk of a heart attack or sleep attack was up to 40% higher than that of people who were not stressed [36] . The result of the INTERHEART study that psychosocial stress is an independent cardiovascular risk factor is only the reminiscence of what is actually familiar [37] .
If one takes into account that chronic stress automatically also causes oxidative stress, ie an increase in reactive oxygen species (ROS) can be expected, stress should be one of the strongest promoters for the aging process [38] . Regardless of this, there is also evidence that chronic stress leads to a shortening of the telomeres, ie the “protective caps” on the chromosomes [39] , [40] , [41] , [42] , [43] . Because every cell division leads to a shortening of the telomeres. If they fall below a certain length, the chromosome is damaged and the cell can no longer divide and is rejected. The stress hormone cortisol, for example, slows down the repair enzyme telomerase, which can counteract telomer shortening [44] .
According to current surveys, the prevalence of chronic stress (without social support) is 32% (women) and 20.8% (men) [45] , which almost inevitably leads to dysregulation of the autonomic nervous system. Usually this means a dominance of the sympathetic nervous system, ie the parasympathetic nervous system leads to a niche existence, which sometimes leads to an increased activation (“discharge”) after a long sympathetic episode.
Typical examples of “parasympathetic disorders” are migraines [46] , [47] and asthma [48] , [49] . Migraines occur frequently on days off and on weekends [50] , [51] , with fewer attacks on Sundays [52] . This is probably related to the fact that Sundays are usually burdened with the anticipation of a “difficult” week and thus the sympathetic nervous system is increasingly activated. A non-allergic asthma attack does not occur during arousal (sympathetic nervous system), but only afterwards.
Sleep disorders are one of the most common health complaints. According to surveys, around 25% of adults suffer from sleep problems, and over 10% often or permanently experience their sleep as not restful [53] . According to other data, the worldwide prevalence is between 10 – 30% [54] , [55] . Although not all sleep disorders can be attributed to chronic stress, a clear relationship can generally be demonstrated [56] , [57] , [58] , [59] . A reduction in the deep sleep phases in favor of the REM phases (dream phases) could be the underlying mechanism for sleep problems [60] .
In this context, it also makes sense to suspect a link between cancer and chronic stress [61] , [62] . This does not mean the fact that further cancer growth and metastasis is triggered via the sympathetic nervous system in an existing cancer [63] , [64] . Rather, in some psychotherapeutic cancer models [65] , [66] a long-term dominance of the sympathetic versus the parasympathetic plays a not unimportant role or in the imbalance of an adaptive oscillation between the two vegetative poles.
To what extent a permanent activation of the sympathetic nervous system leads to a so-called “regulatory stiffness” has not been scientifically investigated, nor does a conclusive counter-model to cancer development result from this. Popular scientific statements that adrenal fatigue can occur after chronic stress (“adrenal fatigue”) are definitely not true. According to a systematic review that analyzed a total of 3 470 studies from the beginning to April 2016, of which only 58 publications met the required evidence criteria, it is said to be a myth [67] .
At present there are only indirect indications that sympathetic dominance prevents the ability to regulate that is essential for the human organism and thus a system-relevant ability to adapt. This is evident, for example, from a weaker immunological response after an infection, or that adults and especially the elderly hardly ever have as high a fever as children. The result – instead of healing – is the tendency to chronify.
Only a few studies have been indexed in the PubMed and Embase databases on influencing the vegetative nervous system or on stress treatment using PEMF. However, it must be taken into account that indications such as insomnia, migraines, myocardial infarction, microcirculation, arterial hypertension, stroke, etc., in which always dysregulation of the autonomic nervous system plays a role, are not explicitly identified as vegetative diseases.
For example, an investigation into different PEMF setting parameters (intensity) showed that a PEMF application mainly affects the sympathetic nervous system [68] . The HRV determination (Heart Rate Variability) showed that the VLF (Very Low Frequencies), which stand for the sympathetic nervous system, recovered faster than placebo after a previous stress exposure under PEMF. Overall, a 20-minute PEMF application led to an improvement in HRV.
Stress and the associated vegetative changes have long been measured using the so-called HRV (heart rate variability). The HRV is now a recognized global indicator of health because it reflects the psycho-physiological balance of people. It describes the rhythmic fluctuations in the heart rate and thus enables an insight into the sympatho-vagal adjustment mechanism [69] . This is based on the fact that the duration of a heartbeat constantly varies in the millisecond range. For example, once 0.812 s, then 0.857, then 0.798, etc.
In sum, this brings a heart rhythm of 72 beats per minute, for example. The more evenly the heart rate in apparently healthy people or figuratively “the more accurate, sensible and stuck a life is”, the more vulnerable the person is. For example, there is a risk of a heart attack, stroke or, in the event of vegetative dysregulation, even cancer. More recent data also show a strong influence on the intestinal microbiome, which in turn affects the permeability of the intestinal barrier [70] .
The consequence is an increased transfer of microbes and toxins into the bloodstream [71] , [72] , [73] . The latter studies would also explain why chronic stress is relatively closely related to chronic polyarthritis [74] .
HRV is also a central marker for determining performance and vigilance (vigilance) [75] . A deterioration in vigilance is very closely linked to changes in the autonomic nervous system, which is very sensitive to internal demands and external influences. In an HRV-controlled study, PEMF use – compared to the control group – led to a significant improvement in vigilance [76] .
In a double-blind, placebo-controlled study, 82 headache and migraine patients were treated with the PEMF system QRS (16 Hz, 5 µT) for 4 weeks. Result: All examined pain parameters improved significantly compared to the placebo group. In 76% of the active group the symptoms improved either clearly or even very strongly. This was reported by only 1 patient in the placebo group, where the symptoms worsened slightly in 8% or the result was significantly worse in 2% than before [77] .
In a further double-blind, placebo-controlled study, a total of 101 patients with sleep disorders (problems falling asleep, problems sleeping through and nightmares) were treated with the PEMF system QRS for 4 weeks. The parameters sleep time, number of sleep interruptions, sleepiness after getting up, daytime tiredness, difficulty concentrating and daytime headache were checked.
Result: 70% of the PEMF group reported a substantial or even complete improvement in their sleep problems. 24% reported a clear improvement and 6% a slight improvement. In contrast, only 2% of the placebo patients had a clear improvement in sleep, 49% reported a slight or clear improvement and 49% the treatment was unsuccessful [78] .
While the approach to osteoarthritis or tendinitis lies, for example, in the inhibition of inflammation, improved microcirculation is crucial for wound healing, or in the case of musculoskeletal pain, the resolution of myofascial syndromes or the activation of the body’s own opioid system is important, it remains unclear how to look directly PEMF effect on the vegetative, the HPA axis or the associated diseases has to be presented.
Basically, dysregulation or an imbalance between the sympathetic and parasympathetic nervous system can always be assumed in the case of vegetative diseases. The sympathetic seems to have become “independent”, ie all structures and organs connected to it are subject to a constant, activating impulse. This can no longer be compensated for by an occasional flashing parasympathetic nervous system. This is often even counterproductive, because a “pent-up” parasympathetic nervous system can react excessively during occasional periods of psychological rest, so that – with the appropriate predisposition – a migraine or non-allergic asthma develops.
On the one hand, there is evidence that cell activity reacts to certain electro-magnetic impulses and that there are even “receiving antennas” (receptors) whose irritation leads to the formation of messenger substances (“second messenger”) Ca ++ or cAMP [79] , [80] and cryptochromes also act as receptors here [81] , [82] , it can be assumed that the neurons of the autonomic nervous system also react identically. Of course, never selectively either on the sympathetic or parasympathetic, but for both opponents always in the same manner and intensity.
While a previously “silent” parasympathetic nervous system experiences the PEMF signals as natural stimulation, an already active, but “stuck” sympathetic nervous system is even pushed to the upper end of its activity potential in order to start up again – similar to a PC removed from the circuit to adjust and, ideally, i.e. after a series of repetitive applications, to re-establish a natural rhythm with its counterpart parasympathetic nervous system. For a better understanding it should be added here that with an increased sympathetic activity a simultaneous activation of the also stimulated parasympathetic nervous system is physiologically excluded.
A short-term push of the sympathetic nervous system should also explain the phenomenon of “initial deterioration” due to PEMF, which is observed in some cases, after an initial magnetic field treatment such as high blood pressure (“peripheral vasoconstriction or blocking of the microcirculation”) initially increases or pain symptoms further intensified ( “Sympathetic or cortisol-related increase in inflammation parameters such as the pro-inflammatory cytokines IL-1, IL-2, TNF-alpha [83] ).
It also explains why geomagnetic storms – statistically speaking – lead to short-term negative physical and psychological changes. Therefore, you should be on the safe side with an application recommendation to choose a rather low intensity and frequency range at the start of a new PEMF treatment. With extremely low-intensity magnetic field therapy systems such as QRS, the risk of initial deterioration is likely to be lower than with mT devices.
PEMF has a fundamental potential for readjusting a dysregulated vegetative nervous system. Despite specific PEMF influencing factors, it thus supports microcirculation, an anti-inflammatory effect, improves sleep problems, reduces the frequency of attacks of a migraine or that of non-allergic asthma – although to date there have been no studies, but only observations of use for the latter indication. The fact that fewer ROS (free radicals) can also result in a not inconsiderable anti-aging effect.
To what extent this also reduces the risk of heart attack or stroke is difficult to assess, since the anti-inflammatory and antiplatelet properties of PEMF are more decisive here. In any case, it does not seem impossible that with a permanent reduction of an excessive stress reaction, cognitive factors such as memory formation and ability to concentrate will benefit from it or will be preserved into old age.
[1] Ghione S et al. Do geomagnetic disturbances of solar origin affect arterial blood pressure. J Hum Hypertens 1998; 12 (11): 749-54
[2] Halberg F et al. Time structures (chronomes) of the blood circulation, populations’ health, human affairs and space weather. World Hear J 2011; 3: 1-40
[3] Stoupel e et al. Ambulatory blood pressure monitoring in patients with hypertension on days of high and low geomagnetic activity. J Hum Hypertens. 1995; 9: 293-294
[4] Cornelissen K et al. Non-photic solar associations of heart rate variability and myocardial infarction. J Atmos Sol Terr Phys. 2003; 64: 707-20
[5] Villoresi G et al. Myocardial infarct and geomagnetic disturbances: Analysis of data on morbiditiy and mortality. Biofizika 1998; 43: 623-632
[6] Malin SRC, Srivatava BJ. Correlation between heart attacks and magnetic activity. Nature 1979; 277: 646-648
[7] Stoupel E. Sudden cardiac deaths and ventricular extrasystoles on days of four levels of geomagnetic activity. J Basic Physiol Pharmacol 1993; 4: 357-366
[8] Knox EG et al. Heart attacks and geomagnetic activity. Nature 1979; 281: 564-565
[9] Persinger MA. Sudden unexpected death in epileptics following sudden, intense, increases in geomagnetic activity: Prevalence of effect and potential mechanisms. Int J Biometeorol 1995; 38: 180-187
[10] Stoupel EG et al. Space weather and human deaths distribution: 25 years’ observation (Lithuania, 1989-2013). J Basic Clin Physiol Pharmacol 2015; 26 (5): 433-41
[11] Tada H et al. Association of geomagnetic disturbances and suicides in Japan, 1999 – 2010. Environ Health Prov Med 2014; 19 (1); 64-71
[12] Feigin VL et al. Geomagnetic Storms Can Trigger Stroke. Stroke 2014; 45: 1639-14
[13] Stoupel EG et al. Traffic accidents and environmental physical activity. Int J Biometeorol 2009; 53 (6): 523-34
[14] Sandyk R. Effects of picotesla flux electromagnetic fields on dopaminergic transmission in Tourette’s syndrome. Int J Neurosc 1996; 84 (1-4): 187-94
[15] Sandyk R. Treatment with weak electromagnetic fields improves fatigue associated with multiple sclerosis. Int J Neurosci 1996; 84 (1-4): 177-86
[16] Seyle H. https://home.cc.umanitoba.ca/~berczii/hans-selye/walter-cannon-fight-or-flight-response.html
[17] Cannon WB. Vodoo death. Am Anthropol 1942. 44 (new series): 169-181
[18] Tachè Y. Hans Selye and the stress response. From “the first mediator” to the identification of the hypothalamic corticotrophin-releasing factor. Ideggyogy Sz 2014; 67 (3-4): 95-8
[19] Rosch PJ. Cholesterol does not cause coronary heart disease in contrast to stress. Scand Cardiovasc J 2008; 42 (4): 244-9. Review
[20] Ramot A et al. Hypothalamic CRFR1 is essential for HPA axis regulation following chronic stress. Nature Neurosci 2017; 20: 385-388
[21] Sapolsky RM et al. Hippocampal damage associated with prolonged glucocorticoid exposure in primates. J Neurosci 1990; 10 (9): 2897-2902
[22] Boscaro M et al. Age-related changes in glucocorticoid fast feedback inhibition of adrenocorticotropin in man. J Clin Endocrinol Metabol 1998 Apr; 83 (4): 1380-3.
[23] Dilman VM. Age related elevation of hypothalamic, threshold to feedback control, and its role in development, ageine, and disease. Lancet 1971; 1 (7711): 1211-9
[24] Dilman VM, Ostroumova MN, Tsyrlina EV. Hypothalamic mechanisms of aging and of specific age pathology – II. On the sensitivity threshold of hypothalamo-pituitary complex to homeostatic stimuli in adaptive homeostasis. Experiment Gerontol 1979; 14 (4): 175-181
[25] Lara VP et al. High cortisol levels are associated with cognitive impairment no-dementia (CIND) and dementia. Clin Chim Acta 2013; 423: 18-22
[26] Newcomer JW et al. Decreased memory performance in healthy humans induced by stress-level cortisol treatment. Arch Gen Psychiatrist 1999; 56 (6): 527-33
[27] Kim JH, McKenzie LA. The impacts of physical exercise on stress coping and well-being in university students in the context of leisure. Health 2014; 6: 2570-2580
[28] Salmon P. Effects of physical exercise on anxiety, depression, and sensitivity to stress. A unifying theory. Clin Psychol Rev 2001; 21: 33-61
[29] Carmeli E. Physical activity reduces stress on anxiety. Aging Sci 2: e108
[30] Heidt T et al. Chronic variable stress activates hematopoietic stem cells. Nat Med 2014; 20 (7): 754-758
[31] Kershaw KN et al Chronic stress and endothelial dysfunction: the multi-ethnic study of atherosclerosis. On J Hypertens 2017; 30 (1): 75-80
[32] Fantidis P. Review. The role of the stress-related anti-inflammatory hormones ACTH and cortisol in atherosclerosis. Curr Vasc Pharmacol 2010; 8 (4): 517-25
[33] Dimsdale JE. Psychological stress and cardiovascular disease. J Am Coll Cardiol 2008; 51 (13): 1237-46
[34] Kotlega D et al. The emotional stress and risk of ischemic stroke. Neurol Neurochir Pol 2016; 50 (4): 265-70
[35] Somervell PD et al. Psychological distress as a predictor of mortality. Am J Epidemiol 1989; 130 (5): 1013-23
[36] Kivimäki M, Kawachi I. Work stress as a risk factor for cardiovascular disease. Curr Cardiol Rep 2015; 17 (9): 630
[37] Yusuf S et al. Effect of potentially modifiable risk factors associated with myocardial infarcation in 52 countries (The INTERHEART study): case-control-study. Lancet 2004; 364 (9438): 937-52
[38] Aschbacher K et al. Good stress, bad stress, and oxidative stress. Insights in anticipatory cortisol reactivity. Psychoneuroendocrinology 2013; 38 (9): 1698-1708
[39] Epel ES, Prather AA. Stress, telomeres, and psychopathology: Toward a deeper understanding of a triad of early aging. Annu Rev Clin Psychol 2018 Mar 1. Epub ahead of print.
[40] Epel ES et al. Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci US A. 2004; 101 (49): 17312-5
[41] Fali T, Vallet H, Sauce D. Impact of stress on aged immune system compartments: Overview from fundamental to clinical data. Exp Gerontol 2018; Feb 7. Epub ahead of print
[42] Mathur MB et al. Perceived stress and telomere length: a systematic review, meta-analysis, and methodologic considerations for advancing the field. Brain Behav Immun 2016; 54: 158-169
[43] Naomi M et al. Telomere shortening and mood disorders: preliminary support for a chronic stress model of accelerated aging. Psychiatry 2006; 60: 432-435
[44] Choi J et al. Reduced telomerase activity in human T lymphocytes exposed to cortisol. Brain Behav Immun 2008; 22 (4): 600-605
[45] Robert Koch Institute. Federal Health Gazette – Health Research – Health Protection 5/6 · 2013, pp. 750. Hapke et al. Chronic stress among adults in Germany
[46] Peroutka SJ. Migraine: a chronic sympathetic nervous system disorder. Headache 2004; 44 (1): 53-64
[47] Shechter A et al. Migraine and autonomic nervous system function: a population-based, case-control study. Neurology 2002; 58 (3): 422-7
[48] Jartti T. Asthma, asthma medication and autonomic nervous system dysfunction. Clin Physiol 2001; 21 (2): 260-9
[49] Scott GD, Fryer AD. Role of parasympathetic nerves and muscarinic receptors in Allergy and Asthma. Chem Immunol Allergy 2012; 98: 48-69
[50] Nattero G et al. Psychological aspects of weekend headache sufferers in comparison with migraine patients. Headache 1989; 29 (2): 93-9
[51] Torelli P, Cologno D, Manzoni GC. Weekend headache: a retrospective study in migraine without aura and episodic tension-type headache. Headache 1999; 39 (1): 11-20
[52] Alstadhaug KB, Salvesen R, Bekkel and S. Weekend migraine. Cephalalgia 2007; 27 (4): 343-6
[53] Federal health reporting. Robert Koch Institute Oct 2005; Volume 27.
[54] Ohayon MM. Epidemiology of insomnia: what we know and what we still need to learn. Sleep Med Rev 2002; 6: 97-111
[55] Ohayon MM. Epidemiological overview of sleep disorders in the general population. Sleep Med Rev 2011; 2: 1-9
[56] Linton SJ. Does work stress predict insomnia. A prospective study. Br J Health Psychol 2004; 9 (Pt2): 127-36
[57] Davidson LM, Fleming R. Baum A. Chronic stress, catecholamines, and sleep disturbance at Three Mile Island. J Human Stress 1987; 13 (2): 75-83
[58] Shaver JL et al. Stress exposure, psychological distress, and physiological stress activation in midlife women with insomnia. Psychosome Med 2002; 64 (5): 793-802
[59] Nakata A et al. Job stress, social support, and prevalence of insomnia in a population of Japanese daytime workers. Soc Sci Med 2004; 59 (8): 1719-30
[60] Hedge P et al. Chronic stress-induced changes in REM sleep on oscillations in the rat hippocampus and amygdala. Brain Res 2011; 1382: 155-64
[61] Saha SK et al. Review. Correlation between Oxidative Stress, Nutrition, and Cancer Initiation. Int Mol Sci. 2017; 18: 1544
[62] Gill JG, Piskounova E, Morrison SJ. Cancer, stress, and metastasis. Cold Spring Harbor Symposia on Quantitative Biology Jan 2017; 81 (1)
[63] Tang J et al. ss-Adrenerg system, a backstage manipulator regulating tumor progression and drug target in cancer therapy. Semin Cancer Biol 2013; 23 (6, Part B): 533-542
[64] Magnon C. Role of the autonomic nervous system in tumorigenesis and metastasis. Mol Cell Oncol 2015; 2 (2): e75643
[65] DEW, Robert A .: The Biopathic Diathesis. Journal of Orgonomy 2-4, 6-8.1O, 12
[66] REICH, Wilhelm: The Bioelectrical Investigation of Sexuality and Anxiety; Farrar, Straus & Giroux, NY 1982
[67] Cadegiani FA, tomcat CE. Adrenal fatigue does not exist: a systematic review. BMC Endocrinol Disord 2016; 16 (1): 48
[68] Grote V et al. Short-term effects of pulsed electromagnetic fields after physical exercise are dependent on autonomic tone before exposure. Eur J Appl Physiol 2007; 101 (4): 495-502
[69] Hughes JW, Stoney CM (Ohio State University, Columbus 43210-1222, USA): Psychosom Med 2000 Nov-Dec; 62 (6): 796-803
[70] De Punder K, Pruimboom L. Stress induces endotoxemia and low-grade inflammation by increasing barrier permeability. Front Immunol 2015 May 15; 6: 223. doi: 10.3389 / fimmu.2015.00223
[71] Smith MD et al. Abnormal bowel permeability in ankylosing spondylitis and rheumatoid arthritis J Rheumatol 1985; 12 (2): 299-305
[72] Yeoh N et al. The role of the microbiome in rheumatic diseases. Curr Rheumatol Rep 2013; 15 (3): 314
[73] Horta-Baas G et al. Intestinal dysbiosis and rheumatoid arthritis: a link between gut microbiota and the pathogenesis of rheumatoid arthritis. J Immunol Res 2017: 4835180
[74] Sturgeon JA et al. Affective disturbance in rheumatoid arthritis: psychological and disease-related pathways. Nat Rev Rheumatol 2016; 12 (9): 532-542
[75] Chua EC, Tan WQ, Yeo SC. Heart rate variability can be used to estimate sleepiness related decrements in psychomotor vigilance during total sleep deprivation. Sleep 2012; 35 (3): 325-334
[76] Cui H et al. Effects of magnetic stimuli on vigilance: a heart rate variability analysis. JPBS 2017; 2 (3): 1
[77] Pelka RB, Jaenicke C, Gruenwald J. Impulse magnetic-field therapy for migraine and other headaches: a double-blind, placebo-controlled study. Adv Ther 2001; 18 (3): 101-9
[78] Pelka RB, Jaenicke C, Gruenwald J. Impulse magnetic-field therapy for insomnia: a double-blind, placebo-controlled study. Adv Therapy 2001; 18 (4): 174-80
[79] Schimmelpfeng J. Dertinger H. The action of 50 Hz magnetic and electric fields upon cell proliferation and cyclic AMP content of cultured mammalian cell. Bioelectrochem Bioenerg 1993; 30: 143-50
[80] Dertinger H, Weiberzahn KF. Treatment of Psoriasis with Interferential Current – New Perspectives of electromagnetic therapy. Act Dermatol 2002: 28: 165-169
[81] Maeda K et al. Magnetically sensitive light-induced reactions in cryptochrome are consistent with its proposed role as a magnetoreceptor. Proc Natl Acad Sci USA 2012; 109 (13): 4774-9
[82] Close J. Are stress responses to geomagnetic storms mediated by the cryptochrome compass system. Proc R Soc B 2012; 279: 2081-2090
[83] Dickerson SS et al. Social-evaluative threat and proinflammatory cytokine regulation. An experimental laboratory investigation. Psychol Sci 2009; 20 (10): 1237-1244