Evidence that dirty electricity is causing the worldwide epidemics of obesity and diabetes

The epidemics of obesity and diabetes most apparent in recent years had their origins with Thomas Edison’s development of distributed electricity in New York City in 1882. His original direct current (DC) generators suffered serious commutator brush arcing which is a major source of high-frequency voltage transients (dirty electricity). From the onset of the electrical grid, electrified populations have been exposed to dirty electricity. Diesel generator sets are a major source of dirty electricity today and are used almost universally to electrify small islands and places unreachable by the conventional electric grid. This accounts for the fact that diabetes prevalence, fasting plasma glucose and obesity are highest on small islands and other places electrified by generator sets and lowest in places with low levels of electrification like sub-Saharan Africa and east and Southeast Asia.     

Electromagnetic hypersensitivity: biological effects of dirty electricity with emphasis on diabetes and multiple sclerosis

Dirty electricity is a ubiquitous pollutant. It flows along wires and radiates from them and involves both extremely low frequency electromagnetic fields and radio frequency radiation. Until recently, dirty electricity has been largely ignored by the scientific community. Recent inventions of metering and filter equipment provide scientists with the tools to measure and reduce dirty electricity on electrical wires. Several case studies and anecdotal reports are presented. Graham/Stetzer (GS) filters have been installed in schools with sick building syndrome and both staff and students reported improved health and more energy. The number of students needing inhalers for asthma was reduced in one school and student behavior associated with ADD/ADHD improved in another school. Blood sugar levels for some diabetics respond to the amount of dirty electricity in their environment. Type 1 diabetics require less insulin and Type 2 diabetics have lower blood sugar levels in an electromagnetically clean environment. Individuals diagnosed with multiple sclerosis have better balance and fewer tremors. Those requiring a cane walked unassisted within a few days to weeks after GS filters were installed in their home. Several disorders, including asthma, ADD/ADHD, diabetes, multiple sclerosis, chronic fatigue, fibromyalgia, are increasing at an alarming rate, as is electromagnetic pollution in the form of dirty electricity, ground current, and radio frequency radiation from wireless devices. The connection between electromagnetic pollution and these disorders needs to be investigated and the percentage of people sensitive to this form of energy needs to be determined.     

Angiostrongylus cantonensis: Biogenic amines in the lungs of infected rats

Levels of histamine, serotonin, norepinephrine, and dopamine were estimated sequentially in rats parasitized by the lungworm, Angiostrongylus cantonensis, between 30 and 75 days postinfection. The highest level of histamine in the infected lungs was 52.19 μg/g wet wt tissue, 13 times higher than the level found in control rats. The level of serotonin rose from the normal level of 6.41 to 10.27 μg/g wet wt tissue after the worms had lodged in the pulmonary artery for 15 days. There were no changes in norephinephrine or dopamine. Studies of host cell response to infection revealed that the increased histamine and serotonin levels corresponded to a rise in the lung population of mast cells, suggesting that these cells produced the amines.     

Repeated Reserpine Increases Striatal Dopamine Receptor and Guanine Nucleotide Binding Protein RNA

Abstract: In the present study the effects of repeated administration of reserpine on striatal dopamine receptor and guanine nucleotide binding protein mRNAs were determined. Twenty-four hours after seven consecutive daily injections of reserpine—a treatment that is known to produce functional sensitization of D₁ and D₂ dopamine receptors—the level of striatal D₁ dopamine receptor mRNA was unchanged. However, the level of mRNA for the G protein G_sα was increased by 127%. After extended reserpine treatment for 14 days, levels of both striatal D₁ DA receptor and G_sα mRNAs were elevated by 99 and 78%, respectively. Seven days of reserpine treatment also increased levels of mRNA of the striatal D₂ dopamine receptor and of G proteins G_i2α and G_oα by 200, 79, and 32%, respectively. After 14 days of reserpine treatment the level of striatal D₂ dopamine receptor mRNA was increased by twofold. In contrast, levels of the mRNAs coding for the G proteins G_i2α and G_oα were unchanged. These data suggest that dopamine receptors and their respective G proteins play important roles in the development of sensitization of striatal dopamine receptors during repeated reserpine treatment. Furthermore, the persistent increase in level of striatal G_sα mRNA suggests that this G protein is necessary to maintain supersensitivity of the striatal D₁ dopamine receptor system following long-term dopamine depletion.     

Dirty electricity elevates blood sugar among electrically sensitive diabetics and may explain brittle diabetes

Transient electromagnetic fields (dirty electricity), in the kilohertz range on electrical wiring, may be contributing to elevated blood sugar levels among diabetics and pre-diabetics. By closely following plasma glucose levels in four Type 1 and Type 2 diabetics, we find that they responded directly to the amount of dirty electricity in their environment. In an electromagnetically clean environment, Type 1 diabetics require less insulin and Type 2 diabetics have lower levels of plasma glucose. Dirty electricity, generated by electronic equipment and wireless devices, is ubiquitous in the environment. Exercise on a treadmill, which produces dirty electricity, increases plasma glucose. These findings may explain why brittle diabetics have difficulty regulating blood sugar. Based on estimates of people who suffer from symptoms of electrical hypersensitivity (3-35%), as many as 5-60 million diabetics worldwide may be affected. Exposure to electromagnetic pollution in its various forms may account for higher plasma glucose levels and may contribute to the misdiagnosis of diabetes. Reducing exposure to electromagnetic pollution by avoidance or with specially designed GS filters may enable some diabetics to better regulate their blood sugar with less medication and borderline or pre-diabetics to remain non diabetic longer.     

Development of an enzyme-linked immunosorbent assay system for the determination of asymmetric dimethylarginine using a specific monoclonal antibody

We produced a monoclonal antibody (mAb) against N(G),N(G)-dimethyl-L-arginine (asymmetric dimethylarginine: ADMA), an endogenous competitive inhibitor of nitric oxide synthase (NOS), and developed an enzyme-linked immunosorbent assay (ELISA). The competitive ELISA method using the mAb determined 5 nM-100 nM ADMA, and ADMA levels in human plasma and urine were found to be 0.78 μM and 51.3 μmol/g of creatinine respectively.     

Relationship among urinary albumin excretion rate, lipoprotein lipase PvuII polymorphism and plasma fibrinogen in type 2 diabetic patients

Plasma fibrinogen level represents a strong cardiovascular risk factor and is regulated by an interplay of genetic and environmental factors. Hyperfibrinogenemia frequently occurs in cluster with dyslipidemia within the frame of insulin resistance syndrome (IRS) and type 2 diabetes mellitus. Genetic variants with a pleiotropic effect have been proposed to cause IRS features including hyperfibrinogenemia. We studied the influence of polymorphisms in lipoprotein lipase (LPL) gene, beta-fibrinogen gene (FIBB) and environmental factors on plasma fibrinogen levels in type 2 diabetes patients. 131 type 2 diabetes patients (mean age 62+/-10 years, 33% male) were genotyped for polymorphisms in LPL gene (intron 6 PvuII, intron 8 HindIII) and FIBB gene (-148C/T, -455G/A) by PCR-RFLP method. Fibrinogen was measured by thrombin coagulation method, albuminuria by immunoturbidimetric assay. Polymorphism LPL PvuII showed a gene-dose effect on fibrinogen levels, with the highest fibrinogen in P-P- homozygotes (p = 0.05, analysis of variance). P-carriers (P-P- and P+P- combined) had significantly higher fibrinogen levels compared with P+P+ homozygotes (3.74+/-1.40 g/l vs 3.06+/-1.20 g/l, p=0.03). Other studied polymorphisms were not significantly related to fibrinogen levels. Age- and sex-adjusted fibrinogenemia correlated significantly with albuminuria (r = 0.48, p=0.001), serum uric acid (r = 0.42, p=0.006) and serum creatinine (r = 0.32, p=0.04). Multiple stepwise linear regression identified interaction term of LPL PvuII and albuminuria as an independent predictor of fibrinogen level, explaining 18% of fibrinogen variance. Albuminuria thus appears to be the best predictor of fibrinogen plasma levels in type 2 diabetic patients. Relationship between albuminuria and fibrinogenemia may be modified by the genotype LPL PvuII, which also shows a weak association with plasma fibrinogen level in type 2 diabetes patients.     

Prevalence of Anemia Among Unselected Adults with Diabetes Mellitus and Normal Serum Creatinine Levels

ObjectiveTo determine the prevalence of anemia in a cohort of patients with diabetes and normal serum creatinine concentration in a primary care clinic.MethodsWe undertook a retrospective cohort study, comparing adult patients who had diabetes, with or without anemia. Patients older than 18 years who had diabetes were identified by using the computerized database for the years 2006 and 2007 in a primary care clinic. Patients with hemoglobin levels < 13.7 g/dL (men < 60 years old), ≤ 13.2 g/dL (men ≥ 60 years old), or < 12.2 g/dL (women) with no known cause of anemia were identified and compared with patients who had diabetes but not anemia. All patients had normal serum creatinine levels (men ≤ 1.5 mg/dL and women ≥ 1.4 mg/dL).ResultsOf 594 eligible patients with diabetes, 192 (32%) had anemia. Older age, higher serum urea and creatinine levels, lower estimated glomerular filtration rates, and reduced serum iron levels were more common in the patients with diabetes who had anemia than in those without anemia. The prevalence of anemia was higher in patients treated with “glitazones,” insulin, and angiotensin receptor blockers in comparison with those receiving other orally administered hypoglycemic medications. In stepwise logistic regression analysis, only serum creatinine, age, and use of glitazones retained statistical significance.ConclusionIn a community clinic, the prevalence of anemia in unselected patients with diabetes and normal serum creatinine levels was 32%. Factors associated with anemia were older age, higher serum creatinine levels, and use of glitazone therapy. (Endocr Pract. 2009;15:714-719)     

Stimulation of ethylene production by catecholamines and phenylethylamine in potato cell suspension cultures

The catecholamines (50 M dopamine, 50 M norepinephrine and 100 M epinephrine) and phenylethylamine (200 M) were found to stimulate ethylene production in potato suspension cultures. When 100 M amino-oxyacetic acid was added together with epinephrine, ethylene release returned to control levels. The endogenous 1-aminocyclopropane-1-carboxylic acid levels were increased in parallel with the release of ethylene, suggesting that the observed effect probably occurs via regulation of aCC synthase. Our results suggest that there is a link between these naturally occurring monoamines and ethylene in plants.Abbreviations AOA amino-oxyacetic acid - ACC 1-aminocyclopropane-1-carboxylic acid - DA dopamine - NE norepinephrine - E epinephrine - CA catecholamines - PEA phenylethylamine     

Direct hypophysial inhibition of luteinizing hormone release by dopamine in the rabbit.

The role and site of action of dopamine in regulating gonadotropin secretion remain unclear. In the present study, we investigated the possibility that dopamine regulates LH secretion by acting directly on the pituitary gland of the rabbit. The effect of dopamine infusion on LHRH-evoked LH release was determined in intact and pituitary stalk sectioned animals. Intravenous injection of LHRH (1 μg) in intact and acutely stalk sectioned rabbits increased peripheral plasma LH levels from a resting value of 0.2 ng/ml to maximal values of 12–14 ng/ml within 10–20 min. When dopamine was infused iv at a dose of 6.6 μg/min/kg BW from 30 min before LHRH injection until 120 min after, the rise in plasma LH levels in intact and stalk sectioned animals was decreased by 50–70%. However, dopamine infused at a lower dose (0.66 μg/min/kg BW) or at a higher dose (66.0 μg/min/kg BW), did not affect the LHRH-induced secretion of LH. These results suggest that dopamine can exert a direct hypophysial inhibitory effect on release of LH. They also demonstrate that dopamine is inhibitory only within a restricted dose-range, extending to the pituitary an established property of dopamine in the cardiovascular system.     

白藜芦醇通过降低galectin-3的表达抑制宫颈癌SiHa细胞的增殖并促进其凋亡

目的：探讨白藜芦醇对人宫颈癌SiHa细胞增殖和凋亡的影响及galectin-3在其中的作用。方法：以体外培养的人宫颈癌SiHa细胞为研究对象,实验分为对照组、白藜芦醇处理组及[白藜芦醇＋galectin-3（5、10、20μg/mL）]共5组,分别给予生理盐水、300μmol/L白藜芦醇及[300μmol/L白藜芦醇＋Galectin-3（5、10、20μg/mL）]处理。48小时后,分别收集各组细胞,采用MTT法检测细胞的增殖情况,Caspase-3活性试剂盒测定细胞的凋亡情况,Western Blot技术测定细胞内galectin-3的蛋白表达水平。结果：300μmol/L的白藜芦醇明显抑制SiHa细胞的增殖,并显著增加其凋亡水平,同时减少了细胞内galectin-3的蛋白表达。在白藜芦醇处理的同时,给予5、10及20μg/mL的Galectin-3,随着Galectin-3蛋白浓度的增加,SiHa细胞的增殖抑制率逐渐降低,凋亡水平也逐渐下降,但是VEGF-R3受体的磷酸化水平却逐渐升高。结论：白藜芦醇通过降低galectin-3的表达抑制宫颈癌SiHa细胞的增殖并促进其凋亡。     

Acute human toxicity and mortality after selenium ingestion: A review

BackgroundAlthough selenium is an essential element for humans, acute toxicity has been reported after high oral exposure.MethodsThe published literature on the acute toxicity of oral selenium was gathered and reviewed.ResultsReported symptoms and signs include abdominal symptoms, such as vomiting, diarrhea, pain, and nausea, as well as garlic-like odor on the breath. In cases of severe toxicity, cardiac and pulmonary symptoms may develop and ultimately lead to mortality. Mortality has been described after the ingestion of gun bluing solutions, which often contain selenous acid among other potentially toxic substances. Mortality has also been reported after the ingestion of other forms of selenium. Ingested doses associated with mortality are in the range of 1–100 mg Se/kg body weight. Blood levels associated with mortality are above 300 μg Se/L (normal level: 100 μg/L), whereas urinary levels associated with the same endpoint are above170 μg Se/L (normal level: 20–90 μg/L).ConclusionThe acute toxicity associated with oral selenium ingestion and the blood and urinary levels of selenium in different cases of poisonings were reviewed. Mortality is a risk of acute selenium poisoning. Concentrations of selenium in blood and urine samples in non-fatal cases are close to those observed in fatal cases.     

Evaluation of blood mercury and serum selenium levels in the pregnant population of the Community of Madrid,Spain

BackgroundThe main exposure route to methylmercury (MeHg) is from eating fish and shellfish containing this compound. Since 2004, women of childbearing age in Spain have been urged not to eat some species (eg, tuna, shark, and swordfish), instead choosing low-MeHg seafood as part of a healthy diet.ObjectiveTo describe maternal total blood mercury (THg) and serum selenium (Se) in a cohort of pregnant women living in Spain as it relates to fish intake during the three trimesters and to assess whether or not Spanish women of childbearing age follow the recommendations listed in fish advisories and choose fish species with lower mercury levels.MethodsWe studied 141 female volunteers of childbearing age (16–45 years), interviewing all participants about their overall eating habits and seafood intake. Hg and Se levels were tested using cold-vapor atomic absorption spectrometry (CVAAS) and electrothermal atomic absorption spectrometry (ETAAS), respectively.ResultsAverage THg levels in pregnant women were 2.89 μg/L (standard deviation [SD], 2.75 μg/L, geometric mean [GM], 2.19 μg/L), and THg GM was positively associated with fish intake. Mean Se levels in pregnant women were 73.06 μg/L (SD, 13.38 μg/L), and Se levels were found to increase with tuna intake. In 16 (12%) pregnant women, THg was higher than the level recommended by the U.S. Environmental Protection Agency (EPA) (6.4 μg/L). A positive association was also found between THg and serum Se.ConclusionWomen of childbearing age in Spain had higher THg levels than women in other Western studies. Our study observed that 12% of women had THg levels above the safety limit set by the EPA (6.4 μg/L), and 31% had levels above the relevant benchmark level of 3.5 μg/L suggested by various researchers.     

The zinc,copper, and manganese status of children with malabsorption syndromes and inborn errors of metabolism

The zinc, copper, and manganese status of seven children with malabsorption syndromes of varied etiology (MVE) and 12 with inborn errors of metabolism (IEM) receiving semi-synthetic diets was investigated using serum and hair trace element concentrations, dietary trace element intakes, and anthropometric measurements as the principal indices. The hair zinc levels of both test groups and hair manganese levels of the IEM group were significantly lower (p<0.05) than those of their respective healthy controls matched by age, sex, and geographic location, despite comparable dietary zinc and manganese intakes in test and control subjects. Four subjects from the malabsorption and five from the inborn errors group had hair zinc levels below 100 μg/g (range 30–88 μg/g). Of these nine subjects, serum zinc levels were determined for six, and five were less than normal (range 64–74 μg/dL). In contrast, the copper status of the MVE and IEM subjects, as indicated by hair and dietary copper levels, was not lower than the controls. Mean serum copper levels were 136±30 and 171±40 μg/dL for the IEM and MVE groups, respectively. Levels for the MVE subjects were higher than published normal values. The suboptimal zinc and manganese status observed in some of these test subjects probably arose from malabsorption and decreased availability of dietary zinc and manganese. However, the zinc depletion was not severe enough to result in linear growth retardation.     

Effect of prolactin and estradiol on rat striatal dopamine receptors

Chronic estrogen treatment has been found to increase the level of rat striatal dopamine receptors. Since it is well known that estrogen treatment increases circulating prolactin levels, we have investigated the possibility that the stimulatory effect of estrogens on dopamine receptors is exerted via prolactin. Ovariectomized female or intact male rats were implanted with three adenohypophyses under the kidney capsule or treated with 17 β-estradiol (10 μg, twice daily) for 2 weeks. In animals of both sexes, the pituitary-implanted and estradiol-treated rats showed higher levels of [³H]spiperone binding to striatal dopamine receptors. This effect of estradiol or pituitary implants on dopamine receptors was further investigated in ovariectomized rats. The pituitary-implanted and estradiol-treated rats had elevated plasma prolactin levels and an increased density of striatal dopamine receptors without alteration of their affinity. The role of the pituitary in the effect of estradiol was next investigated using hypophysectomized female rats treated with 17 β-estradiol (10 μg, twice daily), o-prolactin (500 μg, twice daily) or bearing three anterior pituitary implants. The implants as well as the treatment with estradiol or prolactin increased the level of striatal dopamine receptors in hypophysectomized rats while, as expected, the estradiol-treated animals did not have elevated plasma prolactin levels. The present data indicate that high prolactin levels lead, as observed with chronic estradiol treatment, to an increased density of striatal dopamine receptors. However, the effect of estradiol may not be explained exclusively by increased prolactin levels since a similar stimulatory effect is observed in hypophysectomized animals.     

Relationship between myelin production and dopamine synthesis in the PKU mouse brain

Phenylketonuria is caused by specific mutations in the phenylalanine hydroxylase gene and is characterized by elevated blood phenylalanine levels, hypomyelination in forebrain structures, reduced dopamine levels, and cognitive difficulties. To determine whether brain tyrosine levels and/or myelination play a role in the up-regulation of dopamine, phenylketonuric mice were placed on a low phenylalanine diet for 4 weeks and as blood phenylalanine levels dropped to normal, the relationships between phenylalanine, tyrosine, dopamine, myelin proteins, and axonal proteins in frontal cortex and striatum were determined using gas chromatography mass spectrometry, histology, and western blotting techniques. Blood phenylalanine rapidly decreased from an eight-fold elevation to near control levels, and blood tyrosine gradually rose from about 50% to near normal values. In frontal cortex and striatum, phenylalanine levels dropped to 2- and 1.5-fold elevations above control, respectively, and tyrosine levels increased but remained less than 70% of control in both structures. In frontal cortex, increases in dopamine and myelin basic protein occurred in a similar biphasic pattern, reaching near normal levels by week 4. In striatum, dopamine and MBP dramatically increased to near normal levels in the first week. Myelination was confirmed histologically and by western blot quantification of phosphorylated neurofilaments. In summary, our results showed: (i) an increase in dopamine despite low brain tyrosine levels and (ii) similar recovery patterns for myelination and dopamine. Since myelin/axonal interactions trigger signaling pathways that result in axonal maturation, we speculate that this interaction also may trigger signals that up-regulate neurotransmitter synthesis.     

Changes in calmodulin levels during development of the silkworm,Bombyx mori

Calmodulin levels were measured in various tissues during the larval-adult development of the silkworm, Bombyx mori. In the larval period, calmodulin levels in fat body, midgut and testis were in a range of 0.3–1.7 μg/mg protein and remained almost constant during larval growth. The silk gland contained a relatively high (0.2 μg/mg protein) level of calmodulin early in the fifth instar which gradually decreased during maturation of the larva. At pupation, testis calmodulin dropped from 1.5 to 1.7 μg/mg protein to about 1 μg/mg, and remained constant thereafter. The most striking change occurred in fat body calmodulin which fell from 0.5 to 0.6 μg/mg in the larval stage to 0.01–0.03 μg/mg during pupal-adult metamorphosis. Midgut calmodulin levels were unchanged at pupation and remained constant during pupal-adult development.When expressed on per g wet weight basis, calmodulin levels in silkworm tissues were comparable to mammalian tissue levels. However, only 2–4% of the total calmodulin in silkworm tissues was in a membrane-bound form compared to 20–60% for membrane-bound calmodulin in mammals.     

PAI-1 Gene 4G/5G polymorphism and risk of type 2 diabetes in a population-based sample

Elevated plasma levels of plasminogen activator inhibitor-1 (PAI-1) increase risk for type 2 diabetes. The PAI-1 4G/5G polymorphism is a major genetic determinant of plasma PAI-1 levels, with 4G/4G homozygotes having elevated PAI-1 levels relative to 5G allele carriers. These observations suggest the hypothesis that the PAI-1 4G/5G polymorphism could be a genetic risk factor for diabetes. We tested this hypothesis among 2169 participants of the Framingham Offspring Study followed for seven examinations over 26 years for 216 cases of type 2 diabetes. PAI-1 4G/4G homozygotes (genotype frequency, 27.4%) were not at significantly (p > 0.05) increased risk of incident diabetes compared with 5G allele carriers and did not have elevated levels of diabetes-related quantitative traits including BMI, fasting plasma glucose, or fasting insulin. In proportional hazards regression models accounting for correlation among siblings, with the 5G/5G genotype as the referent, the hazard ratio for incident diabetes for 4G/5G carriers was 0.93 (95% confidence interval, 0.68 to 1.28) and for 4G/4G carriers was 1.20 (95% confidence interval, 0.83 to 1.92). Results were not altered by further adjustment for sex or levels of BMI, triglycerides, or PAI-1. We conclude that the PAI-1 4G/5G polymorphism is not an important genetic risk factor for type 2 diabetes in this community-based sample. Elevated PAI-1 levels may be associated with an increased risk for diabetes as a marker for underlying endothelial dysfunction rather than by a direct effect of genetically mediated elevated levels.     

绵羊皮肤成纤维细胞对G418及Blasticidin S抗性的研究

抗生素常被用于对转基因动物、植物及微生物细胞进行筛选。在进行抗生素抗性筛选前,需要摸索合适的抗生素使用浓度,其原因在于:过低的筛选浓度无法抑制非转基因细胞的生长;反之,过高的筛选浓度会导致转基因细胞死亡。为了摸索绵羊皮肤成纤维细胞(sheep skin fibroblasts, SSFs)对G418及Blasticidin S的抗性,本实验以体外培养的SSFs为实验材料,采用不同浓度的上述两种抗生素处理SSFs,采用活细胞计数的方式检测SSFs对上述两种抗生素的抗性。单独使用G418或Blasticidin S导致SSFs全部死亡的最低致死浓度分别为200μg/mL及4μg/mL;当两种抗生素联合使用时,其最低致死浓度为100μg/mL G418+3μg/mL Blasticidin S或150μg/mL G418+2μg/mL Blasticidin S。该实验为采用这两种抗生素筛选转基因SSFs提供了理论基础。     

Microcentrifuge desalting: a rapid, quantitative method for desalting small amounts of protein

A mass fragmentographic method for the determination of unconjugated homovanillic acid, vanilmandelic acid, and 3-methoxy-4-hydroxyphenylethylene glycol in serum, using deuterated internal standards, is described. Reference values for normal healthy adults were 11.3 + 4.2. μg/liter (homovanillic acid), 5.9 + 2.2 μg/liter (vanilmandelic acid), and 3.3 ± 1.3 μg/liter (3-methoxy-4-hydroxyphenylethylene glycol). Samples obtained from children were found to contain statistically higher values. The clinical importance of these measurements in diseases such as neuroblastoma, pheochromocytoma, Parkinsonism treated with l-3,4-dihydroxyphenylalanine, and renal failure is discussed in relation to the reference values mentioned above and the levels of homovanillic acid and vanilmandelic acid in urine.