Loading ...
Sorry, an error occurred while loading the content.

1824C O'Gorman and SA Broadley, cigarettes cause MS -- give as much methanol as aspartame and unfresh juices, has blood half-life 3 hours, made into rampant formaldehyde inside human cells by ADH1 enzyme -- Prof. WC Monte paradigm: Rich Murray 2014.06.17

Expand Messages
  • Rich Murray
    Jun 17, 2014
    • 0 Attachment
      C O'Gorman and SA Broadley, cigarettes cause MS -- give as much methanol as aspartame and unfresh juices, has blood half-life 3 hours, made into rampant formaldehyde inside human cells by ADH1 enzyme -- Prof. WC Monte paradigm: Rich Murray 2014.06.17


      Some research papers from Berlin about 1926 found that a pack of cigarettes gave 40 mg methanol in the smoke, -- as much as two cans of aspartame diet drink, or 3 cups of unfresh tomato or fruit juice that have been in sealed containers for days at room temperature.

      In humans only, the cells lack an innate biochemical defense system against methanol, which has a half-life in human blood of 3 hours, being swiftly made into rampant formaldehyde right inside cells, via the ADH1 enzyme, at high levels in 20 specific tissues, including the inner walls of blood vessels at the base of the brain and in the retina -- resulting in direct disruption of the blood brain barrier and leading to many scattered complex spots of inflammation.

      Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004,  gives a free bibliography of 782 mostly full text medical research studies at WhileScienceSleeps.com ...





      J Neurol. 2014 Jun 13. [Epub ahead of print]
      Smoking and multiple sclerosis: evidence for latitudinal and temporal variation.
      O'Gorman C 1, Broadley SA.

      1 School of Medicine, Griffith University, Gold Coast, QLD, 4222, Australia.

      Abstract

      There is growing evidence for the role of smoking in the aetiology of multiple sclerosis. We have expanded existing meta-analyses and further explored the roles of study design, gender, latitude and year of study with regression modelling.
      We have found a consistent association between smoking and MS with an odds ratio of approximately 1.5, with males at higher risk.
      This finding is independent of study design.
      However, latitude and year of study may have unexpected influence.
      Smoking appeared to confer a greater risk to females living closer to the equator than to females at higher latitudes.
      The effect of cigarette smoke exposure on MS risk may not be fixed over time, but could be increasing.
      These results suggest a threshold model of MS risk that includes a fairly constant genetic risk (for Caucasian populations) together with variable environmental risks which are dominated by vitamin D deficiency at higher latitudes and are more significant in women who have an intrinsically lower threshold for development of disease.

      PMID: 24923244




      J Clin Neurosci. 2014 Jun 2.
      pii: S0967-5868(14)00168-4.
      doi: 10.1016/j.jocn.2014.01.009.
      published online 07 April 2014.
       [Epub ahead of print]
      Smoking increases the risk of multiple sclerosis in Queensland, Australia.
      O'Gorman C 1, Bukhari W 2, Todd A 3, Freeman S 2, Broadley SA 4.

      Abstract

      There is growing evidence for the role of smoking in the aetiology of multiple sclerosis (MS).
      We have undertaken a large case-control study of smoking in MS and assessed this using a regression model.
      We have confirmed an association between increased risk of MS and smoking in Queensland, Australia, a region of intermediate risk for MS.
      The overall adjusted odds ratio was 1.9 (95% confidence interval 1.5-2.5) for ever smokers.
      There was no statistically significant difference in the risks for males and females.
      A number of potential mechanisms to explain this association have been postulated including direct and indirect (via vitamin D) effects on the immune system.

      Copyright © 2014 Elsevier Ltd. All rights reserved.

      KEYWORDS:
      Case-control studies; Multiple sclerosis; Risk factors in epidemiology
      PMID: 24932591


      1 School of Medicine, Gold Coast Campus, Griffith University, QLD, Australia; Department of Neurology, Mayo Clinic, 200 1st Street SW, Rochester, MN 55905, USA. Electronic address: cullenogorman@...
      2 School of Medicine, Gold Coast Campus, Griffith University, QLD, Australia.
      3 Gold Coast Hospital, Southport, QLD, Australia.
      4 School of Medicine, Gold Coast Campus, Griffith University, QLD, Australia; Gold Coast Hospital, Southport, QLD, Australia

      Cullen O. Gorman ,
      W. Bukhari ,
      Simon A. Broadley    ,




      [ color images ]

      Molecular Pathogenesis of Neuromyelitis Optica
      Bukhari W, Barnett MH, Prain K, Broadley SA - Int J Mol Sci (2012)

      Bottom Line: Like other autoimmune diseases, Th17 cells and their effector cytokines (such as interleukin 6) have been implicated in pathogenesis.
      Despite rapid advances in the understanding of NMO pathogenesis, unanswered questions remain, particularly with regards to disease mechanisms in NMO IgG seronegative cases.Increasing knowledge of the molecular pathology is leading to improved treatment strategies.

      Affiliation: School of Medicine, Gold Coast Campus, Griffith University, QLD 4222, Australia. w.bukhari@...

      ABSTRACT

      Neuromyelitis optica (NMO) is a rare autoimmune disorder, distinct from multiple sclerosis, causing inflammatory lesions in the optic nerves and spinal cord.

      An autoantibody (NMO IgG) against aquaporin-4 (AQP4), a water channel expressed on astrocytes is thought to be causative.

      Peripheral production of the antibody is triggered by an unknown process in genetically susceptible individuals.

      Anti-AQP4 antibody enters the central nervous system (CNS) when the blood brain barrier is made permeable and has high affinity for orthogonal array particles of AQP4.

      Like other autoimmune diseases, Th17 cells and their effector cytokines (such as interleukin 6) have been implicated in pathogenesis.

      AQP4 expressing peripheral organs are not affected by NMO IgG, but the antibody causes extensive astrocytic loss in specific regions of the CNS through complement mediated cytotoxicity.

      Demyelination occurs during the inflammatory process and is probably secondary to oligodendrocyte apoptosis subsequent to loss of trophic support from astrocytes.

      Ultimately, extensive axonal injury leads to severe disability.

      Despite rapid advances in the understanding of NMO pathogenesis, unanswered questions remain, particularly with regards to disease mechanisms in NMO IgG seronegative cases.

      Increasing knowledge of the molecular pathology is leading to improved treatment strategies.




      yet 2 more new laboratory studies on aspartame toxicity, from Turkey and India -- relevance of WC Monte paradigm for harm from methanol, made in  humans only into rampant formaldehyde right inside cells by ADH1 enzyme: Rich Murray 2014.06.16


      Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004 ]


      Aspartame induces angiogenesis in vitro and in vivo models, HETox 2014.06.12 Ankara, Turkey, Yesildal F, Aydin F, Deveci S, Tekin S, Aydin I, Mammadov R, Fermanli O, Avcu F, Acikel C, Ozgurtas T: Rich Murray 2014.06.16


      Hum Exp Toxicol. 2014 Jun 12.
      pii: 0960327114537535.
      [Epub ahead of print]
      Aspartame induces angiogenesis in vitro and in vivo models.
      Yesildal F 1, Aydin F 1, Deveci S 2, Tekin S 3, Aydin I 1, Mammadov R 4, Fermanli O 3, Avcu F 5, Acikel C 6, Ozgurtas T 7.

      1 Department of Biochemistry,
      Gülhane Military Medical Academy, Ankara, Turkey.
      2 Department of Pathology,
      Gülhane Military Medical Academy, Ankara, Turkey.
      3 School of Medicine,
      Gülhane Military Medical Academy, Ankara, Turkey.
      4 National Nanotechnology Research Center,
      Bilkent University, Ankara, Turkey.
      5 Department of Haematology,
      Gülhane Military Medical Academy, Ankara, Turkey.
      6 Department of Public Health and Biostatistics,
      Gülhane Military Medical Academy, Ankara, Turkey.
      7 Department of Biochemistry,
      Gülhane Military Medical Academy, Ankara, Turkey


      Abstract

      Angiogenesis is the process of generating new blood vessels from preexisting vessels and is considered essential in many pathological conditions.

      The purpose of the present study is to evaluate the effect of aspartame on angiogenesis in vivo chick chorioallantoic membrane (CAM) and wound-healing models as well as in vitro 2,3-bis-2H-tetrazolium-5-carboxanilide (XTT) and tube formation assays.

      In CAM assay,aspartame increased angiogenesis in a concentration-dependent manner.
      Compared with the control group, aspartame has significantly increased vessel proliferation (p < 0.001).

      In addition, in vivo rat model of skin wound-healing study showed that aspartame group had better healing than control group, and this was statistically significant at p < 0.05.

      There was a slight proliferative effect of aspartame on human umbilical vein endothelial cells on XTT assay in vitro, but it was not statistically significant;
      and there was no antiangiogenic effect of aspartame on tube formation assay in vitro.

      These results provide evidence that aspartame induces angiogenesis in vitro and in vivo;
      so regular use may have undesirable effect on susceptible cases.

      © The Author(s) 2014.
      KEYWORDS:
      Aspartame; CAM assay; angiogenesis; skin wound healing; tube formation
      PMID: 24925367





      Assistant Prof. R. Harikumaran Nair, Mahatma Gandhi U,  studies on liver and lung harm re aspartame -- human harm re wood and paper mills, home cooking fuels, car exhaust, organic solvents, diabetes, -- which all have methanol/formaldehyde, while MSG is also neurotoxic -- most modern "Diseases of Civilization" are involved via the Monte methanol/formaldehyde paradigm: Rich Murray 2012.03.30


      "Histopathological examination revealed mild vascular congestion in the
      1,000 mg/kg b.w. group of aspartame-treated rats."

      Drug Chem Toxicol. 2012 Mar 2. [Epub ahead of print]
      Long-term consumption of aspartame and brain antioxidant defense status.
      Abhilash M,
      Sauganth Paul MV,
      Varghese MV,
      Nair RH.
      School of Biosciences, Mahatma Gandhi University , Kottayam , India.

      Abstract

      The present study investigated the effect of long-term intake of
      aspartame, a widely used artificial sweetener, on antioxidant defense
      status in the rat brain.

      Male Wistar rats weighing 150-175 g were randomly divided into three
      groups as follows:
      The first group was given aspartame at a dose of 500 mg/kg body weight (b.w.);
      the second group was given aspartame at dose of 1,000 mg/kg b.w., respectively,
      in a total volume of 3 mL of water; and
      the control rats received 3 mL of distilled water.
      Oral intubations were done in the morning, daily for 180 days.

      The concentration of reduced glutathione (GSH) and the activity of
      glutathione reductase (GR) were significantly reduced in the brain of
      rats that had received the dose of 1,000 mg/kg b.w. of aspartame,
      whereas only a significant reduction in GSH concentration was observed
      in the 500-mg/kg b.w. aspartame-treated group.

      Histopathological examination revealed mild vascular congestion in the
      1,000 mg/kg b.w. group of aspartame-treated rats.

      The results of this experiment indicate that long-term consumption of
      aspartame leads to an imbalance in the antioxidant/pro-oxidant status
      in the brain, mainly through the mechanism involving the
      glutathione-dependent system.
      PMID: 22385158



      Aspartame water in rats for 6 months causes liver harm, RH Nair et al, Mahatma Gandhi U, Food Chem Toxicol 2011.03.02: Rich Murray 2011.03.12

      "Histopathological examination revealed leukocyte infiltration in
      aspartame-treated rats (1000 mg/kg.b.wt)."


      Food Chem Toxicol. 2011 Mar 2. [Epub ahead of print]
      Effect of long term intake of aspartame on antioxidant defense status in liver.
      Abhilash M, Paul MV, Varghese MV, Nair RH.
      School of Biosciences, Mahatma Gandhi University,
      Kottayam, Kerala, India, 686560.

      Abstract

      The present study evaluates the effect of long term intake of
      aspartame, the artificial sweetener, on liver antioxidant system and
      hepatocellular injury in animal model.
      Eighteen adult male Wistar rats, weighing 150 - 175 g, were randomly
      divided into three groups as follows:
      first group was given aspartame dissolved in water in a dose of 500 mg/kg.b.wt;
      the second group was given a dose of 1000 mg/kg.b.wt;
      and controls were given water freely.
      Rats that had received aspartame (1000 mg/kg.b.wt) in the drinking
      water for 180 days showed a significant increase in activities of
      alanine aminotransferase (ALT),
      aspartate aminotransferase (AST),
      alkaline phosphatase (ALP) and
      y-glutamyl transferase (GGT).
      The concentration of reduced glutathione (GSH)
      and the activity of glutathione peroxidase (GPx), and
      glutathione reductase (GR)
      were significantly reduced in the liver of rats that had received
      aspartame (1000 mg/kg.b.wt).
      Glutathione was significantly decreased in both the experimental groups.

      Histopathological examination revealed leukocyte infiltration in
      aspartame-treated rats (1000 mg/kg.b.wt).

      It can be concluded from these observations that long term consumption
      of aspartame leads to hepatocellular injury and alterations in liver
      antioxidant status mainly through glutathione dependent system.
      Copyright 2011. Published by Elsevier Ltd. PMID: 21376768

      Souganth Paul, MV - Research Fellow

      Abhilash, M - Research Fellow

      Varghese, Mathews V - Research Fellow



      Chronic Effect of Aspartame on Ionic Homeostasis and Monoamine Neurotransmitters in the Rat Brain. Abhilash M, Alex M, Mathews VV, Nair RH, IJTox 2014.05.28 Mahatma Gandhi U, India: Rich Murray 2014.06.16


      Int J Toxicol. 2014 May 28.
      pii: 1091581814537087.
      [Epub ahead of print]
      Chronic Effect of Aspartame on Ionic Homeostasis and Monoamine Neurotransmitters in the Rat Brain.
      Abhilash M 1, Alex M 1, Mathews VV 1, Nair RH 2.
      1 School of Biosciences, Mahatma Gandhi University, Kottayam, Kerala, India.
      2 School of Biosciences, Mahatma Gandhi University, Kottayam, Kerala, India

      R. Harikumarin Nair  <harinair@...>,


      Abstract

      Aspartame is one of the most widely used artificial sweeteners globally.
      Data concerning acute neurotoxicity of aspartame is controversial, and knowledge on its chronic effect is limited.

      In the current study, we investigated the chronic effects of aspartame on ionic homeostasis and regional monoamine neurotransmitter concentrations in the brain.

      Our results showed that aspartame at high dose caused a disturbance in ionic homeostasis and induced apoptosis [cell death] in the brain.

      We also investigated the effects of aspartame on brain regional monoamine synthesis, and the results revealed that there was a significant decrease of dopamine in corpus striatum and cerebral cortex and of serotonin in corpus striatum.

      Moreover, aspartame treatment significantly alters the tyrosine hydroxylase activity and amino acids levels in the brain.

      Our data suggest that chronic use of aspartame may affect electrolyte homeostasis and monoamine neurotransmitter synthesis dose dependently, and this might have a possible effect on cognitive functions.

      © The Author(s) 2014.
      KEYWORDS:
      Na+-K+-ATPase; apoptosis; aspartame; monoamines; phenylalanine
      PMID: 24872471




      Name: Dr. R. Harikumaran Nair                                                                                  
      Designation: Assistant Professor
      Address: Room No. 5                                                                      
      School of Biosciences,
      Mahatma Gandhi University
      Priyadarshini Hills. P O. , Kottayam-686 560
      Kerala, India
      Phone: +91- 481- 2731035 Extension: 16
      Mobile Phone: +91-94472 60362

      Research Interest
      In our laboratory, we study the effect of food additives such as monosodium glutamate,
      aspartame, drug component arsenic trioxide and other toxins like organic solvents on different physiological mechanisms in rats and tissue culture model systems. Another area of interest is environmental and occupational stress.

      Academic Profile
      Ph. D-Physiology (2001), School of Biosciences, Mahatma Gandhi University, Kottayam,
      Kerala, India
      M. Sc- Zoology (1994) University of Kerala, Thiruvananthapuram, Kerala, India,
      B. Sc-Zoology (1992) University of Kerala, Thiruvananthapuram, Kerala, India,

      Professional Experience:
      *Lecturer in Physiology (Permanent service) - School of Biosciences, Mahatma Gandhi
      University, Kerala, India. 22nd May 2006 to present
      *Lecturer in Physiology (contract service) - School of Biosciences, Mahatma Gandhi
      University, Kerala, India. 20th November 2003 to 21st May 2006
      *Postdoctoral Research fellow- Dept. of Physiology, St. John’s Medical College,
      Bangalore, India. 01st March 2002 to 15th July 2002
      *Research Fellow – School of Biosciences, Mahatma Gandhi University, Kottayam, Kerala,
      India. October 1995- April 2001

      Group Members
      Sagi, T.M- Research Fellow
      Souganth Paul, M.V- Research Fellow
      Abhilash, M.- Research Fellow
      Mathews .V. Varghese- Research Fellow
      Manju Alex- Research Fellow

      Publications:

      Scientific Proceedings
      1. Abhilash M, Shashidhar S, Harikumaran Nair R. The role of electrolytes in
      cataractogenesis and modulation by silver nitrate in albino rats. 22nd Kerala Science
      Congress. 28-31 January 2010. KFRI, Peechi, Thrissur, Kerala, India
      2. Sauganth Paul, Harikumaran Nair R, Shashidhar.S. Lipid peroxidation and
      antioxidant activities in hypertensive subjects of different age group, Indian Science
      Congress, Medical Sciences section. 03.01.2010 to 07.01.2010, University of Kerala,
      Kerala, India

      Publications
      1. Ajitha kumari.R, Shashidar.S and Harikumaran Nair, R. Oxidative stress and lung
      functions in diabetic mellitus. Biomedicine. 2010 (accepted)
      2. Pankajam.K, Harikumaran Nair R, Kesavachandran.C, Rethamma.KV, and
      Shashidhar.S. Effects of Automobile exhaust pollution on the pulmonary functions in
      shopkeepers, Pollution Research. 2005; 24(1): 51-56.
      3. Kesavachandran.C, Harikumaran Nair R. and Shashidhar.S.
      Pulmonary function studies in Kalarypayathu Practitioners. Ind. J. Physiol.
      Pharmacol., 2004, 48(2), 235-240.
      4. Geetha. B., Harikumaran Nair R., Kesavachandran.C.,Susan Chandy and
      Shashidhar. S., Pulmonary functions in workers of fertilizer and chemical
      Industry,Ind.J.Physiol.Pharmacol.2001:45(2):215-221.
      5. Geetha B., Harikumaran Nair R., Kesavachandran,C and Shashidhar, S., Respiratory
      Function Studies in Rare Earth Factory Workers, Pollution Research 2001: 20(1):115-119.
      6. Kesavachandran.C., Harikumaran Nair R.,and Shashidhar.S., Lung Volumes in
      Swimmers performing different strokes, Ind.J.Med.Sci.2001:55(12):669-676.
      7. Reethamma K.V., Harikumaran Nair R., Kesavachandran C and Shashidhar S. Effect
      of Wood Dust on Lung Functions, Pollution Research 2000:19(4):693-699.
      8. Harikumaran Nair R., Kesavachandran C and Shashidhar S., Spirometric
      Impairments in Undernourished Children, Ind.J.Physiol.Pharmacol.1999, 43(4):467-473.
      9. Harikumaran Nair R.,Kesavachandran C.,Sanil R.,Sreekumar R and Shashidhar S.
      Prediction Equation for Lung Functions in South Indian Children,
      Ind.J.Physiol.Pharmacol.1997, 41(4):390-396.
      10. Kesavachandran C., Sanil R., Harikumaran Nair R.,Arun A.Rauf and
      ShashidharS.,PulmonaryFunction Studies in Rowers.Ind.J.Physiol.Pharmacol.1997,41(1):29 –34.
      11. Bindu K.Pazhur,Susan Chandy, Harikumaran Nair R.,and Shadhidhar S. Effect of
      Domestic Cooking Fuels on Lung Functions in Women,
      Pollution Research 1997, 16(3):149-154.

      Scientific Papers in International Conference:
      1. Geetha B, Harikumaran Nair R, Kesavachandran C and Shashidhar S.
      Respiratory Function Studies on Newsprint Factory workers. International
      Conference on Health, Occupation and Environment in Unorganized sector-
      problems and Road maps (ICHOE 2004). November 1-3, 2004, Industrial
      Toxicology Research Centre (ITRC, CSIR), Lucknow, INDIA.
      2. Rethamma K V, Harikumaran Nair R, Kesavachandran C and Shashidhar S.
      Pulmonary function status among Wood workers. International Conference on
      Health, Occupation and Environment in Unorganized sector- problems and Road
      maps (ICHOE 2004). November 1-3, 2004, Industrial Toxicology Research Centre
      (ITRC, CSIR), Lucknow, INDIA.

      Academic & Administrative Duties
      • Chairman, B Sc Biophysics Board of Examinations, University of Calicut,
      Kerala, India
      • Convenor & Member, Institutional Animal Ethics Committee, Mahatma
      Gandhi University, Kerala, India
      • Member Secretary, Institutional Human Ethics Committee, Mahatma Gandhi
      University, Kerala, India
      • External Examiner in Fundamentals of Physiology, School of Medical
      Education, Mahatma Gandhi University, Kerala, India
      • Member, Campus Development Committee, Mahatma Gandhi University,
      Kerala, India

      Training undertaken :( 2007 Onwards)
      • Refresher Course in Lifesciences. 08.12.2009 to 29.12.2009. UGC Academic
      Staff College, University of Kerala, Kerala
      • University workshop on Research Projects, 02.04.2009. Mahatma Gandhi
      University, Kerala
      • UGC sponsored short term course for Research Guides. 23.03.2009 to
      28.03.2009, UGC Academic Staff College, University of Kerala, Kerala.
      • Workshop on Curriculum Design for B.Sc. Biophysics Course. Kerala State
      Higher Education Council and the University of Calicut, Kerala, 24.02.2009 to
      28.02.2009

      Research Collaborations
      IITR- Lucknow,UP, India
      NIIST- Thiruvananthapuram, Kerala, India



      methanol from cigarettes, aspartame, unfresh fruit juice becomes rampant formaldehyde inside human cells via ADH1 enzyme in 20 specific tissues -- WC Monte gives new paradigm with 782 full text references : Rich Murray 2014.06.16

      Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain, Iyaswamy Ashok, Rathinasamy Sheeladevi, U of Madras 2014.04.29 free full text: Rich Murray 2014.05.24

      aspartame harm in rat brain from 75 mg/kg gives human ADI 0.75 mg/kg, 53 times less than EU ADI 40 mg/kg, Ashok Iyyaswamy, SheelaDevi Rathinasamy, U. Madras 2012.08.03 free full text -- main methanol toxin is formaldehyde, not formate: Rich Murray 2013.06.01

      Rathinasamy Sheeladevi
      free full text

      [ See also:

      methanol toxicity, not by formate, but by formaldehyde made inside human cells by ADH1 enzyme -- brief by Woodrow C. Monte, with lengthy references: Rich Murray 2013.05.24

      two studies by Rong-Qiao He teams in China on monkeys and mice show oral methanol leads to specific formaldehyde harm similar to Alzheimers disease, confirming WC Monte paradigm: Rich Murray 2014.05.16


      "As a matter of course, every soul citizen of Earth has a priority to quickly find and positively share evidence for healthy and safe food, drink, environment, and society."

      within the fellowship of service,
      Rich Murray,
      MA Boston University Graduate School 1967 psychology,
      BS MIT 1964 history and physics,
      1039 Emory Street, Imperial Beach, CA 91932
      505-819-7388 cell
      619-623-3468 home