Journal of Neurosurgery: Spine April 5, 2013 [epub] Matthew Grosso, BS; Roy Hwang MD; Thomas Mroz MD; Edward Benzel MD;Michael Steinmetz MD These authors performed a retrospective review of 36 patients with myelopathic symptoms who underwent cervical deformity correction surgery.Preoperative and postoperative radiographic findings of the degree of kyphosis werecompared with functional outcome with minimum follow-up of 2 years. Functionaloutcomes were assessed with the modified Japanese Orthopaedic Association(mJOA). KEY POINTS FROM THIS STUDY: 1) The reversal of normal cervical curvature, as seen in kyphosis, can occurthrough a variety of mechanisms and can lead to mechanical pain, neurologicaldysfunction, and functional disabilities. Kyphosis of the cervical spine can be adebilitating condition that leads to significant neurological dysfunction. 2) Surgical intervention is warranted in patients with sufficiently symptomaticdeformities in an attempt to correct the deformed cervical spine. 3) The results of this study showed significantly improved neurological outcomeswith better correction of focal kyphosis and with attainment of global lordosis. 4) The authors’ results suggest that the degree of correction of focal kyphosisdeformity correlates with improved neurological outcomes. 5) The authors also saw a positive relationship between attainment of globallordosis and improved mJOA scores. 6) The normal lordotic curvature of the cervical spine is critical to maintainingsagittal alignment and spinal balance. 7) It is believed that the neurological symptoms seen in cervical kyphosis are aresult of deformity-induced anatomical changes that apply pressure to the spinalcord and nerve roots. 8) Narrowing of the neuroforamen caused by disc degeneration may result inradiculopathy, while stretching or impingement of the spinal cord, often at the apexof the [kyphotic] deformity, can lead to myelopathic symptoms. 9) As kyphosis progresses, spinal cord and nerve root stresses often increase,leading to further neurological debilitation. 10) It is thought that the tension created from kyphotic deformity on the anteriorspinal cord results in compression on the regional blood supply and nerves. 11) Our study found that the degree of correction of focal kyphosis deformitycorrelates with improved neurological outcomes. 12) The extent of cervical kyphosis is commonly associated with progression ofneurological symptoms. 13) These authors found that a greater degree of focal kyphosis correction wasassociated with a greater degree of neurological improvement. 14) In patients with focal kyphosis, a greater degree of correction may assist inachieving greater neurological improvements. 15) In correction surgery for cervical kyphotic deformity, better outcomes werereported in patients who achieved lordosis than in those who maintained kyphosis. COMMENTS FROM DAN MURPHY: Although this is a surgical study, it has a number of chiropractic applications: 1) Cervical kyphosis adversely affects spinal cord function, probably bycontributing to anterior spinal cord ischemia and pressure on the spinal cord andnerve roots. 2) Cervical kyphosis can cause: A)) Mechanical pain B)) Neurological dysfunction C)) Functional disabilities 3) Correction of cervical lordosis is desirable. 4) The better the correction of focal cervical kyphosis and the better theachievement of global cervical lordosis, the better the improvement of neurologicaloutcomes. Some chiropractic techniques, especially Chiropractic Biophysics, have proveneffective (published in PubMed), nonsurgical clinical protocols to restore cervicallordosis. Chiropractic Biophysics has taught these techniques to chiropractors formore then 30 years.

Journal of Clinical Neuroscience Volume 17, Issue 6, June 2010, Pages 742-745 A. Dimitroulias, C. Tsonidis, K. Natsis, I. Venizelos, S.N. Djau, P. Tsitsopoulos andP. Tsitsopoulos FROM ABSTRACT The aim of our study was to determine the types of mechanoreceptors in the twolower intervertebral discs in normal adult cadaveric donors and to review theliterature.Twenty-five lumbar (L4 – 5 and L5 – S1) intervertebral discs were retrieved from 15fresh cadavers.We utilized immunoreactivity against the S-100 protein to localize specialized nerveendings. Immunoreactivity showed receptors in 92% of discs.The most frequent type had morphology resembling the Ruffini type receptor(88%), followed by the Golgi type.Free nerve fibers were frequently present.All neural structures were found in the superficial layers of the annulus fibrosus, inlongitudinal ligaments, or between these two.The anterior part of the L5 – S1 disc had a greater frequency of encapsulatedreceptors than the other parts, which may be correlated with the high shear forcesto which the lumbosacral junction is subjected. KEY POINTS FROM THIS STUDY: 1) The presence of nerve structures in intervertebral discs is well documentedsince 1932. 2) These receptors have a key role in the perception of joint position andadjustment of the muscle tone of the vertebral column.[Important: these nerves are responsive to changes in joint position andalignment, and they control vertebral column muscle tone]. 3) An important component of low back pain is an intense muscle spasm of thevertebral musculature, elicited through reflex arches mediated by specialized nerveendings. 4) There are four categories of joint receptors: A)) type I: encapsulated mechanoreceptors similar to Ruffini endings B)) type II: encapsulated mechanoreceptors similar to Pacinian corpuscles C)) type III: encapsulated mechanoreceptors similar to Golgi endings D)) type IV: unmyelinated free nerve endings and unencapsulated plexuses thathave nociceptive function. 5) The 25 discs used in this study were harvested from 15 human cadavers withthe mean age of 45.4 years (range, 15 – 66 years). None had any history of chroniclow back pain. 6) Nerves were not found in 2 out of 25 discs (8%). 7) The receptors most frequently encountered showed Ruffini receptormorphology [mechanoreceptors]. Ruffini receptors help maintain muscle tone (lowthreshold, slow adaptation). 8) The second most common receptors found had Golgi tendon organmorphologically [mechanoreceptors]. Golgi receprtors are activated at extremes ofjoint motion (high threshold, slow adaptation). 9) Free nerve fibers [pain afferents] were a frequent finding. In 16 of the 25discs [64%], free nerve fibers were found. It is assumed that those close to bloodvessels have a vasomotor role[sympathetic] while those away from vessels mayhave a nociceptive (small caliber) or a proprioceptive role (large caliber). 10) The neural elements were found in the longitudinal ligaments, the spacebetween the longitudinal ligaments and the annulus fibrosus, and in the outer thirdof the annulus fibrosus. 11) The greatest amount of mechanoreceptors were found at the anterior part ofthe L5 – S1 disc which may be correlated with the high shear forces to which thelumbosacral junction is subjected. 12) All neural structures detected were located either in the longitudinalligaments, or the superficial lamellae of the annulus fibrosus, which are the areassustaining the greatest pressure or tension during extremes of movement. 13) During axial loading of a motion segment, compressive stresses in thenucleus will generate tensile stresses in the peripheral annulus, which is rich inneural receptors. 14) In conclusion, this study confirms the existence of an abundant network ofencapsulated and non-encapsulated receptors in the intervertebral discs of thelower lumbar spine in normal human subjects. The principal role of encapsulatedstructures is assumed to be the continuous monitoring of position, velocity andacceleration (kinesthesia). Free nerve fibers are likely to be involved in nociceptionor regulation of vessel tone (autonomic fibers). COMMENTS FROM DAN MURPHY It is chiropractically important to understand that the intervertebral disc isinnervated with nerves that communicate with the central nervous system. Thesenerves tell the CNS about the mechanical status of spinal function and alignment ofthe spine. Undoubtedly, chiropractic adjustments influence these nerves both during anadjustment and afterwards as a consequence of improved biomechanical functionand posture.

British Medical Journal January 11, 2011; Vol. 342:c7086 Sven Trelle, Stephan Reichenbach, Simon Wandel, Pius Hildebrand, BeatriceTschannen, Peter M Villiger, Matthias Egger FROM ABSTRACT Objective : To analyse the available evidence on cardiovascular safety of non-steroidal anti-inflammatory drugs. Design: Network meta-analysis. Network meta-analysis allows a unified, coherentanalysis of all randomised controlled trials that compare non-steroidal anti-inflammatory drugs head to head or with placebo while fully respectingrandomisation. We analysed the cardiovascular safety of non-steroidal anti-inflammatory drugs by integrating all available direct and indirect evidence innetwork meta-analyses. Data sources: Bibliographic databases, conference proceedings, study registers,the Food and Drug Administration website, reference lists of relevant articles, andreports citing relevant articles through the Science Citation Index. Study selection: All large scale randomised controlled trials comparing any non-steroidal anti-inflammatory drug with other non-steroidal anti-inflammatory drugsor placebo. Data extraction:The primary outcome was myocardial infarction. Secondary outcomes included stroke, death from cardiovascular disease, and deathfrom any cause. Data synthesis: 31 trials in 116,429 patients with more than 115,000 patientyears of follow-up were included.Patients were allocated to naproxen [Aleve], ibuprofen [Motrin, Advil], diclofenac [Voltaren], celecoxib [Celebrex], etoricoxib [Arcoxia], rofecoxib [Vioxx], lumiracoxib[Prexige], or placebo. Compared with placebo, rofecoxib [Vioxx] was associated with the highest risk ofmyocardial infarction (increased risk by 112%), followed by lumiracoxib [Prexige](increased risk by 100%). Ibuprofen was associated with the highest risk of stroke (increase risk by 236%),followed by diclofenac [Voltaren] (increased risk by 186%).Etoricoxib [Arcoxia] (increased risk by 307%) and diclofenac [Voltaren] (increasedrisk by 298%) were associated with the highest risk of cardiovascular death. Conclusions Little evidence exists to suggest that any of the investigated drugs are safe incardiovascular terms.Cardiovascular risk needs to be taken into account when prescribing any non-steroidal anti-inflammatory drug. KEY POINTS FROM THIS STUDY: 1) This study is unique. It is the largest network meta-analysis looking at allrandomized controlled trials that assess the risk of myocardial infarction, stroke,death from cardiovascular disease, and death from any cause, as a consequence oftaking non-steroidal anti-inflammatory drugs (NSAIDs). 2) Non-steroidal anti-inflammatory drugs (NSAIDs) have been the cornerstoneof pain management in patients with osteoarthritis and other painful conditions. 3) In the United States an estimated 5% of all visits to a doctor are related toprescriptions of non-steroidal anti-inflammatory drugs and they are among themost commonly used drugs. 4) Cardiovascular death A)) The analysis showed that cardiovascular death accounted for 46% of alldeaths in those evaluated in this study.3 B)) All drugs except naproxen showed some evidence for an increased risk ofcardiovascular death compared with placebo. 5) Death from any cause A)) All the drugs seemed to be associated with increased risks of death from anycause compared with placebo. B)) All drugs seemed to be associated with increased risks of the composite ofnon-fatal myocardial infarction, non-fatal stroke, or cardiovascular death comparedwith placebo. 6) Discussion A)) Non-steroidal anti-inflammatory drugs are mainly used for symptomatictreatment of musculoskeletal conditions. Clearly, as for any symptomatic treatment,doing more harm than good with this class of drugs should be avoided. B)) Our study confirms previous notions of regulatory bodies, mainly based onobservational evidence, that all non-steroidal anti-inflammatory drugs areassociated with an increased risk of cardiovascular adverse effects. C)) Our results are based on randomised evidence and we therefore believe thatour study provides the best available evidence on the safety of this class of drugs. D)) Naproxen seems to be the safest analgesic for patients with osteoarthritis incardiovascular terms but this advantage has to be weighed against gastrointestinaltoxicity and the need for concomitant prescription of a proton pump inhibitor inmany patients. E)) Paracetamol [acetaminophen] results in only a small reduction in pain and isassociated with clinically relevant hepatotoxicity, even in dosages recommended formusculoskeletal pain. F)) The analgesic effects of opioids are better than acetaminophen, butoutweighed by large increases in the risk of adverse events. G)) In conclusion, the options for the treatment of chronic musculoskeletal painare limited and patients and clinicians need to be aware that cardiovascular riskneeds to be taken into account when prescribing. H)) In 2004, Vioxx, a COX 2 selective inhibitor, was withdrawn from the marketbecause it increased the risk of cardiovascular events. Cardiovascular safety of NSAIDs Editorial British Medical Journal January 11, 2011; Vol. 342:c6618 Wayne A Ray: Professor and Director, Division of Pharmacoepidemiology, Department of Preventive Medicine, Nashville, TN SOME POINTS FROM THIS EDITORIAL: 1) The cardiovascular risks from NSAIDs should prompt evaluation of a broaderrange of alternatives. 2) Millions of patients with chronic musculoskeletal symptoms are long-termusers of non-steroidal anti-inflammatory drugs (NSAIDs). Unfortunately, thesedrugs have common and potentially severe adverse effects, including renalimpairment, gastrointestinal complications, and cardiotoxicity. 3) The cardiotoxicity from NSAIDs is particularly worrying because manypatients with musculoskeletal disease also have cardiovascular disease. 4) All cyclo-oxygenase-2 [COX-2] inhibitors studied in large placebo controlledtrials have been found to confer an increased risk of serious cardiovasculardisease. 5) What does this all mean when prescribing NSAIDs for patients at high risk ofcardiovascular disease? Current data suggest that selective cyclo-oxygenase-2inhibitors, particularly in higher doses, should be avoided. COMMENTS FROM DAN MURPHY: Apparently all pain drugs have serious side effects. The drugs include NSAIDs,acetaminophen, and opiates. The side effects I have reviewed in studies includegastrointestinal bleeding, kidney disease, liver disease, heart attack, stroke,increase in all cause mortality, dementia, Alzheimers dementia, hearing loss, anderectile dysfunction. As noted above, this wake-up information should prompt evaluation of a broaderrange of alternatives. A list of such non-toxic alternatives for pain managementwas presented by Dr. Joseph Maroon, the neurosurgeon for the Pittsburgh Steelers,in the journal Surgical Neurology International, December 2010. I reviewed Dr.Maroons article, its Article Review #8-12. As chiropractors, we should recall that in 2003, Spine published a study comparingchiropractic adjustments to the NSAIDs Celebrex and Vioxx in patients with chronicneck and back pain. Chiropractic was better then 5 times more effective than thesedrugs, caused no side effects, and had a stable therapeutic benefit a year later(Article Reviews 12-03 and 34-04).

Journal of Immunotoxicology January 2011; Vol. 8; No. 1; pp. 68 – 79Helen V. Ratajczak FROM ABSTRACT Autism, a member of the pervasive developmental disorders (PDDs), has beenincreasing dramatically since its description by Leo Kanner in 1943. First estimatedto occur in 4 to 5 per 10,000 children, the incidence of autism is now 1 per 110 inthe United States, and 1 per 64 in the United Kingdom, with similar incidencesthroughout the world. Searching information from 1943 to the present in PubMed and Ovid Medlinedatabases, this review summarizes results that correlate the timing of changes inincidence with environmental changes.Autism could result from more than one cause, with different manifestations indifferent individuals that share common symptoms. Documented causes of autism include genetic mutations and/or deletions, viralinfections, and encephalitis following vaccination. Therefore, autism is the result of genetic defects and/or inflammation of the brain.The inflammation could be caused by a defective placenta, immature blood-brainbarrier, the immune response of the mother to infection while pregnant, apremature birth, encephalitis in the child after birth, or a toxic environment. KEY POINTS FROM THIS AUTHOR: 1) Autism is a neuro-developmental disorder. 2) Genetic, environmental, and immunological factors may play a role in thepathogenesis of Autism. 3) Boys have autism 3-4 times more often than girls. 4) 75% of autistic individuals become either institutionalized as adults or areunable to live independently. 5) The estimated lifetime per capita incremental societal cost of autism is $3.2million per case. Greater than the monetary cost, the emotional devastationcaused by the great difficulties posed by the autistic individual, and the strains onthe family. 6) Autism was first described in 1943, with a prevalence of 1/2500 children. 7) In the 1970s, autism was still 1/2500 children. By the 1990s the rate was1/250 children, a 10-fold increase. 8) The Center for Disease Control and Prevention states that the prevalence ofautism is increasing at epidemic rates. 9) In 2002, the rate for autism was 1/150 children (USA). 10) In 2006, the rate for autism was 1/110 children (USA). 11) A 2007 parent survey showed an autism rate of 1/91 children (USA). 12) The incidence of autism in the United Kingdom is also increasing, with higherrates than in the United States, with a current prevalence of 1/64 children. 13) The autism increase is not a result of reclassification; there have been nochanges in prevalence of mental retardation, speech/language impairment, ortraumatic brain injury, which suggests that the increase in autism is real. Changes in rates of autism incidence 1) In 2004, the flu vaccine containing Thimerosal was recommended for allchildren 6 – 23 months old in the United States. In addition, flu vaccination during alltrimesters of pregnancy is now universally recommended in the United States. Mostflu vaccines contain Thimerosal, despite its implication in autism.[Important: the flu vaccine still contains Thimerosal with mercury, and isrecommended for all children and pregnant mothers, every year] 2) The increase in autism incidence began about 1988 – 1990. 3) The new version of the measles, mumps, rubella vaccine (i.e., MMR II) thatdid not contain Thimerosal was introduced in 1979. By 1983, only the new versionwas available. Autism in the United States spiked dramatically between 1983 and1990 from 1/2500 to 1/500. 4) In 1988, two doses of MMR II were recommended to immunize thoseindividuals who did not respond to the first injection. A spike of incidence of autismaccompanied the addition of the second dose of MMR II. 5) In 1988, MMR II was used in the United Kingdom, which reported a dramaticincrease in prevalence of autism to 1/64. Canada, Denmark, and Japan alsoreported dramatic increases in prevalence of autism. 6) The rubella component of MMR II was propagated in a human cell linederived from embryonic lung tissue. The MMR II vaccine is contaminated withhuman DNA from the cell line. This human DNA could be the cause of the spikes inincidence. 7) An additional increased spike in incidence of autism occurred in 1995 whenthe chicken pox vaccine was grown in human fetal tissue. 8) The human DNA from the vaccine can be randomly inserted into therecipients genes. This insertion occurs primarily on the X chromosome in genesinvolved in nerve cell synapse formation, central nervous system development, andmitochondrial function, accounting for autism primarily in boys. These data supportthe hypothesis that residual human DNA in some vaccines might cause autism. 9) The incidence and prevalence data indicate the timing of introduction ofvaccines and changes in the type and increasing number of vaccines given at onetime implicate vaccines as a cause of autism. 10) The current recommended immunization schedule in the United Statesincludes six vaccines at 2 months. The immune system is particularly sensitive at 2months of age. The immune system of an infant is compromised at 2 months. Achallenge by so many vaccines while the immune system is compromised might contribute to an onset of autism. Vaccine antigens 1) Many parents cite normal development of their children until they receivevaccines at about the age of 18 months. 2) A possible cause of autism is that the pertussis toxin in the DPT vaccinecreates chronic autoimmune damage to the gut, altering immune function. 3) When the measles vaccine is given, it depletes the children of their existingsupply of Vitamin A, which negatively impacts the retinoid receptors, accounting forthe distorted vision in autistic individuals. When the natural form (cis) of Vitamin Awas given to autistic subjects for 2 – 3 months, followed by urocholine, many autisticchildren showed immediate improvement in their autistic behaviors, includingimproved eye contact, ability to socialize, ability to sleep through the night, etc. Vaccine Preservative and Environmental Mercury 1) There is evidence that Thimerosal (which is 49% ethyl mercury) is indeedharmful. Thimerosal is an antibacterial agent in vaccines. Thimerosal has beenimplicated as a cause of autism. 2) Not only is every major symptom of autism documented in cases of mercurypoisoning but also biological abnormalities in autism are very similar to the sideeffects of mercury poisoning itself. 3) Autistic brains show neurotransmitter irregularities that are virtually identicalto those arising from mercury exposure. 4) Due to the extensive parallels between autism and mercury poisoning, thelikelihood of a causal relationship is great. More evidence linking autism withmercury poisoning is the timing of inclusion of Thimerosal in vaccines in the 1930sclosely preceding the discovery of autism in 1943. 5) There are dangerous effects of Thimerosal on the immune system,particularly on T-lymphocytes. Mercury induces glutathione depletion, increasedoxidative stress, and apoptosis in these cells. 6) Thimerosal causes toxic effects on brain cells, affects nerve differentiation,and depletes glutathione. 7) Mercury is both neurotoxic and immunotoxic. 8) Autistic individuals have a 10-fold greater number of hyperactive mast cells.Mercury stimulates to release pro-inflammatory cytokines, which may disrupt theblood – brain barrier and cause brain inflammation. 9) Cumulative mercury exposure results from mercury as a pollutant in air, soil,dust, water, consumer products, dental amalgam and lighting fixtures, foodstuffs,fish, and seafood. Concerning air, for every 1,000 pounds of mercury (all forms),there was a 61% increase in the rate of autism. 10) Mercury is found in many foods, including high-fructose corn syrup. Theconsumption of high-fructose corn syrup could impact the behavior of children withattention deficit hyperactivity disorder (ADHD), which is associated with autism. 11) The consumption of some artificial food color additives has been shown tolead to zinc deficiency. Dietary zinc is essential for maintaining the metabolicprocesses required for mercury elimination. Measles Mumps Rubella Vaccine (MMR) An examination of the continuing increase in prevalence in autism in thecontext of the dates of spikes in increase in prevalence which point to the MMR IIvaccine (which did not contain Thimerosal) suggests that something new causedthe increase in incidence of autism. The new component could be the human DNAfrom the preparation of the rubella component of the MMR II vaccine and thechicken pox vaccine. Metal metabolism disorder 85% of autistic patients have severely elevated Cu:Zn ratios. Genetics There is indisputable evidence for a genetic component in autism, because ifone identical twin is autistic, the likelihood that the other twin will have autism is90%. In great contrast, the likelihood that non-identical twins both have autism isonly 2 – 3%. Yet, the genetic cause of autism is only 1 – 2% of the cases. A reasonto discount an overall genetic cause is that autism is now considered an epidemicand there is no such thing as a genetic epidemic. Age of parents 1) Advanced maternal and paternal ages are independently associated with riskof autism-spectrum disorders. 2) A 10-year increase in maternal age is associated with a 38% increase in theodds ratio for autism. A 10-year increase in paternal age is associated with a 22%increase. 3) The trend toward delaying childbearing contributed about a 4.6% increase ofautism over the decade. Ageing increases cumulative toxic exposure, resulting innucleotide repeat instability. Mitochondrial disease and dysfunction Mitochondrial dysfunction is caused by environmental toxins and cancontribute to the altered energy metabolism in the brains of children with autism. Pregnancy 1) A defective blood-brain barrier is common in autistic patients. 2) A mothers immune response(s) to infection during pregnancy includes theformation/release of antibodies and cytokines that could cross the blood-brainbarrier of the fetus and which, over time, could cause autism. Imbalance in neural systems Autism might be caused by an imbalance between excitation and inhibition inkey neural systems including the cortex. Environment Autism may be a disease of very early fetal development (approximately day20 – 24 of gestation), with environmental exposures during pregnancy causing orcontributing to autism based on the neurobiology of developmental genes. Medications are implicated in autism including: 1) Thalidomide by the mother. 2) Misoprostol, a prostaglandin analogue used for prevention of gastric ulcers. 3) Valproic acid, an anti-convulsant. 4) Acetaminophen has also been suggested to cause autism. 5) Children given acetaminophen after the MMR II vaccine were significantlymore likely to become autistic than children given ibuprofen. 6) During pregnancy, mothers of autistic children commonly suffer morebacterial and viral infections and fevers, which could affect the fetus to predisposethe child for autism. These mothers often take acetaminophen to treat theinfections. Acetaminophen overdose depletes the livers supplies of sulfate andglutathione, impairing its ability to detoxify and excrete harmful substances. Therefore, the fetus could be impaired by the mothers consuming acetaminophen.After birth, if acetaminophen were given to the child, and used repeatedly, the drugcould cause depletion of sulfate and glutathione, and the child could regress intoautism. Low Glutathione Glutathione (GSH) is the most important antioxidant for detoxification andelimination of environmental toxins. GSH is decreased in the plasma of autisticsubjects. In addition, GSH plays a major role in methylation and is intimatelyinvolved in detoxification processes. Phthalates, Polychlorinated Biphenyls (PCBs), Environmental Contaminants 1) Phthalates, an environmental toxin, are implicated in autism. 2) Phthalates are synthetic chemicals with widespread human exposure becauseof their use in plastics and other consumer products. 3) Humans are exposed to phthalates through ingestion, inhalation, and dermalroutes. 4) There is a significant relationship between the concentration of urinaryphthalates and the degree of autism. 5) Polychlorinated biphenyls (PCBs) are a suspected as causes of autism. 6) Environmental contaminants, including PCBs, herbicides, perchlorates,mercury, and coal derivatives interfere with thyroid function, and this can affectfetal brain growth, leading to autism. 7) Organophosphate pesticides may contribute to ADHD prevalence. 8) The highest rate of autism is in schools near EPA Superfund sites. SUMMARY 1) Autism has increased to epidemic proportions, affecting four times as manymales and females. 2) With a prevalence of 1/110 in the United States, 1/64 in the UnitedKingdom, and similar ratios in many other countries, [autism is] a very significantthreat to future generations is evident. 3) This review cites documentation of causes of autism, including geneticmutations/deletions, viral infections (i.e., rubella and herpes), and encephalopathyfollowing vaccination. 4) Autism has been documented to be caused by genetic defects and/orinflammation of the brain. The inflammation could be caused by a wide variety ofenvironmental toxicants, infections, and co-morbidities in individuals geneticallyprone to the developmental disorder.

The New England Journal of Medicine February 24, 2011; Vol. 364, No. 8, pp. 701-9 Markus J. Ege, M.D., Melanie Mayer, Ph.D., Anne-Cécile Normand, Ph.D., JonGenuneit, M.D., William O.C.M. Cookson, M.D., D.Phil., Charlotte Braun-Fahrländer,M.D., Dick Heederik, Ph.D., Renaud Piarroux, M.D., Ph.D., Erika von Mutius, M.D. FROM ABSTRACT: Children who grow up in environments that afford them a wide range of microbialexposures, such as traditional farms, are protected from childhood asthma andatopy. In previous studies, markers of microbial exposure have been inverselyrelated to these conditions. Results In both studies, children who lived on farms had lower prevalences of asthma andatopy and were exposed to a greater variety of environmental microorganisms thanthe children in the reference group.Increased microbial exposure was inversely related to the risk of asthma:Reduced by 38% in one study and 14% in the other study, for an average reductionby 24%. Conclusions Children living on farms were exposed to a wider range of microbes than werechildren in the reference group, and this exposure explains a substantial fraction ofthe inverse relation between asthma and growing up on a farm. KEY POINTS FROM THIS STUDY: 1) This study looked at two groups of children whose exposure to microorganisms was evaluated differently. Each group involved children who grewup on rural farms and a group of controls who were not farm raised children.Combined, the study group consisted of 16,511 children between ages 6-13 years. 2) One study analyzed childrens mattress dust collected with a vacuum cleaner.One study analyzed childrens room dust collected with electrostatic dust collectors. 3) After collection, the dust was incubated for 7 days. The colonies weremicroscopically counted and identified and treated with Grams stain. 4) Environmental exposure to microorganisms has repeatedly been found to beinversely related to the manifestation of atopic diseases such as asthma and hayfever. 5) In the population with higher bacterial exposures, the prevalence of asthmaand atopy was substantially lower. 6) Children living on farms had a lower prevalence of asthma than children in thereference groups in both studies by a combined 25%. 7) Indoor microbial exposure is much more common and diverse in the farmingenvironment than in the nonfarming environment. 8) The risk of asthma decreased significantly with the increase in the number ofdetectable bacteria and fungi. 9) Children growing up on farms were protected from asthma and atopy. Thesechildren were exposed to a greater variety of environmental fungi and bacteria ascompared with children in the reference group who lived in the same regions. 10) These data support the idea that the greater diversity of microbial exposureamong children who live on farms is associated with protection from thedevelopment of asthma. 11) The transport of environmental microorganisms from animal sheds and barnsto the indoor environment has been documented. Even when indoors, childrenliving on farms were exposed to a greater variety of microbes than children who didnot live on farms. 12) Microorganisms may be protective against asthma by triggering the innateimmune system for a prominent Type 1 helper T cell response; predominance oftype 2 helper T cells is characteristic of asthma. [Innate Immune Response] 13) The results of both studied groups showed that children living on farms had awider range of microbial exposures than children in the reference groups, whichlargely explained the protective effect of the farming environment on thedevelopment of asthma in children. A COMMENT FROM DAN MURPHY Recall Article Review 9-12 indicated that early life exposure to antibiotics (which killthese microbes) was associated with a 52% increase in asthma.The book by immunologist Mary Ruebush, PhD, Why Dirt Is Good further detailswhy innately children are meant to come into contact with microbes; when theydont or when the microbes are killed with antibiotics, the immune system does not develop properly, there is a switch to a predominant Th2 response, and atopicdisorders (asthma, hay fever, eczema, etc.) develop.

Brismée, Jean-Michel ScD; Sizer, Phillip S. Jr PhD; Dedrick, Gregory S. ScD;Sawyer, Barbara G. PhD; Smith, Michael P. PhD The authors are from the School of Allied Health Sciences, Texas Tech UniversityHealth Sciences Center KEY POINTS FROM THIS STUDY: 1) There is controversy with regard to the anatomic and histological makeup ofthe uncovertebral joints. Some authors claim it to be a synovial joint; othersconsider it to be disc tissue. In his original findings, Von Luschka suggested that theuncinate processes had a joint cavity that was lined with a synovial membrane that secreted synovial fluid.[Hubert von Luschka was the first to describe the uncinate joints in 1858] 2) No research has investigated the presence of pain generating neurotransmitters within the uncovertebral cartilaginous and capsular tissue. Thisstudy investigated the anatomy and innervation of the uncovertebral joints todetermine if it is synovial in nature and capable of generating pain. 3) This study used 2 unembalmed fresh male human cadavers of a mean age of83 years. Tissue from uncovertebral capsule and cartilage was harvested for eachuncovertebral surface from C2-C3 to C6-C7. 4) Chondrocytes and synoviocytes were identified at the capsular tissue of eachuncovertebral joints. [This indicates that the uncinate joints have articularhyaline cartilage and a synovial capsule]. This suggests that the uncovertebraljoint is synovial in nature. 5) Immunoreactivity indicates the uncinate capsules also have the presence ofboth the somatic and autonomic nerve fibers. These findings suggest that theuncovertebral joints are potential pain generators in the cervical spine.[Free nerve endings (pain afferents) were found]. 6) The uncinate capsules are also innervated with post-ganglionic sympatheticefferents. [Important, as this helps establish the biological plausibility ofsomato-sympathetic reflexes] 7) These capsular and synovial tissue nerve fibers lead to pain perception andreflexive responses associated with synovial pathology.[Important: probably including somato-sympathetic reflexes]. 8) Immunohistologic staining in this study found noradrenergic sympatheticpostganglionic nerve fibers. The sympathetic nervous innervation can causenonsegmental spinal pain patterns. [And has potential visceral consequences]. 9) Biomecahnically, the uncovertebral joint is a major contributor to coupledmotion at the lower cervical spinal segments and serves as a controlling factor ofoverall cervical segmental motion.[These joints are biomechanically important]. 10) A synovial or diarthrodial joint must exhibit a joint capsule, a synovialmembrane, synovial fluid, and articular cartilage. Our present findings support thenotion that the uncovertebral complex includes a synovial joint. 11) Disc degeneration always influences the uncinate joints, their biomechanicsand their degenerative potential. 12) Degenerative changes in the uncinate joints may translate into osteophyticprojections that can compress adjacent cervical segmental nerves as they coursethrough the intervertebral foramen or may cause cervical myelopathy. 13) Due to the close proximity of the uncinate process to the vertebral arterydegenerative changes in the uncovertebral joint have been clinically related tovertebral artery compression, ultimately lending to the onset and severity of clinicalvertebrobasilar insufficiency. COMMENTS FROM DAN MURPHY Many chiropractors, myself included, contend that the uncinate joint can becomesubluxated. The uncinate joint subluxation is distinct from the facet jointsubluxation. The adjustment of the uncinate joint subluxation is quite distinct fromthe facet joint subluxation.This study indicates that the uncinate joint is innervated with pain afferents and isthus a source of neck pain. Since pain perception is controlled by mechanicalintegrity (Melzacks and Walls Gate theory), and a subluxated uncinate joint is aloss of mechanical integrity, one would need to adjust the subluxated uncinate jointto best manage some cases of neck pain. Because the uncinate joints are innervated with post-ganglionic sympatheticefferents nerve fibers, it is easier to explain their involvement in cervical somato-sympathetic reflexes that may influence systemic health and wellbeing.

Journal of Immunotoxicology January 2011; Vol. 8; No. 1; pp. 68 – 79 Helen V. Ratajczak FROM ABSTRACT Autism, a member of the pervasive developmental disorders (PDDs), has beenincreasing dramatically since its description by Leo Kanner in 1943. First estimatedto occur in 4 to 5 per 10,000 children, the incidence of autism is now 1 per 110 inthe United States, and 1 per 64 in the United Kingdom, with similar incidences throughout the world. Searching information from 1943 to the present in PubMed and Ovid Medlinedatabases, this review summarizes results that correlate the timing of changes inincidence with environmental changes. Autism could result from more than one cause, with different manifestations indifferent individuals that share common symptoms.Documented causes of autism include genetic mutations and/or deletions, viralinfections, and encephalitis following vaccination. Therefore, autism is the result of genetic defects and/or inflammation of the brain.The inflammation could be caused by a defective placenta, immature blood-brainbarrier, the immune response of the mother to infection while pregnant, apremature birth, encephalitis in the child after birth, or a toxic environment. KEY POINTS FROM THIS AUTHOR: 1) Autism is a neuro-developmental disorder. 2) Genetic, environmental, and immunological factors may play a role in thepathogenesis of Autism. 3) Boys have autism 3-4 times more often than girls. 4) 75% of autistic individuals become either institutionalized as adults or areunable to live independently. 5) The estimated lifetime per capita incremental societal cost of autism is $3.2million per case. Greater than the monetary cost, the emotional devastationcaused by the great difficulties posed by the autistic individual, and the strains onthe family. 6) Autism was first described in 1943, with a prevalence of 1/2500 children. 7) In the 1970s, autism was still 1/2500 children. By the 1990s the rate was1/250 children, a 10-fold increase. 8) The Center for Disease Control and Prevention states that the prevalence ofautism is increasing at epidemic rates. 9) In 2002, the rate for autism was 1/150 children (USA). 10) In 2006, the rate for autism was 1/110 children (USA). 11) A 2007 parent survey showed an autism rate of 1/91 children (USA). 12) The incidence of autism in the United Kingdom is also increasing, with higherrates than in the United States, with a current prevalence of 1/64 children. 13) The autism increase is not a result of reclassification; there have been nochanges in prevalence of mental retardation, speech/language impairment, ortraumatic brain injury, which suggests that the increase in autism is real. Changes in rates of autism incidence: 1) In 2004, the flu vaccine containing Thimerosal was recommended for allchildren 6 – 23 months old in the United States. In addition, flu vaccination during alltrimesters of pregnancy is now universally recommended in the United States. Mostflu vaccines contain Thimerosal, despite its implication in autism.[Important: the flu vaccine still contains Thimerosal with mercury, and is recommended for all children and pregnant mothers, every year] 2) The increase in autism incidence began about 1988 – 1990. 3) The new version of the measles, mumps, rubella vaccine (i.e., MMR II) thatdid not contain Thimerosal was introduced in 1979. By 1983, only the new versionwas available. Autism in the United States spiked dramatically between 1983 and1990 from 1/2500 to 1/500. 4) In 1988, two doses of MMR II were recommended to immunize thoseindividuals who did not respond to the first injection. A spike of incidence of autismaccompanied the addition of the second dose of MMR II. 5) In 1988, MMR II was used in the United Kingdom, which reported a dramaticincrease in prevalence of autism to 1/64. Canada, Denmark, and Japan alsoreported dramatic increases in prevalence of autism. 6) The rubella component of MMR II was propagated in a human cell linederived from embryonic lung tissue. The MMR II vaccine is contaminated withhuman DNA from the cell line. This human DNA could be the cause of the spikes inincidence. 7) An additional increased spike in incidence of autism occurred in 1995 whenthe chicken pox vaccine was grown in human fetal tissue. 8) The human DNA from the vaccine can be randomly inserted into therecipients genes. This insertion occurs primarily on the X chromosome in genesinvolved in nerve cell synapse formation, central nervous system development, andmitochondrial function, accounting for autism primarily in boys. These data supportthe hypothesis that residual human DNA in some vaccines might cause autism. 9) The incidence and prevalence data indicate the timing of introduction ofvaccines and changes in the type and increasing number of vaccines given at onetime implicate vaccines as a cause of autism. 10) The current recommended immunization schedule in the United Statesincludes six vaccines at 2 months. The immune system is particularly sensitive at 2months of age. The immune system of an infant is compromised at 2 months. Achallenge by so many vaccines while the immune system is compromised mightcontribute to an onset of autism. Vaccine antigens: 1) Many parents cite normal development of their children until they receivevaccines at about the age of 18 months. 2) A possible cause of autism is that the pertussis toxin in the DPT vaccinecreates chronic autoimmune damage to the gut, altering immune function. 3) When the measles vaccine is given, it depletes the children of their existingsupply of Vitamin A, which negatively impacts the retinoid receptors, accounting forthe distorted vision in autistic individuals. When the natural form (cis) of Vitamin Awas given to autistic subjects for 2 – 3 months, followed by urocholine, many autisticchildren showed immediate improvement in their autistic behaviors, includingimproved eye contact, ability to socialize, ability to sleep through the night, etc. Vaccine Preservative and Environmental Mercury: 1) There is evidence that Thimerosal (which is 49% ethyl mercury) is indeedharmful. Thimerosal is an antibacterial agent in vaccines. Thimerosal has beenimplicated as a cause of autism. 2) Not only is every major symptom of autism documented in cases of mercurypoisoning but also biological abnormalities in autism are very similar to the sideeffects of mercury poisoning itself. 3) Autistic brains show neurotransmitter irregularities that are virtually identicalto those arising from mercury exposure. 4) Due to the extensive parallels between autism and mercury poisoning, thelikelihood of a causal relationship is great. More evidence linking autism withmercury poisoning is the timing of inclusion of Thimerosal in vaccines in the 1930sclosely preceding the discovery of autism in 1943. 5) There are dangerous effects of Thimerosal on the immune system,particularly on T-lymphocytes. Mercury induces glutathione depletion, increasedoxidative stress, and apoptosis in these cells. 6) Thimerosal causes toxic effects on brain cells, affects nerve differentiation,and depletes glutathione. 7) Mercury is both neurotoxic and immunotoxic. 8) Autistic individuals have a 10-fold greater number of hyperactive mast cells.Mercury stimulates to release pro-inflammatory cytokines, which may disrupt theblood – brain barrier and cause brain inflammation. 9) Cumulative mercury exposure results from mercury as a pollutant in air, soil,dust, water, consumer products, dental amalgam and lighting fixtures, foodstuffs,fish, and seafood. Concerning air, for every 1,000 pounds of mercury (all forms), there was a 61% increase in the rate of autism. 10) Mercury is found in many foods, including high-fructose corn syrup. Theconsumption of high-fructose corn syrup could impact the behavior of children withattention deficit hyperactivity disorder (ADHD), which is associated with autism. 11) The consumption of some artificial food color additives has been shown tolead to zinc deficiency. Dietary zinc is essential for maintaining the metabolicprocesses required for mercury elimination. Measles Mumps Rubella Vaccine (MMR) An examination of the continuing increase in prevalence in autism in thecontext of the dates of spikes in increase in prevalence which point to the MMR IIvaccine (which did not contain Thimerosal) suggests that something new causedthe increase in incidence of autism. The new component could be the human DNAfrom the preparation of the rubella component of the MMR II vaccine and the chicken pox vaccine. Metal metabolism disorder 85% of autistic patients have severely elevated Cu:Zn ratios. Genetics There is indisputable evidence for a genetic component in autism, because ifone identical twin is autistic, the likelihood that the other twin will have autism is90%. In great contrast, the likelihood that non-identical twins both have autism isonly 2 – 3%. Yet, the genetic cause of autism is only 1 – 2% of the cases. A reasonto discount an overall genetic cause is that autism is now considered an epidemic and there is no such thing as a genetic epidemic. Age of parents 1) Advanced maternal and paternal ages are independently associated with riskof autism-spectrum disorders. 2) A 10-year increase in maternal age is associated with a 38% increase in theodds ratio for autism. A 10-year increase in paternal age is associated with a 22%increase. 3) The trend toward delaying childbearing contributed about a 4.6% increase ofautism over the decade. Ageing increases cumulative toxic exposure, resulting innucleotide repeat instability. Mitochondrial disease and dysfunction Mitochondrial dysfunction is caused by environmental toxins and cancontribute to the altered energy metabolism in the brains of children with autism. Pregnancy 1) A defective blood-brain barrier is common in autistic patients. 2) A mothers immune response(s) to infection during pregnancy includes theformation/release of antibodies and cytokines that could cross the blood-brainbarrier of the fetus and which, over time, could cause autism. Imbalance in neural systems Autism might be caused by an imbalance between excitation and inhibition inkey neural systems including the cortex. Environment Autism may be a disease of very early fetal development (approximately day20 – 24 of gestation), with environmental exposures during pregnancy causing orcontributing to autism based on the neurobiology of developmental genes. Medications are implicated in autism including: 1) Thalidomide by the mother. 2) Misoprostol, a prostaglandin analogue used for prevention of gastric ulcers. 3) Valproic acid, an anti-convulsant. 4) Acetaminophen has also been suggested to cause autism. 5) Children given acetaminophen after the MMR II vaccine were significantlymore likely to become autistic than children given ibuprofen. 6) During pregnancy, mothers of autistic children commonly suffer morebacterial and viral infections and fevers, which could affect the fetus to predisposethe child for autism. These mothers often take acetaminophen to treat theinfections. Acetaminophen overdose depletes the livers supplies of sulfate andglutathione, impairing its ability to detoxify and excrete harmful substances. Therefore, the fetus could be impaired by the mothers consuming acetaminophen.After birth, if acetaminophen were given to the child, and used repeatedly, the drugcould cause depletion of sulfate and glutathione, and the child could regress intoautism. Low Glutathione Glutathione (GSH) is the most important antioxidant for detoxification andelimination of environmental toxins. GSH is decreased in the plasma of autisticsubjects. In addition, GSH plays a major role in methylation and is intimatelyinvolved in detoxification processes. Phthalates, Polychlorinated Biphenyls (PCBs), Environmental Contaminants 1) Phthalates, an environmental toxin, are implicated in autism. 2) Phthalates are synthetic chemicals with widespread human exposure becauseof their use in plastics and other consumer products. 3) Humans are exposed to phthalates through ingestion, inhalation, and dermalroutes. 4) There is a significant relationship between the concentration of urinaryphthalates and the degree of autism. 5) Polychlorinated biphenyls (PCBs) are a suspected as causes of autism. 6) Environmental contaminants, including PCBs, herbicides, perchlorates,mercury, and coal derivatives interfere with thyroid function, and this can affectfetal brain growth, leading to autism. 7) Organophosphate pesticides may contribute to ADHD prevalence. 8) The highest rate of autism is in schools near EPA Superfund sites. SUMMARY 1) Autism has increased to epidemic proportions, affecting four times as manymales and females. 2) With a prevalence of 1/110 in the United States, 1/64 in the UnitedKingdom, and similar ratios in many other countries, [autism is] a very significantthreat to future generations is evident. 3) This review cites documentation of causes of autism, including geneticmutations/deletions, viral infections (i.e., rubella and herpes), and encephalopathyfollowing vaccination. 4) Autism has been documented to be caused by genetic defects and/orinflammation of the brain. The inflammation could be caused by a wide variety ofenvironmental toxicants, infections, and co-morbidities in individuals geneticallyprone to the developmental disorder.