Journal of Neurotrauma October 2011; Vol. 28; No. 10; pp. 2133-2122 Aiguo Wu, Zhe Ying, Fernando Gomez-PinillaDepartment of Integrative Biology and Physiology, University of California at LosAngeles KEY POINTS FROM THIS ARTICLE: 1) Traumatic brain injury (TBI) is one of the most common causes of death anddisability in United States: 220,000 hospitalizations, 52,000 deaths from headtrauma, and 80,000-90,000 patients suffering from permanent disability eachyear. 2) Even though over 30 major clinical trials have been made, no efficienttreatment for TBI has been found to date. 3) TBI results in long lasting consequences on the cognitive ability of patients. 4) The pathology of traumatic brain injury is characterized by membranedamage, oxidative stress, failure in the capacity of neurons to metabolize energy,sustain synaptic function, and likely resulting in cognitive and emotional disorders. 5) These authors assessed the potential of the omega-3 fatty aciddocosahexaenoic acid (DHA) to counteract the effects of concussive injury onimportant aspects of neuronal function and cognition. 6) Fluid percussion injury (FPI) or sham injury was performed on rats whichwere then maintained on a diet high in DHA (1.2% DHA) for 12 days. 7) DHA supplementation improves learning ability in FPI rats. 8) Given the involvement of SOD [superoxide dismutase endogenousantioxidant] and Sir2 [a longevity gene] in promoting metabolic homeostasis, DHAmay help the TBI brain by providing resistance to oxidative stress. 9) The overall results emphasize the potential of dietary DHA to counteractbroad and fundamental aspects of the TBI pathology that can translate in preservedcognitive capacity. 10) Dietary supplementation of fish oil before brain injury can protect the brainfrom the deleterious effects of TBI on cognition and plasticity.2 11) DHA is a crucial omega-3 fatty acid abundant in the brain, is important forbrain development and plasticity, and has been shown to support learning andmemory neurodegerative disorders such as Alzheimers. 12) This study investigated the healing capacity of DHA dietary supplementationwhen provided immediately after a concussive injury in rats. 13) There is a homeostatic effect of DHA dietary supplementation when providedimmediately after TBI. 14) A short period of DHA supplementation significantly counteracted thenegative effects of the injury on cognitive function, neuronal signaling, andmembrane homeostasis. 15) These results indicate that DHA supplementation can provide the type ofbroad protection important for counteracting the effects of TBI. 16) Given the role of DHA in membrane homeostasis and neuronal signaling,these findings implicate dietary DHA as a potential candidate for counteracting theadverse effects of TBI on synaptic plasticity and cognition. 17) Short time feeding of DHA significantly unregulated molecules withrecognized antioxidant capacity such as SOD and Sir2. DHA upregulates SOD andSir2, which may contribute to counteracting oxidative damage to plasma membraneafter TBI. 18) The increase in DHA content may help maintain membrane fluidity, therebypreserving cognitive function in TBI animals. 19) It is known that TBI causes degradation of membrane phospholipids. Synapticmembranes phospholipids are preferentially enriched in omega-3 fatty acid DHA.Increased DHA content helps prevent the loss of DHA from membrane lipids. 20) Our findings suggest that supplementation of DHA may help the TBI brainpreserve synaptic membrane integrity and fluidity, thereby enhancing membranerelated cellular function and subsequent cognitive improvement. 21) Our results demonstrate that DHA dietary supplementation appliedimmediately after TBI counteracts the related cognitive decay.

James B Adams, Tapan Audhy, Sharon McDonough-Means, Robert A Rubin, DavidQuig, Elizabeth Geis, Eva Gehn, Melissa Loresto, Jessica Mitchell, Sharon Atwood,Suzanne Barnhouse and Wondra Lee: From Arizona State University FROM ABSTRACT Background: Vitamin/mineral supplements are among the most commonly usedtreatments for autism, but the research on their use for treating autism has beenlimited. Method: This study is a randomized, double-blind, placebo-controlled three monthvitamin/mineral treatment study. The study involved 141 children and adults withautism, and pre and post symptoms of autism were assessed. Results: The vitamin/mineral supplement was generally well-tolerated. Levels ofmany vitamins, minerals, and biomarkers improved/increased showing goodcompliance and absorption. Statistically significant improvements in metabolic status were many including:Total sulfate +17%Sadenosylmethionine (SAM) +6% Reduced glutathione +17%Ratio of oxidized glutathione to reduced glutathione (GSSG:GSH) -27%ATP +25%NADH +28%NADPH +30% The supplement group had significantly greater improvements than the placebogroup on the Parental Global Impressions-Revised (PGI-R), and on the subscoresfor Hyperactivity, Tantrumming, Overall, and Receptive Language. The degree of improvement of the PGI-R was strongly associated with the initiallevels of biotin and vitamin K; both biotin and vitamin K are made by beneficialintestinal flora. [Important] Conclusions: Oral vitamin/mineral supplementation is beneficial in improving thenutritional and metabolic status of children with autism, including improvements inmethylation, glutathione, oxidative stress, sulfation, ATP, NADH, and NADPH. The supplement group had significantly greater improvements than did the placebogroup on the PGI-R. This suggests that a vitamin/mineral supplement is a reasonable adjunct therapyto consider for most children and adults with autism. [Important] KEY POINTS FROM THIS STUDY: 1) This study presents the effect of nutritional supplements on the nutritional/metabolic status and symptoms of autism in children and adults. It is arandomized, double-blind, placebo-controlled study lasting three months. 2) Inadequate intake of vitamins and minerals due to poor diet is a majorcontributing factor to many child health problems in the US and around the world. 3) Metabolic disturbances may be linked to neuro-developmental disordersincluding attention deficit disorder, learning disorders, and intellectual development. 4) Vitamin/ mineral supplements are among the most widely recommendedmedical interventions for autism, recommended by 49% of physicians. 5) Children with autism have: * Impaired methylation (decreased SAM, [decreased B vitamins]) * Decreased glutathione * Increased oxidative stress [free radical damage] 6) Supplementation with vitamin methyl-B12, folinic acid, and trimethylglycine inautistic children significantly improves methylation, glutathione, and reducesoxidative stress. [Key Point] 7) Supplementation with high-dose vitamin C reduces autism severity. Childrenwith autism have high oxidative stress, and supplementation with vitamin Csignificantly decreases the level of oxidative stress. 8) Supplementation with very high dose vitamin B6 with magnesium, almostalways shows positive behavioral improvements. 9) Subjects and controls were given a liquid supplement or placebo,administered in three equally divided doses with food at breakfast, lunch, anddinner. 10) Both the supplements and placebos formulations were sweetened withsucralose [a known organochloride toxin that also alters gut flora: Article44-09] and contained preservatives potassium sorbate and sodium benzoate[known to cause ADD/ADHD: Article 18-08], and also contained sucrose. 11) The minerals iron and copper were not included in the supplement. 12) The form of vitamin B6 used was pyridoxine, because that form can enter the cell and be converted into the active form, pyridoxal-5-phosphate (P5P); incontrast, P5P cannot enter cells. 13) The amount of vitamin B6 is moderately high because autistic children haveabnormally low B6-dependent biomarkers such as glutathione. 14) Methylsulfonylmethane (MSM) was used as a source of sulfate, becausechildren with autism have very low levels of plasma sulfate. 15) Lithium was included because children with autism and their mothers are lowin lithium, and low lithium is linked to a wide range of psychological disorders. 16) Coenzyme Q-10 was added to support mitochondrial function. 17) A low dose of N-acetylcysteine was included to enhance production ofglutathione. [Important] 18) This formulation contained a water soluble form of vitamin E (d-Alpha-TocopherylPolyethylene Glycol-1000 Succinate) that has shown to improve theabsorption of fat-soluble vitamins in patients with malabsorption. 19) Dosage levels of nutrients in the supplement were significantly higher thanRDA levels. 20) Autism assessment included the revised Parent Global Impressions (PGI-R),which includes:Expressive Language,Receptive Language,General Behavior (Hyperactivity, Tantrums, Cognition, and Play),Gastrointestinal Symptoms, Sleep, Sociability, and Eye Contact. 21) It appears that much higher levels of vitamin D are needed to affect bloodlevels of vitamin D. [They only used 300 IUs; I suggest 2500 IUs] 22) Copper is not included in the supplement since children with autism seem togenerally have adequate or slightly high levels of it. [Important] 23) Supplementation with MSM substantially improved sulfate status, but sulfatelevels were still low, suggesting that higher levels of MSM or other sources ofsulfate such as Epsom salt (magnesium sulfate) baths are needed. 24) Sulfur is important for many reactions including detoxification, inactivation ofcatecholamines, and synthesis of brain tissue. 25) Autistic children have low sulfate levels. Low sulfate decreases the ability todetoxify acetaminophen [Tylenol], which is linked to increased autism.[Important, Article Review 10-12] 26) ATP is required for the kidneys, and low levels of ATP are a contributor todecreased sulfate in children with autism. [The May 2012 Pediatrics indicatesthat pregnant mothers with insulin resistance {reduced ability to makeATP from glucose} increase their babys risk of autism by 61%: ArticleReview 09-13] 27) Autistic children have a problem of converting sulfite to sulfate in themitochondria; the conversion enzyme (sulfite oxidase) contains molybdenum. Theconversion is improved by supplementing with molybdenum (about 150 mcg). 28) The supplement substantially improved glutathione (an important antioxidantand defense against toxic metals). 29) Oral folinic acid, trimethylglycine, and methyl Vitamin B12 greatly improvemethylation, glutathione, and oxidative stress. 30) ATP is the primary energy source for the body and the brain. Supplementingwith CoQ10 significantly increased the levels of ATP. 31) The supplement group had significantly greater improvement than theplacebo group on the Average Change of the PGI-R. 32) The supplement resulted in many significant improvements in nutritional andmetabolic status after three months. 33) Children with low levels of biotin are more likely to benefit fromsupplementation. Biotin is an important cofactor that regulates gluconeogenesis(generation of glucose from non-carbohydrate sources), fatty acid synthesis, andthe Krebs cycle. 34) Approximately half of the biotin and half of the vitamin K in humans comefrom their intestinal bacteria. One of the common causes of biotin or vitamin Kdeficiency is antibiotic usage. One major difference in the medical history ofchildren with autism compared to neurotypical children is a much higher usage oforal antibiotics. Antibiotics lower levels of biotin and vitamin K in children. 35) The correlation of improvement in autism symptoms with biotin and vitamin Kmay relate to a lack of beneficial bacteria which produce biotin and vitamin K. 36) Children with low biotin or low vitamin K were most likely to benefit from themulti-vitamin/mineral supplement. 37) Autistic children have low levels of biotin, glutathione, SAM, plasma ATP,NADH, NADPH, plasma sulfate (free and total), and plasma tryptophan; and highlevels of oxidative stress biomarkers and evidence of impaired methylation (highuridine). By the end of the treatment study, these biomarkers had all improved oreven normalized. 38) Vitamins and minerals are required co-factors for the production of manyneurotransmitters. 39) This study is consistent with several other studies that reported thatvitamin/mineral supplementation is beneficial in treating children with autism. 40) Some children and adults with autism require very high doses of vitamin B6,500-1000 mg/day. [This study used only 40 mg] 41) The length of the study (three months) may not have been long enough toobserve the full-effect of the supplement, and longer treatment may result in largereffect. 42) The supplement group improved significantly more than the placebo groupon the PGI-R Average Change and on several of the PGI-R subscales. 43) The data from this study strongly suggests that oral vitamin/mineralsupplementation is beneficial in improving the nutritional and metabolic status ofchildren with autism, and in reducing their symptoms. 44) Based on the present findings, vitamin/mineral supplementation should beconsidered as an adjunct therapy for most children and adults with autism.The autism pediatric (for 60 lb. child) formula used in this study: VITAMINS Vitamin A (palmitate) 1000 IU Vitamin C (calcium ascorbate) 600 mg Vitamin D3 (cholecalciferol) 300 IU Vitamin E 150 IU Mixed Tocopherols 70 mg Vitamin K2 55 mcg B1 (thiamin HCl) 20 mg B2 (riboflavin) 20 mg B3 (niacin/niacinamide) 15 mg niacin/10 mg niacinamide B5 (calcium d-pantothenate) 15 mg B6 (pyridoxine HCl) 40 mg B12 (cyanocobalamin) 500 mcg Folic Acid 100 mcg Folinic Acid 550 mcg Biotin 150 mcg Choline (choline chloride) 250 mg Inositol 100 mg Mixed Carotenoids 3.6 mg Coenzyme Q10 50 mg N-acetyl cysteine (NAC) 50 mg MINERALS Calcium (calcium ascorbate) 100 mg Chromium (chromium amino acid chelate) 70 mcg Copper NONE Iodine (potassium iodide) 100 mcg Iron NONE Lithium (lithium orotate) 500 mcg Magnesium (magnesium chloride hexahydrate) 100 mg Manganese (manganese amino acid chelate) 3 mg Molybdenum (sodium molybdate dihydrate) 150 mcg Phosphorus NONE Potassium (potassium chloride) 50 mg Selenium (selenomethionine and sodium selenite) 22 mcg Sulfur (MSM) 500 mg Zinc (zinc gluconate) 12 mg

Sharon P. Fowler, Ken Williams, Roy G. Resendez1, Kelly J. Hunt, Helen P. Hazudaand Michael P. Stern; From the Department of Medicine, Division of ClinicalEpidemiology, The University of Texas Health Science Center at San Antonio. FROM ABSTRACT: We have examined the relationship between artificially sweetened beverage (ASB)consumption and long-term weight gain in the San Antonio Heart Study. From 1979 to 1988, height, weight, and ASB consumption were measured among5,158 adult residents of San Antonio, Texas. Seven to eight years later, 3,682participants were re-examined. Outcome measures were incidence of overweight/obesity (OW/OB). A significant positive dose – response relationship emerged between baseline ASBconsumption and all outcome measures. Consuming >21 ASBs/week (vs. none) was associated with almost-doubled risk ofOW/OB (93% increase incidence). Among the baseline normal-weight individuals, a doubled risk of OW/OB was notedat follow-up (103% increased incidence). These findings raise the question whether AS use might be fueling rather thanfighting our escalating obesity epidemic. KEY POINTS FROM ARTICLE: 1) Over 6,000 products including foods, beverages, cosmetics, andpharmaceuticals contain aspartame alone. 2) These authors assessed long-term weight change among participants in theSan Antonio Heart Study who use AS products compared with those who did not. 3) During the past 30 years, people have increasingly turned to artificiallysweetened (AS) foods and beverages in an attempt to lose weight or control it. 4) Manufacturers messages and conventional wisdom suggests that use of ASproducts would enhance weight loss or prevent further gain. 5) Sugar-sweetened beverage consumption was 75% less in ASB userscompared to nonusers. 6) Percent of calories from protein, total fat, and saturated fat were significantlyhigher in AS users. [Suggesting appetite control damage] 7) Dieting rates about the same in both groups. 8) The researchers adjusted the ORs for baseline BMI, age, ethnicity, gender,education, socioeconomic index, baseline and interim change in exercise frequency,baseline smoking status, and interim smoking cessation. 9) Overall, obesity showed significant dose – response relationships with ASBconsumption. 10) For each AS beverage consumed, users experienced significantly higherincrease in BMI. 11) Several studies have described increased appetite, hunger, and foodconsumption following AS exposure. 12) Other studies show that the incidence of metabolic syndrome increases withincreased diet soda consumption (by 34% to 53%). Increased incidence ofmetabolic syndrome has been observed among AS users in two major observationalstudies. 13) The authors suggest that because AS are 180 – 13,000 times sweeter thansugar, their consumption leads to taste distortion, increasing appetite forintensely sweet, highly caloric foods. AS use or sweet taste itself may increasehunger, cravings, or food intake. 14) Studies have shown that AS cause elevated insulin levels. [Important: GaryTaubes (Good Calories Bad Calories {2008}, Why We Get Fat {2011},Newsweek May 14 2012 The New Obesity Campaigns Have It All Wrong)notes that elevated insulin levels upregulates the enzyme lipoproteinlipase which opens the door to the fat cell, increasing fat storage] 15) Aspartame is 40% aspartate. Aspartate is toxic to neurons in the arcuatenucleus of the hypothalamus. The arcuate nucleus of the hypothalamus is a keysite for leptin signaling. Leptin signaling in the arcuate nucleus of thehypothalamus instructs us to reduce food intake. The earlier the exposure to excessaspartate, the more profound the damage to the arcuate nucleus. [ByronRichards (The Leptin Diet {2006}) notes that the hormone leptin is key forturning off our hunger so that we stop eating] 16) Animal experiments show that in utero exposure to aspartate producesoffspring obesity and causes severe loss of neurons in the arcuate nucleus. 3 17) The authors suggest that aspartame exposure may cause neurotoxicity withincreased leptin resistance and obesity. 18) We observed a classic, positive dose – response relationship between ASbeverage consumption and long-term weight gain. 19) Are ASs fueling rather than fighting the very epidemic they were designedto block? These authors suggest the answer is yes. 20) These results, together with findings of increased lymphoma and leukemia inyoung rodents exposed to aspartame, should be carefully considered when policyrecommendations to deter the development of obesity in children and adolescentsare being formulated particularly those recommending increased AS consumption.

The majority of people would say that your medical doctor is the most important person to keeping us healthy. That would be wrong. Here is some history behind what happened when medical doctors went on strike in different areas of the world. In Israel in 1973, the doctors went on strike for a month, and the death rate dropped 50 percent. There had not been a month with so few deaths since the previous doctor’s strike 20 years before. A few years later in Bogota, Columbia, and a two month long strike resulted in a 35 percent drop in the death rate. When Los Angeles county doctors went on a work slowdown to protest high malpractice premiums, the death rate dropped 18 percent, but when the slowdown ended and the medical industry got back to work, the death rate went right back to where it was previously. You and most everybody else would be surprised at what profession is the most important to your health. This profession is overlooked, yet has the greatest impact on our health on a daily basis. The people that pick up your trash have one of the most dangerous jobs and also are life savers. Did you know that sanitation workers have twice the fatality rate of police officers, and nearly seven times the fatality rate of firefighters? A study done in 1851 about the New York City garbage strike concluded that fully a third of the city’s deaths that year could have been prevented if basic sanitary measures had been in place.Rates of preventable disease went down. Mortality rates went down. It also had a ripple effect across all different areas of the city. This is the main reason why third world countries have so many health problems, because they live in unsanitary conditions. They don’t have access to clean drinking water because of people dumping their trash in where their water supply is coming from. The amount of preventable diseases in these countries would go way down just by cleaning up their trash in a more environmental friendly way. Maybe next time you see your garbage man picking up your trash you will say thank you for being such an important person to your health.

Natalie M. Spearing, Luke B. Connelly, Susan Gargett, Michele SterlingFrom the University of Queensland, Australia BACKGROUND FROM DAN MURPHY: CLAIMAINT ONLY STUDY: One that only looks at injured people that are suing. This type of study isconsidered to be of poor quality. These authors excluded these studies. PROXY MEASURES FOR HEALTH STUDIES: This is when determining the health status of an individual is done not by looking attheir health but by looking at something like their ability to return to work or howlong their claim remained open. This type of study is considered bogus. Examples ofthis type of study includes: J. David Cassidy, D.C., Ph.D., Linda J. Carroll, Ph.D., Pierre Côté, D.C., MarkLemstra, M.Sc., Anita Berglund, B.Sc., and Åke Nygren, M.D., Ph.D.; Effect ofEliminating Compensation for Pain and Suffering on the Outcome of InsuranceClaims for Whiplash Injury; New England Journal of Medicine; April 20, 2000; Vol.342; No. 16; pp. 1179-1186. REVERSE CAUSALITY BIAS: This occurs when the results of a study are interpreted to mean that (Whiplash-Injured)people who hire lawyers to obtain compensation have worse healthrecovery outcomes; when in fact it may actually mean that [whiplash-injured]people with greater injuries, more pain and more disability are the ones who seeklawyers to help them obtain the benefits they need. KEY POINTS FROM THIS STUDY: 1) Many believe that compensation [after whiplash injury] does more harm thangood. There is a view that injury compensation leads to worse health; this is calledthe compensation hypothesis. 2) This view that compensation is harmful has been used to argue forreductions to compensation benefits and changes to scheme design, influencejudicial decisions, and advise people that compensation payments will impede theirrecovery. 3) The compensation hypothesis has important implications for injured people,insurers, governments, and health and legal professionals, among others. 4) This systematic review focuses on whiplash, which is a contentious injurybecause there is no gold standard diagnostic test, and its most common symptom,pain, is subjective. These issues have led some to question whether the lure ofcompensation prompts symptom exaggeration. 5) This study systematically reviewed the evidence on the compensationhypothesis using PubMed, CINAHL, EMBASE, PEDro, PsycInfo, CCTR, Lexis, andEconLit. 6) These authors excluded studies using claimants only, or using proxymeasures of health outcome, noting that they were of poor quality and not reliable. 7) 9 of 16 studies used in this review [56%] indicated that compensationadversely influenced health outcomes. However, none evaluated or considered thepotential for reverse causality bias in making their conclusions. Consequently,there is no clear evidence to support the idea that compensation and its relatedprocesses lead to worse health. [Key Point] 8) It is not possible to tell if statistically significant negative associations reflecta compensation effect, or if they simply reflect the pursuit of compensation bythose with comparatively worse health and/or a worse prognosis (a selectioneffect); however, the former is often assumed. 9) Our overall conclusion, that it is currently not possible to determine whetheror not compensation leads to worse health after whiplash because reverse causalitybias has not been addressed, varies from that of earlier systematic reviews onwhiplash as they did not consider this source of bias.[Consequently, these earlier reviews concluding that compensation leadsto worse outcomes may be biased and flawed.] 10) Claiming lawyer involvement leads to worse pain, could also be interpretedas worse pain increases the likelihood of lawyer involvement. [REVERSE CAUSALITY BIAS] 11) The potential for reverse causality bias is largely unacknowledged in thewhiplash literature, and lies similarly unaddressed in studies on other types ofcompensable injuries. [Key Point] 12) It is important to ascertain whether statistically significant negativeassociations between compensation-related factors and health do indeed indicatethat exposure to these factors leads to worse health, or whether they simply reflectthe likelihood that people in comparatively worse health (eg, pain) are more likelyto pursue compensation. Unless the latter possibility is considered, decisions toreduce compensation benefits, for example, may inadvertently disadvantage thosewho are in most need of assistance, which would be an undesirable (andunintended) policy consequence. [Key Point] 13) Statistically significant negative associations between compensation-relatedvariables and health are reported in some studies on whiplash. However, ouranalysis suggests it is inappropriate to interpret these associations as evidence thatcompensation factors lead to worse health because the problem of reverse causalityhas not been addressed. As a result, the magnitude and direction of any observedeffect is unclear and potentially biased. 14) Only when reverse causality is addressed will it be possible to make.

1) An important pathological hallmark of Alzheimer disease (AD) is B-amyloid (AB) peptide (mainly AB40 and AB42) deposition in the brain, resulting in formation of plaques. 2) It is not easy or practical to measure brain AB levels, but plasma AB is easy to obtain and minimally invasive. 3) These authors examined whether dietary intake of nutrients was associated with plasma AB levels in a cross-sectional analysis of 1,219 persons 65 years or older. Participants were in a community based multiethnic cohort. 4) Plasma levels of AB were measured and analyzed against stringent and comprehensive nutrient and supplement data collection. 5) The associations of plasma AB40 and AB42 levels and dietary intake of 10nutrients were examined using linear regression models, adjusted for age, gender,ethnicity, education, caloric intake, apolipoprotein E genotype, and recruitmentwave. 6) Nutrients examined included saturated fatty acid, monounsaturated fatty acid,omega-3 polyunsaturated fatty acid (PUFA), omega-6 PUFA, vitamin E, vitamin C,beta-carotene, vitamin B12, folate, and vitamin D. 7) Higher intake of omega-3 PUFA was associated with lower levels of AB40(24.7% reduced risk) and lower levels of AB42 (12.3% reduced risk). [Total ABreduced risk of 37%] 8) Other nutrients were not associated with plasma AB levels. 9) Our data suggest that higher dietary intake of omega-3 PUFA is associatedwith lower plasma levels of AB42, a profile linked with reduced risk of incident ADand slower cognitive decline in our cohort. 10) There is increasing evidence to suggest that diet may play an important rolein preventing or delaying the onset of Alzheimer disease.

Spinal manipulative therapy (SMT) has been recognized as an effective treatmentmodality for many back, neck and musculoskeletal problems. One of the major issues of the use of SMT is its safety, especially with regards toneck manipulation and the risk of stroke. The vast majority of these accidentsinvolve the vertebro-basilar system, specifically the vertebral artery (VA) betweenC2/C1. Here, we present first ever data on the mechanics between C2/C1 during cervicalSMT performed by clinicians. VA strains obtained during SMT are significantly smaller than those obtained duringdiagnostic and range of motion testing, and are much smaller than failure strains. We conclude from this work that cervical SMT performed by trained clinicians doesnot appear to place undue strain on VA, and thus does not seem to be a factor invertebro-basilar injuries. KEY POINTS FROM THIS STUDY: 1) Spinal manipulative therapy (SMT) is an effective treatment modality formany back, neck and musculoskeletal problems. It has received wide-spreadacceptance in a variety of disciplines including chiropractic, physiotherapy, nursing,and mainstream health care. 2) One of the major issues of the use of SMT is its safety, especially withregards to neck manipulation and the risk of stroke. 3) The estimate of stroke associated (but not necessarily caused) by SMT issmall – about one in a million. 4) It has been assumed [wrongly as per this study] that the VA experiencesconsiderable stretch during extension and rotation of the neck, which may lead toocclusions and damage to the VA, predisposing the patient to stroke. 5) Recent evidence indicates that vertebral artery damage is unlikely to occurbetween C1 to the foramen magnum, and between VAs origin from the subclavianartery to C6. 6) Here, we review the results of existing studies on human VA strains duringhigh-speed, low-amplitude SMTs administered by qualified clinicians and comparethem to the strains encountered during full range of motion (ROM) tests, andfurthermore, add the summarized results of unpublished works from strainsmeasured from all sections of 8 VAs using data from 3 clinicians, resulting in a totalof 3,034 segment strains obtained during SMTs and 2,380 segment strains obtainedduring full ROM testing. 7) Tests were performed on 12 human cadavers, 2 embalmed and 10 fresh. AllROM and SMT testing was performed by three licensed chiropractors. The SMT wasa diversified lateral/rotational maneuver applied to the recorded spinal regions. 8) The force measurements were performed and measured in such a mannerthat if anything at all, the strains during SMTs measured here are likely greaterthan those one would obtain in a patient. 9) The mean [not maximum] failure strains of VAs are reported previously to be58%. All maximum values documented here are clearly below the mechanicalfailure strains of VAs with the largest measured value of 22.9% for ROM testing inthe V3 region representing about 39% of the failure strain. 10) These authors found that the length change of the VA during SMT is muchsmaller than that observed during the range of motion testing. 11) These authors did additional experiments to conclude that repeatedtreatments, as may occur in clinical practice, could not cause micro-structuraldamage and failure strain to the vertebral artery. 12) In summary, the maximal strain values for the ROM testing at eachsegmental level were always greater than the corresponding strain values for theSMTs, suggesting that neck SMTs impose less stretch than turning your head, orextending your neck while looking up at the sky. 13) The results of this study suggest that neck SMTs impose stretches on the VAthat are maximally 55% of the passive range of motion achieved with normalmovements of the head and neck and are maximally 22% of the observed meanmechanical failure strain of human VAs. Therefore, based on the mechanical testsperformed here, one should be able to conclude that stretching of VA during neckSMTs does not cause any damage of the VAs. 14) The VA is never really strained during spinal manipulative treatments butthat the VA is merely taking up slack as the neck and head are moved during SMT,but that there is no stress and thus no possibility for microstructural damage. 15) These authors also argue and state that the increased rate of stretch of theVA during SMT was not able to injury the VA. 16) The results from this study demonstrate that average and maximal VAstrains during high-speed low-amplitude cervical spinal manipulation aresubstantially less than the strains that can be achieved during ROM testing for allvertebral artery segments. 17) We conclude that cervical spinal manipulations, as tested here, are safe froma mechanical point of view for normal, healthy VA.

1) Recently reported associations between synovitis, cartilage damage andplasma levels of omega-3 and omega-6 fatty acids in patients with osteoarthritissuggest that fish oil supplements might be beneficial additions to the therapeuticregime in this disease. 2) Osteoarthritis (OA) is characterized by degeneration and loss of articularcartilage, and accompanying synovial inflammation (synovitis). 3) Synovitis can cause swelling, tenderness and restricted movement in OApatients. 4) In OA, inflammatory cytokines (IL-1B, TNF, IL-6)amplify the pathophysiologicalprocesses that result in joint damage. 5) In OA, low-grade inflammation influences the long-term outcomes in patients. 6) Treatments that safely reduce the inflammation underlying cartilagedegeneration in OA are important. 7) Plasma levels of long chain omega-6 (n-6) and omega-3 (n-3) fatty acidscorrelate with MRI evidence of synovitis in the knees of patients with OA. 8) The inflammatory effects of omega-6 eicosanoids derived from arachidonicacid are greater than the anti-inflammatory effects derived from the omega-3 fattyacids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). 9) The availability of arachidonic acid for production of inflammatoryeicosanoids could be a predisposing factor for synovitis in early OA. 10) The n-6 (AA) and n-3 (EPA) fatty acid ratios could be more important thanthe absolute amounts of these fatty acids. 11) EPA and DHA reduced expression of degradative enzymes and inflammatorycytokines. 12) Long-term fish oil treatment at anti-inflammatory doses inhibits prostaglandinE2 synthesis. 13) Established benefits for omega-3-rich supplements in patients withrheumatoid arthritis include: * Reduced symptom severity * Increased remission * Improvement in markers of cardiovascular risk * Decreased use of NSAIDs 14) The reduced use of NSAIDs is important as these drugs whilst providing aprompt analgesic effect have not been shown to improve long-term outcomes inRA, and their use can distract clinicians from prescribing more effective long-term disease-suppressing agents. 15) Moreover, NSAIDs are associated with an increased risk of potentially life threateninggastrointestinal bleeding and serious thrombotic cardiovascular events,including myocardial infarction and stroke. 16) The NSAID-sparing effect and the direct collateral cardiovascular benefits areimportant potential advantages of fish oil use for long-term analgesia in a diseasesuch as osteoarthritis. 17) Treatment with omega-3 fatty acids has the potential to play a key part inthe management of patients with osteoarthritis. 18) The omega-3 fats in dietary fish oil, EPA and DHA, inhibit the omega-6 fattyacid arachidonic acid cascade into the inflammatory prostaglandins and leukotrienessuch as PGE2 and LTB4. 19) Competitive inhibition of arachidonic acid metabolism by EPA and DHA couldreduce inflammation, pain and synovitis. 20) EPA and DHA suppress chondrocyte metalloproteinases production, anddietary fish oil has a protective effect on cartilage and subchondral bone in OA.