Journal of Alzheimers Disease October 16, 2012 [epub] Natividad Lopez, Consuelo Tormo, Isabel De Blas, Isabel Llinares, Jordi AlomFree Radical Damage=Oxidative Stress=Reactive Oxygen Species (ROS)=LipidPeroxidation KEY POINTS FROM THIS STUDY: 1) Oxidative stress may be a decisive factor in Alzheimers disease (AD) and inthe initial phase of mild cognitive impairment (MCI). 2) This study measured blood oxidative stress using the following: A)) Levels of malondialdehyde (MDA), a marker of oxidative damage to thedouble bonds of lipids; a marker for oxidative degradation of cellular membranes. B)) Levels of superoxide dismutase (SOD), an enzymatic, endogenousantioxidant; blocks the conversion of superoxide radicals into hydrogen peroxide. C)) Levels of ceruloplasmin, another endogenous antioxidant. D)) Level of copper, a powerful pro-oxidant metal ion; a driver of free radicalproduction. 3) The study group consisted of 36 patients with AD, 18 patients with MCI, and33 healthy aged subjects. Blood samples were obtained from each subject. 4) A significantly higher copper level was found in patients with AD and MCIcompared to the control group. [Important point] 5) Levels of MDA were higher in patients from the AD and MCI groups than inthe control group. 6) Our findings support the hypothesis that oxidative stress might represent asign of AD pathology and could be an early event in the progression of MCI to AD. 7) Previous research suggests that oxidative stress may contribute to thepathogenic cascade in Alzheimers disease (AD). 8) Oxidative damage to essential biomolecules (nucleic acids, lipids, proteins, orcarbohydrates) alter the biological role that these play in physiological conditions. 9) The presence of high levels of unsaturated lipid content (that are readilyattacked by free radicals) coupled with high oxygen utilization, high level of redoxtransition metal ions, and relatively poor antioxidant systems makes the brainparticularly vulnerable to oxidative damage. 10) In the brain, due to its high lipid content, the most important mechanism inthe damage due to free radicals is the peroxidation of lipids. 2 11) Cu imbalance contributes to the oxidative stress that is part of thepathogenesis of AD and can play an important role in the development of AD. 12) Mild cognitive impairment (MCI) may be the earliest stage of AD. 13) Cu levels showed a significant increase in the serum of AD and MCI patients,compared to the control group. Cu showed a clear gradient from healthy to ADpatients passing through MCI subjects. 14) Our data show a steady increase in serum Cu levels from healthy subjects toMCI and AD patients. 15) Our findings could support the hypothesis that an increase in serum Culevels could be related to lipid peroxidation due to its correlation with MDA levels,resulting in an involvement of Cu in oxidative damage. 16) Plasma levels of MDA were significantly higher in subjects with AD and MCI, incomparison to healthy controls. 17) Previous studies reported increased oxidative damage in patients with MCI.Plasma in MCI patients is known to have lower levels of non-enzymatic antioxidants[exogenous antioxidants, like vitamin E and C] and decreased activity of antioxidantenzymes [endogenous antioxidants like superoxide dismutase, catalase, andglutathione peroxidase], increased oxidative damage in nuclear and mitochondrialDNA, and higher levels of isoprostanes compared to that of the healthy subjects. 18) The current results suggest that oxidative stress [free radical damage] maybe present in early cognitive decline. 19) In conclusion, we found that lipid peroxidation occurs in patients with MCIand AD in a similar way, suggesting that oxidative stress might represent a signalof the AD pathology and could be an early event in the progression of MCI to AD. KEY CONCEPTS FROM DAN MURPHY *The brain is primarily composed of fat, especially unsaturated fats. *The unsaturated fats of the brain are particularly vulnerable to oxidative stress(free radicle damage). This process is called lipid peroxidation. *Copper significantly accelerates lipid peroxidation (free radical damage) and istherefore a factor in accelerating mild cognitive impairment (MCI) and Alzheimersdisease. Other studies we have reviewed [AR 49-11 and 3-12] concur and indicatethat the primary source of such copper is municipal drinking water and copperfound in dietary supplements; suggesting that our municipal drinking water shouldbe reversed osmosis and our supplements should essentially be copper free. *Both exogenous and exndogenous antioxidants are important in reducing brainfree radical damage. My protocol for doing such is attached. *One should probably not consume fish oil without also increasing consumption ofantioxidants [Article Review 30-12].Supplements That Everyone Should TakeEvery Day All People(Nutri-West: 800-443-3333) 1) Vitamin D3800 IU per day for infants (1 Vitamin D 400) 2,500 IU – per day for children (1 Complete Immuno D3) 5,000 IU per day (1 Complete Hi D3) 2) Multiple Vitamin-MineralShould be copper free (less than 100 micrograms) and iron free(3 Core Level Health Reserves) 3) Omega-3 fatty acids Children: The DHA should be greater than the EPA (2.6/1) 900 mg of EPA + DHA per day (8 Complete Childrens EPA/DHA) Adults: Has an ideal ratio of ALA, EPA, DHA, and GLA; EPA should be double DHA3,000 mg of EPA + DHA per day (6 Complete Omega-3 Essentials)(or 1 teaspoon of Complete Hi-Potency Omega-3 Liquid) 4) Omega-3 antioxidants (1 Complete Omega-3 Co-Factors per gram of EPA + DHA) 5) Mitochondrial Health (adults only): A) Acetyl-l-carnitine 680 mg per day B) Alpha-lipoic acid 240 mg per day (4 Complete AG) C) CoQ 10 10 mg per day 6) Increase Glutathione A) N-Acetyl Cysteine, or NAC: (Complete Glutathione)Children 120 mg per day 2 per dayAdults 240 mg per day 4 per day B) Undenatured Whey Protein: (Complete Whey-G)Children 7 grams per day 1 scoop per dayAdults 21 grams per day 3 scoops per day 7) Resveratrol (adults only)100 mg per day(4 Complete Neuro) 8) Curcumin (Tumeric) (adults only)200 mg per day AntioxidantsExogenous EndogenousMust Come Made by ourFrom Diet DNAVitamin C SuperoxideDismutaseVitamin E CatalaseFruits GlutathionePeroxidaseVegetablesEtc.Endogenous antioxidants have anenormous advantage over exogenousantioxidants Sally Nelson, The induction of human superoxide dismutase and catalase invivo: A fundamentally new approach to antioxidant therapy, Free RadicalBiology & Medicine, 2006, from the Webb-Warning Institute for Cancer,Aging and Antioxidant Research, University of Colorado, and theDepartment of Medicine University of ColoradoATP95 %O2 + Glucose5 %Free RadicalsOxygen Free RadicalsReactive Oxygen Species(ROS)Superoxide RadicalSuperoxideDismutase H2O2 + H2OCatalase GlutathionePeroxidaseO2 + H20
il/May/June 2012; 4:2, 81 – 83; William B. Grant and Vin Tangpricha KEY POINTS FROM THIS ARTICLE: 1) Evidence that vitamin D reduces the risk of many types of disease isincreasing exponentially. 2) In 2011, the Institute of Medicine (IOM) of the US National Academiesreviewed the evidence for beneficial effects of vitamin D for skeletal health, and setthe daily recommended intake of vitamin D at 600 – 800 IU for most children andadults; and defined vitamin D sufficiency as a serum 25(OH)D level above 20 ng/ml(50 nmol/l). They also set a daily upper intake of 4,000 IU of vitamin D3. 3) More than 130 journal publications have criticized the IOM report as beingtoo conservative. One summarized the problems succinctly: The IOMrecommendations for vitamin D fail in a major way on logic, on science, and oneffective public health guidance. 4) The importance of vitamin D is underscored by the fact that skinpigmentation varied as humans moved out of Africa, becoming very pale innorthern Europe. 5) The authors cite evidence of the relationship between low vitamin D levelsand cancers (bladder, brain, colon, gastric, prostate, and rectal cancer; multiplemyeloma; and non-Hodgkin lymphoma), and their survivability rates. 6) The beneficial effects of vitamin D may be much higher than is apparentaccording to prospective studies (perhaps a 28% reduction in all-cause mortalityrate.) 7) Vitamin D may reduce the risk of the metabolic syndrome and its sequelae,type-2 diabetes mellitus and cardiovascular disease (CVD). 8) Several human skin diseases, including psoriasis, vitiligo, atopic dermatitisand localized scleroderma, can be treated with solar radiation (heliotherapy) orartificial UV radiation (phototherapy). 9) One non-vitamin D effect of UVA is liberation of nitric oxide (NO), which canlower blood pressure, has antimicrobial effects and acts as a neurotransmitter.2 10) Ultraviolet light releases endorphins, which may be one reason that being inthe sun is pleasurable. 11) Ultraviolet light may reduce the risk of multiple sclerosis through non-vitaminD mechanisms. 12) Vitamin D deficiency may be a risk factor for erectile dysfunction. 13) Vitamin D deficiency is linked to the risk of CVD and taking vitamin Dsupplements can reduce the risk of CVD. 14) Optimal vitamin D levels appear to help in the prevention and treatment ofinfections. 15) 250,000 IU of cholecalciferol rapidly restores vitamin D status into the optimalrange in subjects with cystic fibrosis acute respiratory infection and is associatedwith improved survival and improved recovery of lung function. 16) There is epidemiologic and intervention studies pointing to an important rolefor vitamin D in the critically ill patient with infection. 17) Vitamin D deficiency is a common feature of chronic kidney disease (CKD).Ergocalciferol [vitamin D2] was less effective than cholecalciferol [vitamin D3],and correcting vitamin D status required a daily dose of greater than 2,000 IU. 18) Vitamin D can improve the efficacy and reduce some of the adverse sideeffects of antiepileptic glucocorticoids, bisphosphonates, antiretroviral drugs, anti-estrogens,cytostatic agents, antihypertensive drugs, and antituberculotic drugs.This action occurs through the Pregnane X receptor (PXR), which plays an importantrole in detoxifying xenobiotics [chemicals that are found in the body but notproduced or expected to pre present in it] and drugs. 19) Vitamin D appears to reduce the risk of hospital-acquired infections, such aspneumonia, bacteremias, urinary tract infections, and surgical site infections.Therefore, vitamin D status should be assessed and corrected in hospital patients. 20) Low vitamin D levels may increase two immune-mediated diseases, asthmaand lupus. Studies of pregnant women and their offspring suggest that vitamin Ddeficiency may predispose an infant to future risk of wheezing disorders. COMMENTS FROM DAN MURPHY We test vitamin D levels on nearly all of our patients. We target 50 ng/ml asoptimal. It is difficult to achieve these levels without consuming at least 5,000 IU ofVitamin D3 per day.
Journal of Clinical Epidemiology November 2012; Vol. 65; No. 11; pp. 1219-1226 Natalie M. Spearing, Luke B. Connelly, Hong S. Nghiem, Louis Pobereskin BACKGROUND FROM DAN MURPHY Reverse causality refers to a direction of cause-and-effect contrary to a commonpresumption. Reverse causality is cause and effect in reverse. That is to say theeffects precede the cause. The problem is when the assumption is A causes B whenthe truth may actually be that B causes A. It is usually stated in published studies, by insurance companies, and by theirrepresentatives (lawyers, claims adjusters, IME doctors, etc.) that injured patientswho seek compensation (ask for compensation, hire a lawyer, etc.)(A), have worsehealth outcomes and slower recovery rates (B). However, such adverse health outcomes do not consider or evaluate the concept ofReverse Causality: slower recovery (B) leads individuals to claim, seek legaladvice, and litigate (A). In my experience, which is extensive, many injured people feel compelled to seeklegal counsel because it is their belief that their insurance company is treating themunfairly, hindering them from obtaining the treatment they need to recover. KEY POINTS FROM THIS STUDY: 1) This study highlights the serious consequences of ignoring reverse causalitybias in studies on compensation-related factors and health outcomes. 2) These authors evaluated reverse causality using a sophisticated (andingenious) evaluation of compensation claims associated with recovery from neckpain (whiplash) after rear-end collisions. 3) Although it is commonly believed that claiming compensation leads to worserecovery, it is also possible that poor recovery may lead to compensation claims apoint that is seldom considered and never addressed empirically. 4) When reverse causality is ignored, claimants appear to have a worserecovery than nonclaimants; however, when reverse causality bias is addressed,claiming compensation appears to have a beneficial effect on recovery. [Key] 5) Reverse Causality must be evaluated to avert biased policy and judicialdecisions that might inadvertently disadvantage people with compensable injuries. 6) There is a prevailing belief that compensation does more harm than good,and this idea that claimants are worse off influences decisions about injurycompensation laws. 7) An assumed belief is that the lure of compensation prompts individuals toexaggerate subjective symptoms. But, no studies have examined the effect ofcompensation payments per se on health. 8) In assessing injury outcomes, reverse causality must also be consideredbecause the causal relationship between compensation factors and health isambiguous. Claiming compensation, lawyer involvement, and litigation, may leadto slower recovery, but it is also possible that slower recovery leads individuals toclaim, seek legal advice, and litigate. 9) The consequences for statistical inference of ignoring reverse causality biasare potentially serious: if negative associations between compensation-relatedfactors and health status actually reflect worse health among those pursuingcompensation (a rarely considered, but entirely plausible proposition), thendecisions to limit access to compensation benefits may do more harm than good. *This study used a source population of 1,174 adults with injuries arising from arear-end vehicle collision. *Of these, 503 agreed to participate in the study. *80% (403/503) developed neck pain within 7 days of collision (early whiplash). *[This means that 20% (100/503) developed neck pain after 7 days of collision]. *65% of those with early whiplash symptoms became claimants (265/403). *35% of those with early whiplash symptoms were non-claimants (138/403). Variable Claimant Non-claimant Number 265 (65%) 138 (35%) Age (mean) 41 43 Female 71% 62% Married 71% 70% Neck Pain 1 wk post MVC 99% 50% Neck Pain, baseline 41.8 19.5 Neck Pain, 6 months 34.7 4.3 Neck Pain, 1 year 26.6 3.3 Neck Pain, 2 years 15.6 1.9 Headache at Baseline 84% 75% Prior Neck Pain 23% 19% Went to ER 75% 61% Went to GP 84% 75% Car Drivable yes 64% 63% Aware yes 25% 25% Prior Collision(s) 20% 17% Not Working at 6 Months 38% 2% 10) Neck pain at 24 months was selected as the primary health outcome. Neckpain severity was measured using the visual analogue scale (VAS) score (0 – 100).Higher VAS scores indicate worse pain: a score of 100 represents the worst painimaginable and zero represents no pain. 11) The analysis offered by these authors is extremely mathematical. They notethat the standard method used to declare compensation negatively affectsrecovery uses a standard single equation approach. However, to assess reversecausality, a simultaneous equations techniques must be used. When thesimultaneous equations techniques are used, the results tell a different story. 12) The usual approach to analyzing the effect of compensation-related healthfactors using the single equation approach is inappropriate and gives rise tobiased and inconsistent results. 13) These authors reject the hypothesis that the decision to claim compensationnegatively affects recovery. 14) Once reverse causality bias is addressed, people who claim compensationappear to experience a better recovery from neck pain at 24 months compared withnon-claimants. [Key Point] 15) The results of this study suggest that compensation claiming may not bedisadvantageous to injured parties after all and that it may even have a beneficialeffect, because access to financial assistance and/or treatment may indeed relievepain and suffering. This is, after all, one of the motivations for compensating peoplewho have sustained an insult to their health. [Key Point] 16) Neck pain is significantly worse at baseline among claimants compared withnon-claimants, which suggests that claims are more likely to be made by individualswhose initial neck pain is worse. [Key Point] 17) Reverse causality is largely overlooked in studies on compensation-relatedfactors. Yet, this study shows that people with worse health tend to claimcompensation. [Key Point] 18) Policies that restrict access to compensation benefits or legal advice mayinadvertently disadvantage people who need financial or legal assistance. [Key] 19) This study serves as a reminder of the dangers of drawing causalinterpretations from statistical associations when the causal framework isambiguous. It establishes, empirically, that reverse causality must be addressed instudies on compensation-related factors and health outcomes. WHAT IS NEW: POINTS FROM AUTHORS: * Reverse causality bias has never been addressed empirically in studies onthe relationship between compensation factors and health outcomes. In spite ofthis, the results of these studies are consistently interpreted as evidence thatexposure to compensation-related factors is harmful to health outcomes. * This study confirms that reverse causality is an important source of bias incompensation research. * Unless all sources of bias, including reverse causality bias, have beenconvincingly addressed, one cannot draw conclusions about the relationshipbetween injury compensation and health outcomes. * The quality of research in this field must be improved to avert decisions thatwill inadvertently disadvantage people with compensable injuries.
Food and Chemical Toxicology 2012 [epub] Gilles-Eric Séralini, Emilie Clair, Robin Mesnage, Steeve Gress, Nicolas Defarge,Manuela Malatesta, Didier Hennequin, Joël Spiroux de VendômoisKEY POINTS FROM THIS ARTICLE: 1) This study represents the first detailed documentation of long-termdeleterious effects arising from the consumption of a GM Roundup-tolerant maizeand of Roundup, the most used herbicide worldwide. 2) Monsanto produced the Roundup-tolerant GMO corn and the Roundup used inthis study. The chemical name for Roundup is glyphosate. 3) These authors evaluated the health effects on rats with the consumption of: A) Roundup-tolerant genetically modified corn grown with applied Roundup[this group is being exposed to BOTH GMO corn and to Roundup] B) Roundup-tolerant genetically modified corn grown without applied Roundup[this group is being exposed to GMO corn but NOT to Roundup] C) Water with Roundup in it at 0.1 ppb (parts per billion) at very lowenvironmentally relevant doses starting below the range of levels permittedby regulatory authorities in drinking water and in GM feed[this group is being exposed ONLY to Roundup] 4) All 3 groups of animals died 2 – 3 times more than controls [at the same timemarker], and died more rapidly, especially the females. 5) Females in all 3 groups developed large mammary tumors almost alwaysmore often than and before controls. 6) The pituitary was the second most disabled organ in all 3 female groups. 7) The sex hormonal balance was modified by GMO and Roundup treatments inall 3 female groups. 8) In treated males, liver congestions and necrosis were 2.5 – 5.5 times higher. 9) Males presented 4 times more large palpable tumors than controls whichoccurred up to 600 days earlier. 10) Biochemistry data confirmed very significant kidney chronic deficiencies; forall treatments and both sexes, 76% of the altered parameters were kidney related. 11) These results can be explained by the endocrine-disrupting effects ofRoundup, and by the overexpression of the transgene in the GMO and its metabolicconsequences. [Important] 12) GM soy and corn that are rendered tolerant to the herbicide Roundup containmore herbicide residues. [Very Important] 13) Chronic diet ingestion of Roundup pesticide residues in GM feed may causeearly alterations in kidney and liver functions. 14) Roundup concentrations about 103 times below the maximal residual levelsinduces endocrine disturbances in human cells. 15) Today, Roundup residues are found in tap water, food and animal feed. 16) Up to 14 months, no animals in the control groups showed any signs oftumors whilst 10 – 30% of treated females per group developed tumors. 17) By the 24th month, 50 – 80% of female animals had developed tumors in alltreated groups, with up to 3 tumors per animal, whereas only 30% of controls wereaffected. 18) The second most affected organ in females was the pituitary gland, ingeneral around 2 times more than in controls for most treatments. 19) The big palpable tumors in males (in kidney, and mostly skin) were by theend of the experimental period on average twice as frequent as in controls. 20) The most affected organs in males were the liver, together with thehepatodigestive tract and kidneys. Hepatic congestions, macroscopic andmicroscopic necrotic foci were 2.5 – 5.5 times more frequent in all treatments than incontrol groups. 21) Degenerating kidneys with marked and severe chronic progressivenephropathies were about twice as high in the treated groups. 22) In summary, for all treatments and both sexes, 76% of the discriminantvariables versus controls were kidney related. 23) The first large detectable tumors occurred at 4 and 7 months into the studyin males and females respectively, underlining the inadequacy of the standard 90day feeding trials for evaluating GM crop and food toxicity. [Important] 24) Currently, no regulatory authority requests mandatory chronic animalfeeding studies to be performed for edible GMOs and formulated pesticides. 25) We observed a strikingly marked induction of mammary tumors by Roundupalone, a major formulated pesticide, even at the very lowest dose administered. 26) Roundup disrupts estrogen synthesis and interferes with estrogen andandrogen receptors. Roundup appears to be a sex endocrine disruptor. 27) Roundup enhances pituitary dysfunction, especially in females. 28) It appears that consumption of Roundup-tolerant corn provokes early aging ofkidney physiology through oxidative stress. 29) Very low dilutions of Roundup are toxic to liver mitochondrial function, andcause cell membrane degradation. 30) In conclusion, it was previously known that glyphosate [Roundup]consumption in water above authorized limits may provoke hepatic and kidneyfailures. 31) The results of the study presented here clearly demonstrate that lower levelsof complete agricultural glyphosate [Roundup] herbicide formulations, atconcentrations well below officially set safety limits, induce severe hormone-dependentmammary, hepatic and kidney disturbances. 32) Roundup and Roundup-tolerant GMO corn cause significant biochemicaldisturbances and physiological failures. COMMENTS FROM DAN MURPHY This study indicates that consumption of GMO Roundup-tolerant corn, whether it isexposed to Roundup or not, or any exposure to Roundup, alters biologicalphysiology. Such exposures damage the pituitary gland, breast, liver, kidney, andhormonal systems; such exposures appear to be carcinogenic.
Archives of Internal Medicine; Vol. 172; No. 15; August 13/27, 2012; pp.1180-118 Beatrice A. Golomb, MD, PhD; Marcella A. Evans, BS; Joel E. Dimsdale, MD; HalbertL. White, PhDUniversity of California, San Diego No drug is without adverse effect potential, and fatigue and exertionalintolerance are adverse effects reported by patients receiving statins. These authors evaluated whether moderate dose statins affected energy andexertional fatigue in a primary prevention population of 1016 subjects (692 menand 324 women), taken for 6 months. Both fatigue and exertional intolerance were significantly higher in both menand women, but women were disproportionately affected: * 40% of treated women cited worsening in either energy or exertional fatigue * 20% of treated women characterized both energy or exertional fatigue asworse or as much worse * 10% of treated women characterized both energy or exertional fatiguecomponents as much worse To our knowledge, this is the first randomized evidence affirming unfavorablestatin effects on energy and exertional fatigue. Effects were seen in a generallyhealthy sample given modest statin doses, and both simvastatin [Zocor] and pravastatin [Pravachol] contributed to the significant adverse effect of statins onenergy and fatigue with exertion. Particularly for women, these unfavorable effectswere not uncommon. These findings are important, given the central relevance of energy andfunctional status to well-being. These effects, germane to quality of life, merit consideration when prescribing or contemplating use of statins, particularly in groups without expectednet morbidity/mortality benefit, extending to high-risk primary prevention andwomen and elderly persons (including those with coronary artery disease). Physicians should be alert to patients reports of exertional fatigue ordiminished energy during statin use. COMMENTS FROM DAN MURPHY Documenting the exertional fatigue and diminished energy with statin use shouldsurprise no one. Energy and exertional activities require ATP. One cannot make adequate levels ofATP without CoQ10. Standard biochemistry texts (I like Salway, 2004, below) show that cholesterol ismade from glucose, primarily in the liver. Statin drugs block this process. Importantly, statin drugs also block the production of CoQ10. Hence, leading toexertional fatigue and diminished energy. Keshav Singhs 2006 book Oxidative Stress, Disease and Cancer states: CoQ10 is a lipid-soluble antioxidant and an integral component of themitochondrial respiratory chain for oxidative energy production. Statins are at present one of the most widely prescribed drugs in the Westernworld. Statins not only reduce the synthesis of cholesterol but also of CoQ10. Statins…deplete body CoQ10 levels.
Physical Medicine and Rehabilitation (PM&R) Volume 4, Issue 6, June 2012, Pages 394 – 401 Ronald Donelson MD, Greg McIntosh MS; Hamilton Hall MD The purpose of this study was to determine the frequency and the characteristics of low back pain (LBP) recurrences by asking these questions: 1) Are low back pain (LBP) recurrences common? 2) Do episodes worsen with multiple recurrences? 3) Does pain change location in any recognizable pattern during an episode? The questionnaire was given to 589 LBP patients from 30 clinical practices(primary care [7%], physical therapy [67%], chiropractic [19%], and surgical spine[7%]) in North America and Europe. There were no exclusions based on type of LBP,history of onset, or comorbidities. Results: 1) Are low back pain (LBP) recurrences common?: [rounded] 73% had suffered a previous episode of LBP 54% had experienced ≥10 episodes of prior LBP in their lifetime 20% had experienced >50 episodes of prior LBP in their lifetime 27% with a previous episode of LBP had 5 or more episodes of LBP per year 2) Do LBP episodes worsen with multiple recurrences? [rounded] 61% reported that at least one of the survey domains was worse 37% reported that recent LBP episode was not worse 21% were worse in all domains 9% were better or the same in all domains 3) Does LBP pain change location in any recognizable pattern during anepisode? [rounded] 76% yes 63% reported that their pain first spread distally then retreated proximallyduring recovery; there was a strong trend toward those reportingworsening episodes also reporting proximal-to-distal-to-proximalchanges in pain location during their episodes. KEY POINTS FROM THIS ARTICLE: 1) Recurrent LBP episodes were common and numerous. Recurrences oftenworsened over time. It seems inappropriate to characterize the typical course of LBPas benign and favorable. [KEY POINT] 2) Sadly, LBP clinical guidelines are unequivocal in their position that the naturalhistory is highly favorable. 3) It is often stated that LBP is normal; has an excellent prognosis, with 90% ofindividuals recovering within 3 months of onset in most cases; and is not debilitatingover the long term. One guideline states that recovery usually takes place within aslittle as 6 weeks. 4) Acute LBP is perceived as largely self-limiting and requiring little if any formaltreatment. This benign view justifies what has become the standard clinical guidelinerecommendation that clinicians often need do nothing more than simply reassurepatients that they will likely recover. 5) Few clinicians [or insurance companies and their representatives]realize that this positive recovery prognosis was derived from a 1966 UK study thatnever collected data on the natural history of LBP; and that when patients with LBPdid not return for follow-up, the researchers assumed that the patients hadrecovered. 6) It is known that the failure of a patient with acute LBP to return to the samedoctor does not necessarily indicate recovery. A patient’s disappearance from thepractice is a poor proxy for recovery. When persistent LBP does not respond to adoctor’s care, the patient tends to drop out of care. 7) These authors cite a handful of studies that showed these numbers: * 69% of patients with recent LBP were still experiencing LBP pain 1 year later. * 82% of patients with non-recent onset of back pain were still experiencingLBP pain 1 year later. * 20-25% of recent LBP patients were still reporting substantial activity limitations1 year later. * Only 21% of LBP patients reported complete recovery at 3 months.[Key Point: note 33%, not 90% as often stated] * 90% of LBP patients had stopped consulting with their doctor within 3 months,further discrediting the termination of care seeking from a single source as asurrogate for recovery; yet 75% had not returned to their pre-episodelevel of function or achieved symptom-free status a year later. * LBP and disability often persist beyond the often-quoted 6-week mark. 8) A review of 36 articles about the long-term course of LBP concluded that theoverall picture is clearly that LBP is not a self-limiting condition. 9) There is no evidence supporting the claim that 80%-90% of patients with LBPbecome pain free within 1 month. 10) Recurrences of back pain are widely recognized as common, reported asoccurring in 60%-73% of individuals within 1 year after recovery from an acuteepisode. 11) In any one year, recurrences, exacerbations, and persistence dominate theexperience of low back pain in the community. This clinical picture is very differentfrom what is typically portrayed as the natural history of LBP in most clinicalguidelines. 12) Considerable clinical experience, contemporary research, and published dataindicate that recurrences of LBP often worsen over time. 13) Most persistent disabling back pain is preceded by episodes that, although theymay resolve completely, may also increase in severity and duration over time. 14) 84% of total medical costs for patients with LBP are related to a recurrence. 15) Many persons with back pain that extends into the buttock or leg report thattheir episode begins with only axial LBP that subsequently spreads distally. 16) Many patients report that, before complete pain abolition, their buttock or legpain retreats or returns to their low back and centralizes, which may represent animportant element of the natural history of LBP in a substantial subset of individuals. 17) In this study, 83% had back and/or buttock pain, 17% had leg pain only. 18) The conventional view of the natural history of acute LBP is that it is self-limitingand that 90% of patients experiencing LBP recover within 90 days or less, butthere is no evidence to suggest that either of these statements is accurate. In reality,the recovery rates reported in population studies and in our survey data are far lessoptimistic. 19) Consistent with many other published studies, the recurrence rate among ourrespondents with LBP was 73%. 20) Many respondents had numerous recurrences, with 27% reporting 5 or moreepisodes per year and [20%] having had more than 50 episodes in their lifetime." 21) Patients whose recurrences are worsening, their underlying condition may bedeteriorating over multiple recurrences. [Important] 22) Recurrent episodes of LBP should not be routinely viewed as independentevents. It appears, as a rule, that LBP recurrences grow progressively worse. 23) Many patients with chronic LBP had prior recurrent episodes that had becomelonger and more severe until the most recent episode did not resolve and thusbecame chronic. [Important] 24) Most disabling back pain episodes increase in severity and duration over time. 25) Could the underlying pain generator(s) responsible for episodic acute LBPprogressively deteriorate over multiple recurrences, finally reaching the point wherereversal is impossible and the pain becomes chronic? If so, then any pain-free periodbetween acute episodes would indicate that the underlying problem is still capable ofrecovery and would accentuate the need for effective preventive measures.Alternatively, worsening recurrent pain would suggest that the repeated insults on theunderlying pain generator carry an increasing risk of non-recovery. 26) When considering the multitude of studies, including our own, that indicate thatmany patients experience LBP episodes that worsen over time, guideline panelsshould begin to incorporate these data and acknowledge the impact of recurrence onthe true natural history of LBP. 27) These authors cite evidence that implicates the intervertebral disk as theprimary low back pain generator. [Important] 28) We hypothesize that the specific pattern of change in pain location within eachepisode reflects pain arising from a particular physical structure that is usually able torecover but that also progressively deteriorates over many episodes to the point thatit can no longer recover. [like the disc] 29) Collectively, our findings, and those of other studies, indicate that it may beinaccurate to characterize LBP as having an excellent prognosis. Recurrences arefrequent and are often progressively worse over time. Recovery from acute LBP is notas favorable as is routinely portrayed. 30) Eventually, there may be no recovery, and the underlying condition maybecome chronically painful. In light of these characteristics, it seems inappropriate tocharacterize the natural history of LBP as benign and favorable.These authors specifically bad-mouth two practice guidelines as beingincorrect and overly optimistic in their view of the natural history of LBP: *Practice guidelines low back disorders K. Hegmann, J. Talmage (Eds.), OccupationalMedicine Practice Guidelines (Revised ed.), American College of Occupational andEnvironmental Medicine, Elk Grove Village, IL (2007), p. 368. *M. van Tulder, A. Becker, T. Bekkering et al.; European guidelines for themanagement of acute non-specific low back pain in primary care; 2004. COMMENTS FROM DAN MURPHY: These authors suggest that the generators of LBP (primarily the intervertebral disc)deteriorate with successive recurrences of LBP until the patient suffers from constantchronic LBP. Consequently, they stress the importance to accentuate the need foreffective preventive measures. Remember the Cifuentes study (Journal of Occupational and Environmental Medicine, 2011) clearly showed that LBPpatients who remained under chiropractic maintenance care after an episode of acuteLBP incurred significantly fewer (and significantly delayed) episodes of LBPrecurrences (Article Review #16-12). Also recall that David Taylor presented anexcellent academic and case review article suggesting that the frequency of suchchiropractic maintenance care should be once every 2 to 4 weeks (Article Review#23-23). Practice guidelines, insurance companies and their representatives that indicate thenatural history of acute LBP is 6-12 weeks with good clinical outcomes are bogus andshould be challenged as being bogus. This study is excellent for that purpose. A number of years ago I investigated the 90% recovery rate for acute LBP andauthored an article on the topic; it is also an excellent review. I have been asked forthousands of reprints of that article. If anyone wants a copy, email my professional assistant, Michelle Schaer, DC, at [email protected] and ask for the 90% article.