American Journal of Epidemiology December 29, 2010; Vol. 173, No. 3; pp. 310-318 Kari R. Risnes, Kathleen Belanger, William Murk, and Michael B. Bracken The authors are from Yale University This analyses of a cohort included 1,401 US children, assessed the associationbetween antibiotic use within the first 6 months of life and asthma and allergy at 6years of age. KEY POINTS FROM THIS STUDY 1) 25% of urban children in the developed world have asthma. 2) Many studies have reported that antibiotic use may be associated withincreased risk of childhood asthma. 3) Many studies report a positive association between antibiotic use andchildhood asthma, including a large prospective cohort study with more than 5,000cases of childhood asthma that determined early antibiotic exposure to be one ofthe most important predictors of childhood asthma. 4) The hygiene hypothesis is a frequently cited explanation for the increasingprevalence of allergic diseases, suggesting that reduced exposure to bacteria andviruses may delay development of the immune system and promote atopic immuneresponses. [including the use of antibiotics and vaccines] 5) Gastrointestinal flora are important for developing a healthy immune systemwith resistance to allergic sensitization, and antibiotic exposure in early life mightincrease the risk of atopic diseases through altered microbial exposure. RESULTS FROM THIS STUDY: 1) One third of the children had been exposed to antibiotics by 6 months ofage. 2) Nearly 70% of children with a history of lower respiratory infections andmore than 50% with otitis in the first year of life had received antibiotics. 3) Children of African-American or Hispanic mothers had twice the risk ofasthma compared with children of white mothers. 4) If one parent had a history of asthma, the increased risk of asthma was 140%compared with children with no history of parental asthma. If both parents had ahistory of asthma, the increased risk was 257%. 5) The number of antibiotic courses before 6 months of age and asthma showa dose-response relation. 6) One course of antibiotic exposure increased the risk of asthma by 40%. 7) Two or more courses of antibiotic exposure increased the risk of asthma by72%. 8) The increased risk for asthma in children who had no parental history ofasthma was 89%. DISCUSSION 1) The association of antibiotics and asthma in the present study wasparticularly strong in children with no family history of asthma. 2) The hygiene hypothesis suggests that microbial exposure [becominginfected] in early life enhances postnatal maturation of the immune system thatmay protect against development of allergic diseases. 3) Normal postnatal development incurs a change from fetal predominantly Thelper 2 (known as TH2) to more mature T helper 1 (known as TH1) immunity.This is important because Overexpression of TH2 responses to allergens is thehallmark of allergic diseases. 4) Microbial exposure, particularly in the intestinal tract, is necessary forpostnatal transition to a balanced immune response in healthy children. 5) The early postnatal period is particularly vulnerable to imbalances in immuneresponse, and that delayed postnatal maturation of TH1 cell function is a keycomponent of genetic risk for atopy. 6) Children with no family history of asthma are more susceptible to the effectsof antibiotics than children with a genetic predisposition to asthma. 7) We found a strong association between early antibiotic exposure withreported positive immunoglobulin E blood or skin test reactivity. 8) We conclude that antibiotic exposure before 6 months of age is associatedwith asthma and allergy at 6 years of age. 9) The adverse effect of antibiotics on asthma risk was particularly strong inchildren with no parental history of asthma, which should encourage physicians toavoid unnecessary antibiotic use in low-risk children with no genetic predispositionto asthma. 10) Antibiotic exposure is associated with increased risk of asthma by 52%.
Monthly Archives: September 2014
Natural anti-inflammatory agents for pain relief
Surgical Neurological International December 2010 Joseph C. Maroon, Jeffrey W. Bost, and Adara Maroon Department of Neurosurgery, University of Pittsburgh Medical Center, Pittsburgh,PA, and Vanderbilt University, Nashville, TN FROM ABSTRACT: The use of both over-the-counter and prescription nonsteroidal medications isfrequently recommended in a typical neurosurgical practice. But persistent long-term use safety concerns must be considered when prescribing these medicationsfor chronic and degenerative pain conditions.Although nonsteroidal medications can be effective, herbs and dietary supplementsmay offer a safer, and often an effective, alternative treatment for pain relief,especially for long-term use. THESE AUTHORS ALSO NOTE: In most cases, the genesis of pain is inflammatory, regardless of theetiology. This inflammation has 2 primary causes: 1) Inflammatory hormones (PGE2, LTB4, etc.)[derived from the omega-6 fatty acid arachidonic acid] 2) Inflammatory cytokines (interleukin ((IL))-1a, IL-1b, IL-6 and tumor necrosisfactor ((TNF-a)).[proteins that are derived form the immune system cells] The use of non-steroidal anti-inflammatory drug (NSAID) medication is stillthe mainstay of most classically taught clinicians for joint and spine relatedinflammatory pain, despite their commonly known side effects.The pro-inflammatory cytokines stimulate the production of the pro-inflammatory hormone prostaglandin E2 (PGE2).NSAIDs ability to interfere with the production of prostaglandin E2 (PGE2) isthe major mechanism for the anti-inflammatory success of these drugs. INFLAMMATORY PATHWAYS Prostaglandins act as short-lived localized hormones that can be released byany cell of the body during tissue, chemical, or traumatic injury, and can inducefever, inflammation, and pain, once they are present in the intercellular space.Thromboxane hormones increase the inflammatory response. A major component of the inflammatory pathway is called the arachidonicacid pathway because arachidonic acid is immediately released from traumatizedcellular membranes.Cell membrane trauma releases arachidonic acid. Arachidonic acid is thentransformed into the pro-inflammatory hormones prostaglandins and thromboxanesthrough the enzymatic action of cyclooxygenase. Nonselective NSAIDs major side effects include significant gastrointestinalupset, gastritis, ulceration, hemorrhage, and even death. By blocking COX-1, whichalso normally acts to protect the gastrointestinal mucosa, nonselective NSAIDs andaspirin can cause significant gastric tissue damage. NSAIDs can delay muscle regeneration and may reduce ligament, tendon,and cartilage healing.NSAIDs also have adverse effects on kidney function. The National KidneyFoundation asserts that approximately 10% of kidney failures per year are directlycorrelated to substantial overuse of NSAIDs. Selective COX-2 inhibiting NSAIDs were thought to reduce inflammatory painwithout enhancing GI bleeding. Celebrex was FDA approved in 1998, followed bythe approval of Vioxx and Bextra in 1999. These drugs quickly became themainstay for the treatment of chronic pain conditions related to inflammation. On September 30, 2004, Vioxx was withdrawn because it doubled the risk ofserious thromboembolic events, including myocardial infarction.Natural compounds for inflammation Because of the significant side effect profiles of steroidal and NSAIDmedications, there is a greater interest in natural compounds, such as dietarysupplement and herbal remedies, which have been used for centuries to reducepain and inflammation.Nuclear Factor kappa-B (Nf-kB) controls the transcription of DNA for theperpetuation of the inflammatory immune response. It acts as a switch to turninflammation on and off in the body. Plant- and animal-derived nutraceutical preparations have been used forhundreds and even thousands of years to obtain effective pain relief. Herbalmedications are becoming increasingly popular because of their relatively few sideeffects. The US governmental agencies, through the FDA and others, routinelyinspect the manufacture of vitamins or supplements made in this country, as theydo for any other food product. Products such as omega-3 essential fatty acids (EFAs) (O3) do have strongscientific support to be considered as an alternative and/or complementary agent toNSAIDs. Published studies have shown the effectiveness of O3 to successfully treatspine-related pain. Omega-3 EFAs (fish oil)The use of fish oil for the treatment of muscular, skeletal, and discogenicdiseases, can be traced back to the late 18th century. Research has shown that the omega-3 polyunsaturated fatty acids are someof the most effective natural anti-inflammatory agents available. [7 references] With the discovery that vascular inflammation is the underlying cause ofcoronary artery disease, fish and fish oil supplements are now recommended by theAmerican Heart Association for the prevention of this disease. Countries that have the highest fish consumption also have a lower incidenceof neurodegenerative disease and depression. The biological basis for the effectiveness of fish oil in treating arthritis hasbeen well documented with many positive clinical studies, when compared totraditional pharmaceutical anti-inflammatory agents. The active ingredients in fish oil, eicosapentaenoic acid (EPA) anddocosahexaenoic acid (DHA), enhance the conversion of COX to prostaglandin E3. Anatural anti-inflammatory agent, prostaglandin E3 competitively inhibits the effectsof the arachidonic acid conversion to prostaglandin E2, a highly inflammatorysubstance. Prostaglandin E3 also inhibits the synthesis of TNF-a and IL1b, both of whichare inflammatory cytokines. The EPA and DHA can inhibit the 5-LOX pathway, which convertsarachidonic acid to inflammatory leukotrienes. When EPA and DHA are incorporated into articular cartridge chondrocyte cellmembranes, there is a dose-dependent decrease in the expression and activity ofthe enzymes that degrade cartilage.Omega-3 EFA, found in fish oil, can directly reduce the degenerative enzymesand reduce the inflammation in synovial cartilage.Belching may occur if fish oil supplements are not taken with meals. Persons on a regimen of anticoagulant medications should not take omega-3EFAs because of the possibility of increasing the bleeding potential. White willow barkBark from the white willow tree has analgesic and antipyretic properties.Salicin from white willow bark is converted to salicylic acid by the liver and isconsidered to have fewer side effects than aspirin. White willow bark should not be used in children (to avoid the risk of Reyessyndrome), or in patients with peptic ulcer disease, poorly controlled diabetes,hepatic or renal disorders, or other conditions in which aspirin would becontraindicated. The usual dose of white willow bark is 240 mg/day.Curcumin (turmeric) Curcumin is a naturally occurring yellow pigment derived from turmeric, aflowering plant of the ginger family. It has traditionally been used as a coloring andflavoring spice in food products. Curcumin is an anti-inflammatory agent, and hasantioxidant, anti-inflammatory, and antineoplastic effects. Curcumin is known to inhibit inflammation by suppressing NF-kB and COXenzymes, and it may be considered a viable natural alternative to nonsteroidalagents for the treatment of inflammation. The usual dosage of standardized turmeric powder is 400 – 600 mg takenthree times per day. Green tea Green tea has cardiovascular and cancer preventative characteristics due toits antioxidant properties; its use in the treatment of arthritic disease as an anti-inflammatory agent is more recent. The constituents of green tea include polyphenolic compounds calledcatechins; epigallocatechin-3 galate is the most abundant catechin in green tea.Epigallocatechin-3 galate inhibits NF-kB and the production of pro-inflammatory cytokines.Green tea inhibits the aggrecanases that degrade cartilage.Green tea has both anti-inflammatory and chondroprotective effects.Increased green tea consumption in Asia may lead to significantcardiovascular, neuroprotective and cancer prevention properties. The recommendation for green tea consumption is 3 – 4 cups a day, or greentea extract dosage of 300 – 400 mg a day. Pycnogenol (maritime pine bark) Pycnogenol is derived from the bark of the maritime pine tree and has beenused for more than 2000 years.Pycnogenol is helpful for wound healing, treating scurvy, healing of ulcers,and reducing vascular inflammation.Pycnogenol contains a potent blend of active polyphenols, which includescatechin, taxifolin, procyanidins, and phenolic acids. It is one of the most potentantioxidant compounds currently known.Pycnogenol inhibits NF-kB production of pro-inflammatory cytokines. Studies have shown that pycnogenol is 50 – 100 times more potent thanvitamin E in neutralizing free radicals and that it helps to recycle and prolong theactivity of vitamins C and E. Studies have shown pycnogenol to be effective in reducing blood pressureand reducing the risk of venous thrombosis by its effect on vascular endothelium.The usual dosage is 100 – 200 mg daily.Because pycnogenol enhances immune system function, it should not betaken by patients who are being treated with immunosuppressants or by thosereceiving corticosteroid drugs, both of which have the opposite effect on theimmune system.Boswellia serrata resin (Frankincense) Boswellia possesses anti-inflammatory, anti-arthritic, and analgesicproperties.Boswellia can inhibit the leukotriene biosynthesis, thus affecting variousinflammatory diseases that are perpetuated by leukotrienes.Clinically, Boswellia is used in the treatment of degenerative andinflammatory joint disorders. A combination of Boswellia and curcumin showed superior efficacy andtolerability compared with nonsteroidal diclofenac for treating active osteoarthritis. Boswellia typically is given as an extract standardized to contain 30-40%boswellic acids (300-500 mg two or three times/day). Resveratrol Resveratrol is a plant-based polyphenol molecule that is found in manydifferent plant sources, but the skins of red wine grapes are believed to have thehighest concentration.In plants, resveratrol protects the plant from infection, excessive UV radiationand aids in general plant defense. Resveratrol has also been found to have significant anti-mutation, anti-inflammatory, antioxidant and DNA protective actions, when consumed by animalsand humans. Most of the active research with resveratrol has been done in neuro andcardioprotection, but several studies are being reported on resveratrols use forarthritic joint pain.Resveratrol inhibits NFkB and the production of pro-inflammatory cytokines.The typical dose for Resveratrol is 50 to 500 mg daily. Uncaria tomentosa (cats claw) The bark of cats claw is used to treat arthritis, bursitis, and intestinaldisorders. The active ingredients appear to be polyphenols (flavonoids,proanthocyanidins, and tannins), alkaloids, and sterols.Cats claw inhibits NFkB and the production of pro-inflammatory cytokines. Cats claw can be consumed as a tea (1000 mg root bark to 8 oz water), oras a dry, standardized extract in a capsule (20-60 mg daily).Capsaicin (chili pepper)Capsicum accentuates chilis stinging pungency.Capsaicin produces highly selective regional anesthesia by causingdegeneration of capsaicin-sensitive nociceptive nerve endings which can producesignificant and long-lasting increases in nociceptive thresholds.Capsaicin inhibits NF-kB, thus producing an anti-inflammatory effect. CONCLUSIONS Anti-inflammatory agents such as NSAIDs can have undesirable side effectssuch as gastric ulceration and, infrequently, myocardial infarction and stroke. For centuries, natural anti-inflammatory compounds have been used tomediate the inflammatory process and often with fewer side effects [than NSAIDs]. PLA2 = Phospholipase A2 (the enzyme that cleaves AA from the cell membrane following trauma / injury) AA = Arachidonic Acid (an omega-6 fatty acid commonly found in cellmembranes) LOX = Lipoxygenase (the enzymes that converts AA into pro-inflammatory LThormones) COX = Cycloxygenase (the pro-inflammatory enzymes that convert AA into thepro-inflammatory PG and TXA hormones) LT = Leukotrienes TXA = Thromboxanes PG = Prostaglandins Interleukin-1a = IL1a (a pro-inflammatory cytokine protein) Interleukin-1b = IL1b (a pro-inflammatory cytokine protein) Interleukin-6 = IL6 (a pro-inflammatory cytokine protein) Tumor Necrosis Factor alpha = TNFa (a pro-inflammatory cytokine protein) NF-kB= Nuclear Factor kappaB (pro-inflammatory protein that lives in the cellcytoplasm) IkB = Inhibitory kappaB ( a protein that when attached to NFkB inhibits itspro-inflammatory influence; consequently its an anti-inflammatoryprotein) IkBK = Inhibitory kappaB Kinase (an enzyme that cleaves NFkB away from itsinhibitory Ikb protein, allowing NFkB to cross into the nucleus andactivate the genes that produce pro-inflammatory cytokines) CK = Cytokines (pro-inflammatory proteins made by immune system cells) EPA = Eicosapentaenoic Acid (anti-inflammatory omega-3 fatty acid)8 These authors indicate that the inflammatory mediators above can be triggered asa consequence of: Stress Infection Radiation Trauma/Injury Arachidonic Acid Inflammatory Diet Allergic Immune Response This inflammation is a factor in: Pain Cancer Thrombosis Atherosclerosis Insulin Resistance Neurodegeneration
Efficacy and safety of corticosteroid injections for management of tendinopathy: A systematic review of randomised controlled trials
Lancet November 20, 2010; Vol. 376; pp. 1751 – 67 Brooke K Coombes, Leanne Bisset, Bill Vicenzino FROM ABSTRACT: Background Few evidence-based treatment guidelines for tendinopathy exist. We undertook asystematic review of randomised trials to establish clinical efficacy and risk ofadverse events for treatment by injection. Methods We searched eight databases without language, publication, or date restrictions. Weincluded randomized trials assessing efficacy of one or more peritendinousinjections with placebo or non-surgical interventions for tendinopathy, scoring morethan 50% on the modified physiotherapy evidence database scale. We undertook meta-analyses with a random-effects model, and estimated relative risk andstandardised mean differences. The primary outcome of clinical efficacy was protocol-defined pain score in the shortterm (4 weeks, range 0 – 12), intermediate term (26 weeks, 13 – 26), or long term(≥52 weeks). Findings 3824 trials were identified and 41 met inclusion criteria, providing data for 2672participants. We showed consistent findings between many high-quality randomisedcontrolled trials that corticosteroid injections reduced pain in the short termcompared with other interventions, but this effect was reversed at intermediate and long terms. THESE AUTHORS ALSO NOTE: 1) Overuse disorders of tendon or tendinopathies affect active young people(20 – 30 years old) and middle-aged people (40 – 60 years old) and are often difficultto manage successfully. 2) These disorders are characterized by angiofibroblastic hyperplasia, includinghypercellularity, neovascularisation, increased protein synthesis, anddisorganisation of matrix, but not inflammation. [The Fibrosis of Repair] 3) This absence of inflammation, along with poor long-term outcomes andadverse effects, has led investigators to question the use of corticosteroid injectionsfor treatment. RESULTS 4) Compared with non-injection interventions, there was strong evidence forbenefit of corticosteroid injections in the short term across all outcome measuresfor treatment of lateral epicondylalgia. 5) Strong evidence suggests that corticosteroid injections are less beneficialthan are other interventions for treatment of lateral epicondylalgia at 26 weeks. 6) Inferior reductions in pain were reported after corticosteroid injectioncompared with no intervention, NSAIDs, physiotherapy, and platelet-rich plasmainjections. 7) Repeated corticosteroid injections (average of 4 injections, range of 3-6 in18 months) were associated with a poorer long-term effect on reduction in painthan were interventions with one injection. DISCUSSION 8) We have shown strong evidence that corticosteroid injection is beneficial inthe short term for treatment of tendinopathy, but is worse than other treatmentoptions in the intermediate and long terms. 9) Use of corticosteroid injections, which are potent anti-inflammatories, posesa clinical dilemma because consistent findings suggest good short-term effects buttendinopathy does not have an inflammatory pathogenesis. Altered release oftoxins and inhibition of collagen, extracellular matrix molecules, and granulationtissue might provide a biological basis for this effect. 10) Our systematic review challenges continued use of corticosteroid injectionsby providing strong evidence that they are worse in the long term than are mostconservative interventions for tendinopathy. 11) Injection into the tendon might weaken its structure and increase probabilityof rupture. 12) Moderate evidence of harmful effects of repeated corticosteroid injection onpain was noted. COMMENT FROM DAN MURPHY Many of our patients are advised to have their tendinopathies treated withcorticosteroid injection, and consequently they ask us for advice. This systematicreview of randomized controlled trials indicates that these injections are beneficialin the short term (at 8 weeks), but are worse than conservative treatments in theintermediate (26 weeks) and long (≥52 weeks) terms. In addition, Injection intothe tendon might weaken its structure and increase probability of rupture.
Fruit and Type 2 Diabetes
Convential wisdom recommends against fruit consumption for type2 diabetics, the concern beingthat fruit would have a negative impact on glycemic control. A study published in 2013 indicatesfruit consumption might not have an impact. This was an open randomized controlled trial with two parallel groups. The primary outcome wasa change in HbA1c during 12 weeks of intervention Participants were randomized to one of twointerventions; medical nutrition therapy + advice to consume at least two pieces of fruit a day(high fruit) or medical nutrition therapy + advice to consume no more than two pieces of fruit a day (low fruit). All participants had two consultations with a registered dietitian. Results:The study population consisted of 63 men and women with newly diagnosed type 2diabetes. All patients completed the trial. HbA1c decreased in both groups with no differencebetween the groups. Both groups reduced body weight and waist circumference, however therewas no difference between the groups. Conclusions:A recommendation to reduce fruit intake as part of standard medical nutritiontherapy in overweight patients with newly diagnosed type 2 diabetes resulted in eating less fruit.It had however no effect on HbA1c, weight loss or waist circumference. We recommend that theintake of fruit should not be restricted in patients with type 2 diabetes.Source: Christensen et al. Nutrition Journal 2013, 12;29.
Meriva Curcumin Suppresses Effects of Chemotherapy
A new study reports Meriva Curcumin alleviates adverse effects of cancer treatment.Abstract: "A proprietary lecithin delivery system of curcumin (Meriva) was evaluated in acontrolled study to assess its efficacy in alleviating the side effects of cancer chemo- andradiotherapy in 160 patients undergoing these treatments. In both cases, a semi-quantitaveevaluation of the side effects was carried out using a visual analogue scale, assessing also theplasma free radical status in all patients. Results showed that lecithinized curcumin mightalleviate the burden of side effects associated to chemo- and radiotherapy, suggesting that theanecdotal use of various preparations of curcumin as a supportive agent for cancer treatment iswell worth a systemic investigation in larger scale clinical trials. The capacity of curcumin toupregulate anti-oxidative responses and downregulate inflammatory pathways could explain itsbeneficial effect in tempering the prolonged and systemic oxidative and inflammatory effects of cancer treatment, and the beneficial effects observed in the plasma oxidative status in allpatients of the treatment group support this view.2013, Velcaro, Hosoi, Pellegrini, et al., Phytotherapy Research published by John Wiley & Sons, Ltd.
Omega 6 to Omega 3 Ratios May Not Be Important
Conventional paleo philosophy stresses the importance of balancing intake of essential fattyacids, i.e. that dietary ratios should be anywhere from 1:1 to 4:1 to properly regulate pro-inflammatory fatty acid synthesis. It turns out that ratios may not be as important as the totalamount of omega-3s in the diet. Loren Cordain explains, "Newer research suggests both omega-6 and omega-3 FAs reduce therisk of heart disease, and the ratios of these fatty acids is not useful and can be misleading. Onestudy reported that omega-6 FAsdo not inhibit the beneficial effects of omega 3 FAs and thecombination of both fatty acids leads to the greatest reduction in levels of inflammation. . . .However, the real issue here is that omega-3 FAs bind to G coupled-protein receptors, andcause broad anti-inflammatory effects. If you remove the 3s from your diet, inflammationreturns. This means that adequate omega-3 intake alone, regardless of omega-6 intake, is enough to sto inflammation in the body. The same is apparent when you look at the biochemicalpathway of omega-6 and omega-3 FAs. They compete for the same enzyme through a processknown as competitive inhibition." Cordain continues with recomendations, "The best method of action to pursue, is to simply followa Paleo Diet and eat plenty of fish rich in omega-3. If you want to avoid dietary intake of omega-3, and obtain requirements from a supplement, DHA is preferable to all other forms of omega-3,since it can be retro converted into EPA. Only in the context of a very inflammatory diet (like thestandard Western diet) does the ratio of omega-3 to 6 matter. . . This isn’t to say that the omega- 3 to omega-6 ratio is completely irrelevant, but if you’re consuming a Paleo Diet, you will likely begetting the right amounts of these essential fatty acids for optimial health." Source, Loren Cordain, Thepaleodiet.com.
Synovial folds – A pain in the neck?
Manual Therapy April 2011; Vol. 16; No. 2; pp. 118-124 Alexandra L. Webb, Patricia Collins, Hamid Rassoulian, Barry S. Mitchell FROM ABSTRACT The synovial folds of the cervical spine are regarded as a potential source of neckpain and headache, especially following whiplash injury.Damage to the synovial folds following motor vehicle trauma has been welldocumented in post-mortem studies.However, methods of identifying injury to the synovial folds in the survivors ofmotor vehicle trauma have proven elusive to date. Recently, it has beenmade possible to image the synovial folds in vivo using magnetic resonanceimaging. This now makes it feasible to investigate the potential involvement ofsynovial folds in the generation of neck pain and headache and its relief using spinal manipulation. This paper reviews critically the morphology of the synovial folds of the cervicalspine that underpins the hypotheses proposed to explain their functional and clinicalsignificance and a new system of naming and classifying the synovial folds ispresented. These findings have implications for understanding the anatomical basis of neckpain and headache and the rationale for the use of spinal manipulation in theirmanagement. KEY POINTS FROM THIS ARTICLE: 1) Intra-articular synovial folds are formed by folds of synovial membrane(synovium) that project into the joint cavity and are found in synovial articulationsthroughout the vertebral column. 2) The earliest description of synovial folds in the vertebral column occurred in1855. 3) The published literature uses a number of names to identify these synovialfolds, including: * Synovial fold is the most accurate name to apply to these structures. * Meniscus / Menisci * Meniscoid * Intra-articular inclusions * Intra-articular discs 4) Cervical synovial folds extend 1 – 5 mm between the articular surfaces. 5) Synovial folds have been identified in all synovial articulations of the cervicalspine. 6) Synovial folds are most commonly found in adult lateral atlanto-axial andcervical zygapophysial joints. 7) Synovial folds contain an abundant vascular network. 8) With repeated mechanical impingement between the articular surfaces, thesynovial fold may differentiate into fibrous tissue to varying degrees. Collagen-producing,activated fibroblasts have been observed within synovial folds.Consequently, the process of fibrous change may involve inflammation and repair. 9) The presence of nerve fibers and endings has been demonstrated in synovialfolds. These nerve fibers have been identified both alongside and independent ofblood vessels in the cervical synovial folds. The function of these nerves may benociceptive, proprioceptive and/or vasomotor. There are a number of studiessupporting the nociceptive function in particular for these joint structures. 10) The synovial folds are believed to adapt themselves intimately to the contourof the joint space in all positions of the joint and act as passive space-fillers thatfill peripheral non-congruent parts of the joint in its neutral position but displacewhen the joint moves. 11) The synovial folds may protect and/or lubricate the articular surfaces,enhance joint congruity and stability, assist weight-bearing or dissipate stress. 12) The synovial folds may have a mechanosensory role. The synovial fold tissuesare fibro-fatty in composition, and innervated adipose tissue is thought to beimportant in giving proprioceptive feedback for sensorimotor control which would beespecially important in the upper cervical spine which has direct neurophysiologicalconnections via cervical proprioceptors to the vestibular and visual systems. 13) Disturbances in balance and vision have been reported to accompany uppercervical pain and dysfunction and are areas of increasing interest particularly inrelation to whiplash. 14) The entrapment hypotheses, is usually proposed to explain the clinicalpresentations of the synovial fold syndrome. 15) Intra-articular adhesions and synovial fold impingement following whiplashmay cause deformation and/or inflammation within the synovial folds, irritating thesensory nerves. Consequently, spinal manipulation and mobilization may effectivelytreat the associated spinal pain and disability. [Important] 16) An abnormal joint movement may cause a synovial fold to move from itsnormal position at the articular margins to become imprisoned between thearticular cartilage surfaces causing pain and articular hypomobility accompanied byreflex muscle spasm. 17) Synovial fold entrapment has been used to explain the pathophysiology oftorticollis and the relief of pain and disability following spinal manipulation. Thetraction forces generated during manipulation would cause rupture of a trappedfibro-adipose synovial fold from the fibrous capsule causing intra-articularhaemarthrosis and loose body formation. 18) In habitually immobilised or under-used joints, the synovial folds may act asa nidus for fibrous tissue proliferation resulting in the formation of adhesions thatreduce joint motion. [Reduced motion resulting in fibrosis] 19) The majority of evidence regarding the possible role of synovial folds in thegeneration of neck pain relates to their potential to become injured during whiplashassociated with motor vehicle trauma. 20) Contusions, rupture and displacement of the synovial folds have beenreported at autopsy following fatal motor vehicle trauma in addition to jointhaemarthrosis caused by synovial fold disruption. Such injuries are not visible atpost-mortem using conventional X-ray, CT or MRI. 21) Discolouration of the dorsal synovial folds has been observed months afterthe initial injury in post-mortem studies of motor vehicle trauma survivors who diedlater from other causes. Therefore injury to the synovial folds following whiplashmay be a potential source of both acute and chronic neck pain. COMMENTS FROM DAN MURPHY: My orthopedic training (from the late, great Richard Stonebrink, DC) advises thatthe best adjustment approach for the synovial fold entrapment syndrome is toadjust on the low side of the rainbow, i.e. to make the antalgic lean worse. Thisapproach is most likely to gap the contralateral facet joint, freeing the entrappedsynovial fold. The result is immediate improvement of antalgic lean and improvement in the range of motion. Dr. Stonebrink referred to the synovial foldentrapment syndrome as a meniscoid block.
Analgesic Use and the Risk of Hearing Loss in Men
The American Journal of Medicine March 2010; Vol. 123; No. 3; pp. 231-237 Sharon G. Curhan, MD, ScM, Roland Eavey, MD, Josef Shargorodsky, MD, Gary C.Curhan, MD, ScD These authors are from Brigham and Women’s Hospital in Boston, Vanderbilt University, and Harvard School of Public Health. FROM ABSTRACT TO BACKGROUND: Hearing loss is a common sensory disorder, yet prospective data on potentially modifiable risk factors are limited. Regularly used analgesics, the most commonly used drugs in the US, may beototoxic and contribute to hearing loss. METHODS: We examined the independent association between self-reported professionally diagnosed hearing loss and regular use of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and acetaminophen in 26,917 men aged 40-74 yearsat baseline in 1986. Study participants completed detailed questionnaires at baseline and every 2 years thereafter. RESULTS: Regular use of each analgesic was independently associated with an increased risk of hearing loss. Multivariate-adjusted hazard ratios of hearing loss in regular users (2 times times/week) compared with men who used the specified analgesic 2 times/week were 1.12 for aspirin, 1.21 for NSAIDs, and 1.22 for acetaminophen. The magnitude of the association was substantially higher in younger men. For men younger than age 50 years, the hazard ratio for hearing loss was 1.33 for regular aspirin use, 1.61 for NSAIDs, and 1.99 for acetaminophen. CONCLUSIONS: Regular use of aspirin, NSAIDs, or acetaminophen increases the risk of hearing loss in men, and the impact is larger on younger individuals. Increased Risk of Hearing Loss From Analgesic Consumption Compared to Consuming Analgesics. KEY POINTS FROM THIS STUDY: 1) Hearing loss is the most common sensory disorder in the US and afflicts over 36 million people. 2) Aspirin, acetaminophen, and ibuprofen are the 3 most commonly used drugs in the US: * 17% of the population use aspirin at least weekly * 17% of the population use ibuprofen at least weekly * 23% of the population use acetaminophen * 28% of men aged 45 years and above are aspirin users 3) It is well documented that salicylates [aspirin] have ototoxic effects such as hearing loss and tinnitus. 4) High doses of nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to be ototoxic in animals and in human case reports, potentially through a reduction in cochlear blood flow. 5) Acetaminophen depletes glutathione; glutathione protects the cochlea from noise-induced damage. RESULTS FROM THIS STUDY: 1) Hypertension was more common among regular analgesic users. 2) It was common for an individual to use more than one type of analgesic regularly. 3) Regular analgesic use was independently associated with an increased risk of hearing loss for all 3 types of analgesics. 4) For NSAIDs and acetaminophen, the risk of hearing loss increased with longer duration of regular use. 5) Those who used aspirin regularly for 1-4 years were 28% more likely to develop hearing loss than those who did not use aspirin regularly. 6) Those who used NSAIDs regularly for 4 or more years were 33% more likely to develop hearing loss than those who did not use NSAIDs regularly. 7) Those who used acetaminophen for 4 or more years were also 33% morelikely to develop hearing loss than low-level users ( 2X/wk). 8) The association between hearing loss and concomitant use of more than one class of analgesic appeared to be approximately additive. DISCUSSION: 1) Regular analgesic use was independently associated with an increased risk of hearing loss. The increased risk of hearing loss seen with regular analgesic use was greatest among younger men, particularly those below age 60 years. 2) Frequent use of acetaminophen causes hypertension and chronic renal dysfunction because acetaminophen use depletes glutathione. Acetaminophen also might deplete endogenous cochlear glutathione, which is present in the cochlea in substantial amounts and protects the cochlea from noise-induced damage. 3) The impact of regular use of multiple analgesics appeared to be additive. 4) 58% of older men use aspirin for cardiovascular prophylaxis. 5) Regular use of analgesics, specifically aspirin, NSAIDs, and acetaminophen,might increase the risk of adult hearing loss, particularly in younger individuals. Given the high prevalence of regular analgesic use and health and social implications of hearing impairment, this represents an important public health issue. KEY POINTS FROM THE AUTHORS: * Regular use of aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs, the most commonly used drugs in the US, increase risk of hearing loss. * The increased risk of hearing loss associated with regular analgesic use is greater among younger men, particularly those below age 50 years. COMMENTS FROM DAN MURPHY: Acetaminophen (found in Tylenol) was associated with the highest risk of hearing loss. Acetaminophen also damages the kidneys and causes hypertension. Glutathione protects the kidney from Tylenol and protects the hearing apparatus from loud noises. Strategies to increase glutathione are quite important: N-acetyl cysteine (NAC), undenatured whey protein, pomegranate juice, low-level laser, etc. Most men who take aspirin do so for cardiovascular prophylaxis.
Can an Unhealthy Spine Affect Internal Organs?
A the University of Pennsylvania, Dr. Henry Winsor conducted an experiment based on chiropractors claim that by adjusting the vertebrae they can relieve stomach troubles, ulcers, menstrual cramps, thyroid conditions, kidney disease, constipation, heart disease, lung and other diseases. In this experiment he dissected both human and animal cadavers to see if there was any relationship between any diseased internal organs discovered on autopsy and the vertebrae and nerves that went to the organs. Dr. Winsor dissected 75 human and 72 cat cadavers. He found nearly 100% correlation between minor curvatures of the vertebrae and diseases of the internal organs. RESULTS Heart Disease All 20 cases with heart and pericardium conditions had the upper five thoracic vertebrae misaligned (T1-T5). Lung Disease All 26 cases of lung disease has spinal misalignments in the upper thoracic area. Stomach Disease All 9 cases of stomach disease had spinal misalignment in the mid-thoracic (T5-T9) area. Liver Disease All 13 cases of liver disease had misalignments in the mid-thoracic area (T5-T9). Gallbladder All 5 cases with gallstone disease had spinal misalignments in the mid-thoracic area (T5-T9). Pancreas All 3 cases with pancreas disease had spinal misalignments in the mid-thoracic area (T5-T9). Spleen All 11 cases with spleen disease had spinal misalignments in the mid-thoracic area (T5-T9). Kidney All 17 cases with kidney disease were out of alignment in the lower thoracic area (T10-T12). Prostate and Bladder Disease All 8 cases with prostate disease had the lumbar vertebrae misaligned. Uterus 2 cases with uterine conditions had the second lumbar misaligned.