Keep High-Risk Civil Workers Healthy and Limber for Work

Police officers, firefighters and military personnel all lead active lives, spending a good deal of their time training to stay in top shape to commit to their life’s work. Their work is–along with their personal lives–often fraught with physical and mental stress, thanks to the high-risk nature of their work.

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Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize

Food and Chemical Toxicology 2012 [epub] Gilles-Eric Séralini, Emilie Clair, Robin Mesnage, Steeve Gress, Nicolas Defarge, Manuela Malatesta, Didier Hennequin, Joël Spiroux de Vendômois KEY POINTS FROM THIS ARTICLE: 1) This study represents the first detailed documentation of long-term deleterious effects arising from the consumption of a GM Roundup-tolerant maize and of Roundup, the most used herbicide worldwide. 2) Monsanto produced the Roundup-tolerant GMO corn and the Roundup used in this 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 low environmentally relevant doses starting below the range of levels permitted by 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 time marker], and died more rapidly, especially the females. 5) Females in all 3 groups developed large mammary tumors almost always more 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 in all 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 which occurred up to 600 days earlier. 10) Biochemistry data confirmed very significant kidney chronic deficiencies; for all treatments and both sexes, 76% of the altered parameters were kidney related. 11) These results can be explained by the endocrine-disrupting effects of Roundup, and by the overexpression of the transgene in the GMO and its metabolic consequences. [Important] 12) GM soy and corn that are rendered tolerant to the herbicide Roundup contain more herbicide residues. [Very Important] 13) Chronic diet ingestion of Roundup pesticide residues in GM feed may cause early alterations in kidney and liver functions. 14) Roundup concentrations about 103 times below the maximal residual levels induces 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 of tumors whilst 10 – 30% of treated females per group developed tumors. 17) By the 24th month, 50 – 80% of female animals had developed tumors in all treated groups, with up to 3 tumors per animal, whereas only 30% of controls were affected. 18) The second most affected organ in females was the pituitary gland, in general around 2 times more than in controls for most treatments. 19) The big palpable tumors in males (in kidney, and mostly skin) were by the end of the experimental period on average twice as frequent as in controls. 20) The most affected organs in males were the liver, together with the hepatodigestive tract and kidneys. Hepatic congestions, macroscopic and microscopic necrotic foci were 2.5 – 5.5 times more frequent in all treatments than in control groups. 21) Degenerating kidneys with marked and severe chronic progressive nephropathies were about twice as high in the treated groups. 22) In summary, for all treatments and both sexes, 76% of the discriminant variables versus controls were kidney related. 23) The first large detectable tumors occurred at 4 and 7 months into the study in males and females respectively, underlining the inadequacy of the standard 90 day feeding trials for evaluating GM crop and food toxicity. [Important] 24) Currently, no regulatory authority requests mandatory chronic animal feeding studies to be performed for edible GMOs and formulated pesticides. 25) We observed a strikingly marked induction of mammary tumors by Roundup alone, a major formulated pesticide, even at the very lowest dose administered. 26) Roundup disrupts estrogen synthesis and interferes with estrogen and androgen 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 of kidney physiology through oxidative stress. 29) Very low dilutions of Roundup are toxic to liver mitochondrial function, and cause cell membrane degradation. 30) In conclusion, it was previously known that glyphosate [Roundup] consumption in water above authorized limits may provoke hepatic and kidney failures. 31) The results of the study presented here clearly demonstrate that lower levels of complete agricultural glyphosate [Roundup] herbicide formulations, at concentrations well below officially set safety limits, induce severe hormonedependent mammary, hepatic and kidney disturbances. 32) Roundup and Roundup-tolerant GMO corn cause significant biochemical disturbances and physiological failures. COMMENTS FROM DAN MURPHY This study indicates that consumption of GMO Roundup-tolerant corn, whether it is exposed to Roundup or not, or any exposure to Roundup, alters biological physiology. Such exposures damage the pituitary gland, breast, liver, kidney, and hormonal systems; such exposures appear to be carcinogenic.

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I Don’t Believe In Chiropractic

There are so many times when somebody asks me what I do for a living and I tell them that I am a Chiropractor. Then they tell me that they believe in Chiropractic and it is meant as a compliment or supporting my profession. I reply back to them that I don’t believe in Chiropractic and they look at me perplexed. What do you mean you don’t believe in Chiropractic? but you’re a Chiropractor! I am a Chiropractor, but it is not a belief it is a law. What do you mean by that? It is a law of having a clear nervous system of any interference. These interferences are called subluxations. A subluxation is the condition of a vertebra that has lost its proper position with the one above or the one below or both; which occludes an opening, impinges nerves and interferes with the transmission of the nerve impulses of the brain. If you have any subluxations your body is not going to function at its optimum, because your body is under total control by your nervous system. Your nervous system controls all the organs, muscles, tissues, and cells in the body. It’s like believing if there is gravity or not. There is the law of gravity. Trust me you don’t believe if there is gravity or not. If you were on a tall building and jumped from it you would feel the effects of gravity in a very sudden and dangerous way. Your belief doesn’t affect if you or going to fall or not, it is a law just like the law of nerve interference. In a more dramatic example of the law of nerve interference, if your spinal cord was severed your body would never function at its optimum because the messages from the brain down the spinal cord and branching out the spinal nerves could never send the proper messages to all the organs, muscles, tissues, and cells in the body again. Dr. Suh, a research doctor from the University of Colorado did a study on nerve conduction and he found out that putting only 20 mm of Hg pressure would reduce the communication from the brain, through that nerve by an astonishing 50%. 20 mm of Hg pressure is the equivalent of the amount of pressure that a weight of a dime would have on a nerve. How painful is that? Not very painful right, so waiting until you’re in pain to see your Chiropractor is a poor indicator for any nerve interference. Remember just like the law of gravity there is a law of nerve interference. Stop believing in Chiropractic and know that it is a fact that a nervous system with no interference will let your body function at its optimum the way it should all the time. Dr. Kevin Kita

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Research on injury compensation and health outcomes: Ignoring the problem of reverse causality led to a biased conclusion

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 common presumption. Reverse causality is cause and effect in reverse. That is to say the effects precede the cause. The problem is when the assumption is A causes B when the truth may actually be that B causes A. It is usually stated in published studies, by insurance companies, and by their representatives (lawyers, claims adjusters, IME doctors, etc.) that injured patients who seek compensation (ask for compensation, hire a lawyer, etc.)(A), have worse health outcomes and slower recovery rates (B). However, such adverse health outcomes do not consider or evaluate the concept of Reverse Causality: slower recovery (B) leads individuals to claim, seek legal advice, and litigate (A). In my experience, which is extensive, many injured people feel compelled to seek legal counsel because it is their belief that their insurance company is treating them unfairly, 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 causality bias in studies on compensation-related factors and health outcomes. 2) These authors evaluated reverse causality using a sophisticated (and ingenious) evaluation of compensation claims associated with recovery from neck pain (whiplash) after rear-end collisions. 3) Although it is commonly believed that claiming compensation leads to worse recovery, it is also possible that poor recovery may lead to compensation claims a point that is seldom considered and never addressed empirically. 4) When reverse causality is ignored, claimants appear to have a worse recovery 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 judicial decisions 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 injury compensation laws. 7) An assumed belief is that the lure of compensation prompts individuals to exaggerate subjective symptoms. But, no studies have examined the effect of compensation payments per se on health. 8) In assessing injury outcomes, reverse causality must also be considered because the causal relationship between compensation factors and health is ambiguous. Claiming compensation, lawyer involvement, and litigation, may lead to slower recovery, but it is also possible that slower recovery leads individuals to claim, seek legal advice, and litigate. 9) The consequences for statistical inference of ignoring reverse causality bias are potentially serious: if negative associations between compensation-related factors and health status actually reflect worse health among those pursuing compensation (a rarely considered, but entirely plausible proposition), then decisions 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 a rear-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). 10) Neck pain at 24 months was selected as the primary health outcome. Neck pain 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 pain imaginable and zero represents no pain. 11) The analysis offered by these authors is extremely mathematical. They note that the standard method used to declare compensation negatively affects recovery uses a standard single equation approach. However, to assess reverse causality, a simultaneous equations techniques must be used. When the simultaneous equations techniques are used, the results tell a different story. 12) The usual approach to analyzing the effect of compensation-related health factors using the single equation approach is inappropriate and gives rise to biased and inconsistent results. 13) These authors reject the hypothesis that the decision to claim compensation negatively affects recovery. 14) Once reverse causality bias is addressed, people who claim compensation appear to experience a better recovery from neck pain at 24 months compared with non-claimants. [Key Point] 15) The results of this study suggest that compensation claiming may not be disadvantageous to injured parties after all and that it may even have a beneficial effect, because access to financial assistance and/or treatment may indeed relieve pain and suffering. This is, after all, one of the motivations for compensating people who have sustained an insult to their health. [Key Point] 16) Neck pain is significantly worse at baseline among claimants compared with non-claimants, which suggests that claims are more likely to be made by individuals whose initial neck pain is worse. [Key Point] 17) Reverse causality is largely overlooked in studies on compensation-related factors. Yet, this study shows that people with worse health tend to claim compensation. [Key Point] 18) Policies that restrict access to compensation benefits or legal advice may inadvertently disadvantage people who need financial or legal assistance. [Key] 19) This study serves as a reminder of the dangers of drawing causal interpretations from statistical associations when the causal framework is ambiguous. It establishes, empirically, that reverse causality must be addressed in studies on compensation-related factors and health outcomes. WHAT IS NEW: POINTS FROM AUTHORS: * Reverse causality bias has never been addressed empirically in studies on the relationship between compensation factors and health outcomes. In spite of this, the results of these studies are consistently interpreted as evidence that exposure to compensation-related factors is harmful to health outcomes. * This study confirms that reverse causality is an important source of bias in compensation research. * Unless all sources of bias, including reverse causality bias, have been convincingly addressed, one cannot draw conclusions about the relationship between injury compensation and health outcomes. * The quality of research in this field must be improved to avert decisions that will inadvertently disadvantage people with compensable injuries.

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Vitamin D Its role in disease prevention

Dermato-Endocrinology April/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 is increasing exponentially. 2) In 2011, the Institute of Medicine (IOM) of the US National Academies reviewed the evidence for beneficial effects of vitamin D for skeletal health, and set the daily recommended intake of vitamin D at 600 – 800 IU for most children and adults; 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 being too conservative. One summarized the problems succinctly: The IOM recommendations for vitamin D fail in a major way on logic, on science, and on effective public health guidance’. 4) The importance of vitamin D is underscored by the fact that skin pigmentation varied as humans moved out of Africa, becoming very pale in northern Europe. 5) The authors cite evidence of the relationship between low vitamin D levels and cancers (bladder, brain, colon, gastric, prostate, and rectal cancer; multiple myeloma; and non-Hodgkin lymphoma), and their survivability rates. 6) The beneficial effects of vitamin D may be much higher than is apparent according to prospective studies (perhaps a 28% reduction in all-cause mortality rate.) 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 dermatitis and localized scleroderma, can be treated with solar radiation (heliotherapy) or artificial UV radiation (phototherapy). 9) One non-vitamin D effect of UVA is liberation of nitric oxide (NO), which can lower blood pressure, has antimicrobial effects and acts as a neurotransmitter. 10) Ultraviolet light releases endorphins, which may be one reason that being in the sun is pleasurable. 11) Ultraviolet light may reduce the risk of multiple sclerosis through non-vitamin D 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 D supplements can reduce the risk of CVD. 14) Optimal vitamin D levels appear to help in the prevention and treatment of infections. 15) 250,000 IU of cholecalciferol rapidly restores vitamin D status into the optimal range in subjects with cystic fibrosis acute respiratory infection and is associated with improved survival and improved recovery of lung function. 16) There is epidemiologic and intervention studies pointing to an important role for 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 side effects of antiepileptic glucocorticoids, bisphosphonates, antiretroviral drugs, antiestrogens, cytostatic agents, antihypertensive drugs, and antituberculotic drugs. This action occurs through the Pregnane X receptor (PXR), which plays an important role in detoxifying xenobiotics [chemicals that are found in the body but not produced or expected to pre present in it] and drugs. 19) Vitamin D appears to reduce the risk of hospital-acquired infections, such as pneumonia, 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, asthma and lupus. Studies of pregnant women and their offspring suggest that vitamin D deficiency 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 as optimal. It is difficult to achieve these levels without consuming at least 5,000 IU of Vitamin D3 per day.

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Oxidative Stress in Alzheimer’s Disease and Mild Cognitive Impairment

Journal of Alzheimers Disease October 16, 2012 [epub] Natividad Lopez, Consuelo Tormo, Isabel De Blas, Isabel Llinares, Jordi Alom Free Radical Damage=Oxidative Stress=Reactive Oxygen Species (ROS)=Lipid Peroxidation KEY POINTS FROM THIS STUDY: 1) Oxidative stress may be a decisive factor in Alzheimers disease (AD) and in the 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 the double bonds of lipids; a marker for oxidative degradation of cellular membranes. B)) Levels of superoxide dismutase (SOD), an enzymatic, endogenous antioxidant; 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 radical production. 3) The study group consisted of 36 patients with AD, 18 patients with MCI, and 33 healthy aged subjects. Blood samples were obtained from each subject. 4) A significantly higher copper level was found in patients with AD and MCI compared to the control group. [Important point] 5) Levels of MDA were higher in patients from the AD and MCI groups than in the control group. 6) Our findings support the hypothesis that oxidative stress might represent a sign 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 the pathogenic cascade in Alzheimers disease (AD). 8) Oxidative damage to essential biomolecules (nucleic acids, lipids, proteins, or carbohydrates) alter the biological role that these play in physiological conditions. 9) The presence of high levels of unsaturated lipid content (that are readily attacked by free radicals) coupled with high oxygen utilization, high level of redox transition metal ions, and relatively poor antioxidant systems makes the brain particularly vulnerable to oxidative damage. 10) In the brain, due to its high lipid content, the most important mechanism in the damage due to free radicals is the peroxidation of lipids. 11) Cu imbalance contributes to the oxidative stress that is part of the pathogenesis 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 AD patients passing through MCI subjects. 14) Our data show a steady increase in serum Cu levels from healthy subjects to MCI and AD patients. 15) Our findings could support the hypothesis that an increase in serum Cu levels 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, in comparison 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 antioxidant enzymes [endogenous antioxidants like superoxide dismutase, catalase, and glutathione peroxidase], increased oxidative damage in nuclear and mitochondrial DNA, and higher levels of isoprostanes compared to that of the healthy subjects. 18) The current results suggest that oxidative stress [free radical damage] may be present in early cognitive decline. 19) In conclusion, we found that lipid peroxidation occurs in patients with MCI and AD in a similar way, suggesting that oxidative stress might represent a signal of 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 is therefore a factor in accelerating mild cognitive impairment (MCI) and Alzheimers disease. Other studies we have reviewed [AR 49-11 and 3-12] concur and indicate that the primary source of such copper is municipal drinking water and copper found in dietary supplements; suggesting that our municipal drinking water should be reversed osmosis and our supplements should essentially be copper free. *Both exogenous and exndogenous antioxidants are important in reducing brain free radical damage. My protocol for doing such is attached. *One should probably not consume fish oil without also increasing consumption of antioxidants [Article Review 30-12].

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Scar Formation and Ligament Healing [Surgical Biology for the Clinician]

Canadian Journal of Surgery December 1998; Vol. 41; No. 6; pp. 425-429 Kevin Hildebrand, MD and Cyril Frank, MD KEY POINTS FROM THIS ARTICLE 1) Ligaments are fibrous connective tissues that provide stability to joints. 2) Ligaments have a vascular network with an accompanying nerve supply. 3) Ligaments also participate in joint proprioception. [Key Point] 4) Injuries to ligaments induce a healing response that is characterized by the formation of a scar. This scar tissue is weaker. [Key Points] 5) Ligament healing is characterized by the formation and remodeling of scar tissue that is weaker than normal ligament owing to alterations in biochemical composition and structural organization. The scars have a greater amount of inferior strength tissue compared with that of normal ligaments. 6) Ligaments are composed of: 70% water 25% collagen protein 05% other matrix components 7) Ligament collagen fibers are arranged longitudinally but not in parallel. 8) When forces to the ligament are increased more fibers are recruited, allowing the ligament to accommodate greater physiologic forces. If forces beyond this range are applied, progressive sequential failure of fibers occur, leading to complete disruption of the ligament. 9) Ligaments and ligament scars have the ability to biomechanically adapt to changes in length or force (viscoelastic behavior, creep). [Adjustment?] 10) Ligaments are dynamic participants in joint function, helping to balance compressive and tensile forces. 11) Ligaments are part of a neurophysiological mechanism involved with joint function. They contain specialized neurological receptors that play a role in a proprioceptive ligamentomuscular reflex loop. [Subluxation] 12) There is evidence that autonomic nerves control blood flow in normal and healing ligaments. Regulation of blood flow could be an important mechanism for inflammation or repair in ligaments and periarticular tissues. [Key Point] 13) Ligament healing culminates in the formation of a scar that bridges the torn ends. Ligament healing follows these steps: A)) A fibrin clot is formed within minutes. B)) An inflammatory response ensues over the next 3-5 days, removing debris and attracting fibroblasts. C)) For the next 6 weeks, the fibroblasts produce a collagen matrix. D)) The healing tissue is remodeled over the next several months and years leading to better collagen alignment. 14) The structural strength and stiffness, stress and tissue quality continue to improve up to 12 months after injury, but after that time only relatively small increases are made. However, the material properties of the ligament scar do not return to normal even after 2 years. 15) Residual scar tissue behaves with abnormal biomechanical, biochemical and ultrastructural properties. 16) The return of joint function after injury does not mean that the ligament has healed. [Very Important] 17) Motion in stable joints improves the biomechanical properties of healing ligaments compared with immobilization of joints. The mechanism presumably involves the application of controlled forces; too little or too much force is detrimental. [Very Important] [Adjustment?] 18) Clinically, it can be difficult to accurately classify ligament injuries as stable or unstable. 19) Biomechanically, ligament scars are weaker because of inferior material quality. 20) Ligament healing in what may be considered to be the best case scenario is characterized by a scar material with inferior tissue quality, with changes in biochemical and histologic properties, that does not regenerate a normal ligament even after 2 years of healing. 21) The ligament scar affects the associated joint function. [Key Point] COMMENTS FROM DAN MURPHY These concepts on ligament repair have important applications for chiropractors that treat spinal trauma patients: * Even healed ligament injury leaves residual weakness and altered proprioception. * The altered proprioception function of injured and healed ligaments not only alters joint protective reflex muscle tone, but also alters the autonomic control of blood flow, which further impairs the ligament healing. [Not to mention that alters the autonomic control of blood flow has the potential to adversely affect systemic health including immunology]. * Controlled motion [chiropractic adjustment] is the best approach to enhance the quality of ligament healing, especially in the remodeling phase.

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The Basics of Soft Tissue Healing and General Factors that Influence Such Healing

Sports Medicine Arthroscopic Review September 2005; Vol. 13; No. 3; pp. 136 – 144 Kevin A. Hildebrand, MD, Corrie L. Gallant-Behm, BSc, Alison S. Kydd, BSc, and David A. Hart, PhD: From the University of Calgary, Alberta, Canada. KEY POINTS FROM THIS ARTICLE: 1) Wound healing following overt injury to a tissue follows general rules irrespective of the tissue involved. 2) Wound healing and repair of injured tissues follows several steps in the healthy individual. The process is initiated by the inflammatory response and subsequent steps are based on this initial response. 3) Whereas wound healing generally leads to a repair of the injured site, it does not lead to tissue regeneration. This difference between repair and regeneration has influence on tissues such as ligaments and tendons that function in a mechanically active environment. 4) The dynamic interface between mechanics and biology influence the effectiveness of the healing response. [Important] 5) Factors that impact the outcome of the healing response include the biology of the host, such as: A)) Age B)) Sex C)) Genetics D)) Tissue history (prior injuries, scar tissue, and disease states) 6) The repair process can lead to a loss of function, primarily from scar tissue, and this can occur in both musculoskeletal and visceral tissue (heart, lung, kidney, liver). 7) Recent investigations have detailed the healing response of many connective tissues (ligaments, tendons, menisci, joint capsules) that function in mechanically diverse environments. 8) The functional outcome of the healing process depends on the extent of repair versus regeneration. 9) The basic steps in the repair or healing of a tissue following overt injury are: A)) Hemostasis and a rapid inflammatory phase B)) A phase of cell proliferation and matrix deposition C)) A slow remodeling phase, which may take months to years A)) The Inflammatory Phase *Following acute injury there is bleeding into the area of injury and pain. *Hemostasis is restored by the formation of a fibrin clot, which prevents further bleeding and serves as a provisional matrix for migrating cells. *This clotting cascade results in the release of inflammatory molecules and inflammatory cytokines from cells such as platelets. *There is an influx of fibroblasts, which sets the stage for the second phase (B) of the repair process. B)) The Matrix Deposition Phase *Deposition of matrix molecules [fibroblasts] produce collagen proteins that bridge the damaged area with the residual endogenous ligament tissue. *If the matrix deposited early during the healing or repair process is altered compared with normal, the organization of the repair tissue is also likely to be altered. [Important: early best treatment is critical for ultimate quality of healing] *The organization of the matrix deposited early following injury is disorganized compared with normal tissue. [The Fibrosis Of Repair] *The tissue deposited early after injury appears to be an attempt to bridge the damaged area without regard to what was present before injury. *Not only does this provisional matrix have a different structural and cellular composition as compared with normal tissue, but in the case of ligament injury, this tissue is not necessarily even localized to the injury gap but also may extend to surround the entire remaining ligament midsubstance. *This somewhat amorphous material, resulting from the initiation of an overt inflammatory response and subsequent events is compromised at both the organizational and functional levels, independent of whether it is a ligament, tendon, or skin. C)) The Remodeling Phase *The remodeling phase is a slow process and is accompanied by alterations not only in matrix remodeling, but also gene expression, cellularity, vascularity, and innervation. *The scar tissue in a ligament undergos a protracted process where the initially deposited material seems to be turning over and the organization of collagen fibrils become more oriented along the long axis of the ligament. *Because the remodeling phase occurs slowly, and may take months (i.e., skin) or years (i.e., tendon and ligament). [Important] *A number of variables seem to influence the rate of remodeling and the final outcome, and it is not always possible to assign potential cause and effect relationships. *Even after protracted time post-injury, the mechanical properties of a scar tissue in a ligament … is still compromised compared with normal. *The scar tissue may be functional for most activities even though it is not normal. [Fails during high demand activities] 10) Normal tissues are organized with respect to collagen alignment and collagen fibril assembly, whereas collagen expressed early following injury is not aligned and heterogeneous with regard to orientation in the tissue. Because the latter is critical for function in a mechanically active environment such as a ligament, it is not surprising that the mechanical properties of the healing ligament are severely compromised compared with normal tissue. [The Fibrosis Of Repair] 11) The scar cells in the healing ligament are different from normal cells and therefore the scar is intrinsically different. [Key Point] 12) Tissues that do not have an influx of new microvasculature, like the disc and meniscus, do not heal well. [Very Important] 13) Not all ligaments heal to the same degree, and healing of ligament injuries seems to be influenced by various factors including location (i.e. extra-articular vs. intra-articular), intrinsic aspects (which are largely unknown), mechanical environment, as well as factors discussed in more detail in the following sections. 14) The large scar tissue mass gradually remodels, likely under the influence of the mechanical environment. [Very Important: supports the contention that the mechanics of the chiropractic adjustment can enhance the timing and quality of scar remodeling] 15) Scar-like tissue is functionally ineffective. 16) Maturation of the scar tissue requires mechanical loading to continue the remodeling phase of healing. [Very Important] 17) Normal connective tissues that function in a mechanically active environment (actually most tissues) subscribe to the use it or lose it paradigm of tissue 4 integrity. Increased loading leads to adaptation, whereas decreased loading below a threshold leads to atrophy. The same principle likely also holds for scar tissue and immobilization beyond the initial phases of healing could have a detrimental impact on outcome. [Very Important] 18) Too much loading of a scar at too early a time point may have a detrimental impact on the maturation of the scar. 19) Post healing joint instability and the loss of function leads to increased expression of inflammatory mediators, likely caused by microinjuries to the scar tissue, and resulted in a protracted healing response. There is a delicate balance between biology and mechanical environment when it comes to optimizing the basic healing response in tissues such as ligaments, tendons, or skin. 20) Some tendon and ligament injuries lead to formation of scar tissue that is partially functional, but to regain as much function as possible requires physiotherapy to facilitate the return to function after the scar tissue has formed. [Very Important] 21) The inflammatory response associated with overt injury or surgery can lead to formation of adhesions, where the ligament/tendon scar tissue is bonded to the surrounding tissue and thus, such restrictions compromise function in situations where movement is required. [Adhesions, Fibrosis Of Repair] 22) This emphasizes the need to minimize the induction of a vigorous inflammatory response in some environments to assist in the repair process without side effects such as adhesions. [Very Important: the resolution of inflammation is fibrosis; reducing inflammation reduces the fibrosis] 23) It is clear that the outcome is repair and not regeneration in all soft connective tissues, except for muscle and of course the hard tissue, bone. [Most Important: ligaments and tendons repair (with scar tissue) rather than regenerate (heal with normal pre-injury tissue)]. 24) Writings from ships captains from the 17th to 19th centuries whose men suffered from scurvy noted: Under conditions of vitamin C deficiency, scars on men that had formed greater than 20 years prior seemed to dissolve before normal skin was affected, leaving gaping wounds where once there were scars. Thus, even after many years, scar tissue is more ascorbate dependent than normal skin for maintenance of integrity in humans. [Both acute injury and the long-term integrity of healed tissues are Vitamin C dependent]. 25) The healing process is influenced by age. 26) It is known that the biomechanical properties of ligaments and tendons change with age (become stiffer) because of accumulated stresses and the 5 incidence of injuries, and degenerative processes in many of these tissues increase with age (aside from those associated with athletics). [Very Important] 27) The authors present evidence that indicates that different tissues and different individual [animals] have phenotypes that allow them to genetically heal better or worse. Apparently, genetics in part, determines if the healing occurs by regeneration or by scar tissue, which is linked to the severity and extent of the inflammatory response. [Very Important] 28) Women tend to have a more vigorous inflammatory response than males, [and therefore more fibrotic and mechanical (scar) healing residuals]. This response is probably linked to estrogen levels. 29) Normal ligament and joint function (laxity) can be influenced by the menstrual cycle in some women. 30) Pregnancy is associated with changes in several hormones qualitatively and quantitatively, impairing the metabolism of cells in the healing ligament, and also affecting the functioning of the normal ligament (i.e. laxity). 31) Genetic factors play a role in some pathologic scarring or wound healing such as keloid formation. 32) It is apparent from talking with orthopedic surgeons that there is a body of anecdotal information that has implicated genetics in wound healing following ligament injuries and surgical interventions. 33) The quality of the tissue prior to overt injury may play a role in the wound healing process and the final outcome, and therefore should be considered. The presence of previous injury, either overt or subclinical, could also impact the healing outcome. The healing outcome following re-injury could impact both the quality of the outcome and the functioning of the healed tissue.[Very Important] 34) Mechanobiology is likely important in the healing outcome in tissues such as ligaments, tendons, and related tissues. That is, depriving healing ligaments of mechanical loading likely has a detrimental impact on healing outcome. [Very Important: improved with chiropractic adjustments] 35) Ligaments and tendons adapt to increases in mechanical loading within a physiologic window; therefore, decreased loading decreases function. [Important] 36) When loading is consistently decreased, the quality of the tissue is decreased; this may influence the ability of these injuries to heal and their functional residuals. 37) Aging influences healing outcomes. [Very Important] 38) Re-injury of an acutely healing ligament increases inflammatory molecules, which could worsen the long-term consequence of the mechanical properties of the tissue. [Very Important] 39) Because not all injuries to a tissue are overt, it is possible that the accumulated cycles of injury and repair to a tissue could impact the starting material following an overt injury. If one extends this to the situation of a second acute injury, the starting material following a second injury is really scar tissue rather than normal tissue. This could impact the functional outcome in at least 2 ways; first, the quality of the scar may be compromised compared with the original scar tissue; and second, the size of the scar may be increased and thus could impact the functional outcome. [Very Important] 40) The size of the wound and the resulting scar tissue has a dramatic impact on the biomechanical outcome. 41) Diabetes can impact the healing outcome. 42) Many patients with diabetes have a compromised wound healing response due in part to an impaired inflammatory response and elaboration of growth factors. 43) In conditions such as diabetes, the disease could affect the quality of the connective tissue directly via derivatization of the tissues and formation of advanced glycation endproducts [AGEs] by carbohydrates. 44) Many individuals with diabetes exhibit impaired wound healing and can develop chronic wounds that do not readily heal. 45) In animals, a single local glucocorticoid treatment of a healing ligament resulted in reduced biomechanical properties of the scar, possibly because of a delay in the maturation/remodeling of the healing tissue. 46) It is readily apparent that wound healing in the adult under the most optimal conditions should be considered tissue repair not regeneration. For tissues like a ligament or tendon, the mechanical outcome may be less than ideal, depending on the expectations of tissue use post-injury and the occurrence of side-effects such as adhesions. [Very Important] 47) Improved understanding and application of the regulation of the inflammatory response may improve the subsequent healing processes improving the functionality of the reparative outcome. [Lasers, Omega-3, Antioxidant Status, etc.] 48) Regulation of the interface between biology and biomechanics (i.e. mechanobiology) may also affect the functionality of the reparative outcome. [Chiropractically Very Important] 7 COMMENTS FROM DAN MURPHY This article reiterates that ligaments are important sources of proprioception. This is important because proprioceptive afferents control joint muscle tone; there is appreciative evidence from other sources that indicate that joint proprioception influences sympathetic autonomic tone and immunology. This article reiterates that soft tissue healing occurs over a period of 12 months or more. Ligaments and tendons heal with scar tissue (repair) as a rule, and not with normal pre-injury tissue (regeneration). This scar tissue causes permanent loss of function. Scar tissue is mechanically and neurologically functionally inferior to normal tissue. Its inherent weakness makes the tissue prone to failure at previously normal load levels, and subsequent new trauma to scarred tissue will result in greater injury. Scar tissue (fibrosis) is linked to the intensity of the initial inflammatory response. Consequently, early inflammation control could improve the timing and quality of healing. Scar tissue, to varying degrees, is remodelable with the application of controlled motion, which I believe includes and even requires chiropractic adjustment. Mechanical loading is critical for scar tissue remodeling and maturation. Lack of symptoms is not synonymous with full healing and functional recovery. There are definitive reasons as to why some patients heal slowly or incompletely with functional residuals. These reasons include: A)) Age B)) Female Sex C)) Genetics D)) Tissue history (prior injuries, scar tissue, and disease states) E)) Diabetes F)) Disc injuries heal poorly, primarily as a consequence of poor blood supply G)) Pregnancy H)) Vitamin C levels I)) Menstrual cycle hormonal changes J)) Any reason that deprives the healing tissues from mechanical loading K)) Re-injury of a prior injury or prior tissue that has sustained repetitive stress L)) Excess carbohydrates that increase glycation (AGEs) [Hb-A1c] M)) Any treatment with corticosteroids N)) Anything that exaggerates the inflammatory response [omega-6/omega-3 or AA/EPA ratio]

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The startle response during whiplash: a protective or harmful response?

15, 2012; Vol. 113; No. 4, pp. 532-540 Daniel WH Mang, Gunter P Siegmund, J Timothy Inglis, JS Blouin KEY POINTS FROM THIS STUDY: 1) During whiplash collisions, initially relaxed occupants exhibit brisk, stereotypical muscle responses consisting of postural and startle responses that may contribute to the injury. 2) The neck neuromuscular response to a rear-end impact consists of a postural response and a startle response elicited by a multisensory stimulus (somatosensory, acoustic, and vestibular) associated with the vehicle impact. 3) During a rear-end collision, afferents from the somatosensory, acoustic, and vestibular systems are activated and trigger a startle response in the neck muscles. 4) These authors sought to determine if the startle response elicited during a rear-end collision contributes to head stabilization or represents a potentially harmful, overreaction of the body. In the context of a rear-end collision, it is not clear whether these reflex actions are protective and thus beneficial or potentially injurious and therefore harmful. 5) Three experiments were performed using 33 different subjects. The analysis included the use of surface electromyography, and head accelerations were measured using an accelerometer array. 6) The startle response represents an overreaction that increases the kinematics in a way that potentially increases the forces and strains in the neck tissues. [Key] 7) Neck muscle activity begins about 50 – 100 ms after vehicle acceleration onset, early enough to influence peak head and neck kinematics. There is evidence that neck muscles are a contributor to other neck tissue injuries during whiplash mechanism. 8) The time period over which the neck muscles are active overlaps the time period during which peak acceleration and displacement of the head and neck occur. This overlap suggests that muscle-induced strains and motion-induced strains in the posterior neck tissues potentially coincide and cause more severe whiplash injury and related symptoms following a rear-end collision. 9) In experimental rear-end collisions, subjects who reported temporary neck pain exhibited larger startle responses in their posterior neck muscles than did subjects who did not report neck symptoms. 10) Based on prior studies, injuries sustained during a rear-end car collision could be exacerbated by a startle response that increases neck muscle activity during a time when the posterior neck tissues may be vulnerable. 11) During whiplash, the startle response inhibits muscle tone; therefore, the startle response is potentially harmful and ill-adapted for whiplash collision exposures. 12) The startle response during a rear-end collision decreased the whiplashevoked neck muscle response by 16 – 29%. [Muscles protect joints. Joint injuries (facet/disc) are primarily responsible for chronic whiplash pain. Startle reduces muscle protection of joints, increasing whiplash injury and chronicity]. 13) These kinematic differences suggest that the startle response evoked by a rear-end collision may be more harmful than protective. 14) Our findings suggest that the startle response evoked by a rear-end collision may increase the risk of certain whiplash injuries. 15) The cervical facet joints are a source of neck pain in 40 – 68% of patients with chronic whiplash injuries, and excess strain in the facet joint capsule can occur during whiplash exposures. The neck multifidus muscles insert directly onto the [facet] capsule. 16) Posterior neck muscle activity, and multifidus muscle activity in particular, elicited by the collision may exacerbate cervical facet capsular ligament strain at a moment when the ligament is already being strained by the collision-induced intervertebral motion. 17) Our results provide additional support for the potential role of the startle response in exacerbating certain whiplash-related neck injuries. 18) Although startle responses are generalized body reactions to intense stimuli and are generally thought to protect the body from potential injury by drawing in the limbs and stiffening the body, during whiplash they tend to inhibit cervical muscle tone and increase cervical spine injury. COMMENTS FROM DAN MURPHY This article may help explain why some patients can be injured in very low impact scenarios; they are injured as a consequence of the startle response, caused by a cervical neuromuscular multisensory response from somatosensory, acoustic, and vestibular afferents associated with the vehicle impact.

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Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure Entropy

Stephanie Seneff, Robert M. Davidson and Jingjing Liu This article is 27 pages long and has 121 references November 7, 2012; 14; pp. 2227-2253 BACKGROUND FROM DAN MURPHY: FROM Salway, Metabolism at a Glance, Blackwell, 2004: Glutathione is a tripeptide that is formed from glutamate, cysteine and glycine. Glutathione protects cells against oxidative damage. Glutathione conjugates with toxins and drug metabolites to form water-soluble products for excretion. FROM Dan, an over simplication: Vaccine producers have a problem. Using a weakened live virus increases risk of giving the person the disease. Using a completely dead virus does not work very well unless the vaccine is coupled with something that ramps up the immunological response, an adjuvant, such as mercury or aluminum. The problem is that these adjuvants, like mercury or aluminum are extremely toxic to the nervous system, especially the developing nervous system of a child. This is further complicated by the fact that the blood-brain barrier is not fully complete until after many such vaccines are administered (around age 2 or so). KEY POINTS FROM THIS ARTICLE: 1) The Vaccine Adverse Event Reporting System (VAERS) is a surveillance system implemented by the U.S. government, which allows doctors and/or patients to report any adverse reactions observed in association with vaccines. 2) Autism (ASD) is a condition characterized by impaired cognitive and social skills, associated with compromised immune function. The incidence is alarmingly on the rise, and environmental factors are increasingly suspected to play a role. 3) This paper investigates word frequency patterns in the U.S. Centers for Disease Control (CDC) VAERS database. Results provide strong evidence supporting a link between autism and the aluminum in vaccines. A literature review showing toxicity of aluminum in human physiology offers further support. [Key Point] 4) Mentions of autism in VAERS increased steadily at the end of the last century, during a period when mercury was being phased out, while aluminum adjuvant burden was being increased. [Key Point] 5) After 2000, vaccines have been associated with increased cellulitis, seizure, depression, fatigue, pain and death, which are also significantly associated with aluminum-containing vaccines. 6) These authors propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione. [Key Point] 7) A strong correlation between autism and the MMR (Measles, Mumps, Rubella) vaccine is also observed, which may be partially explained via an increased sensitivity to acetaminophen given to control fever. [Key Point] 8) While it has been suggested that the observed increase in [Autism] rates may be due mainly to a change in diagnosis criteria, the actual criteria have changed very little from 1943. 9) The fact that ASD rates have been rapidly increasing over the last two decades strongly points to an environmental component. [Key Point] 10) The ASD community has maintained a long-standing conviction that vaccination plays a causative role in ASD, an idea that has been vehemently denied by the vaccine industry. 11) A study published in 2011 has confirmed a positive correlation between the proportion of children who received vaccinations in each state over the interval from 2001 to 2007 and the incidence of autism or speech and language impairment. For each 1% increase in vaccination rate, 680 additional children were diagnosed with autism or speech delay. [Key Point] 12) In 2012, we proposed that a causative factor in autism is an inadequate supply of cholesterol sulfate, both in utero and postnatally. Cholesterol sulfate synthesis in the skin is catalyzed by sun exposure. We hypothesized that autism may be induced by a combination of inadequate dietary sulfur and insufficient sun exposure to the skin, for both the mother and the child. [Key Point] [We have reviewed a number of studies linking low glutathione levels to autism: glutathione contains the sulfur containing amino acid cysteine] [We have reviewed a number of studies linking low vitamin D levels to autism: insufficient sun exposure causes low levels of vitamin D] 13) In autism there is a consistent deficiency in glutathione, an important sulfurbased antioxidant that plays a role in detoxifying aluminum. [Key Point] 14) Cysteine is the rate-limiting amino acid in the synthesis of glutathione and sulfate. 15) ASD individuals have reduced levels of glutathione, cysteine, and sulfate, impeding the detoxification and excretion of mercury. 16) Glutathione and sulfate are essential for the detoxification of xenobiotics and commonly administered drugs like acetaminophen in the liver. [Glutathione attaches to toxins so that the body can eliminate them. Acetaminophen 3 {like in Tylenol} is a toxin and depletes body stores of glutathione during detoxification, leaving inadequate levels of glutathione to detoxify toxins metals, like mercury and/or aluminum, etc. in vaccines] 17) Cholesterol sulfate deficiency provides an explanation for the link between autism, acetaminophen, asthma, and eczema. 18) Many children with autism have a low amount of serum glutathione. 19) Increased use of antibiotics leads to an alteration in gut flora which impairs the ability to detoxify toxic metals like mercury. 20) Vitamin D deficiency has been hypothesized to be a risk factor for autism. The over-zealous application of sunscreen is strongly implicated in autism, not only because sunscreen interferes with the production of vitamin D3 and cholesterol sulfate but also because it often contains aluminum, particularly the high Sun Protection Factor (SPF) sunblock products. [Wow] 21) Aluminum, due in part to its +3 ionic charge, is highly toxic to biological systems. [Key Point] There are no known life forms that utilize aluminum in any biological systems. 22) Autistic children accumulate aluminum that would almost certainly interfere with neuron function through these mechanisms: A)) Absorption through the skin because of poorly developed epidermis barrier. B)) As a consequence of their serum sulfate deficiency that leads to an impaired ability to dispose of aluminum. C)) Due to their increased permeability of the blood brain barrier. 23) It has recently been proposed that aluminum, commonly used in vaccines as an adjuvant, may be the most significant factor in adverse reactions, and, furthermore, that the nervous system is especially vulnerable to aluminum toxicity. 24) Vaccine clinical trials often include aluminum in the placebo, at the same or greater concentrations than the amount found in the vaccine. [This is crazy] 25) A highly informative study [Aluminum and Alzheimer’s disease: after a century of controversy, is there a plausible link? Journal of Alzheimers Disease: 2011] reviews the relationship between aluminum toxicity and Alzheimer’s disease. It also discusses issues the aluminum burden in children’s vaccines. It was pointed out that children today receive a cumulative aluminum burden from vaccines that may exceed the FDA limit by a factor of 50. [Wow!] 26) The vaccine industry has a difficult task in designing vaccines that are both safe and effective. The use of weakened but live pathogens can lead to vaccineinduced disease in children with an impaired immune system, yet debris from dead pathogens may not always cause a sufficient reaction to induce the required for protection against future exposure. Therefore the vaccine industry increasesimmunologic success in using vaccines with dead pathogens by adding adjuvants such as [very toxic] aluminum. 27) Also, adding aluminum or mercury to vaccines increases the stability of the antigen for long-term storage. 28) Glass contains aluminum oxide. When mercury in vaccines began to be phased out in the late 1990s, they began storing them in glass vials, yet aluminum can be leached out of the glass vial and the rubber stopper during storage. 29) Aluminum is one of the most common elements on Earth, yet no biological system has yet found a use for it. Its +3 charge makes it extremely destructive in water-based biological systems. 30) Aluminum is a known neurotoxin and there is no safe level. The central nervous system is particularly susceptible to the deleterious effects of aluminum. 31) Exposure to low concentrations of aluminum sulfate may be associated with Alzheimer’s disease. [This is the stuff municipalities put in water to filter it; aluminum sulfate causes debris to clump for easy removal, but aluminum sulfate residuals remain. Aluminum sulfate is often called alum.] 32) Aluminum exposure induces significant reactive oxygen species (ROS), even more than mercury (7X more) or lead (3X more). [Wow] 33) Aluminum damages the mitochondria, causing impaired ATP synthesis and excess production of reactive oxygen species. 34) Mercury [and aluminum] has a great predilection for bonding to reduced sulfur atoms, especially those in thiol-containing molecules such as glutathione, cysteine, homocysteine, and albumin. 35) Methylmercury is eliminated by binding to bio-organic sulfates. Newborns are much more susceptible to mercury toxicity than adults. 36) Impaired disposal of mercury and aluminum is due to insufficient glutathione. 37) Mercury builds up to toxic levels and further reduces sulfate bioavailability in the child with autism. 38) The measles, mumps, and rubella (MMR) vaccine may be contributing to the increased prevalence of autism. Unlike many vaccines, MMR contains neither thimerosal nor aluminum. MMR is often administered simultaneously with DTaP, an aluminum-containing vaccine. The synergistic and cumulative effects of multiple vaccines would likely lead to nonlinear enhancement of adverse events. 39) In the U.S., thimerosal still appears in several vaccinations given to young children, including Hep-B and HiB Titer. Aluminum is present in several of the vaccines, for example, Hep-B, PREVNAR, all of the DTaP formulations, and H1N1 flu vaccine multidose vials. 40) Recent published studies seriously addresses the question of the safety of aluminum adjuvants in vaccines, pointing out the neurotoxicity of aluminum. 41) There is a three-fold increased risk to autism associated with neonatal administration of Hepatitis B (Hep-B) vaccine prior to 1999, compared with either no vaccination or a delay until after the first month of age. Notably, Hep-B contains both aluminum and mercury. 42) Several researchers have reported increased frequencies of either sudden death or other health crises such as anaphylaxis or cardiorespiratory problems in association with vaccines. 43) Adults given the Hepatitis B vaccine show a significant number of adverse reactions. 44) Adults show profound adverse reaction to multiple vaccinations containing aluminum, including debilitating muscle pain and weakness associated with chronic fatigue syndrome and myofascitis. 45) MMR is significantly more likely to be associated with autism. MMR contains neither aluminum nor mercury. An interesting theory relating the MMR vaccine to ASD involves a proposed toxic reaction to the acetaminophen (paracetamol) administered to control fever following vaccination. [Key Point] 46) Acetaminophen may mediate oxidative stress and neurotoxicity in autism. 47) An impaired ability to metabolize toxic substances via a sulfation pathway contributes to autism. If the MMR vaccine is administered simultaneously with DTaP, an aluminum-containing vaccine (as is often the case), then the acetaminophen would likely interfere with the childs ability to dispose of the aluminum. [Key Point] 48) Hep-B is administered usually within 24 hours of birth, and most definitely in the first two months of life, and HiB Titer is administered three or four times before the age of 15 months. These two vaccinations would thus cause an accumulation of mercury and aluminum along with a depletion of the bioavailability of sulfate prior to the MMR vaccine in the vulnerable child, leaving them more susceptible to an infection arising from the live virus administered in MMR, and a subsequent dose of Tylenol (acetaminophen) to curb fever. 49) In the U.S., aluminum was allegedly phased in at the same time that mercury was phased out. [Key Point] 50) If the current CDC immunization schedule is followed, babies are injected with nearly 5 mg of aluminum by 18 months of age. 51) Symptoms associated with aluminum-containing vaccines include: fatigue, seizure, blister, cellulitis, pain, swelling, injection site macule, insomnia, injection site reaction, infection, depression, and uveitis. 52) The increased sensitivity to aluminum in the population is possibly due to a synergistic effect of cumulative exposure to multiple [vaccine] toxins. 53) When MMR fever is treated with acetaminophen, it becomes toxic to the brain of the child predisposed toward autism because of their inability to dispose of it. 54) Acetaminophen would also deplete sulfate needed to detoxify aluminum in any concurrent aluminum-containing vaccine such as DTaP. 55) In 1991, the Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control (CDC) recommended that all infants be injected with the first dose of hepatitis B vaccine at birth. Since Hep-B contains both mercury and aluminum, and since it is administered at birth, it is likely to be a major factor contributing to the steady rise in autism-related events in the latter half of the 1990’s. The practice of requiring Hep-B administration at birth is likely to be extremely dangerous to children who are born with a sulfur deficiency. 56) Aluminum in these vaccines administered to young children may be even more toxic than the mercury. 57) The autistic child cannot adequately detoxify acetaminophen. 58) ASD is a condition characterized by a serum deficiency in sulfur metabolites, particularly the sulfate anion, which results in an inability to safely dispose of mercury, aluminum, and acetaminophen. [Key Point] 59) While the autism community has focused on the mercury in thimerosal as the main culprit in vaccines, our studies with the VAERS database have identified aluminum and acetaminophen as being likely even more damaging than mercury. Because of the sulfur deficiencies, aluminum, mercury and acetaminophen likely accumulate in the autistic brain, leading to further damage. [Key Point] 60) We hypothesize that this unanticipated consequence is due to simultaneous increases in the aluminum content, attributed to an increased number of required vaccines, intentional addition of aluminum to achieve an adjuvant effect, as well as the likely further accumulation of aluminum as a consequence of leaching, given the new practice of storage in individual glass vials with rubber stoppers. 61) Oral antibiotics dramatically inhibit mercury excretion to 10% of normal levels. [Important] 62) Further aluminum exposure comes from aluminum in skin products such as high SPF sunscreen, particularly for the child whose barrier function is defective due to inadequate cholesterol sulfate and filaggrin in the epidermis. Other potential sources of aluminum are aluminum flocking agents in municipal water supplies, aluminum leaching from aluminum baby formula cans, and aluminum in the human milk supply to the breastfeeding infant, absorbed by the mother from sunscreen, antiperspirants, antacid medications, cooking utensils, etc. 63) The high fever associated with a reaction to MMR led to the administration of acetaminophen, whose safe disposal, like that of aluminum, depends on an adequate serum supply of bio-sulfates. The frequent presence of concurrent aluminum-containing vaccines would contribute synergistically to toxicity. 64) We hypothesize that the fever associated with MMR results in the administration of acetaminophen, which, in conjunction with the intense immune response to live viruses, becomes toxic to the vulnerable child. 65) Both women of childbearing age and children should be encouraged to consume foods that are rich in sulfur and to spend considerable time outdoors without sunscreen on sunny days. It might be prudent to implement a screening test for sulfate and/or glutathione concentration in the blood prior to administration of an aluminum-containing vaccine, and to waive the vaccine or consider a nonaluminum-containing alternative if sulfate or glutathione levels are insufficient. 66) The practice of including aluminum in the so-called placebo in vaccine trials should be abolished, so that the effects of aluminum adjuvant can be formally measured in a premarket phase. 67) Based upon our statistical research of the VAERS database, we would encourage the vaccine industry to consider omitting aluminum adjuvant doping of all vaccines for both children and adults. 68) Neuronal damage due to aluminum penetration into the nervous system may be a significant factor in autism. The fact that mentions of autism rose steadily concomitant with significant increases in the aluminum burden in vaccines, is highly suggestive. 69) Autism may be linked to other environmental toxins, like herbicides or pesticides, or aluminum in other products such as antiperspirants and antacids. 70) We observed a strong correlation between the MMR vaccine and autism, which we suggest could be explained by the effects of acetaminophen. 71) We propose that simple corrective measures such as increased sunlight exposure and decreased use of sunscreen may help protect a child from a severe reaction to aluminum-containing vaccines, but we also feel that the vaccine industry should find a way to reduce or even eliminate the aluminum content in vaccines.

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