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.
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.
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
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.
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.
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].