2009, Vol. 73, pp. 438 – 440 Rodney Philip Kinvig Ford The Childrens Gastroenterology and Allergy Clinic, Christchurch, New Zealand KEY POINTS FROM DAN MURPHY: 1) Gluten grains (wheat, rye, and barley) have become staples in our diet. Thequantity of gluten in our daily food intake has been steadily increasing withadvances in food processing. 2) Gluten instigates celiac disease (gluten-sensitive enteropathy), which affectsone in every hundred people. Celiac disease is a gastro-intestinal disease;symptoms are due to mucosal damage or malabsorption. In celiac disease there ishistological evidence of mucosal damage. 3) Gluten causes symptoms, in both celiac disease and non-celiac gluten-sensitivity, by its adverse actions on the nervous system. Gluten harms thenervous system. Gluten is linked to neurological harm in patients, both with andwithout evidence of celiac disease. 4) Many celiac patients experience neurological symptoms, frequentlyassociated with malfunction of the autonomic nervous system. 5) Gluten-sensitivity can be associated with neurological symptoms in patientswho do not have any mucosal gut damage (that is, without celiac disease). 6) Gluten can cause neurological harm through a combination of cross-reactingantibodies, immune complex disease and direct toxicity. 7) A host of symptoms outside the gut (extraintestinal symptoms) have beenobserved in gluten sensitive people. 8) Gluten is responsible for significant ill health other than celiac disease (non-celiac gluten-sensitivity or The Gluten Syndrome), such as: Ataxia Eczema Irritable bowel disease Hypotonia Developmental delay Learning disorders Attention deficit hyperactivity disorder Migraine 2 Headache Epileptic disorders Many patients with these problems respond favorably to a gluten-free diet. 9) Gluten intolerance gives rise to a variety of dermatological manifestationswhich may benefit from a gluten-free diet. 10) The smooth uninterrupted function of the body relies upon the autonomicnervous system. The sympathetic and parasympathetic pathways are driven by therespective neuro-transmitters. The regulation of the cardiovascular system, gut,bladder, uterus, and glands (pancreas, gall bladder, sweat, and saliva) all dependson this vast autonomic nerve network. There is evidence that gluten causesintestinal autonomic neuropathy. 11) Gluten-sensitivity without histological gut damage may provoke neurologicaldysfunction; such nerve damage might be through autoimmune damage. 12) Celiac disease is not a mandatory requirement for gluten-sensitivity. This iswhy more than half of patients with negative gut IgG-gliadin antibody tests reportimprovements in a variety of symptoms with a gluten-free diet. These includetiredness, lethargy, irritability, and sleep disturbance. These are likely to beneurological symptoms generated by gluten-sensitivity. 13) Evidence points to the nervous system as the prime site of gluten damage. 14) The histological gut damage in celiac disease is not mediated through thisneurologic system. It is caused by local toxicity to the bowel in susceptible people. 15) Non-gut symptoms related to gluten are mediated through neural networks. COMMENTS FROM DAN MURPHY All of my family and close friends and many patients are gluten free as aconsequence of our direction. My immediate family has been gluten free for manyyears. All of us have noticed substantial improvements in our health and we allavoid gluten like the plague. There are many excellent books of this topic. Myfavorite most recent book is Wheat Belly, by William Davis, MD, 2011. For a number of reasons, wheat has been significantly genetically modified over thepast half century. Reasons include increased crop yields, improved harvestingefficiency, and desirable palliative and baking aesthetics. Sadly, these modificationshave significantly raised modern wheats Glycemic Index and reduced thedigestibility of its gluten.

November 1993; Vol. 18; No. 15; pp. 2355-2357 Toshihiro Ando, MD and Kentaro Mimatsu, MD Department of Orthopedic Surgery, Nagoya University School of Medicine, Japan KEY POINTS FROM DAN MURPHY 1) This case of serial MRI studies shows clear evidence that lumbar discherniation can occur over a period of up to 20 months following a single traumaticinjury:A 16-year-old girl with no history of back pain, riding a motor scooter, was struckby an automobile, striking the pavement hard on her lower back.She experienced immediate low back pain.Initial exam (same day) showed no neurological signs/symptoms.Initial x-rays (same day) were normal.Initial MRI (same day) was normal.Through the entire follow-up period (20 months) she engaged in no sports of otherphysical activities.A very small signal change at L4-5 disc was observed with MRI at 2 months afterinjury.MRI at 11 months after injury showed L4-5 disc height narrowing along with anextruded disc fragment.MRI at 20 months after injury showed additional disc height reduction and thesignal intensity had decreased further. 2) MRI studies clearly showed the disc herniation to be progressing as a resultof the trauma, leading to a diagnosis of traumatic lumbar disc herniation. 3) Disc extrusion became clearly visible on MRI obtained 11 months after theaccident. It is thought that the direct impact of an external force created a ruptureof incomplete rupture of the annulus fibrosis, which represented a weak spotmechanically to release stress on the disc, leading to gradual extrusion of thenucleus pulposus. 4) It is necessary to carefully observe changes in other cases such as this one,in which disc degeneration progresses steadily for months after trauma, even whensymptoms are minor. 5) If any signs of change on MRI, patients should be repeatedly observed withcaution. COMMENTS FROM DAN MURPHY These authors are clearly advocating repeated MRI on patients with persistentsymptoms, and not to rely on the initial or early MRIs when they appear to be non-revealing. This is a 2nd study (of 3) I found doing a search for a PI attorney (plaintiff) fromSalt Lake City. The primary perspective is: It is often (essentially always) claimed by insurance defense attorneys andtheir experts that if the MRI is normal that there is no injury. This studyclearly shows that is not the case because a traumatized disc candegenerate and herniate over a period of time (months, up to 20 months). A plaintiff attorney might use such a study to ask a defense expert something like: Doctor… * After a disc is injured, can the immediate MRI be essentially normal? * After a disc is injured, can an MRI taken 2 months after injury be essentiallynormal? * After a disc is injured, can sequential MRIs, taken over a period of 20 months,show progressive disc degeneration and eventually herniation, even without anyensuing injury or physical stress? * In order for an expert to give his/her best opinion, should one not first haveobtained the best possible evidence? * Because you did not have sequential MRIs in this case, you really do not havethe best evidence as to whether this injury is responsible for the eventualdegeneration and herniation or not, do you doctor?

Markus Kornberg, MD KEY POINTS FROM DAN MURPHY: 1) The most useful modality for assessing symptomatic degeneration of thelumbar intervertebral disc is discography. 2) With aging, intervertebral discs lose water. Determination of discdegeneration with magnetic resonance imaging (MRI) depends on the loss of watercontent in the disc. 3) Four trauma case histories are presented of patients with negative MRIstudies but with abnormal discography: #1: 35-year-old man fell while roller-skating, developed low back and right legpain. MRI and Discogram performed at 2 years: MRI normalDiscogram L5-S1 annular disruption, injection reproduced pain #2: 27-year-old man fell a short distance off scaffolding, developed low back andbilateral leg pain. MRI and Discogram performed at 4 months:MRI normalDiscogram L5-S1 disc degeneration, injection reproduced pain #3: 41-year-old woman tripped and fell to pavement, injuring spine.Myelogram normal CT normalAfter 2.5 years of continuous symptoms, MRI and Discogram:MRI normalDiscogram L5-S1 annular disruption, injection reproduced pain #4: 37-year-old man thrown against wall by a pressure hose, developed LBP andleft leg pain. MRI and Discogram performed at 2 years:MRI normalDiscogram L5-S1 disc degeneration, injection reproduced pain 4) Normal lumbar disc MRI does not necessarily rule out [symptomatic] discdegeneration. 5) A normal MRI does not rule out early disc degeneration.2 6) There is an interval of time between the development of traumaticdisruption of the annulus and loss of sufficient water content to be reflected on MRIas decreased signal intensity. 7) If MRI fails to demonstrate evidence of disc degeneration, then discographyis indicated to determine the status of the annulus and for pain provocation. COMMENTS FROM DAN MURPHY I found this study doing a search for a PI attorney (plaintiff) from Salt Lake City. Itwas important in his case. The primary perspective is: It is often (essentially always) claimed by insurance defense attorneys andtheir experts that if the MRI is normal that there is no injury. This studyclearly shows that is not the case. A discogram is clearly more accurate than MRI is documenting symptomatic discinjury and degeneration. A plaintiff attorney might use such a study to ask adefense expert something like: Doctor… * Can a discogram prove post-traumatic symptomatic disc degeneration incases where the MRI appears to be normal? * To give a more complete opinion in this case, would you have liked to haveseen the results of a discogram? * In order for an expert to give his/her best opinion, should one not first haveobtained the best possible evidence? * Because you did not have the results of a discogram in this case, you reallydo not have the best evidence as to whether the disc is injured or not, do youdoctor? Although I believe these concepts are important, I am not in favor of routinediscograms as there is evidence that disrupting the integrity of the annular ring ofthe disc with a needle, either for diagnostics or for treatment, tends to acceleratedisc degenerative disease. [Article Review 11-11: Does Discography Cause Accelerated Progression of Degeneration Changes in the Lumbar Disc: A Ten-YearMatched Cohort Study; Spine; October 1, 2009, Volume 34, Number 21, pp. 23382345:2009 ISSLS Prize Winner (International Society for the Study of the LumbarSpine).]

The American Journal of Emergency Medicine August 3, 2012 [epub] Michael Lewis, MD; Parviz Ghassemi; Joseph Hibbeln, MD BACKGROUND: On January 2, 2006, in Upshur County, West Virginia, USA, there was an explosionin the Sago Coal Mine. The blast trapped 13 miners for nearly two days; only oneminer survived. The lone survivor was Randal L. McCloy, Jr., age 26. He was found practically dead, unconscious and suffering from carbon monoxide poisoning, acollapsed lung, brain hemorrhaging, edema, muscle injury, faulty liver and heartfunction, and almost no brain electrical activity. His initial prognosis for recoverywas grim, expecting permanent damage to his brain. However, McCloy recovered almost fully. McCloy is the longest exposure to carbon monoxide poisoning to have survived. Hisdoctors predicted that if he did survive, he would be severely brain damaged sincethe carbon monoxide had stripped the protective myelin sheath from most of hisbrain’s neurons. McCloys neurosurgeon started to enternally feed him a daily dose of 15,000milligrams (mg) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) fishoil. Soon, his brain electrical activity returned and he emerged from his coma, graduallyregaining his ability to walk, talk, and see. Apparently the omega-3s helped rebuildthe damaged gray and white matter of his brain. McCloy is now married, haschildren, and is largely functioning normally. The authors of this study state: We are aware of only one report where n-3FA were used, that being thesurvivor of the Sago Mine accident in January 2006 suffering from hypoxiaand exposure to toxic gases, dehydration, and rhabdomyolysis.[Roberts L, Bailes J, Dedhia H, et al.; Surviving a mine explosion; J Am Coll Surg,207 (2) (2008), pp. 276 – 283] {Dr. Bailes was McCloys neurosurgeon} These authors then present a case study stating:To our knowledge, this is the first report of specific use of substantial amounts ofn-3FA following severe TBI. * A teenager sustained a severe TBI in a motor vehicle accident. 2 * His extrication prolonged, he was in a coma, he sustained a subduralhematoma that was surgically decompressed. * The attending neurosurgeons believed the injuries were likely fatal. * On day 10, (still in a coma), MRI showed significant subdural hemorrhageand diffuse axonal injury. His doctors believed him to be in a permanentvegetative state. * A tracheotomy and percutaneous endoscopic gastrostomy (PEG) tube wereplaced for custodial care and enteral feedings were started. * On Day 11, 9,756 mg eicosapentaenoic acid (EPA) and 6,756 mg docosahexaenoic acid (DHA) per day were added to enteral feedings. * On day 21, he was weaned off the ventilator and transported to a specializedrehabilitation institute 3 days later. * 3 months after the injury the patient attended his high school graduation toreceive his diploma. * 4 months after the injury the patient was discharged to home. * For the following year, the patient continued to take 16,500 mg of EPA + DHAfish oil supplements per day along with 6000 IU of vitamin D3; hisimprovement continued and he experienced no adverse effects.

1) Occipital neuralgia is defined as paroxysmal stabbing pain, with or withoutpersistent aching between paroxysms, in the distributions of the greater, lesser,and third occipital nerves. 2) Occipital neuralgia is a cause of protracted or severe intractable headaches,which occur more frequently in women. 3) Entrapped peripheral nerves typically have increased cross-sectional area.Increases in the cross-sectional areas of nerves in cases of peripheral neuropathyhave been well described. 4) Occipital neuralgia is a headache that may result from greater occipital nerveentrapment. 5) Possible zones of greater occipital nerve irritation and entrapment include thefollowing: A)) Where the greater occipital nerve emerges from the C2 dorsal ramus betweenthe atlas and the axis. B)) Where the nerve courses between the obliquus capitis inferior andsemispinalis capitis muscles. [Its like a sandwich: the 2 muscles are the bread and the nerve is between them] C)) Where the nerve pierces the belly of the semispinalis capitis. D)) Where the nerve exits from the tendinous aponeurosis of the trapezius. 6) The purpose of this study was to measure the cross-sectional area andcircumference of symptomatic and asymptomatic greater occipital nerves inpatients with unilateral occipital neuralgia. Measurements were done withsonography in 17 patients. 7) Persons with a greater body mass index (BMI) had larger cross-sectionalnerves. [This suggests that increased BMI people may be more prone to peripheralnerve entrapment]. 8) This article reports sonographic evidence showing significant increased cross-sectional area and circumference of the symptomatic greater occipital nerve inpatients with unilateral occipital neuralgia: with unilateral occipital neuralgia: Ultrasound Measurements of the Greater Occipital Nerve Symptomatic Side Asymptomatic Side Cross Section 4.1 ± 2.6 mm 2.0 ± 0.7 mm Circumference 8.5 ± 2.7 mm 5.6 ± 1.4 mm 9) There were significant differences between the symptomatic andasymptomatic cross-sectional areas. 10) A significant difference was also noted between the symptomatic andasymptomatic circumferences. 11) A usual site of greater occipital nerve entrapment was within the tight fasciasurrounding the belly of the obliquus capitis inferior near the C2 spinous process[E]. 12) There was a significant difference in the cross-sectional areas andcircumferences of the greater occipital nerves between the symptomatic andasymptomatic sides. These findings are consistent with typical swelling of peripheralneuropathy. [Remember: minor compression collapses the intraneural vein,causing neural swelling, resulting in more internal pressure]. 13) We report sonographic data showing a significant increase in the cross-sectional area and circumference of the greater occipital nerve in patients withoccipital neuralgia.

1) The purpose of this article is to discuss a theoretical basis for wellnesschiropractic manipulative care. 2) A search of PubMed and of the Manual, Alternative, and Natural TherapyIndex System was performed with a combination of key words: chiropractic,maintenance and wellness care, maintenance manipulative care, preventive spinalmanipulation, hypomobility, immobility, adhesions, joint degeneration, andneuronal degeneration, 1970-2011. 3) The search revealed surveys of doctors and patients, an initial clinical pilotstudy, randomized control trials, and laboratory studies that provided correlativeinformation to provide a framework for development of a hypothesis for the basis ofmaintenance spinal manipulative therapy. 4) Maintenance care optimizes the levels of function and provides a process ofachieving the best possible health. It is proposed that this may be accomplished byincluding chiropractic manipulative therapy in addition to exercise therapy, diet andnutritional counseling, and lifestyle coaching. 5) It is hypothesized that because spinal manipulative therapy brings a joint tothe end of the paraphysiological joint space to encourage normal range of motion,routine manipulation of asymptomatic patients may retard the progression of joint degeneration, neuronal changes, changes in muscular strength, and recruitmentpatterns, which may result in improved function, decreased episodes of injuries,and improved sense of well-being. 6) This article considers the scientific basis of the commonly practicedprocedure of chiropractic maintenance care and whether a hypothesis of aphysiological basis can be generated to explain findings and practice.Dr. Taylor cites studies to support these concepts: A)) Acute chiropractic care for the management of acute conditions. B)) Care for chronic/recurrent conditions is defined as medically necessary carefor conditions that are not expected to completely resolve, but in which one canprovide documented improvement. 2 [Chronic/recurrent care is medically necessary, even though the condition is notexpected to completely resolve] [Use measurement outcomes to document improvements] C)) Wellness or maintenance care may not be defined as being medicallynecessary for a current condition.However, this type of care optimizes the levels of function and provides a processof achieving the best possible function and health. This care includes chiropracticmanipulative therapy in addition to exercise therapy, diet and nutritionalcounseling, and lifestyle coaching.[Use measurement outcomes to show functional improvement which may qualifysuch care as being medically necessary] 7) The purpose of chiropractic maintenance care is to optimize spinal functionand decrease the frequency of future episodes of back pain. 8) Other definitions for chiropractic maintenance care include: A)) Appropriate treatment directed toward maintaining optimal body function.This is treatment of the symptomatic patient who has reached pre-clinical status ormaximum medical improvement, where condition is resolved or stable. B)) A regimen designed to provide for the patient’s continued wellbeing or formaintaining the optimum state of health while minimizing recurrences of the clinicalstatus. 9) The medical profession uses wellness as providing diagnostic tests for earlydetection of disease processes. 10) For this article, maintenance care and wellness care are used synonymouslyto represent the process of spinal manipulative therapy for an asymptomatic patientor a patient that has reached maximum therapeutic improvement. 11) Some insurance companies have defined maintenance care as care providedfor a stable condition without any functional improvement of the patient net healthoutcome over a 4-week period and further determine it as not being medicallynecessary. 12) In published surveys, 90+% of chiropractors opined that the purpose ofmaintenance care was to minimize recurrences or exacerbations; 80+% ofchiropractors responded that it would optimize the patients’ health. 13) 97% of American and 85% of the Australian chiropractors use manipulativetherapy as a component of the maintenance care. 14) 95% of chiropractors recommended maintenance care to minimizerecurrences or exacerbations of conditions and 90% recommended the care tooptimize the health of the patient. 15) In a study 96% of elderly patients who received maintenance care believedthat it was either considerably or extremely valuable. 16) It has been reported that 79% of patients in chiropractic offices arerecommended maintenance care and nearly half of those patients elect to receivethese services. 17) In animal studies, fixation of facet joints for 4-8 weeks causes degenerativechanges and osteophyte formation of the articular surfaces. These findings mayprovide an explanation to the anecdotal findings reported in clinical practice inwhich patients report increased well-being and decreased incidence of spinalcomplaints with once per month preventive wellness manipulation. 18) Sadly, facet articular surface degeneration began at less than 1 week. Thecommon clinical treatment frequency at every 4 weeks correlates with the findingsof the threshold of 4 weeks for irreversible degenerative osteophyte formation.This finding correlates with the common practice pattern of progressive decreasingof the frequency of manipulation as the patients progress in recovery from an acuteincident. It also indicates that even when patients present for once per monthasymptomatic preventive manipulation, the process of degeneration of the articularsurfaces may have already begun. 19) Facet joint fixation also resulted in synovial fold fibrotic adhesions thatprogressed to mild adhesions in 4 weeks, moderate adhesions in 8 weeks, andsevere adhesions after 12 weeks. In humans, it can be hypothesized that there isa period where the adhesions are forming without clinical symptoms. This wouldalso support the common once per month maintenance spinal manipulation. 20) It has also been demonstrated that lumbar spinal manipulation gaps the facetjoints which may break up adhesions. This would lend additional support for theonce per month clinically recommended spinal manipulative therapy. 21) Four weeks of joint immobilization has been found to cause a time dependentloss of neurons that becomes progressively worse thereafter. An increase inneurons occurs after release of the fixation. 22) Such immobilization also causes time dependent muscle weakness, atrophyand fatty deposition of the multifidi muscles. The time-dependent factor progressedfrom normal muscles to mild, moderate, and severe muscular atrophy. 23) There may also be a possibility of reversal of the neuronal degeneration andmuscular weakness through manipulation and remobilization of the joint.4 24) These progressive adverse physiological consequences of joint immobility,create a line of reasoning arises that generates a theoretical framework for aphysiological hypothesis of the basis of maintenance manipulative therapy. 25) Evidence clearly demonstrates that the clinical consensus of dosage ofmaintenance manipulative therapy has been found to be most beneficial at anaverage of once every 2 to 4 weeks. We also see here that it closely correlates withthe studies that show onset of facet joint degeneration, neural degeneration,neuroplastic changes, and muscular atrophy and weakness at an average of 2 to 4weeks. 26) Taking into account the neurological and biomechanical consequences ofmanipulative therapy, it is plausible to hypothesize that monthly manipulativetherapy retards the progression of adhesion formation, joint degeneration, neuronalchanges, and changes in muscular strength and recruitment patterns. This couldresult in improved function, decreased episodes of injuries, and improved sense ofwell-being. 27) A 2004 chiropractic study of chronic low back pain showed that the group ofpatients who received 9 months of maintenance manipulation at the frequency ofonce per every 3 weeks maintained their initial clinical improvement while thecontrol group returned to their previous levels of disability. The authors concludedthat there were positive effects of preventive maintenance chiropractic spinalmanipulation in maintaining functional capacities and reducing the number andintensity of pain episodes after the acute phase of treatment of low back painpatients. 28) Swedish surveys of chiropractors find consensus on providing maintenancecare to prevent disability relapses. 29) There is a common thread of the time dependency noted in all the laboratoryand clinical studies. The periods of onset of the anatomical and physiologicalchanges ranged from 2 to 4 weeks. The clinical studies also provided MMT every 4weeks and noted positive changes in the pain and disability measures. This timeinterval also correlates with the common recommendations found in the surveys ofchiropractic physicians.

OBESITY: excess body fat that adversely effects health; it is a leading cause ofpreventable death in the world and its prevalence is increasing. OVERWEIGHT: having more body fat than is optimally healthy. More people are overweight than obese; obesity is worse than being overweight. This study only looked at obesity rates. 1) This is a prospective study examining whether in-utero exposure to magneticfields (MFs) increases the risk of childhood obesity. 733 pregnant women carried ameter measuring MF levels during pregnancy and their children were followed up to 13 years to collect clinically recorded information on growth patterns and weight. This is the first prospective study to look at this association. 2) The prevalence of childhood obesity is increasing rapidly and has reachedepidemic proportions in both industrialized and newly industrialized countries. 3) It is estimated that this increase in childhood obesity will increase medicalcost by up to $66 billion per year in the U.S. alone. 4) About 20% of US children are obese. [significantly more are overweight] 5) The World Health Organization considers increased obesity the top publichealth challenge. 6) While the efforts to reduce obesity have focused on changing diets andincreasing physical activity with limited success, the causes of the obesity epidemicduring the last several decades remain unclear. 7) Diet and sedentary life style cannot totally explain such a steep world-wideincrease in obesity across countries with vastly differing dietary patterns anddegrees of physical activity. Otherenvironmental factors should be seriouslyexamined, especially in pregnancy, that may damage the formation anddevelopment of fetal endocrine and metabolic systems, predisposing offspring to ahigher risk of developing childhood obesity or becoming overweight. 8) A potential invisible physical risk factor influencing life-long health duringpregnancy is exposure to man-made electromagnetic fields (EMFs) from microwaveovens to countless wireless devices. This parallel in the epidemic ofobesity/overweight with massively increased use of EMF-generating appliances, andwireless networks and devices during the last a few decades warrants closer examination. 9) EMFs exposures during pregnancy have been linked to: * asthma (5 references) * diabetes / overweight/ insulin resistance (2 references) * altered glucose metabolism (2 references) * ADHD (1 reference) * adverse offspring neurological development (1reference) 10) Exposure to EMFs during pregnancy could potentially impact the fetaldevelopment including fetal endocrine and metabolic systems, predisposingoffspring to a higher risk of obesity. 11) EMFs consists of both electric and magnetic fields, but the authors measuredonly magnetic fields. 12) Maternal MF exposure was measured objectively by a MF meter worn byparticipants during pregnancy. 13) The authors controlled for child gender, maternal age, maternal pre-pregnancy BMI, race/ethnicity, education level, smoking during pregnancy, andbreastfeeding, maternal parity, preexisting or gestational diabetes, family income,preterm delivery, and childhood behaviors such as fruit and vegetable intake, TVwatching time, and amount of exercise. 14) In-utero exposure to medium/high MF level was associated with 69%increased risk of being obese or overweight during childhood. 15) There was a dose-response relationship with increasing in-utero MF levelbeing associated with increased risk of obesity/overweight, which was highlystatistically significant. 16) In this prospective cohort study, we present a new finding that a high in-utero MF exposure level in pregnancy is associated with an increased risk ofchildhood obesity. 3 17) The observed association and supporting evidence provide the firstepidemiological link between ever increasing exposure to environmental MFs(especially in-utero exposure) in the last few decades and the rapid rise inchildhood obesity during the corresponding decades. Given the world-wide epidemicof childhood obesity/overweight as a leading public health challenge, our findingshave the potential to reveal a new environmental risk factor for childhood obesity,which may lead to prevention of childhood obesity. 18) The authors hypothesize that the association between MF exposure andchildhood obesity, is linked to altered glucose metabolism [insulin resistance]. 19) It is biologically plausible that in-utero MF exposure have an adverse effecton fetal development including the metabolic and endocrine systems. 20) Both maternal high BMI and diabetes are known risk factors for childhoodobesity/overweight, and the association between in-utero MF exposure andchildhood obesity was much stronger in the presence of these known risk factors. 21) In conclusion, our study provides the first epidemiologic link between in-utero MF exposure and childhood obesity/overweight. Given the worldwide epidemicof childhood obesity and ubiquitous MF exposure, this finding, could haveimplications for possibly reducing childhood obesity and understanding the obesityepidemic. 22) Prenatal exposure to high MF level was associated with increased risk ofbeing obese in offspring than those with lower MF level [69% increased risk]. Theassociation demonstrated a dose-response relationship and was stronger (morethan 2.3 fold increased risk) among children who were followed up to the end of thestudy. 23) Maternal exposure to high MF during pregnancy may be a new andpreviously unknown factor contributing to the world-wide epidemic of childhoodobesity/overweight.