Medical Hypotheses RSS feed: Current Issue. Medical Hypotheses is a forum for ideas in medicine and related biomedical sciences. It will publish interesting and important theoretical papers that foster the diversity and debate upon which the scientific process thrives. The Aims and Scope of Medical Hypotheses are no different now from what was proposed by the founder of the journal, the late Dr David Horrobin. In his introduction to the first issue of the Journal, he asks 'what sorts of papers will be published in Medical Hypotheses? and goes on to answer 'Medical Hypotheses will publish papers which describe theories, ideas which have a great deal of observational support and some hypotheses where experimental support is yet fragmentary'. (Horrobin DF, 1975 Ideas in Biomedical Science: Reasons for the foundation of Medical Hypotheses. Medical Hypotheses Volume 1, Issue 1, January-February 1975, Pages 1-2.). Medical Hypotheses was therefore launched, and still exists today, to give novel, radical new ideas and speculations in medicine open-minded consideration, opening the field to radical hypotheses which would be rejected by most conventional journals. Papers in Medical Hypotheses take a standard scientific form in terms of style, structure and referencing. The journal therefore constitutes a bridge between cutting-edge theory and the mainstream of medical and scientific communication, which ideas must eventually enter if they are to be critiqued and tested against observations. Submitted manuscripts will be reviewed by the Editor and external reviewers to ensure their scientific merit. All reviewers will be fully aware of the Aims and Scope of the Journal and will be judging the premise, originality and plausibility of the hypotheses submitted. Abstracting/indexing Medical Hypotheses is indexed and abstracted in: Science Citation Index, Index Medicus/Medline, Adonis, BIOSIS, Chemical Abstracts, Elsevier BIOBASE/Current Awareness in Biological Sciences, Current Contents/Clinical Medicine, Current Contents/Life Sciences, EMBASE/Excerpta Medica, Medical Documentation Service, Reference Update, Research Alert, SciSearch, UMI (Microfilm), Russian Academy of Sciencehttp://www.medical-hypotheses.com/?rss=yesElsevier Inc.en © 2010 Published by Elsevier Inc. All rights reserved. Medical Hypotheses0306-9877754October 2010 © 2010 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.medical-hypotheses.com/article/PIIS030698771000277X/abstract?rss=yesTitle page/Editorial Board10.1016/S0306-9877(10)00277-XMedical Hypotheses 75, 4 (2010)2010-10-01Medical Hypotheses2010-10-01754S0306-9877(10)X0009-3iihttp://www.medical-hypotheses.com/article/PIIS0306987710001301/abstract?rss=yesSummary: The hypothesis proposed in this article is that a haemodynamic mechanism may cause Amyotrophic Lateral Sclerosis (ALS). The hypothesis is synthesized from three separate streams of medical research: (1) multiple sclerosis (MS) research; (2) ALS research; (3) atherosclerosis research. Each research stream was reviewed as prerequisite for proposing the hypothesis. A vascular mechanism for MS was first advanced in the medical literature 130years ago. Seventy years ago researchers knew that the plaques aligned along a central vein, and the wall of that central vein was damaged and leaky. Twenty-five years ago the refluxing blood mechanism was proposed. Zamboni imaged the veins of MS patients in 2007 and saw stenoses, twistings, and membrane blockages in the jugular, azygous, and vertebral veins, and refluxing venous blood upstream of the constrictions. The refluxing blood damages the blood–brain–barrier (BBB) of the veins. Leakage of blood components into the central nervous system then causes the plaques in the brains of MS people. Zamboni dilated the venous constrictions endovascularly, and the MS symptoms and brain plaques diminished dramatically. ALS research has recently revealed that this disease is started by blood–spinal cord–barrier (BSCB) damage. The ALS mutant mouse shows BSCB damage and down regulation of tight junction proteins Occludin and ZO-1 before motor neuron harm. Samplings of ALS patients’ spinal cords show downregulation of mRNA for tight junction proteins compared to controls. Atherosclerosis research provides the mechanism for how the refluxing blood breaks the tight junctions between the endothelial cells of the veins. Atherosclerosis research on blood flow effects shows that normal pulsatile laminar blood flow is necessary for maintenance of the tight junctions between endothelial cells. Abnormal flow conditions, such as turbulent, stopped, or reversed flow, cause downregulation of tight junction proteins Occludin and ZO-1. Blood flow (haemodynamic) effects explain the BBB damage in MS and may explain the BSCB damage in ALS. The hypothesis: ALS is caused by constrictions in veins draining the spinal cord and brain, which cause venous reflux, which downregulates tight junction proteins Occludin and ZO-1, which leads to breaks in the tight junctions between endothelial cells in the veins, which leads to leakage of toxic blood components into CNS tissue. The consequences of the hypothesis are discussed. If a venous constriction can be reached endovascularly it can be dilated, and such dilation may constitute cure of ALS.A possible haemodynamic mechanism for Amyotrophic Lateral SclerosisRoger W. Arhart10.1016/j.mehy.2010.03.017Medical Hypotheses 75, 4 (2010)2010-04-20Medical Hypotheses2010-04-20754S0306-9877(10)X0009-3Articles341346http://www.medical-hypotheses.com/article/PIIS0306987710001313/abstract?rss=yesSummary: Cerebral ischemia, a phenomenon of reduction in cerebral blood flow, accounts for approximately 80% of all strokes, the third leading cause of death and the leading cause of adult disability. Cerebral ischemia causes heterogeneous changes in tissue oxygenation and cellular metabolism. Focal brain ischemia induces a profound and long-lasting inflammatory reaction which is dominated by macrophages derived from both resident microglia and circulating monocytic precursors.Bone marrow and spleen serve as a reservoir for hematopoietic progenitor cells, especially in rodents. Spleen-derived mononuclear cells home to the site of vascular injury and reduced neointima formation. The migration and engraftment of systematically administered spleen-derived mononuclear cells can be visualized in the post-ischemic brain. Therefore, we hypothesise that removal of the spleen may possibly decrease the production of mononuclear cells, and thus hinder or relieve the inflammatory reaction occured after cerebral ischemia/reperfusion injury. So, the splenectomy may be a prophylactic treatment method for cerebral ischemia.Splenectomy may be a prophylactic treatment for cerebral ischemia?Yusuf Izci10.1016/j.mehy.2010.03.018Medical Hypotheses 75, 4 (2010)2010-04-09Medical Hypotheses2010-04-09754S0306-9877(10)X0009-3Articles347349http://www.medical-hypotheses.com/article/PIIS0306987710001350/abstract?rss=yesSummary: Obesity represents a crucial social problem in developed countries as a cause of multiple metabolic abnormalities. The exact etiology of this multifactorial disease is still unknown. The impact of dietary habits and lifestyle is currently under investigation but the role of other predisposing factors, such as genetic determinants and familial history, needs still to be elucidated. Significant alterations in the composition of the intestinal microbiota have been recently identified in obese mice, suggesting an involvement of gut microbes in obesity. In humans, obese subjects are supposed to have a more efficient flora in energy extraction from food, due to the detection of quantitative differences in the major bacterial groups in obese subjects compared to lean ones. Despite these observations, the homologies in gut microbiota between obese adults and their lean relatives have never been investigated in details. Few reports about the detection of common microbial profiles between members of the same family have been published in the past but only one recent scientific article, investigating the presence of a common core microbiota between obese and lean twins, correlates genetic background and gut microflora as significant variables in obesity.The hypothesis suggested herein is that the identification of a familial-specific core microbiota could be precious in order to identify key-bacterial groups to be used as biomarkers for the evaluation of predisposition to obesity.A common core microbiota between obese individuals and their lean relatives? Evaluation of the predisposition to obesity on the basis of the fecal microflora profileM. Elli, O. Colombo, A. Tagliabue10.1016/j.mehy.2010.03.022Medical Hypotheses 75, 4 (2010)2010-04-12Medical Hypotheses2010-04-12754S0306-9877(10)X0009-3Articles350352http://www.medical-hypotheses.com/article/PIIS0306987710001507/abstract?rss=yesSummary: Tungsten filament lamps are rapidly being displaced from the market-place by compact fluorescent lamps. Although the colour temperature and total luminous output of a fluorescent lamp may be similar to that of an incandescent lamp, the output spectrum is very different. The peaks of the mercury vapour spectrum at 365.4nm (UV) and at 435.8nm (blue) are close to the peak fluorescence excitation wavelengths in the human lens, and it has been shown that such fluorescence can lower sensitivity to low contrast objects. This effect could also explain the reported preference for brown, red and yellow tinted lenses often reported by elderly patients, as these coincidentally block the ultraviolet and blue exciting wavelengths.Low energy lamps and eye lens autofluorescenceGlyn Walsh, E Ian Pearce10.1016/j.mehy.2010.03.024Medical Hypotheses 75, 4 (2010)2010-04-14Medical Hypotheses2010-04-14754S0306-9877(10)X0009-3Articles353355http://www.medical-hypotheses.com/article/PIIS0306987710001556/abstract?rss=yesSummary: Neuronal mechanisms underlying addiction have been attracting attention in neurobiology, economics, neuropsychiatry, and neuroeconomics. This paper proposes a possible link between economic theory of addiction and neurobiological theory of bidirectional synaptic plasticity based on recent findings in neuroeconomics and neurobiology of addiction. Furthermore, it is suggested that several neurobiological substrates such as cortisol (a stress hormone), NMDA and AMPA receptors/subunits and intracellular calcium in the postsynaptic neurons are critical factors determining parameters in Becker and Murphy’s economic theory of addiction. Future directions in the application of the theory to studies in neuroeconomics and neuropsychiatry of addiction and its relation to stress at the molecular level are discussed.A neuroeconomic theory of bidirectional synaptic plasticity and addictionTaiki Takahashi10.1016/j.mehy.2010.03.029Medical Hypotheses 75, 4 (2010)2010-04-15Medical Hypotheses2010-04-15754S0306-9877(10)X0009-3Articles356358http://www.medical-hypotheses.com/article/PIIS0306987710001581/abstract?rss=yesSummary: Bayesian phylogenetic analysis of the haemagglutinin and neuraminidase proteins of influenza A virus demonstrates that their respective most recent common ancestors (MRCAs) both existed approximately 1000years ago. Most of the bifurcations within the haemagglutinin and neuraminidase phylogenetic trees occurred within a time window that can be dated with 95% confidence to the years 1411–1932 of the Common Era (AD) for haemagglutinin and 1366–1874 AD for neuraminidase. This subtype diversification episode is temporally congruent with the “Little Ice Age”, a period of climatic cooling over the northern hemisphere. Furthermore, Bayesian probability mean ages for the bifurcation points within the haemagglutinin tree indicate two bursts of diversification from 1672 to 1715 AD and from 1825 to 1868 AD. The first of these follows in the wake of the coldest epoch in the Little Ice Age, and the second overlaps a later cooling episode. Since climate change is known to affect migration patterns in the reservoir host of influenza A, the aquatic wildfowl, and allopatric cladogenesis following population disruption is well supported in the evolutionary literature, a mechanism is proposed linking the Little Ice Age to influenza subtype diversification via ecological disruption of the wildfowl annual cycle. The suggestion that past climate change has impacted on influenza evolution implies that current global warming may cause a further burst of influenza subtype diversification with possible serious epidemiological consequences becoming apparent in the 22nd and 23rd centuries.The Little Ice Age and the emergence of influenza ADerek Gatherer10.1016/j.mehy.2010.03.032Medical Hypotheses 75, 4 (2010)2010-04-20Medical Hypotheses2010-04-20754S0306-9877(10)X0009-3Articles359362http://www.medical-hypotheses.com/article/PIIS0306987710001593/abstract?rss=yesSummary: There are several hypotheses which explain the de-pigmentation of humans. The most prominent environmental explanation is that reduced endogenous vitamin D production due to diminished radiation at higher latitudes had a deleterious impact on fitness. This drove de-pigmentation as an adaptive response. A model of natural selection explains the high correlations found between low vitamin D levels and ill health, as vitamin D’s role in immune response has clear evolutionary implications. But recent genomic techniques have highlighted the likelihood that extreme de-pigmentation in Eurasia is a feature of the last 10,000years, not the Upper Pleistocene, when modern humans first settled northern Eurasia. Additionally the data imply two independent selection events in eastern and western Eurasia. Therefore new parameters must be added to the model of natural selection so as to explain the relatively recent and parallel adaptive responses. I propose a model of gene-culture co-evolution whereby the spread of agriculture both reduced dietary vitamin D sources and led to more powerful selection on immune response because of the rise of infectious diseases with greater population densities. This model explains the persistence of relatively dark-skinned peoples at relatively high latitudes and the existence of relatively light-skinned populations at low latitudes. It also reinforces the importance of vitamin D as a micronutrient because of the evidence of extremely powerful fitness implications in the recent human past of pigmentation.Diet, disease and pigment variation in humansR. Khan, B.S. Razib Khan10.1016/j.mehy.2010.03.033Medical Hypotheses 75, 4 (2010)2010-04-21Medical Hypotheses2010-04-21754S0306-9877(10)X0009-3Articles363367http://www.medical-hypotheses.com/article/PIIS0306987710001623/abstract?rss=yesSummary: Ventricular tachyarrhythmias are life threatening cardiac arrhythmias and are the most common causes of sudden cardiac death. Greater post-infarction left ventricular remodeling has been shown to have a greater preponderance of ventricular arrhythmias. The hypothesis herein is that adverse structural and electrophysiological remodeling at non-infarcted regions after myocardial infarction constitutes the arrhythmogenic substrate responsible for clinically occurring ventricular arrhythmias leading to sudden cardiac death. Post-infarction patients with more severe left ventricular remodeling (regional hypertrophy) at sites remote to infarction scar might have the highest risk for sudden cardiac death due to lethal ventricular arrhythmias. In the hypertrophic non-infarcted zone, larger action potential duration and repolarization heterogeneity is not in self arrhythmogenic, but can predispose towards arrhythmia development under certain condition, such as transient myocardial ischemia. We should draw more attention to apparently “normal” non-infarction region for further understanding the mechanism of sudden cardiac death.Remodeled left ventricular myocardium remote to infarction sites is the arrhythmogenic substrate for sudden cardiac deathChin-Feng Tsai, Kwo-Chang Ueng, Der-Jinn Wu, Tsung-Po Tsai, Chung-Sheng Lin10.1016/j.mehy.2010.03.036Medical Hypotheses 75, 4 (2010)2010-04-20Medical Hypotheses2010-04-20754S0306-9877(10)X0009-3Articles368371http://www.medical-hypotheses.com/article/PIIS0306987710001635/abstract?rss=yesSummary: “President John F. Kennedy’s death was a neurotoxin-assisted homicide” is the hypothesis of this study.A review of medical evidence demonstrates evidence of a neurotoxin-assisted homicide. The convergence of three independent actions, or the signature traits of a neurotoxin-assisted homicide- the emergence of neurological signs consistent with a neurotoxin-induced paralysis, the induction of a small neck wound consistent with a flechette-transported neurotoxin entry wound, and the execution of a coverup to eliminate neurotoxin evidence, supports this hypothesis.This review suggests, JFK’s death had all the signature traits of a neurotoxin-assisted homicide.President Kennedy’s death: A poison arrow-assisted homicideAlen J. Salerian10.1016/j.mehy.2010.03.037Medical Hypotheses 75, 4 (2010)2010-05-24Medical Hypotheses2010-05-24754S0306-9877(10)X0009-3Articles372377http://www.medical-hypotheses.com/article/PIIS0306987710001751/abstract?rss=yesSummary: A whole host of epidemiological studies have reported lower cancer rates and mortality in high-altitude regions. These studies are reviewed and discussed in detail. Evidence for the salutary role of vitamin D in protecting against cancer and other maladies will also be reviewed and discussed. The dependence of vitamin D production on sunlight and its enhancement with altitude will be demonstrated. The hypothesis is advanced and developed that the lower cancer rates observed at high altitudes arise from enhanced sunlight-induced vitamin D production levels. Protective vitamin D mechanisms which support this hypothesis as well as other supportive medical evidence are also presented.Cancer protection related to solar ultraviolet radiation, altitude and vitamin DDaniel P. Hayes10.1016/j.mehy.2010.04.001Medical Hypotheses 75, 4 (2010)2010-04-20Medical Hypotheses2010-04-20754S0306-9877(10)X0009-3Articles378382http://www.medical-hypotheses.com/article/PIIS0306987710001763/abstract?rss=yesSummary: Thyroid changes are considered to be normal events that happen as a large maternal multiorganic adjustment to pregnancy. However, hyperthyroidism occurs in pregnancy with clinical presentation similar to hyperemesis gravidarum (HG) and pregnancy itself. Moreover, 10% of women with HG will continue to have symptoms throughout the pregnancy suggesting that the underlying cause might not be elevation of human chorionic gonadotropin in the first trimester. Variable frequency of both hyperthyroidism and HG worldwide might suggest the puzzlement of inclusion criteria for both diagnoses enhanced by the alternation of thyroid hormone levels assessed in normal pregnancy. Increased number of hyperthyroidism among women population without the expected rise in gestational hyperthyroidism encouraged us for creating the hypotheses that hyperthyroidism could be underestimated in normal pregnancy and even misdiagnosed as HG. This hypothesis, if confirmed, might have beneficial clinical implications, such as better detection of hyperthyroidism in pregnancies, application of therapy when needed with the reduction of maternal or fetal consequences.Is hyperthyroidism underestimated in pregnancy and misdiagnosed as hyperemesis gravidarum?Ana Tikvica Luetic, Berivoj Miskovic10.1016/j.mehy.2010.04.002Medical Hypotheses 75, 4 (2010)2010-05-17Medical Hypotheses2010-05-17754S0306-9877(10)X0009-3Articles383386http://www.medical-hypotheses.com/article/PIIS0306987710001775/abstract?rss=yesSummary: Einstein is often quoted to have said that without the bee, mankind would have but 4years to live. It is highly unlikely that he made this comment, which was even mentioned in a Lancet article on honey bees. However, the current vanishing of the bees can have serious consequences for human health, because 35% of the human diet is thought to benefit from pollination. Colony collapse disorder (CCD) in honey bees is characterized by the rapid decline of the adult bee population, leaving the brood and the queen poorly or completely unattended, with no dead bodies in or around the hive. A large study found no evidence that the presence or amount of any individual pesticide or infectious agent occurred more frequently or abundantly in CCD-affected colonies. The growing consensus is that honey bees are suffering from comprised immune systems, which allow various infectious pathogens to invade. The question remains, what causes immunosuppression in many colonies of Apis mellifera in North America and Europe? Telomeres are protective DNA structures located at eukaryotic chromosome tips that shorten in the somatic tissues of animals with age. Lifelong tissue regeneration takes place in Apis mellifera, and worker bees have been shown to senesce. In humans, a vast amount of literature has accumulated on exhausted telomere reserves causing impaired tissue regeneration and age-associated diseases, specifically cancer and immunosuppression. Therefore, we propose a new causative mechanism for the vanishing of the bees: critically short telomeres in long-lived winter bees. We term this the telomere premature aging syndrome.Vanishing honey bees: Is the dying of adult worker bees a consequence of short telomeres and premature aging?Reinhard Stindl, Wolfgang Stindl10.1016/j.mehy.2010.04.003Medical Hypotheses 75, 4 (2010)2010-05-18Medical Hypotheses2010-05-18754S0306-9877(10)X0009-3Articles387390http://www.medical-hypotheses.com/article/PIIS0306987710001799/abstract?rss=yesSummary: Bacterial biofilms have been found in many human bacterial infectious processes including chronic rhinosinusitis. It was found also at the surface of nasal polyps, and both at the surface of the nasal part and the stalk of the antrochoanal polyp.However, our recent research clearly demonstrated the presence of the biofilm at the surface of the mucosa of the healthy paranasal sinuses as well.Our hypothesis therefore is that the biofilm in the nose and paranasal sinuses is nothing else but regular respiratory mucosal blanket, a part of the mucociliary system itself, containing variable number of bacteria.Biofilm – The other name for the regular mucosal blanketRanko Mladina, Neven Skitarelić10.1016/j.mehy.2010.04.005Medical Hypotheses 75, 4 (2010)2010-05-13Medical Hypotheses2010-05-13754S0306-9877(10)X0009-3Articles391392http://www.medical-hypotheses.com/article/PIIS0306987710001805/abstract?rss=yesSummary: Because obesity is a risk factor for many serious illnesses such as diabetes, better understandings of obesity and eating disorders have been attracting attention in neurobiology, psychiatry, and neuroeconomics. This paper presents future study directions by unifying (i) economic theory of addiction and obesity , and (ii) recent empirical findings in neuroeconomics and neurobiology of obesity and addiction. It is suggested that neurobiological substrates such as adiponectin, dopamine (D2 receptors), endocannabinoids, ghrelin, leptin, nesfatin-1, norepinephrine, orexin, oxytocin, serotonin, vasopressin, CCK, GLP-1, MCH, PYY, and stress hormones (e.g., CRF) in the brain (e.g., OFC, VTA, NAcc, and the hypothalamus) may determine parameters in the economic theory of obesity. Also, the importance of introducing time-inconsistent and gain/loss-asymmetrical temporal discounting (intertemporal choice) models based on Tsallis’ statistics and incorporating time-perception parameters into the neuroeconomic theory is emphasized. Future directions in the application of the theory to studies in neuroeconomics and neuropsychiatry of obesity at the molecular level, which may help medical/psychopharmacological treatments of obesity (e.g., with sibutramine), are discussed.Toward molecular neuroeconomics of obesityTaiki Takahashi10.1016/j.mehy.2010.04.006Medical Hypotheses 75, 4 (2010)2010-05-12Medical Hypotheses2010-05-12754S0306-9877(10)X0009-3Articles393396http://www.medical-hypotheses.com/article/PIIS0306987710001817/abstract?rss=yesSummary: There is a rising interest towards the old drug, nicotinic acid (niacin, vitamin B3), because at pharmacological concentrations it has a beneficial effect on HDL cholesterol. Its use, however, was limited due to its adverse effect, flushing. When the mechanism of flushing was solved, a combination of niacin and DP1 receptor antagonist or prostaglandin inhibitor is used, there has been a comeback of niacin with extensive clinical trials. This paper argues that the new strategy with niacin for the prevention of atherosclerosis should be re-evaluated, because vasodilatation of the peripheral vessels might be crucially important in the early primary prevention according to our “vasa vasorum hypoxia” hypothesis.Niacin in the prevention of atherosclerosis: Significance of vasodilatationP. Tuohimaa, M. Järvilehto10.1016/j.mehy.2010.04.007Medical Hypotheses 75, 4 (2010)2010-05-10Medical Hypotheses2010-05-10754S0306-9877(10)X0009-3Articles397400http://www.medical-hypotheses.com/article/PIIS0306987710001829/abstract?rss=yesSummary: Sleep is an enigma because we all know what it means and does to us, yet a scientific explanation for why animals including humans need to sleep is still lacking. However, the enigma can be resolved if the animal body is regarded as a purposeful machine whose moving parts are coordinated with spatial information provided by a disparate array of sense organs. The performance of all complex machines deteriorates with time due to inevitable instrument drift of the individual sensors combined with wear and tear of the moving parts which result in declining precision and coordination. Peak performance is restored by servicing the machine, which involves calibrating the sensors against baselines and standards, then with one another, and finally readjusting the connections between instruments and moving parts. It follows that the animal body and its sensors will also require regular calibration of sense organs and readjustment of brain–body connections which will need to be carried out while the animal is not in functional but in calibration mode. I suggest that this is the core function of sleep.This recalibration hypothesis of sleep can be tested subjectively. We all know from personal experience that sleep is needed to recover from tiredness that sets in towards the end of a long day. This tiredness, which is quite distinct from mental or muscular exhaustion caused by strenuous exertion, manifests itself in deteriorating general performance: the sense organs lose precision, movements become clumsy and the mind struggles to maintain focus. We can all agree that sleep sharpens the sense organs and restores agility to mind and body. I now propose that the sense of freshness and buoyancy after a good night’s sleep is the feeling of recalibrated sensory and motor systems.The hypothesis can be tested rigorously by examining available data on sleep cycles and stages against this background. For instance, REM and deep sleep cycles can be interpreted as successive, separate calibration runs of the vestibulo-ocular reflex and the sensory-motor systems, respectively, amongst other functions running in parallel, such as dreaming. Because the split-second connections between sensory information and emotional responses will also require calibration, some aspects of dreaming could be interpreted in this light. Much of the baffling behaviour and patterns of brain activity of sleeping animals and humans make sense in the framework of this technological paradigm since different animal lineages will have evolved different techniques to achieve calibration.Recalibrating sleep: Is recalibration and readjustment of sense organs and brain–body connections the core function of sleep?Victor Smetacek10.1016/j.mehy.2010.04.008Medical Hypotheses 75, 4 (2010)2010-05-12Medical Hypotheses2010-05-12754S0306-9877(10)X0009-3Articles401404http://www.medical-hypotheses.com/article/PIIS0306987710001842/abstract?rss=yesSummary: Tooth movement occurs as a consequence of periodontal tissue remodeling. The goal of every orthodontist is to investigate better approaches to accelerate tooth movement. Estrogen, by binding with its receptors in periodontal tissue, regulates the remodeling of alveolar bones, promotes bone formation, and inhibits bone resorption. Estrogen secretion in vivo is characterized by a nearly lunar rhythm. The estrogen expression level is low during menstruation and the luteal phase, and reaches the highest at 1–2days before ovulation. Estrogen physiological fluctuations can cause physiological fluctuations in the serum markers of bone turnover. Therefore, orthodontic therapy should be planned according to the menstrual cycle since tooth movement, under the application of force, is faster during low estrogen levels. In this paper, we propose a hypothesis that application of orthodontic force after each ovulation may promote tooth movement, thereby shortening the course of orthodontic treatment.A new approach to accelerate orthodontic tooth movement in women: Orthodontic force application after ovulationXiaomei Xu, Qing Zhao, Siwei Yang, Guangxin Fu, Yangxi Chen10.1016/j.mehy.2010.04.010Medical Hypotheses 75, 4 (2010)2010-05-18Medical Hypotheses2010-05-18754S0306-9877(10)X0009-3Articles405407http://www.medical-hypotheses.com/article/PIIS0306987710001787/abstract?rss=yesThere are studies on laterality of sleeping positions and their association with diseases on a particular side of the body. What draws our interest is the fact that, the preferred sleeping position keeps changing as the age advances. Children prefer to sleep in prone position than the adults. Adults spend more time sleeping in the lateral position . Supine position is usually preferred by the elderly. Supine position is understood to be a position of ‘easily’ resting on the back, especially during sleep. Elderly people prefer this position for the reason of resting is understandable. The reason why elderly people avoid sleeping in prone position, while young adults do not, is not clear. Obesity, short durations of sleep, age related muscular and skeletal changes, are the probable reasons, which will never completely justify their preference to sleep in supine position.Sleeping position and the functioning of the brain: Is there a link?Jyothi M.P. D’Souza, Deepak Herald D’Souza10.1016/j.mehy.2010.04.004Medical Hypotheses 75, 4 (2010)2010-05-19Medical Hypotheses2010-05-19754S0306-9877(10)X0009-3Letter to the Editor408408