Medical Hypotheses Journal Impact Factor & Information

Publisher: Elsevier

Journal description

The purpose of Medical Hypotheses is to provide a forum for the presentation and criticism of ideas in medicine and the related biomedical sciences. Most biomedical journals will publish ideas only in papers which also report observations. As the best scientists have repeatedly emphasized, this gives a misleading impression of the process of discovery. The ideas usually come first and they determine what observations should and will be made. Although fully acknowledged in other sciences, this central role of ideas in scientific progress is only now beginning to be widely recognized in medicine. Ideas occur to many people not in a position to test them experimentally. Ideas frequently require much fuller exposition than is allowed in the discussion section of an experimental paper. Ideas should be open to comment by scientists who have not done experimental work in the field. Medical Hypotheses will publish ideas or criticisms of ideas from any person, irrespective of whether any experimental testing of the ideas has been performed by the writer. Medical Hypotheses will also publish letters which comment on articles in the journal. Medical Hypotheses is the only journal fully devoted to the publication of ideas in the biomedical sciences. The justification for its existence is discussed in the editorial printed at the beginning of the first issue (January-February, 1975). If you feel that the aims of Medical Hypotheses are important and worthwhile, please encourage your library to subscribe to it.

Current impact factor: 1.07

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 1.074
2013 Impact Factor 1.152
2012 Impact Factor 1.054
2011 Impact Factor 1.15
2010 Impact Factor 1.389
2009 Impact Factor 1.393
2008 Impact Factor 1.416
2007 Impact Factor 1.276
2006 Impact Factor 1.299
2005 Impact Factor 0.92
2004 Impact Factor 0.607
2003 Impact Factor 0.684
2002 Impact Factor 0.725
2001 Impact Factor 0.745
2000 Impact Factor 0.76
1999 Impact Factor 0.678
1998 Impact Factor 0.628
1997 Impact Factor 0.53

Impact factor over time

Impact factor

Additional details

5-year impact 1.13
Cited half-life 6.90
Immediacy index 0.24
Eigenfactor 0.01
Article influence 0.29
Website Medical Hypotheses website
Other titles Medical hypotheses
ISSN 0306-9877
OCLC 1357097
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The etiology of myalgic encephalomyelitis also known as chronic fatigue syndrome or ME/CFS has not been established. Controversies exist over whether it is an organic disease or a psychological disorder and even the existence of ME/CFS as a disease entity is sometimes denied. Suggested causal hypotheses have included psychosomatic disorders, infectious agents, immune dysfunctions, autoimmunity, metabolic disturbances, toxins and inherited genetic factors. Clinical, immunological and epidemiological evidence supports the hypothesis that: ME/CFS is an infectious disease; the causal pathogen persists in patients; the pathogen can be transmitted by casual contact; host factors determine susceptibility to the illness; and there is a population of healthy carriers, who may be able to shed the pathogen. ME/CFS is endemic globally as sporadic cases and occasional cluster outbreaks (epidemics). Cluster outbreaks imply an infectious agent. An abrupt flu-like onset resembling an infectious illness occurs in outbreak patients and many sporadic patients. Immune responses in sporadic patients resemble immune responses in other infectious diseases. Contagion is shown by finding secondary cases in outbreaks, and suggested by a higher prevalence of ME/CFS in sporadic patients’ genetically unrelated close contacts (spouses/partners) than the community. Abortive cases, sub-clinical cases, and carrier state individuals were found in outbreaks. The chronic phase of ME/CFS does not appear to be particularly infective. Some healthy patient-contacts show immune responses similar to patients’ immune responses, suggesting exposure to the same antigen (a pathogen). The chronicity of symptoms and of immune system changes and the occurrence of secondary cases suggest persistence of a causal pathogen. Risk factors which predispose to developing ME/CFS are: a close family member with ME/CFS; inherited genetic factors; female gender; age; rest/activity; previous exposure to stress or toxins; various infectious diseases preceding the onset of ME/CFS; and occupational exposure of health care professionals. The hypothesis implies that ME/CFS patients should not donate blood or tissue and usual precautions should be taken when handling patients’ blood and tissue. No known pathogen has been shown to cause ME/CFS. Confirmation of the hypothesis requires identification of a causal pathogen. Research should focus on a search for unknown and known pathogens. Finding a causal pathogen could assist with diagnosis; help find a biomarker; enable the development of anti-microbial treatments; suggest preventive measures; explain pathophysiological findings; and reassure patients about the validity of their symptoms.
    Medical Hypotheses 10/2015; 85(6). DOI:10.1016/j.mehy.2015.10.011
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    ABSTRACT: Atherosclerosis is one of the major cause of mortality in developed countries. The characteristic lesion of atherosclerosis is the atheroma or plaque that forms through thickening of the inner layer of the vessel wall (called the intima). The development of stent in 1980s revolutionised treatment of cardiovascular diseases, including atherosclerosis. However the advent of stenting was hindered by the new problem of in-stent restenosis. It was demonstrated that in-stent restenosis was the result of a new pathology in the form of neointimal hyperplasia, which was a maladaptive healing response to bare-metal stent implantation. Recent evidence suggests that although drug-eluting stent (DES) have reduced restenosis rates, important concerns have been raised regarding increased late stent thrombosis, myocardial infarction and death. With advances in nanotechnology and smart materials, covered stents has been proposed to overcome this problem. This is due to in-stent late restenosis and thromboses are mainly caused by smooth muscle cells (SMC) proliferation. Studies showed that there is a relation between high low-density lipoprotein (LDL) and lipoprotein (a) [Lp(a)] level in blood stream and chance of in-stent restenosis, moreover studies show that Lp(a) could stimulate SMC proliferation. We hypothesis development of covered stent with novel design and use of smart materials which could adsorb cholesterol and prevent contact between Lp(a) and vessel wall to overcome problem indicated in DES. In addition cost of stents will significantly reduce by elimination of drugs as well as complex manufacturing of the drug incorporation.
    Medical Hypotheses 09/2015; 85(6). DOI:10.1016/j.mehy.2015.08.023
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    ABSTRACT: Patients with essential hypertension may show neurovascular compression (NVC) at the rostral ventrolateral medulla oblongata (RVLM). Ectatic loops of the vertebral artery (VA) or the inferior posterior cerebellar artery (PICA) cause NVC. This study aims to show the existence and morphology of NVC in patients with gestation-induced hypertension. 17 females were prospectively examined between 19 + 0 and 35 + 6 weeks of gestation. 3 patients with chronic hypertension (group A), 10 patients with preeclampsia (group B), 3 patients with superimposed preeclampsia (chronic hypertension with preeclampsia; group C) and one normotensive patient were included. Groups B and C represented patients with gestation-induced hypertension. All 17 patients underwent imaging by high resolution magnetic resonance imaging (MR-CISS, constructive interference in the steady state). Image processing was done with segmentation and three-dimensional (3D)-visualization was implemented with direct volume rendering of the individual neurovascular details of each patient. 9 of 17 patients (53%) showed NVC of the RVLM. Right-sided NVC was seen in 7 patients (41%). Left-sided NVC was seen in 6 patients (35%). Bilateral NVC was seen in 4 patients (24%). NVC was missing in 8 of the examined 17 patients (47%). The existence of NVC with high-resolution MRI was analyzed in gestation-induced hypertensive pregnant females for the first time. Neurovascular conflicts were seen in hypertensive pregnants. It is possible that NVC is potentially associated in patients with gestation-induced hypertension.
    Medical Hypotheses 06/2015; 84(6). DOI:10.1016/j.mehy.2015.03.024
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    ABSTRACT: Spermatogenesis is a highly regulated process that takes place in the seminiferous tubules of testis. This process initiates at puberty with differentiation of spermatogonia and their meiotic entry. The initiation of spermatogenesis depends on gonadotropins secreted by the pituitary gland; i.e., follicle-stimulating hormone (FSH) and luteinizing hormone (LH). In the absence of FSH and LH only premeiotic germ cells are present in the testis. The prepubertal development phase in juvenile testis is characterized by a protracted hypogonadotropic state, which only consists of Sertoli and undifferentiated germ cells in the seminiferous epithelium. All germ cells in the juvenile testis are undifferentiated spermatogonia, which are proliferating in a relatively gonadotropin-independent manner. It has been revealed that vitamin A deficient (VAD) animals are also infertile, and only premeiotic germ cells (undifferentiated spermatogonia) are present in their seminiferous tubules. The developmental block in VAD animal can be removed by administration of retinol and germ cell differentiation reinitiates in a synchronous manner. Recent studies have revealed that the biologically active form of vitamin A, retinoic acid (RA), regulates germ cell differentiation and lead to the generation of the cycle of the seminiferous epithelium and normal spermatogenic wave. Recent study has shown that synchronous spermatogenesis at neonatal mouse, but not after initiation of meiosis, can be induced by treating vitamin A sufficient males with RA. The treatment of neonatal males at different ages with exogenous RA has revealed that although RA is sufficient to induce differentiation of spermatogonial at 4dpp and earlier, it fails to alter asynchrony and it does not irreversibly cause a spermatogonial differentiation. These observations led us to suggest that gonadotropins trigger differentiation of spermatogonia and spermatogenesis through regulation of RA signaling in the seminiferous epithelium of the adult testis. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Medical Hypotheses 06/2015; 85(3). DOI:10.1016/j.mehy.2015.05.021
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    ABSTRACT: Epidemiological studies have found a negative association between cigarette smoking and Parkinson's disease (PD): PD patients are approximately 50% less likely to have smoked cigarettes than age- and sex-matched controls. In both women and men, the PD protection effect of smoking may be explained by higher levels of phosphate in serum (S-P) and triglycerides (S-TG) in smokers compared to non-smokers. That is, the protecting effect from smoking could be mediated by either a high S-P or high S-TG levels. I suggest that higher S-P as the result of smoking may be associated with intracellular depletion of Pi in skeletal muscle and that this depletion of Pi is associated with increased availability of phosphate for the brain. This increased phosphate availability would protect against PD, as oxidative phosphorylation in the mitochondria is a central and persistent phenomenon in the pathogenesis cascade of PD. Phosphate is necessary for energy production in the form of creatine phosphate (CP) and adenosine-tri-phosphate (ATP) in the brain and skeletal muscle. As such, hypophosphatemia increases risk of cell death. In some clinical instances, this energy depletion may pre-dispose to dopamine neuron death. Mitochondrial dysfunction is associated with the generation of oxidative stress and mediates the induction of apoptosis. Studies with NMR spectroscopy reveal that an energy deficit in brain cells is a strong mark for PD although this differed for men and women. Compared to women, men had lower serum phosphate and ATP levels in the brain (about 15% lower). In addition to sex differences, age, stress, and malnutrition may cause low serum phosphate levels, a situation that could contribute to the lack of energy available to the brain and the risk of PD. As hypophosphatemia is present in overnutrition and has an inverse relation with a high BMI, both obesity and malnutrition are considered to be presumptive risk factor for PD. Copyright © 2015. Published by Elsevier Ltd.
    Medical Hypotheses 06/2015; 85(3). DOI:10.1016/j.mehy.2015.05.017
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    ABSTRACT: Inspite of having so much sunshine, Saudi Arabian population is suffering from the deficiency of the 'sunshine vitamin', vitamin D, measured in the serum as 25-OHD level. According to a recent report, about 83.6% of Saudi population is vitamin D deficient. 31.9% have severe, 32% have moderate and 19.7% have mild vitamin D deficiency (VDD). The severity of VDD differs with age, gender and region. Females are more severely vitamin D deficient than males. Various factors contributing towards it deficiency are linked to their housing designs, religious practices, lifestyle choices and dark skin color. The increasing incidences of breast, prostate and colon cancer among this society are also raising an alarm. The presence of vitamin D receptor (VDR) and the enzyme responsible for conversion of the 25(OH)D in its active metabolite 25(OH)2D3 in extra renal tissue shows the involvement of vitamin D in other diseases like cancer, diabetes, multiple sclerosis etc. About 2000 genes related to various types of diseases are found to be regulated by VDRs. These genes possess vitamin D responsive elements (VDREs) in their promoters. Studies on population of other regions also have shown correlation with low serum levels of 25(OH)D and certain diseases So, we hypothesized that vitamin D deficiencies might cause a higher prevalence of these diseases in the Kingdom. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Medical Hypotheses 04/2015; 85(2). DOI:10.1016/j.mehy.2015.04.006