Best Research Articles
Acta Clin Croat. 2013 Dec;52(4):464-71.
The role of complementary and alternative medicine in therapy of multiple sclerosis.
Kes VB, Cesarik M, Matovina LZ, Zavoreo I, Corić L, Drnasin S, Demarin V.
In the abstract found through the link located below, complementary and alternative therapies are sighted as being used by 70% of MS sufferers. The most common therapists provided are nutrition based focusing on reducing inflammation and resulting neurological damage. The therapies identified with the highest potential were those encouraging low fat diet, increased omega 3 fatty acids, increased antioxidant intake such as lipoic acid, and increased vitamin D.
http://www.ncbi.nlm.nih.gov/pubmed/24696997
The role of complementary and alternative medicine in therapy of multiple sclerosis.
Kes VB, Cesarik M, Matovina LZ, Zavoreo I, Corić L, Drnasin S, Demarin V.
In the abstract found through the link located below, complementary and alternative therapies are sighted as being used by 70% of MS sufferers. The most common therapists provided are nutrition based focusing on reducing inflammation and resulting neurological damage. The therapies identified with the highest potential were those encouraging low fat diet, increased omega 3 fatty acids, increased antioxidant intake such as lipoic acid, and increased vitamin D.
http://www.ncbi.nlm.nih.gov/pubmed/24696997
Mult Scler Relat Disord. 2013 Oct 1;2(4). doi: 10.1016/j.msard.2013.04.002.
Promoting return of function in multiple sclerosis: An integrated approach.
Gacias M1, Casaccia P2.Author information
Multiple sclerosis is a disease characterized by inflammatory demyelination, axonal degeneration and progressive brain atrophy. Most of the currently available disease modifying agents proved to be very effective in managing the relapse rate, however progressive neuronal damage continues to occur and leads to progressive accumulation of irreversible disability. For this reason, any therapeutic strategy aimed at restoration of function must take into account not only immunomodulation, but also axonal protection and new myelin formation. We further highlight the importance of an holistic approach, which considers the variability of therapeutic responsiveness as the result of the interplay between genetic differences and the epigenome, which is in turn affected by gender, age and differences in life style including diet, exercise, smoking and social interaction.
KEYWORDS: Axonal damage, Epigenetics, Multiple sclerosis, Neurodegeneration, Repair, Therapy, myelin
Promoting return of function in multiple sclerosis: An integrated approach.
Gacias M1, Casaccia P2.Author information
- 1Department of Neuroscience, Friedman Brain Institute, United States.
- 2Department of Neuroscience, Friedman Brain Institute, United States ; Department of Genetics and Multiscale Biology, Department of Neurology Icahn School of Medicine at Mount Sinai, United States.
Multiple sclerosis is a disease characterized by inflammatory demyelination, axonal degeneration and progressive brain atrophy. Most of the currently available disease modifying agents proved to be very effective in managing the relapse rate, however progressive neuronal damage continues to occur and leads to progressive accumulation of irreversible disability. For this reason, any therapeutic strategy aimed at restoration of function must take into account not only immunomodulation, but also axonal protection and new myelin formation. We further highlight the importance of an holistic approach, which considers the variability of therapeutic responsiveness as the result of the interplay between genetic differences and the epigenome, which is in turn affected by gender, age and differences in life style including diet, exercise, smoking and social interaction.
KEYWORDS: Axonal damage, Epigenetics, Multiple sclerosis, Neurodegeneration, Repair, Therapy, myelin
Genelabs Technologies, Inc., 505 Penobscot Drive, Redwood City, CA 94063
GL701 (DHEA, prasterone) for the Treatment of Systemic Lupus Erythematosus (SLE) in Women
6.2.11 Study 95-02 Conclusion
With respect to the objective of the study, improving SLE signs and/or symptoms, the GL701 group had
approximately a 35% increase in the proportion of responders, and a 24% decrease in proportion of
patients with definite flares. A responder in this study was defined as a patient whose disease activity was
stable or improved over the one year duration of study. Analysis of the individual components of the
responder definition demonstrated that not one of the 4 scoring instruments dominated the analysis, and
that those patients who were non-responders generally had worsening in 1 or 2 of the instruments. Therefore, the treatment effect resulted from the impact of all 4 scoring instruments, with the placebo patients having a higher rate of worsening on any one of the instruments. This suggests that the GL701 treatment effect was relatively broad, showing benefit in constitutional symptoms as well as various manifestations of disease activity. A general trend in favor of GL701 is seen for each of the four instruments used in the responder definition, with Patient VAS approaching statistical significance.
http://www.fda.gov/ohrms/dockets/ac/01/briefing/3740b1_01_gendlabs.pdf
GL701 (DHEA, prasterone) for the Treatment of Systemic Lupus Erythematosus (SLE) in Women
6.2.11 Study 95-02 Conclusion
With respect to the objective of the study, improving SLE signs and/or symptoms, the GL701 group had
approximately a 35% increase in the proportion of responders, and a 24% decrease in proportion of
patients with definite flares. A responder in this study was defined as a patient whose disease activity was
stable or improved over the one year duration of study. Analysis of the individual components of the
responder definition demonstrated that not one of the 4 scoring instruments dominated the analysis, and
that those patients who were non-responders generally had worsening in 1 or 2 of the instruments. Therefore, the treatment effect resulted from the impact of all 4 scoring instruments, with the placebo patients having a higher rate of worsening on any one of the instruments. This suggests that the GL701 treatment effect was relatively broad, showing benefit in constitutional symptoms as well as various manifestations of disease activity. A general trend in favor of GL701 is seen for each of the four instruments used in the responder definition, with Patient VAS approaching statistical significance.
http://www.fda.gov/ohrms/dockets/ac/01/briefing/3740b1_01_gendlabs.pdf
Am J Gastroenterol. 2000 Dec;95(12):3503-6.
Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome.
Pimentel M1, Chow EJ, Lin HC.Author information
METHODS: Two hundred two subjects in a prospective database of subjects referred from the community undergoing a lactulose hydrogen breath test for assessment of overgrowth were Rome I criteria positive for irritable bowel syndrome. They were treated with open label antibiotics after positive breath test. Subjects returning for follow-up breath test to confirm eradication of overgrowth were also assessed. Subjects with inflammatory bowel disease, abdominal surgery, or subjects demonstrating rapid transit were excluded. Baseline and after treatment symptoms were rated on visual analog scales for bloating, diarrhea, abdominal pain, defecation relief, mucous, sensation of incomplete evacuation, straining, and urgency. Subjects were blinded to their breath test results until completion of the questionnaire.
RESULTS: Of 202 irritable bowel syndrome patients, 157 (78%) had overgrowth. Of these, 47 had follow-up testing. Twenty-five of 47 follow-up subjects had eradication of small intestinal bacterial overgrowth. Comparison of those that eradicated to those that failed to eradicate revealed an improvement in irritable bowel syndrome symptoms with diarrhea and abdominal pain being statistically significant after Bonferroni correction (p < 0.05). Furthermore, 48% of eradicated subjects no longer met Rome criteria (chi2 = 12.0, p < 0.001). No difference was seen if eradication was not successful.
CONCLUSIONS: Small intestinal bacterial overgrowth is associated with irritable bowel syndrome. Eradication of the overgrowth eliminates irritable bowel syndrome by study criteria in 48% of subjects.
http://www.ncbi.nlm.nih.gov/pubmed/11151884
Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome.
Pimentel M1, Chow EJ, Lin HC.Author information
- 1Department of Medicine, Cedars-Sinai Medical Center, CSMC Burns & Allen Research Institute, and School of Medicine, University of California, Los Angeles, 90048, USA.
METHODS: Two hundred two subjects in a prospective database of subjects referred from the community undergoing a lactulose hydrogen breath test for assessment of overgrowth were Rome I criteria positive for irritable bowel syndrome. They were treated with open label antibiotics after positive breath test. Subjects returning for follow-up breath test to confirm eradication of overgrowth were also assessed. Subjects with inflammatory bowel disease, abdominal surgery, or subjects demonstrating rapid transit were excluded. Baseline and after treatment symptoms were rated on visual analog scales for bloating, diarrhea, abdominal pain, defecation relief, mucous, sensation of incomplete evacuation, straining, and urgency. Subjects were blinded to their breath test results until completion of the questionnaire.
RESULTS: Of 202 irritable bowel syndrome patients, 157 (78%) had overgrowth. Of these, 47 had follow-up testing. Twenty-five of 47 follow-up subjects had eradication of small intestinal bacterial overgrowth. Comparison of those that eradicated to those that failed to eradicate revealed an improvement in irritable bowel syndrome symptoms with diarrhea and abdominal pain being statistically significant after Bonferroni correction (p < 0.05). Furthermore, 48% of eradicated subjects no longer met Rome criteria (chi2 = 12.0, p < 0.001). No difference was seen if eradication was not successful.
CONCLUSIONS: Small intestinal bacterial overgrowth is associated with irritable bowel syndrome. Eradication of the overgrowth eliminates irritable bowel syndrome by study criteria in 48% of subjects.
http://www.ncbi.nlm.nih.gov/pubmed/11151884
Clinics (Sao Paulo). June 2010; 65-(6): 635-643
Possible Links Between Intestinal Permeability and Food Processing. A Potential Therapeutic Niche for Glutamine.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898551/
Possible Links Between Intestinal Permeability and Food Processing. A Potential Therapeutic Niche for Glutamine.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898551/
Can J Anaesth. 2012 Sep;59(9):875-81. doi: 10.1007/s12630-012-9748-y. Epub 2012 Jul 14.
Update on the pathogenesis of complex regional pain syndrome: role of oxidative stress.
Taha R1, Blaise GA.Author information
PURPOSE: Complex regional pain syndrome (CRPS) is a chronic inflammatory pain syndrome that affects one or more extremities of the body. It is characterized by burning pain and abnormalities in the sensory, motor, and autonomic nervous systems. This review illustrates how oxidative stress and nuclear factor erythroid 2-related factor (Nrf2) activation might contribute to understanding the etiopathogenesis of CRPS.
PRINCIPAL FINDINGS: The precise cause of CRPS remains unclear, and current treatments are not effective in many patients. The mechanism underlying CRPS may differ across patients and even within a single patient over time. Inflammatory and neuronal mechanisms have been suggested as key contributors to CRPS. Recent evidence demonstrates that oxidative stress is associated with clinical symptoms in patients with CRPS-I. Oxidative stress plays a key role in CRPS pathogenesis. The Nrf2 factor is a master regulator of the transcription of multiple antioxidants, which protects against oxidative stress and inflammation by inducing antioxidant and detoxifying genes through binding with an antioxidant response element. It has antinociceptive effects against inflammatory pain in an animal model.
CONCLUSION: This review summarises the effect of oxidative stress and mitochondrial dysfunction in the pathogenesis of CRPS. It also addresses the question of whether there is a potential role for Nrf2 (activated by pharmacological or nutritional activators) in alleviating the clinical features of CRPS or preventing its progression.
PMID: 22798149 [PubMed - indexed for MEDLINE]
Update on the pathogenesis of complex regional pain syndrome: role of oxidative stress.
Taha R1, Blaise GA.Author information
- 1Multinnova Medical Centre, Université de Montréal, Montreal, QC, Canada.
PURPOSE: Complex regional pain syndrome (CRPS) is a chronic inflammatory pain syndrome that affects one or more extremities of the body. It is characterized by burning pain and abnormalities in the sensory, motor, and autonomic nervous systems. This review illustrates how oxidative stress and nuclear factor erythroid 2-related factor (Nrf2) activation might contribute to understanding the etiopathogenesis of CRPS.
PRINCIPAL FINDINGS: The precise cause of CRPS remains unclear, and current treatments are not effective in many patients. The mechanism underlying CRPS may differ across patients and even within a single patient over time. Inflammatory and neuronal mechanisms have been suggested as key contributors to CRPS. Recent evidence demonstrates that oxidative stress is associated with clinical symptoms in patients with CRPS-I. Oxidative stress plays a key role in CRPS pathogenesis. The Nrf2 factor is a master regulator of the transcription of multiple antioxidants, which protects against oxidative stress and inflammation by inducing antioxidant and detoxifying genes through binding with an antioxidant response element. It has antinociceptive effects against inflammatory pain in an animal model.
CONCLUSION: This review summarises the effect of oxidative stress and mitochondrial dysfunction in the pathogenesis of CRPS. It also addresses the question of whether there is a potential role for Nrf2 (activated by pharmacological or nutritional activators) in alleviating the clinical features of CRPS or preventing its progression.
PMID: 22798149 [PubMed - indexed for MEDLINE]
J Immunol. 2012 Mar 1;188(5):2070-3. doi: 10.4049/jimmunol.1102835. Epub 2012 Jan 30.
Cutting edge: fasting-induced hypoleptinemia expands functional regulatory T cells in systemic lupus erythematosus.
Liu Y1, Yu Y, Matarese G, La Cava A. Author information
Fasting is beneficial in the prevention and amelioration of the clinical manifestations of autoimmune diseases including systemic lupus erythematosus. The mechanisms responsible for these effects are not well understood. During fasting, there is a dramatic reduction of the levels of circulating leptin, an adipokine with proinflammatory effects. Leptin also inhibits CD4(+)CD25(+)Foxp3(+) regulatory T cells, which are known to contribute significantly to the mechanisms of peripheral immune tolerance. In this study, we show that fasting-induced hypoleptinemia in (NZB × NZW)F(1) lupus-prone mice induced an expansion of functional regulatory T cells that was reversed by leptin replacement. The specificity of the findings was indicated by the lack of these effects in leptin-deficient ob/ob mice and leptin receptor-deficient db/db mice. These observations help to explain the beneficial effects of fasting in autoimmunity and could be exploited for leptin-based immune intervention in systemic lupus erythematosus.
PMID: 22291185 [PubMed - indexed for MEDLINE] PMCID: PMC3288569
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3288569/
Cutting edge: fasting-induced hypoleptinemia expands functional regulatory T cells in systemic lupus erythematosus.
Liu Y1, Yu Y, Matarese G, La Cava A. Author information
- 1Division of Rheumatology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.
Fasting is beneficial in the prevention and amelioration of the clinical manifestations of autoimmune diseases including systemic lupus erythematosus. The mechanisms responsible for these effects are not well understood. During fasting, there is a dramatic reduction of the levels of circulating leptin, an adipokine with proinflammatory effects. Leptin also inhibits CD4(+)CD25(+)Foxp3(+) regulatory T cells, which are known to contribute significantly to the mechanisms of peripheral immune tolerance. In this study, we show that fasting-induced hypoleptinemia in (NZB × NZW)F(1) lupus-prone mice induced an expansion of functional regulatory T cells that was reversed by leptin replacement. The specificity of the findings was indicated by the lack of these effects in leptin-deficient ob/ob mice and leptin receptor-deficient db/db mice. These observations help to explain the beneficial effects of fasting in autoimmunity and could be exploited for leptin-based immune intervention in systemic lupus erythematosus.
PMID: 22291185 [PubMed - indexed for MEDLINE] PMCID: PMC3288569
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3288569/
Meadia (Buchar). Mar. 2013; 8(1): 68-74
The Role of Leptin in Autoimmune disease
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749767/
The Role of Leptin in Autoimmune disease
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749767/
J Autoimmun. May 2012; 38(2-3): J177–J186. Published online Dec 3, 2011. doi: 10.1016/j.jaut.2011.11.007PMCID: PMC3302961NIHMSID: NIHMS342469
Gender differences in autoimmunity associated with exposure to environmental factors
K. Michael Pollard
Conclusion
Autoimmunity in humans often, but not always, has a female bias. The mechanisms for gender bias in human autoimmunity are not clear and studies which further our understanding of sex differences will be highly rewarding. This will include an understanding of the contribution of sex chromosomes particularly the X chromosome in modulating the innate and adaptive immune pathways involved in autoimmunity [10, 113].
Numerous epidemiological studies have demonstrated an association between environmental factors and increased risk of autoimmunity in humans. This is most clearly demonstrated by drug-induced autoimmunity. For some environmental exposures there is a female gender bias (e.g. Toxic Oil Syndrome, eosinophilia-myalgia syndrome, coeliac disease), others show increased risk for both sexes (e.g. smoking and RA), and others increase the risk of gender biased diseases (e.g. cosmetics and increased risk of SLE, PBC, RA). However, underlying many of these studies is the likelihood that the presence or absence of gender bias is influenced by occupation (e.g. silica), sex biased activity (e.g. cosmetics) or non-conventional therapeutic/cosmetic exposure (e.g. mercury). Nonetheless the recognition of potential gender bias in autoimmunity associated with environmental factors identifies potential areas of investigation regarding possible mechanisms.
Animal model studies have proven of great use in defining disease mechanisms in environmentally-induced autoimmunity [11]. However examination of gender bias has been limited because many studies have been restricted to female animals because of the known female bias in human autoimmune diseases. Restriction of gender and/or strain in animal model studies does not help confirm gender bias and may actually obscure gender effects. This is because it is clear that gender bias can be strain specific [163] suggesting an interaction between sex chromosome complement and background genes [113]. This observation has significant implications for human studies as it suggests that even within gender biased autoimmunity there may be individuals in which gender does not contribute to disease and vice versa. Environmental exposure likely adds an additional layer of complexity. Determining the interaction between environmental factors and sex hormones and sex chromosome function will be essential in defining the contribution that sex differences play in environmentally-induced autoimmunity.
Gender differences in autoimmunity associated with exposure to environmental factors
K. Michael Pollard
Conclusion
Autoimmunity in humans often, but not always, has a female bias. The mechanisms for gender bias in human autoimmunity are not clear and studies which further our understanding of sex differences will be highly rewarding. This will include an understanding of the contribution of sex chromosomes particularly the X chromosome in modulating the innate and adaptive immune pathways involved in autoimmunity [10, 113].
Numerous epidemiological studies have demonstrated an association between environmental factors and increased risk of autoimmunity in humans. This is most clearly demonstrated by drug-induced autoimmunity. For some environmental exposures there is a female gender bias (e.g. Toxic Oil Syndrome, eosinophilia-myalgia syndrome, coeliac disease), others show increased risk for both sexes (e.g. smoking and RA), and others increase the risk of gender biased diseases (e.g. cosmetics and increased risk of SLE, PBC, RA). However, underlying many of these studies is the likelihood that the presence or absence of gender bias is influenced by occupation (e.g. silica), sex biased activity (e.g. cosmetics) or non-conventional therapeutic/cosmetic exposure (e.g. mercury). Nonetheless the recognition of potential gender bias in autoimmunity associated with environmental factors identifies potential areas of investigation regarding possible mechanisms.
Animal model studies have proven of great use in defining disease mechanisms in environmentally-induced autoimmunity [11]. However examination of gender bias has been limited because many studies have been restricted to female animals because of the known female bias in human autoimmune diseases. Restriction of gender and/or strain in animal model studies does not help confirm gender bias and may actually obscure gender effects. This is because it is clear that gender bias can be strain specific [163] suggesting an interaction between sex chromosome complement and background genes [113]. This observation has significant implications for human studies as it suggests that even within gender biased autoimmunity there may be individuals in which gender does not contribute to disease and vice versa. Environmental exposure likely adds an additional layer of complexity. Determining the interaction between environmental factors and sex hormones and sex chromosome function will be essential in defining the contribution that sex differences play in environmentally-induced autoimmunity.
Int Immunopharmacol. 2014 May;20(1):124-30. doi: 10.1016/j.intimp.2014.02.026. Epub 2014 Mar 6.
Polyphenolics isolated from virgin coconut oil inhibits adjuvant induced arthritis in rats through antioxidant and anti-inflammatory action.
Vysakh A1, Ratheesh M2, Rajmohanan TP3, Pramod C4, Premlal S5, Girish kumar B6, Sibi PI4.
http://www.ncbi.nlm.nih.gov/pubmed/24613207
Br J Nutr. 2014 May 28;111(10):1782-90. doi: 10.1017/S000711451400004X. Epub 2014 Feb 11.
Polyphenolics isolated from virgin coconut oil inhibits adjuvant induced arthritis in rats through antioxidant and anti-inflammatory action.
Vysakh A1, Ratheesh M2, Rajmohanan TP3, Pramod C4, Premlal S5, Girish kumar B6, Sibi PI4.
http://www.ncbi.nlm.nih.gov/pubmed/24613207
Br J Nutr. 2014 May 28;111(10):1782-90. doi: 10.1017/S000711451400004X. Epub 2014 Feb 11.
Minerva Pediatr. 2005 Aug;57(4):173-80.
The almond milk: a new approach to the management of cow-milk allergy...
Salpietro CD1, Gangemi S, Briuglia S, Meo A, Merlino MV, Muscolino G, Bisignano G, Trombetta D, Saija A.
http://www.ncbi.nlm.nih.gov/pubmed/16172596
The almond milk: a new approach to the management of cow-milk allergy...
Salpietro CD1, Gangemi S, Briuglia S, Meo A, Merlino MV, Muscolino G, Bisignano G, Trombetta D, Saija A.
http://www.ncbi.nlm.nih.gov/pubmed/16172596
Arch Dermatol. 1998 Nov;134(11):1349-52.
Randomized trial of aromatherapy. Successful treatment for alopecia areata.
Hay IC1, Jamieson M, Ormerod AD.Author information
OBJECTIVE: To investigate the efficacy of aromatherapy in the treatment of patients with alopecia areata.
DESIGN: A randomized, double-blind, controlled trial of 7 months' duration, with follow-up at 3 and 7 months.
SETTING: Dermatology outpatient department.
PARTICIPANTS: Eighty-six patients diagnosed as having alopecia areata.
INTERVENTION: Eighty-six patients were randomized into 2 groups. The active group massaged essential oils (thyme, rosemary, lavender, and cedarwood) in a mixture of carrier oils (jojoba and grapeseed) into their scalp daily. The control group used only carrier oils for their massage, also daily.
MAIN OUTCOME MEASURES: Treatment success was evaluated on sequential photographs by 2 dermatologists (I.C.H. and A.D.O.) independently. Similarly, the degree of improvement was measured by 2 methods: a 6-point scale and computerized analysis of traced areas of alopecia.
RESULTS: Nineteen (44%) of 43 patients in the active group showed improvement compared with 6 (15%) of 41 patients in the control group (P = .008). An alopecia scale was applied by blinded observers on sequential photographs and was shown to be reproducible with good interobserver agreement (kappa = 0.84). The degree of improvement on photographic assessment was significant (P = .05). Demographic analysis showed that the 2 groups were well matched for prognostic factors.
CONCLUSIONS: The results show aromatherapy to be a safe and effective treatment for alopecia areata. Treatment with these essential oils was significantly more effective than treatment with the carrier oil alone (P = .008 for the primary outcome measure). We also successfully applied an evidence-based method to an alternative therapy.
http://www.ncbi.nlm.nih.gov/pubmed/?term=rosemary+hairloss
http://www.ncbi.nlm.nih.gov/pubmed/17314444 (garlic gel)
http://ijdvl.com/article.asp?issn=0378-6323;year=2007;volume=73;issue=1;spage=29;epage=32;aulast=Hajheydari
Randomized trial of aromatherapy. Successful treatment for alopecia areata.
Hay IC1, Jamieson M, Ormerod AD.Author information
- 1Department of Dermatology, Aberdeen Royal Infirmary, Foresterhill, Scotland. [email protected]
OBJECTIVE: To investigate the efficacy of aromatherapy in the treatment of patients with alopecia areata.
DESIGN: A randomized, double-blind, controlled trial of 7 months' duration, with follow-up at 3 and 7 months.
SETTING: Dermatology outpatient department.
PARTICIPANTS: Eighty-six patients diagnosed as having alopecia areata.
INTERVENTION: Eighty-six patients were randomized into 2 groups. The active group massaged essential oils (thyme, rosemary, lavender, and cedarwood) in a mixture of carrier oils (jojoba and grapeseed) into their scalp daily. The control group used only carrier oils for their massage, also daily.
MAIN OUTCOME MEASURES: Treatment success was evaluated on sequential photographs by 2 dermatologists (I.C.H. and A.D.O.) independently. Similarly, the degree of improvement was measured by 2 methods: a 6-point scale and computerized analysis of traced areas of alopecia.
RESULTS: Nineteen (44%) of 43 patients in the active group showed improvement compared with 6 (15%) of 41 patients in the control group (P = .008). An alopecia scale was applied by blinded observers on sequential photographs and was shown to be reproducible with good interobserver agreement (kappa = 0.84). The degree of improvement on photographic assessment was significant (P = .05). Demographic analysis showed that the 2 groups were well matched for prognostic factors.
CONCLUSIONS: The results show aromatherapy to be a safe and effective treatment for alopecia areata. Treatment with these essential oils was significantly more effective than treatment with the carrier oil alone (P = .008 for the primary outcome measure). We also successfully applied an evidence-based method to an alternative therapy.
http://www.ncbi.nlm.nih.gov/pubmed/?term=rosemary+hairloss
http://www.ncbi.nlm.nih.gov/pubmed/17314444 (garlic gel)
http://ijdvl.com/article.asp?issn=0378-6323;year=2007;volume=73;issue=1;spage=29;epage=32;aulast=Hajheydari
Eur. J. Nutr. Feb. 2013; 52(1): 337-345
Consumption of Red Meat and whole grain bread in relation to biomarkers of obesity, inflammation, glucose metabolism, and oxidative stress
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3549403/
Consumption of Red Meat and whole grain bread in relation to biomarkers of obesity, inflammation, glucose metabolism, and oxidative stress
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3549403/