Agus Siswanto, Ahmad Husain Asdie, Rico Novyanto, Laode Kardin, Yohana Sahara, David Yosua Kaban, Harik Firman Thahadian, Rakhmat Tajudin, Heriyanto Hidayat, Michael Dwinata
{"title":"The Impact of Latihan Pasrah Diri / Self Surrender Practice (LPD) in Sleep Quality and Inflammatory Markers in Diabetes Mellitus Type 2 Patients Without Depression: A Randomized Controlled Trial.","authors":"Agus Siswanto, Ahmad Husain Asdie, Rico Novyanto, Laode Kardin, Yohana Sahara, David Yosua Kaban, Harik Firman Thahadian, Rakhmat Tajudin, Heriyanto Hidayat, Michael Dwinata","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>Insomnia is more frequent in type 2 diabetes mellitus (T2DM) patients. Both conditions are known to cause low-grade inflammation and an independent risk factor for cardio-cerebrovascular events (CCDs) and overall mortality. Relaxation, mindfulness, breath control, and spiritual-based therapies such as Latihan Pasrah Diri / Self Surrender Practice (LPD) have been known to induce relaxation, improve depressive symptoms and sleep quality, inflammatory markers, glycemic control, Daily Living Activities (DLA), and Quality of Life (QoL) in T2DM patients. It is currently unknown whether LPD can improve sleep quality in patients with T2DM without depression and its association with inflammation.</p><p><strong>Objectives: </strong>Determine the effect of LPD on sleep quality and inflammatory markers in T2DM patients without depression.</p><p><strong>Method: </strong>This is a prospective, single-blind, randomized controlled trial. Patients aged 30-60 years old, Muslim, diagnosed with type 2 diabetes mellitus and who were not currently experiencing depression (Beck Depression Inventory-II Score <17) were eligible to be included in the study. We assessed the changes in the value of the ΔInsomnia Severity Score (ΔISI) and inflammatory markers (Δhs-CRP, ΔMPV, and ΔNLR). The intervention group was the group with standard therapy of DM and LPD, while the control group was the group with standard therapy of DM without LPD. The intervention was carried out 2 times a day with 20 minutes for each session, for 8 weeks.</p><p><strong>Result: </strong>A total of 44 subjects were randomized 1: 1 into intervention (n = 22) and control (n = 22) groups. In the intervention group, only 12 subjects met the minimum frequency of intervention, thus being included in the statistical analysis. There was a statistically significant decrease of ΔISI score by 2.58 compared to 0.04 (<i>P</i> = .003; 95% CI -4.15, -0.92), decrease of ΔMPV by 0.41 and 0.03 (<i>P</i> = .001; 95% CI -0.59, -0.18), and change of ΔNLR by -0.4 compared to 0.15 (<i>P</i> = .035; 95% CI -0.93, -0.03) in the intervention group compared to the control group. There was no significant change in Δhs-CRP (<i>P</i> = .762; 95% CI -5.44, 4.02) in the intervention group compared to control.</p><p><strong>Conclusion: </strong>Eight weeks of LPD improves sleep quality and reduces inflammatory markers (MPV and NLR) in T2DM patients without depression. Whether changes in inflammatory markers and insomnia are related and whether improvements in insomnia lead to improvements in inflammatory markers or vice versa requires further study.</p><p><strong>Limitations: </strong>Direct supervision on the diet and physical activity of the subjects was not done due to some obstacles in the field.</p>","PeriodicalId":13593,"journal":{"name":"Integrative medicine","volume":"23 4","pages":"16-22"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11441587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Microbiome's Role in Chronic Pain and Inflammation.","authors":"Shawn Manske","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Context: </strong>Pain is a universal experience, one that is meant to protect people from further harm or injury, and chronic pain is prominent worldwide. Inflammation plays a central role in chronic pain.</p><p><strong>Objective: </strong>The review intended to examine the epidemiology of chronic pain, the ways in which inflammation contributes to it, and the microbiome's role in it, evaluating the function of the oral microbiome and dietary factors.</p><p><strong>Results: </strong>The inflammatory response plays a pivotal role in the transition from acute to chronic pain, with various mediators orchestrating a cascade of events that perpetuate pain signaling and sensitization. The microbiome interacts directly with the immune system and plays a fundamental role in addressing inflammation and chronic pain. Dysbiosis within the gut and oral microbiota can fuel systemic inflammation, exacerbating pain symptoms and influencing pain perception through the gut-brain axis. Additionally, microbial metabolites can influence immune function, reducing or perpetuating inflammation, which can further affect the experience of pain. Dietary factors also contribute significantly to inflammation and pain, and poor nutritional choices can exacerbate immune responses and trigger low-grade inflammation, perpetuating chronic-pain conditions.</p><p><strong>Conclusions: </strong>Moving forward, a holistic approach to chronic pain management is imperative, addressing not only the symptoms but also the underlying inflammatory processes and systemic contributors. Embracing interdisciplinary collaboration and personalized treatment tailored to the individual patient's needs will be essential in alleviating chronic pain and improving overall quality of life. Through continued research and clinical innovation, healthcare practitioners can work towards more effective and compassionate care for those living with chronic pain.</p>","PeriodicalId":13593,"journal":{"name":"Integrative medicine","volume":"23 4","pages":"10-15"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11441585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Christopher R D'Adamo, DeAunne Denmark, Natàlia Carreras-Gallo, Varun Dwaraka, Ryan Smith, Tom Blue, Helen Messier
{"title":"A Pilot Study Evaluating the Feasibility and Efficacy of an In-Home Resonance-Based Electromagnetic Field Protection Device on Improving Markers of Health and Cognitive Function Among a Sample of Healthy Adults.","authors":"Christopher R D'Adamo, DeAunne Denmark, Natàlia Carreras-Gallo, Varun Dwaraka, Ryan Smith, Tom Blue, Helen Messier","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>The dramatic increase in exposure to non-native sources of electromagnetic fields (EMF) in recent years has given rise to numerous human health concerns. The near pervasive exposure to radiofrequency (RF) emanating from wireless technologies inside the home (e.g., cell phones, wireless routers, \"Smart\" devices) and outside of the home (e.g., cell towers, automobiles, computers at work, tablets at school) is particularly troubling. While epidemiological studies are somewhat conflicting to date, RF exposure is currently classified by the World Health Organization as a Class 2B carcinogen. Mechanisms of activity of the deleterious effects of RF exposure on human health include the generation of excessive oxidative stress, chronic inflammation, and disruption of the production of melatonin and other hormones, all of which are believed to be due largely to the activation of voltage-gated calcium channels (VGCC). Mitigation strategies are currently generally limited to wireless device hygiene (e.g., hard-wired ethernet, turning off wireless routers at night, keeping cellphones away from the body) and metal-based shielding in the home, which can be expensive and not feasible for many. The goal of this pilot and feasibility trial was to evaluate the feasibility and preliminary signs of efficacy of an in-home resonance-based electromagnetic field protection device (BluShield) on various physiological and patient-reported outcomes commonly affected by excessive RF exposure.</p><p><strong>Methods: </strong>A sample of relatively healthy adults was enrolled in a single arm, 12-week pilot and feasibility study. The intervention consisted of plugging in the BluShield device at home or at the participant's residence when traveling. Outcomes included laboratory panels assessing overall physiological health (CBC & CMP), blood markers related to inflammation, oxidative stress, DNA damage, and cellular senescence (Jinfiniti), a high-resolution genome-wide assessment of DNA methylation (TruDiagnostic), a validated questionnaire to assess cognitive function (CNS - Vital Signs), a wearable device to assess sleep and other physiological parameters (Oura ring), and a single-item assessment of overall health. Outcomes were compared before and after the intervention with paired <i>t</i> tests or Wilcoxon signed rank tests, depending upon the distribution of data.</p><p><strong>Results: </strong>25 participants enrolled in the study. All participants reported compliance with the EMF mitigation device throughout the course of the study, and no adverse events were reported. There were limited changes in conventional labs (decrease in glucose, increase in monocytes; <i>P</i> < .04]), but modest improvement in self-reported health (<i>P</i> = .02), improvements on numerous domains of the CNS - Vital Signs questionnaire (Composite Memory, Cognitive Flexibility, Executive Function, and Processing Speed; <i>P</i> < .02), wearable device parameters ","PeriodicalId":13593,"journal":{"name":"Integrative medicine","volume":"23 4","pages":"23-28"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11441584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Carolyn F Aldendail, Pinyu Chen, Hannah S Dibble, Vanessa Baute Penry
{"title":"A Comprehensive Review of Safety, Efficacy, and Indications for the Use of Alpha-Lipoic Acid and Acetyl-L-Carnitine in Neuropathic Pain.","authors":"Carolyn F Aldendail, Pinyu Chen, Hannah S Dibble, Vanessa Baute Penry","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The debilitating, chronic symptoms of neuropathic pain result in decreased quality of life, depressed mood, and anxiety in patients suffering from neuropathic pain. Despite hundreds of dollars in monthly treatment-related costs, more than half of the patients report inadequate pain relief. Traditional first-line agents are expensive and may have disruptive side effects. Given the disease burden of neuropathic pain, many patients turn to over-the-counter supplements. Here we review two supplements, alpha-lipoic acid (ALA), also known as thioctic acid, and acetyl-L-carnitine (ALC), and data of treatment outcomes from the available literature suggest comparable efficacy to currently available pharmaceuticals for the treatment of neuropathic pain. Meta-analysis of randomized controlled trials demonstrates that ALA can significantly improve neuropathic pain and nerve conduction velocity. ALA has been evaluated in the treatment of multiple sources of neuropathic pain, including chemotherapy-induced peripheral neuropathy, entrapment neuropathies, radicular nerve pain, and burning mouth syndrome. Common dose-dependent side effects include nausea, vomiting, and vertigo. Cost analysis from June 2022 indicates that a clinically effective dose (600 mg/day) of ALA costs patients $14.40 monthly. Two randomized control trials demonstrate that ALC exhibits neuroprotective effects, can regenerate nerves, and improve vibratory perception in the early stages of DPN. In terms of adverse reactions, no significant differences were observed between treatment and placebo groups, implying that ALC is generally well-tolerated. Cost analysis from June 2022 indicates that a clinically effective dose of ALC (2000 mg/day) costs patients $27.60 monthly. Comparable efficacy in clinical trials, minimal side effects, and lower monthly costs suggest that ALA and ALC should be considered among the accepted first-line treatment options for neuropathic pain.</p>","PeriodicalId":13593,"journal":{"name":"Integrative medicine","volume":"23 3","pages":"32-39"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11302972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hypothesis: 2 Major Environmental and Pharmaceutical Factors-Acetaminophen Exposure and Gastrointestinal Overgrowth of Clostridia Bacteria Induced By Ingestion of Glyphosate-Contaminated Foods-Dysregulate the Developmental Protein Sonic Hedgehog and Are Major Causes of Autism.","authors":"William Shaw","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Epidemiological studies have found 2 significant factors associated with the increased incidence of autism spectrum disorder (ASD): the increased use of acetaminophen in the 1970s when this drug largely replaced the use of aspirin for many patients because of a fear of Reye syndrome, and the agricultural use in the 1990s of the herbicide glyphosate on crops that were genetically modified (GM) to tolerate glyphosate. The incidence of autism in the United States, where acetaminophen is widely available, is more than 1000 times greater than in Cuba, where acetaminophen is available only by prescription. Metabolites of both glyphosate and acetaminophen likely alter the function of the developmental protein sonic hedgehog (SHH). Glyphosate likely affects SHH indirectly by decreasing the beneficial flora of the gastrointestinal tract and increasing pathogenic Clostridia bacteria, which are resistant to glyphosate. The marked increase of certain Clostridia species caused by glyphosate results in Clostridia production of large amounts of 3-(3-hydroxyphenyl)-3-hydroxypropionate (HPHPA) and 4-cresol (<i>p</i>-cresol). The 4-cresol metabolite 4-methyl-o-hydroquinone and the acetaminophen metabolite <i>N</i>-acetyl-<i>p</i>-benzoquinone imine (NAPQI) likely react with the sulfhydryl group of the N-terminal cysteine of SHH, blocking the function of this critical amino acid required for the activation of SHH. HPHPA and 4-cresol also inhibit dopamine β-hydroxylase, resulting in overproduction of dopamine and its toxic metabolites, such as aminochrome, that cause biochemical damage to mitochondria and structural proteins in brain cells. Elevated amounts of these Clostridia products in body fluids in people with autism and in animals with autistic signs have been documented in laboratories throughout the world. The synthesis of the HPHPA molecule in extremely large quantities depletes the body of free coenzyme A, which is needed for the palmitoylation of SHH. SHH covalently coupled to palmitic acid is 30 times more active than SHH without palmitic acid. These possible modifications of SHH help to explain the significantly altered quantities of SHH in the blood serum of patients with autism. The severity of autism is related to the degree of SHH abnormality. The spread of pathogenic Clostridia worldwide from soil to food animals to humans, which may be promoted by glyphosate use, is a great public health concern, not only for autism but perhaps for all the neuropsychiatric diseases that appear to be related to gastrointestinal Clostridia overgrowth These diseases include seizures, tremors, tic disorders, Parkinson disease, chronic fatigue syndrome, obsessive compulsive disorder, schizophrenia, bipolar and unipolar depression, ADHD, and anorexia nervosa.</p>","PeriodicalId":13593,"journal":{"name":"Integrative medicine","volume":"23 3","pages":"12-23"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11302971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Continuing the Conversation About Arsenic.","authors":"Joseph Pizzorno","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Chronic low-level arsenic exposure is a significant contributor to ill health and disease. However, at this time, quantification of the effects of this exposure appears virtually impossible. In a continuation of my editorial on arsenic published earlier this year, this editorial looks at arsenic's mechanisms of damage, more disease correlations, sources of exposure, and early signs for detection of arsenic toxicity.</p>","PeriodicalId":13593,"journal":{"name":"Integrative medicine","volume":"23 3","pages":"6-10"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11302974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}