Integrative medicine最新文献

This case series aims to describe the clinical presentation of three PCOS patients with primary dysmenorrhea and report the outcomes of a tailored naturopathy, yoga, and dietary modification intervention on sleep quality and pain intensity. Primary dysmenorrhea is pain associated with the menstrual cycle without any underlying pathology. It ranks among the primary contributors to the health burden of women worldwide, with a prevalence of 71% globally. This case series included three diagnosed cases of PCOS with dysmenorrhea. Detailed histories and details of daily routine, sleep, and dietary habits were recorded. Patients were prescribed a daily 45-minute yoga protocol, 15-minute naturopathy therapy (hip-bath), and dietary advice such as avoiding eating junk, oily, spicy food and consumption of packaged juices and beverages, including more fruits, vegetables, and sprouts in diet along with min 2 litters of water intake. They were also asked to avoid eating before bed and late at night. Outcomes were compared from the previous menstrual cycle before the intervention to the subsequent menstrual cycle after the intervention. Patients reported a significant decrease in pain intensity measured by Visual Analog Scale (VAS), improvement in sleep quality measured Pittsburgh Sleep Quality Index (PSQi), and overall day-to-day functioning during the menstrual cycle after the intervention. These findings indicate that a regular yoga regime and naturopathy, along with dietary modifications, can be beneficial for the management of dysmenorrhea. Further research is needed, including longitudinal studies and clinical trials with larger sample sizes, to confirm these findings and explore the mechanisms behind this improvement.

Background: 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.

Objectives: Determine the effect of LPD on sleep quality and inflammatory markers in T2DM patients without depression.

Method: 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.

Result: 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 (P = .003; 95% CI -4.15, -0.92), decrease of ΔMPV by 0.41 and 0.03 (P = .001; 95% CI -0.59, -0.18), and change of ΔNLR by -0.4 compared to 0.15 (P = .035; 95% CI -0.93, -0.03) in the intervention group compared to the control group. There was no significant change in Δhs-CRP (P = .762; 95% CI -5.44, 4.02) in the intervention group compared to control.

Conclusion: 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.

Limitations: Direct supervision on the diet and physical activity of the subjects was not done due to some obstacles in the field.

Context: 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.

Objective: 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.

Results: 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.

Conclusions: 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.

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.

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 (p-cresol). The 4-cresol metabolite 4-methyl-o-hydroquinone and the acetaminophen metabolite N-acetyl-p-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.

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.