Complete remission of depression and anxiety using a ketogenic diet: case series

Front. Nutr., 14 May 2024 Sec. Clinical Nutrition Volume 11 - 2024 https://doi.org/10.3389/fnut.2024.1396685
Background: There is little data that describe the use of ketogenic metabolic therapy to achieve full remission of major depression and generalized anxiety disorder in clinical practice. We present a retrospective case series of three adults with major depression and generalized anxiety disorder with complex comorbidity, treated with personalized ketogenic metabolic therapy, who achieved complete remission of major depression and generalized anxiety disorder and improvements in flourishing, self-compassion, and metabolic health.
Methods: Three adults, ages 32–36, with major depression, generalized anxiety, other anxiety disorders, and comorbid psychiatric conditions were treated for 12–16 weeks with personalized whole food animal-based ketogenic metabolic therapy (1.5:1 ratio) in a specialized metabolic psychiatry practice. Interventions included twice-weekly visits with an experienced ketogenic registered dietitian; daily photo journaling and capillary blood BHB/glucose/GKI monitoring; virtual groups; family/friends support; nature walks and talks several times per week, and community building. Successful adoption of the ketogenic diet was defined as the achievement and maintenance of capillary BHB ≥ 0.8 mmol/L and GKI < 6. Remission was assessed by GAD-7 and PHQ-9, and quality of life was assessed subjectively and with validated scales for flourishing and self-compassion. Metabolic health was assessed by laboratories/biometric measures.
Results: Two patients achieved remission of major depression (PHQ-9 ≤ 4) and generalized anxiety (GAD-7 ≤ 4) within 7 weeks of therapeutic nutritional ketosis; one required 12 weeks. Anxiety responded and remitted more quickly than major depression. Flourishing and self-compassion increased steadily. Patients lost 10.9 to 14.8% of their initial body weight within 12 weeks and improved metabolically; one achieved optimal metabolic health.
Conclusion: Complete remission of major depression and generalized anxiety disorder occurred within 7–12 weeks of therapeutic nutritional ketosis during treatment with a personalized animal-based ketogenic diet (ratio 1.5:1) in adults with complex comorbid depression and anxiety engaged in a specialized metabolic psychiatry program.

Introduction

Emerging brain-based research in psychiatry and neurology has focused on identifying fundamental metabolic disturbances within neurons and throughout the body involving insulin resistance, inflammation, oxidative stress, and alterations of the gut microbiome (1). All four of these fundamental metabolic disturbances are present in major depression (2), and underlying anxiety disorders (3) and can be directly modulated through the use of ketogenic metabolic therapy (KMT) (4).
As psychiatric disorders have risen over the past several decades, the prevalence of metabolic syndrome has sharply increased, with only 12.2% of U.S. adults meeting the criteria for optimal metabolic health, leaving 87.8% metabolically compromised (5, 6).
Metabolic syndrome affects almost a third of individuals with major depression (7). It is a significant contributor to their morbidity and mortality (8) and is rooted in impaired glucose metabolism and utilization. Insulin resistance has been well described in many tissues, including the brain (9), where it is being investigated as a link between metabolic health and mental health conditions. Preclinical models demonstrate that glucose intolerance is directly associated with anxiety and that insulin resistance triggers depressive behaviors (9). In brain tissue, insulin resistance results in cerebral glucose hypometabolism and a vicious cycle of unmet energy needs (10). In human studies, cerebral glucose hypometabolism is a feature of major depression (11, 12) and generalized anxiety disorder (GAD) (13).
KMT, also known as the therapeutic ketogenic diet, or KD, is a low carbohydrate, moderate-protein, high-fat diet that supports a fundamental metabolic shift from glucose to ketone bodies as the primary fuel source (14). Classic KMTs are formulated with strict macronutrient ratios, most commonly 4:1 and 3:1 (fat: protein + carbohydrates), and have demonstrated efficacy in intractable epilepsy and genetic disorders. More recently, modified classic KMTs with lower macronutrient ratios of 2.5:1, 2:1, and 1.5:1 have been utilized in research and clinical practice (15, 16). These allow more variety in the diet, meet micronutrient needs except vitamin D (17), and are easier to sustain for extended periods of time.
KMT exploits the body’s natural ability to produce ketone bodies (d-beta-hydroxybutyrate (BHB), acetoacetate, and acetone) in the liver from fatty acids by keeping carbohydrate consumption very low. Acute and sustained production of ketone bodies produces a fundamental shift in fuel energetics within cells, particularly neurons, which can radically re-route and quickly rely on readily available BHB and acetoacetate for cellular energy (18). Ketone bodies also increase vascular density at the blood–brain barrier, which can strikingly increase the availability of ketone bodies for brain energy metabolism by 40-fold (19). Ketones are a preferred energy source in the CNS (20) and neurons will choose ketones over glucose when available.
Nutritional ketosis (10) using a KMT is a natural, not pathological, state (21) where the body’s energy and protein synthesis needs are met with a high-fat/moderate-protein/low-carbohydrate diet, resulting in sustained elevations of serum ketones and fatty acids and normal glucose without acidemia. In both acute and long-term nutritional ketosis, ketone bodies have a number of biological effects that directly change the brain’s cellular energy status (15), increase mitochondrial density (22), and improve mitochondrial morphology, which has been shown to be altered in mood disorders (23, 24). Mitochondrial abnormalities have also been postulated to be responsible for changes in synaptic function and neuroplasticity, potentially associated with symptoms of depression and anxiety (19).
Recent research shows that a ketogenic diet (KD) reduces neuronal firing rates, modulates ion channels and cell signaling cascades, and stimulates the biochemical synthesis and neurotransmission of GABA by inhibiting glutamate decarboxylase, a major inhibitory neurotransmitter involved in neuronal firing and anxiogenesis (25, 26). BHB activates the transcription of antioxidant-related genes by inhibiting histone deacetylases, triggering long-term adaptive changes in gene expression. In addition, at physiologic concentrations, ketone bodies reduce neuroinflammation through direct action at G-protein coupled receptors (25). KD also favorably alters the gut microbiome (27). Perhaps most importantly, KD directly increases NAD+, which reduces reactive oxygen species and increases mitochondrial ATP production. It is also utilized as a substrate for sirtuins and PARP enzymes associated with DNA repair and longevity. A sustained increase in NAD+ may underlie the pleiomorphic benefits of KMT across multiple neuropsychiatric conditions (28). In terms of the frequent abnormal alarms set off in the amygdala during anxiety, nutritional ketosis may provide an acute and long-term intervention to reduce generalized anxiety, panic attacks, obsessive doubt, and symptoms of post-traumatic stress disorder (PTSD). For apathy, anhedonia, amotivation, and abulia seen in major depression, therapeutic nutritional ketosis may provide higher and more sustained intraneuronal energy and repair (29, 30).
There is no published data that describes the implementation and use of personalized KMT for adults in real-world clinical practice who present with major depression comorbid with GAD and complex psychiatric comorbidity.
The aim of this case series is to examine the response to the treatment of major depression and generalized anxiety with whole-food animal-based personalized KMT in adults with complex psychiatric comorbidity and varied metabolic status. We conducted a retrospective review of three cases from our Metabolic Psychiatry Registry that demonstrate a consistent response and remission of major depression and generalized anxiety among patients who are psychiatrically and metabolically complex, despite differences in the initiation and adoption of KMT, and varied metabolic dysfunction. We describe the evaluation process and prescription of KMT, baseline metabolic workup and monitoring, elements that fostered treatment engagement and adherence, and challenges encountered during 12 weeks of KMT. We correlated capillary BHB/GKI with time to the remission of major depression and GAD and the achievement of metabolic health.

Discussion

Although KD was first shown to produce antidepressant effects and alleviate “behavioral despair” in preclinical studies more than 20 years ago (20), there is little clinical data regarding KD in major depression and anxiety disorders.
A retrospective analysis of 31 individuals with primary diagnoses of major depression (N = 7), bipolar II disorder (N = 13), and schizoaffective disorder (N = 12) who had failed to respond to conventional psychiatric care was treated with KD (75%–80% fat, 15%–20% protein, 5% carbohydrate) for 12 weeks in a psychiatric hospital (31). Of these patients, 22 were voluntarily admitted for the initiation of KD, and the remainder were offered KD during their inpatient hospital course. Change in depression was measured by HAM-D and MADRS in 6 of 7 patients with major depression and 12 of 13 patients with bipolar disorder. Notably, 100% of patients given the HAM-D showed statistically significant improvement in depressive symptoms (mean HAM-D decreased from 25.4 to 7.7; mean MADRS decreased from 29.6 to 10.1). However, serum ketones were not measured; urinary ketone measures were obtained once in 28 patients during the 12-week intervention; 18 patients (64%) showed positive urine ketones (31).
Bipolar depression was included in a recent randomized controlled pilot study assessing the safety and feasibility of KMT as adjunctive therapy, and reported safety and feasibility with excellent adherence and maintenance of ketosis (mean BHB 0.88 ± 0.99 mmol/L for 12 weeks) (32).
One case report utilized KD (65% fat, 25% protein, 10% carbs) with a time-restricted feeding window in a 65-year-old woman with major depression and type II diabetes and reported remission of depression (PHQ-9 17 to 0), normalization of HbA1c, decrease in estimated average glucose from 216 to 96 mg/dL, improvement in HOMA-IR from 9.4 to 2.3, and TG/HDL ratio from 4.7 to 1.2 over 12 weeks. The only measured serum BHB reported in the case was a mean of 1.5 mmol/L by week 12 (30).
A recent meta-analysis of low carbohydrate diets used in controlled trials that evaluated symptoms of depression and anxiety, not disorders, in varied metabolic and inflammatory conditions reported that the symptomatic response of these symptoms was inconclusive (33). The conclusions may not apply to KMTs; the meta-analysis was limited by grouping varied diets with higher carb intake and higher protein intake than usually associated with diets formulated to induce nutritional ketosis; serum or capillary BHB was not reported; and primary and secondary outcomes varied across studies.
In anxiety, preclinical research shows that exogenous ketone supplementation reduces anxiety behaviors (34). There is one case report of a self-administered Atkins Diet for weight loss in a woman with panic disorder (35) but no reports of KMT in panic disorder, OCD, or PTSD. Case reports of KD addressing anxiety describe two cases of decreased anxiety symptoms in a woman with women, one with bipolar I disorder and another with unspecified mood disorder, comorbid emotional dysregulation, body dysmorphic disorder, and eating disorder (36, 37), and one case report that describes the elimination of anxiety symptoms in a man with bipolar disorder (38). Anxiety and obsessive preoccupations improved in weight-restored anorexic women, in one case report describing complete remission of anorexia (39) and in a retrospective case series where animal-based KD was adopted without dietary prescription and monitoring (2); however, ketone measures were not reported. One small pilot trial where KD was followed by ketamine infusions reported a significant lessening of obsessive preoccupations in weight-recovered women with chronic anorexia; here, ketosis was measured by breath acetone (40).
Finally, all three patients had comorbid ADHD, which may be important. Approximately 65–89% of adults with ADHD experience one or more comorbid psychiatric conditions, and ADHD often occurs comorbid with anxiety and depression (41). Preclinical studies in murine models (42) of ADHD with hyperactivity suggest that KD may improve symptoms via alteration of the gut microbiome. Preclinical studies in dogs with epilepsy displaying ADHD-like behaviors treated with a medium-chain triglyceride KD have shown decreased pathological behaviors (43). Further research exploring the effect of KMT in humans with ADHD should be considered to understand the mechanisms of action and assess short- and long-term risks and benefits.
There is little research regarding the selection, implementation, and treatment course for KMT use as adjunctive or sole treatment in individual psychiatric conditions. Given the potential benefits of therapeutic nutritional ketosis and the restoration of metabolic health (44), there is a pressing need to identify the biological underpinnings of KD in psychiatric disorders and delineate factors associated with the successful adoption and adherence of KMT and responses in common psychiatric disorders such as depression and anxiety. In clinical practice and real-world settings, where patients often present with multiple comorbidities, consideration of KD can seem daunting to clinicians.
Despite that, this case series illustrates complete remission of both major depression and GAD in three adults with complex psychiatric comorbidity and previously unrecognized metabolic dysfunction using whole-food, animal-based personalized KMT. Anxiety responded first and time to remission occurred rapidly within 7–12 weeks, despite varied challenges, including preferences for time-restricted eating, slow adoption, inconsistent monitoring, and emergent fatigue during strenuous exercise, which occurred many weeks into KMT due to low serum carnitine and spontaneous reduction of protein intake rather than keto-adaptation or “keto-flu.” All patients improved metabolically, and one patient achieved optimal metabolic health (6).
These patients were representative of many adults in clinical psychiatric practice who present with persistent, serious symptoms interfering with several life domains. They each had five DSM-V psychiatric disorders: severe unipolar major depression, GAD, at least one other anxiety disorder (OCD, PTSD, and/or panic disorder), and ADHD, and two had binge eating disorder. They had all failed at least two previous adequate trials of medications and psychotherapy and were seeking relief. All had family histories of mood and anxiety disorders and documented metabolic disease in first-degree relatives. Extensive laboratory testing and bioimpedance evaluations were eye-opening because, although they were overweight, they were not aware of the extent to which they were already metabolically ill; we suspect it enhanced their motivation to adopt and maintain KMT.
This case series is limited by describing only three patients, which limits the generalizability of our results as well as the inherent selection bias, as they were interested in KMT after failing standard therapies. In addition, they were selected because their complex psychiatric comorbidity reflects the complexity seen in the majority of our outpatient psychiatric practice. This degree of complexity may limit the generalization of these findings, although it is important to note that outpatient clinical psychiatric practice as a whole has seen an increase in complex psychiatric comorbidity over the past two decades (44).
As a retrospective case series, there may be additional limiting and confounding factors, including the lack of a control group. Some rating scales and digital data are missing, which may impact the completeness of the analysis. Time to consistent nutritional ketosis and delays in obtaining necessary labs requiring intervention may have contributed to a longer time to response and remission; response and remission may occur earlier than reported here, and this deserves further research. Finally, it is not clear to what extent immersive treatment (see Supplementary material 1) and additional interventions during KMT, such as close digital monitoring, frequent clinical contact, group supports, and nature walks, contributed to the rapidity of response/remission of anxiety and depression, or to overall treatment success, independent of the biological effects of KMT, and which of these elements were most critical; more research is needed. Carefully designed prospective studies and randomized controlled trials providing higher levels of evidence are needed to examine the use of KMT and time to response and remission in individuals without comorbidity and determine the extent to which comorbidity may confound or alter these (8).
As metabolic psychiatry moves forward, we need both preclinical and larger, well-controlled clinical studies examining the pleiomorphic effects of ketone bodies in the brain and in the body to understand how we can best leverage whole foods to optimize brain energy, enhance genetic expression, reduce neuroinflammation, optimize metabolic health, and safeguard the promise of our future.

I started having immediate inflammation on the tip of my penis after oral sex while traveling out of the country. Went to a pharmacy and was given fucidin as an antibiotic/steroid cream. This calmed the irritation but about a week later I noticed some redness inside the urethra. Was given a medication for gonorrhea without testing. About 5 days later I had a fever, pain in my testicles and some clear discharge. I completed my 5 day course of antibiotics and gave it another week to see if symptoms got better.
I still had clear discharge and went to urgent care in my home country. Tested negative for gonorrhea and chlamydia but was given rocephrin injection and doxycycline for a week. Urine culture came back negative as well as nothing for urine analysis. I had terrible inflammation and stinging for another month. Went to primary care Doctor and ran more tests with nothing coming up. Saw a urologist next did PCR testing for chlamydia, gonorrhea, syph, mycoplasma, ureaplasma, HIV, HSV1+2 igg. More urine cultures all negative.
I've repeated all tests at the 4 month mark, still nothing positive. I have 2 spots on my penis that experience intense burning everyday for the last 5 months. I gets worse when I pee, it gets better when I don't walk around and cause any friction in the area. One of the spots is barely visible just inside the urethra. It doesn't photograph well and shrunk in size from 2 months ago but has halted progress. The pain is relentless and I'm not sure what to do. I've had my prostate checked and I do not have any pelvic floor tightness. I do not think its prostatitis.
I've seen an infectious disease doctor that basically said he can't do anything without a positive test, which I understand.
I have another urology appointment this week and wanted to know if there are any other tests I should push for to get a diagnosis. I've seen PCR testing that may be more sensitive for UTIs? Semen analysis? If you have any ideas please send them my way. Thanks!

i smoke montego red 100s, i have a lot of experience with a wide variety of substances and firmly believe there is something off about montegos. They occaisionally taste very off, one of my friends describes the weird taste as being extremely similar to spice(k2) when the cigarettes feel weird they tend to make me feel slightly impaired they often cause a strange spacey almost trippy mindset that lasts up to 15 minutes after i smoke them, the effects and tastes seem to vary and not all the cigarettes in a pack will do this, i have an extemely high tolerance to nicotine and dont get a buzz even from the first cigarette of the day anymore. the weird feeling i get is nothing like a nic buzz. i take a full spectrum urine analysis multiple times a week and dont test positive for any of the 93 drugs they test for so i think its some strange research chemical or a variety of unregulated chemicals. i dont get these effects from any other cigarettes i smoke. does anyone here have similar experiences?

~Kidney function tests market~ is anticipated to grow at a CAGR of 6.8% during the forecast period (2024-2031). Kidney function tests market is driven by the increasing prevalence of kidney diseases, such as chronic kidney disease, diabetic nephropathy, and glomerulonephritis, in addition to the diagnostic significance of these tests. Key players include diagnostic companies, laboratory equipment manufacturers, and healthcare institutions. Technological advancements, such as automation and molecular diagnostics, have improved the accuracy and accessibility of these tests. Investments in healthcare infrastructure, particularly in emerging economies, support the expansion of kidney function testing services. Preventive healthcare initiatives, public health campaigns, and community outreach programs also contribute to the demand for kidney function tests. Healthcare policy and reimbursement policies additionally influence the adoption and utilization of these tests. Public health awareness and education also play an essential role in promoting kidney health and early detection of kidney diseases.
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The market is expanding as a result of improvements in kidney function tests' accessibility, speed, and accuracy provided by advancements in diagnostic technologies, such as molecular diagnostics and point-of-care devices. According to the Centers for Disease Control and Prevention (.gov), in May 2023, chronic kidney disease (CKD) is a prevalent condition among US adults, with an estimated 35.5 million individuals, or 14.0% of the population, being affected. The prevalence of CKD varies across age groups, with higher rates observed in individuals aged 65 years or older (34.0%) compared to those aged 45-64 (12.0%) and 18-44 (6.0%). Furthermore, CKD is slightly more common in women (14.0%) than in men (12.0%), and non-hispanic black adults have the highest prevalence (20.0%) compared to non-hispanic Asian adults (14.0%), non-hispanic white adults (12.0%), and hispanic adults (14.0%).
full report of Kidney Function Tests Market available @ https://www.omrglobal.com/industry-reports/kidney-function-tests-market
o Market Coverage
o Market number available for – 2024-2031
o Base year- 2024
o Forecast period- 2024-2031
o Segment Covered- By Source, By Product Type, By Applications
o Competitive Landscape- Archer Daniels Midland Co., Ingredion Inc., Kerry Group Plc, Cargill
o Inc., and others
Market Segmentation
Global Kidney Function Tests Market by Product Type
o Dipsticks
o Reagents
o Disposables
Global Kidney Function Tests Market by Test Type
o Urine Tests
o Urine Protein Tests
o Microalbumin Tests
o Creatinine Clearance Tests
o Blood Tests
o Serum Creatinine Tests
o Blood Urea Nitrogen Tests
o Glomerular Filtration Rate Tests
Global Kidney Function Tests Market by End-user
o Hospitals
o Diagnostic Laboratories
o Research Laboratories And Institutes
o Others (Clinics, Home Care Settings, and Outpatient Centers)
Regional Analysis
o North America
o United States
o Canada
o Europe
o UK
o Germany
o Italy
o Spain
o France
o Rest of Europe
o Asia-Pacific
o China
o India
o Japan
o South Korea
o Rest of Asia-Pacific
o Rest of the World
o Latin America
o Middle East & Africa
Company Profiles
o ACON Laboratories, Inc.
o Amgen Inc.
o ARKRAY, Inc.
o BIOMÉRIEUX
o Danaher Corp.
o Diasorin S.p.A.
o Laboratory Corp. of America
o Medtronic plc
o Merck KGaA
o Nephrology Associates
o Nipro
o Nova Biomedical
o Quest Diagnostics
o Randox Laboratories Ltd.
o Siemens Healthineers AG
o Sysmex Corp.
o Thermo Fisher Scientific Inc.
o URIT Medical Electronic Co., Ltd.
The Report Covers

• Market value data analysis of 2023 and forecast to 2031.
• Annualized market revenues ($ million) for each market segment.
• Country-wise analysis of major geographical regions.
• Key companies operating in the global kidney function test market. Based on the availability of data, information related to new product launches, and relevant news is also available in the report.
• Analysis of business strategies by identifying the key market segments positioned for strong growth in the future.
• Analysis of market-entry and market expansion strategies.
• Competitive strategies by identifying ‘who-stands-where’ in the market.

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All of these are applicable to both men and women.

1. Hormonal Assessment https://discord.com/channels/1169738819688468501/1179956664221311066:

• Androgens: Elevated levels can stimulate sebum production, leading to acne.
  
• Estrogens (particularly Estradiol) and Progesterone: Imbalances can affect skin health.
  
• Hormone (LH) and Follicle-Stimulating Hormone (FSH): Important for understanding overall hormonal balance.
  
• Cortisol
  

1. Nutritional Status https://discord.com/channels/1169738819688468501/1179948530878648430:

• Vitamin D: Deficiency can impact skin health.
  
• Vitamin A: Essential for skin repair and maintenance.
  
• Serum Iron, Ferritin
  
• Zinc: Low levels can exacerbate acne.
  
• Selenium
  
• B12
  
• Magnesium
  

1. Blood Sugar and Insulin Sensitivity https://discord.com/channels/1169738819688468501/1179956411858427954:

• Fasting Blood Sugar: To check for glucose levels.
  
• HbA1c: Provides an average of your blood sugar levels over the past 2-3 months.
  
• Fasting Insulin: High levels can influence androgen production and are linked to acne.
  
• Fasting IGF-1: Implicated in stimulating sebaceous gland activity and increasing sebum production, which are key factors in acne development.
  
• Lipids
  

1. Inflammation Markers https://discord.com/channels/1169738819688468501/1179979315622973490:

• C-Reactive Protein (CRP): Elevated CRP can indicate systemic inflammation.
  
• Erythrocyte Sedimentation Rate (ESR): Another marker for inflammation.
  

1. Liver Function Tests https://discord.com/channels/1169738819688468501/1179964185203974204:

• Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST), ALP: Liver health can influence hormonal balance and detoxification.
  
• Bilirubin: High levels might indicate liver dysfunction.
  

1. Thyroid Function Tests https://discord.com/channels/1169738819688468501/1179956298041807009:

• TSH, Free T3, Free T4: Thyroid imbalances can affect skin health.

1. Gut Health https://discord.com/channels/1169738819688468501/1179978160717172776 https://discord.com/channels/1169738819688468501/1179948878267678832:

• Stool tests:
  
  • Fecal occult blood test
  • Stool pH test
  • Comprehensive stool analysis
  • Gut microbiome tests
• Intestinal Permeability Tests
  
• Celiac disease tests (blood)
  
• Urine tests:
  
  • Organic acids test
  • Intestinal permeability (leaky gut) tests
• Endoscopy and colonoscopy
  
• Hydrogen and methane breath tests: These tests can diagnose SIBO (small intestinal bacterial overgrowth), which has been linked to increased inflammation and may contribute to acne.
  

1. Food/General Sensitivity/Allergy Tests - although elimination of that food is key to determining if you have an intolerance#"Consumption - Food Intolerances (allergens and/or sensitivities)":

• IgE tests (allergies) - blood and skin prick
  
• IgG tests (sensitivies, controversial)
  

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Blog:
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Hello
25F, 130lbs, 5’10”, no tobacco, MMJ user, hydrocodone and oxyxodone as needed, cyclobenzaprine, protonix
If you read this thank you so much because I’m absolutely desperate and my doctors are tired of me and I think they think I only want pain meds. I don’t, I just want to feel better. I have a huge stash of emergency oxycodone anyway so I barely even need them for that.
On 12/15 I fell down the stairs and hit the lower of my middle back quite hard. 12/19 I had a LEEP done, 01/06 I came down with extreme urinary issues and between then and now have been back 6 times, seen 4 specialists and have seen my PCP at least ten times for urine samples. I’ve also only been able to attend my full time job for 43 days so far this year and have no more money for copays and if it weren’t for my ADA paperwork, I’d have been fired a long time ago
Over the last two weeks, it’s been taking me up to two hours to produce urine while having a full (and very sore - mostly left side) bladder. This is infuriating. When I do end up finally feeling the need to release, I have less than 3 minutes to get to a restroom before my vision starts going spotty from the bladder pressure pain.
My urologist ordered a cystoscopy, but has been blaming my 3mm kidney stone until I begged for an ultrasound last month of my bladder. Found bladder wall thickening and bladder cyst / possible urachal remnant.
I found out what Cuada equina is today. I learned that it is very very commonly missed. I can barely walk, and at the music festival I went to over the weekend I had to use ADA for just about everything. I look completely normal so I got judged pretty hard, but I do have paperwork. I have been losing weight without much diet change and my back has been killing me as well. I feel so weak. My urine flow is so small compared to what it used to be. I had a period of time where the pain was so bad, I couldn’t feel my clitoris or labia at all so sex was pointless as well, and I thought I’d lose my relationship and be alone forever. They send me to an OB-Oncologist who said not to come back, which is why my urologist finally agreed to check my bladder.
Is it possible that all my issues are related to the cyst and thickening, or could this be cuada equina that was missed on multiple CT’s? I can’t find info on bladder cysts. using retention. When is the appropriate time to go to the hospital? I can barely walk without pain meds. I urinated about 40 times on Saturday, with my usual being 10-20 times, and some days there’s very little pain or urgency at all, but the retention is almost always there to some extent.
It almost feels like the part of my brain that controls my bladder doesn’t work anymore because no matter how hard I tell my bladder to release, it just doesn’t happen sometimes and I can’t get comfortable after that. I’ve slept a total of 4 hours since Saturday morning and I only have one hydrocodone left. Pyridium does NOTHING except for when burning pain presents, and I can’t take NSAIDS until my GI clears me due to extreme gas, constipation and bloating / belching thought to be caused by peptic ulcers. I can’t walk at this point without pain meds, but the ER always releases me with the same DX of cyst and bladder wall thickening and tells me they have no clue what that means. But I’m in so much pain I feel like there has to be something they can do other than give me fluids and monitor me for an hour or two until I can get to my cystoscopy next week.
If you have any advice for me I really appreciate it. I don’t want to die but I feel the only way out of lifelong urinary pain after 6 months now is suicide. The only time suicide doesn’t cross my mind a couple times is when I do end up having to take a pain pill. In March, I had to take oxy every day. I only take them now when I can’t walk because the effects are too strong for me to keep my life in order while taking them every day. But this weekend I have had the most trouble walking, and using the restroom, since all of these issues began.
I can’t afford any more specialists visits after my procedure, so I really wish the ER could do something for me as they’re the only ones who won’t turn me away for not having money at this point. My GI doc actually canceled my appointment because I don’t have $20 and I’ve been putting off another ultrasound because it’s $200 up front. IDK what to do but I’m pretty sure this is how a lot of people end up on fent and heroin - if I had been denied pain meds this far I would have turned to the streets, and that’s coming from someone who has chosen - on their own - to quit most drug related and extracurricular activities to better their life at a young age and is much happier for it.
I can’t even get the ER to catheterize me when I can’t urinate for 6+ hours at a time. What gives? Why won’t they run a different imaging test? They wouldn’t even give me a breath test for h pylori recently and now I’m waiting a month for an appointment I can’t even afford.
TL;DR extreme bladder pain, nobody understands why, extreme difficulty urinating, ER can’t do anything for me and awaiting surgery. Is there anything I can say or do to get proper medical attention or can the ER really not touch your bladder like they say? Is there a way I can convince them to admit me so I could see a urologist before my procedure? My urologist is unavailable until my follow-up and I don’t think the company they work for allows them to Rx narcotics and I’m against taking more than 1 oxycodone a week at this point but so far have been unsuccessful in getting something weaker like hydro or tramadol.

I have recently sustained an injury at my place of employment back in December of 2023 and found out I was terminated. I worked at a place that specializes in selling chicken wings and worked forty plus hours every week. I pulled something in my neck and back trying to pull out the flat top grill and refrigeration unit combo to spray down the floors and clean underneath the units as it was a daily task. I felt a discomfort that first night and thought nothing of it. As the week progress I was having tingling, burning, pin like, and numbness in my right arm and shoulder. I mentioned the discomfort and the night I starting feeling it to my manager which he wrote up the incident report. I was referred to their primary care doctor to submit an urine analysis and a check up. Once I arrived at the clinic and waited to be seen I told the clinic several times I was here for workman comp claim and needed to pee. They took me back to a room to see a doctor. I explained the problem and issues I was experiencing which she wrote me a work note for work restrictions believing it was my elbow and called it tennis elbow. I was out a week due to the restriction and rested. Once a week had passed I asked to be placed back on the work schedule and was told I never submitted the urine analysis and I stated I told the clinic I was there for a workman comp claim and was there to pee and be checked out by a doctor. My manager said I couldn't return to work until I submit the urine analysis. I returned to the clinic and told them I needed to submit the urine analysis and was seen that day to be tested. I dropped off the paperwork from the clinic and went home. I had to wait another week til I was allowed to return to work. I work for about two and a half weeks of working doubles before the pain returned but was much more intense. I mentioned the pains I was getting again and asked to be moved to a different station because I had been working the same station for the last couple of weeks and would like to work in a different station in the kitchen and the manager ignored my request. One night during my shift I left work to go to the E.R. because if felt like someone was taking a dull blade and digging it into my shoulder blade and my right hand had swelled up. After sitting in the E.R. bed for a couple of hours I was released from the hospital with another work restrictions stating not to use my right arm as much. I returned to work to drop off the note and see if my employer could accommodate my restrictions such as a different position within the business and was told no they couldn't. immediately they deleted my login to all platforms such as schedules, pay stubs, employee clock in number. I have several pictures of my trying to log into my payroll site and scheduling site and text box telling me to contact management. I have an audio recording of one the managers telling me I was fired immediately after the incident. I believe they terminated me as a retaliation for the workman comp claim and didn't expect me to follow through. I have mediation on the 28th of this month and not sure was I should ask for. Sorry for the awful grammar and spelling this is my first time posting anything

Domestic shorthair cat; 1 years old; spayed; 8 lbs No hx Clinical signs: peed outside the litter box for the first time last week. She also loves running water and playing in her water bowls if that’s relevant. Labs: blood draw with elevated muscle enzymes (vet stated this is typical just from the experience of going to get bloodwork)
My cat peed outside the litter box once last week so I took her to the vet to check. She didn’t have a full bladder so they gave me some plastic pellet things and a cup to get a pee sample from her.
It didn’t work for the 8 hours each day I had her separated from my other cat for 2 days. I had a litter box with the pellets and food/water in there. The second day, she ran out of the room to the real litter boxes and peed. As I stood disappointed. But I don’t want to make her hold her pee - that seems just as bad.
I think she’s fine and I probably overreacted. She peed on a piece of plastic and the vet said cats like to do that. I gave them a stool sample. But I’d like to be thorough and get the urine analysis done. Any other ways?

Species: cat Age: 1 years old Spayed Breed: Domestic short hair Weight: 8 pounds No hx Clinical signs: peed outside the litter box for the first time last week. She also loves running water and playing in her water bowls if that’s relevant. Labs: blood draw with elevated muscle enzymes (vet stated this is typical just from the experience of going to get bloodwork)
My cat peed outside the litter box once last week. I don’t like to wait and see so I took her to the vet. She didn’t have a full bladder so they gave me some plastic pellet things and a cup to get a pee sample from her.
It didn’t work for the 8 hours I had her separated from my other cat for 2 days. (8 hours each day). I had all her items, a litter box with the pellets and food in there. The second day, she ran out of the room to the real litter boxes and peed. As I stood disappointed. But I don’t want to make her hold her pee - that seems just as bad.
I think she’s fine and I probably overreacted. She peed on a piece of plastic and the vet said cats like to do that. I gave them a stool sample. But I’d like to be thorough and get the urine analysis done. Any other ways?

A lot of people from this subreddit have been asking this question and i got this article together to answer that question. I hope it helps. Cheers.

I honestly have found great help when i started taking Omega 3 in a daily basis, Vitamin B1 B6 B12, enough zinc, magnesium and Vitamin D.
PS : for those who also want to increase their testosterone, improving your mood and lowering Cortisol greatly helps.

Stress Reduction

Our bodies release cortisol when stressed. Cortisol decreases serotonin levels in the body, by increasing serotonin reuptake. Too much cortisol can increase your risk of developing mental health disorders. That is why reducing mental stress can help balance cortisol levels and increase serotonin
Many of the lifestyle changes below can be used to decrease stress.

Mood Improvement

Serotonin impacts our mood, but mood also affects serotonin production. Studies using brain imaging (PET), showed that brains of people who are happy produce more serotonin than brains of people who are sad
Therefore, engaging in activities and doing things that make you happier can help boost serotonin production.
In addition, studies show that social interactions also influence serotonin levels. Spend more time with people who make you feel good in general

Exercise

Fatigue, as a result of exercise, increases the amount of tryptophan that can cross the blood-brain barrier (by decreasing BCAA levels) and thereby boosts serotonin production. Psychological benefits of physical exercise can be more readily achieved with consistent aerobic exercise training
Mice that ran on treadmills had higher levels of serotonin compared to mice that remained inactive. Brain tryptophan remained high even after exercise

Getting More Sun

It has been long known that bright light helps treat seasonal depression. But several studies suggest that light is also an effective treatment for other forms of depression
People have higher serotonin levels in the summer compared to winter
In fact, our modern way of life, in which we spend a lot of time indoors, may be depleting our serotonin levels, thereby making us more vulnerable to mood disorders
Pioneer studies suggest that our skin may produce serotonin when exposed to sunlight
In addition, you need vitamin D to produce serotonin, and sun to produce vitamin D
Therefore, going outside and spending more time in the sun on a regular basis is a great way to boost your serotonin levels.

Yoga and Meditation

A review of over 200 peer-reviewed RCTs, clinical trials, and meta-analyses studying complementary and alternative medicine suggest that yoga and meditation may help uplift mood and improve symptoms of mild, moderate, and treatment-resistant depression
In fact, meditation activates many parts of the brain important for understanding the self, emotions, problem-solving, adaptability, and increasing awareness. Serotonin plays a role in wakefulness, along with other neurotransmitters, which are all raised in meditators
Thirty minutes of yoga and breathing exercises improved mood in a study of 71 healthy adults

Psychotherapy

Psychotherapy or counseling may change brain chemistry and even increase serotonin activity (by increasing serotonin receptors). In a (DB-RCT) study of 23 patients with depression who participated in psychotherapy for 4 months, therapy significantly increased serotonin activity and improved symptoms of depression

Eat to Increase Serotonin

Tryptophan is the amino acid building block for serotonin. Tryptophan is not produced by the body, so it must be taken in through diet.
Current research shows that unlike purified tryptophan, consuming tryptophan-rich foods does not necessarily increase brain serotonin. That’s because tryptophan-rich foods, such as meat, dairy, fruits, and vegetables, also contain many other amino acids. Tryptophan has to compete with these other amino acids for transport across the blood-brain barrier
On the other hand, lack of dietary tryptophan (compared to other amino acids) may lead to lower blood and brain tryptophan levels, decreasing serotonin production. Increased BCAAs also lower tryptophan and serotonin, as well as dopamine in the brain. This may be especially problematic for people who take protein powders to enhance exercise performance

Carbs

Consuming carbs increases serotonin levels by increasing the transport of tryptophan into the brain
However, you should use other methods to boost your serotonin, as increasing carbs in your diet can have a plethora of negative effects.

which Supplements can Increase Serotonin?

L-Tryptophan and 5-HTP

In the body, L-tryptophan is used to make 5-HTP from which serotonin is made. Taking L-tryptophan may raise plasma serotonin, improving cognitive, motor, or gut issues in those who are deficient
A protein called alpha-Lactalbumin from milk contains more tryptophan than many other proteins. In a (DB-RCT) study of 18 inpiduals, 12 grams of alpha-Lactalbumin increased the amount of tryptophan in blood plasma by 16% after 90 minutes
In another (DB-RCT) study, 12.32 grams of tryptophan increased blood tryptophan by 43% after 1.5 hours and improved memory in 23 subjects vulnerable to high stress
In a pilot study of 13 female patients experiencing premenstrual syndrome (PMS), 6 grams of L-tryptophan taken daily for 14 days improved mood, irritability, difficulty sleeping, and carbohydrate craving
Tryptophan can be purchased in the form of L-tryptophan supplements. 5-HTP (5-hydroxytryptophan) supplements are also available. It is important to note that 5-HTP is not the same as 5-HT, which is the chemical name for serotonin. 5-HTP freely crosses the blood-brain barrier (serotonin itself does not) to be converted into serotonin

Probiotics

In the digestive tract, probiotics restore the gut microbiome and influence the gut-brain axis. Gut bacteria are important because they can produce tryptophan, from which serotonin is made. Many mental health disorders, such as Parkinson’s disease, are linked to less perse or fewer gut bacteria
In a study (DB-RTC), an 8-week probiotic regimen (2.0 x 109 CFU/g of Lactobacillus helveticus and 2.0 x 109 CFU/g of Bifidobacterium longum) increased tryptophan levels in 110 inpiduals with depression. Increased tryptophan can increase serotonin production
A probiotic (Bifidobacteria infantis) given to rats for 14 days raised levels of blood tryptophan

Vitamin D

Vitamin D helps the body make, release, and use serotonin in the brain. Vitamin D activates an enzyme that converts tryptophan into serotonin. If vitamin D levels are low, our brains make less serotonin. Thus, increasing vitamin D intake increases serotonin levels, reducing the risk of mental health disorders
A cohort study of over 9K subjects demonstrated that taking vitamin D supplements during the first year of life was correlated with a 77% reduced risk of schizophrenia. In other words, preventing low vitamin D levels early in life may reduce the chance of having schizophrenia later in life

Omega-3 Fatty Acids

While vitamin D helps neurons make serotonin, the omega-3 fatty acids, EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), help neurons release serotonin and improve its activity (increasing serotonin receptor sensitivity). Fish, such as salmon or trout, are high in omega-3 fatty acids. The omega 3 fatty acid supplements are also sold as fish oil capsules
Inadequate omega-3 fatty acids intake may increase susceptibility to psychiatric illnesses, including depression
In a (DB-RCT) study of 49 patients that repeatedly self-harm themselves, 1.2 grams of EPA and 0.9 grams of DHA capsules daily for 12 weeks reduced suicidal thinking by 45% and depression by 30%
An observational study of 256,118 Japanese participants, discovered that people who ate fish daily had lower rates of suicidal thoughts compared to people who did not eat fish daily. In another observational study of 1,767 Finnish subjects, consuming fish less than twice a week was associated with a higher risk of depression and suicidal thinking
In rats, low levels of omega-3 fatty acids (specifically alpha linoleic acid) are associated with lower serotonin activity, while DHA deficiency reduces brain serotonin in piglets
Reduced intake of both EPA and DHA by pregnant rats resulted in less production, storage, release, and activity (receptor function) of serotonin in the brains of their offspring. Serotonin was not only reduced in the mothers’ brains but also its availability and production were reduced by (65% and 29%, respectively) in the brains of newborn rats

St. John’s Wort

St. John’s Wort is a popular medicinal plant (Hypericum perforatum) used as an antidepressant for mild depression.
The plant increases serotonin in animals, similar to typical antidepressants, but with fewer side effects
In a review (of 35 studies) of 6,993 patients with depression, St. John’s Wort standalone therapy improved mild to moderate symptoms as well as antidepressants and better than placebo. The typical dose is 300 mg of the extract 3 times per day for at least 4 weeks

S-Adenosyl Methionine (SAMe)

SAMe is needed to produce serotonin
It is a naturally occurring compound that plays a role in methylation, energy breakdown and may help patients with major depressive disorder (MDD) who are not responding to conventional, synthetic antidepressants
In a (DB-RCT) study involving 73 MDD inpiduals unresponsive to drug therapy, 800 mg twice a day improved symptoms of depression compared to the placebo
In a (DB-RCT) study of 144 inpiduals with MDD, 1,600 – 3,200 mg of SAMe daily for 12 weeks significantly improved mood
A review of 132 studies (115 CT and 17 preclinical) concluded that SAMe can be useful not just for depression, but for an array of mental health disorders, such as substance abuse and psychosis

Vitamin B

Lack of vitamin B may be associated with the onset of mental health disorders. The body needs Vitamin B6 to make neurotransmitters like serotonin from 5-HTP (Vitamin B acts as enzyme cofactor)
Vitamin B12 and folate (vitamin B9) are necessary for the folate cycle, which helps convert tryptophan into serotonin (by producing and recycling essential co-factors)
In a cohort study of 549 community-dwelling seniors, those with low vitamin B12 and B9 blood levels were more likely to have irreversible problems with cognition (memory, attention, and thought)
In Rhesus monkeys, a single dose of vitamin B6 increased serotonin production in the brain
In addition, treatment of healthy adult rats with a vitamin B mixture raised serotonin levels in the brain

Vitamin C

Vitamin C supplements over a period of 6 weeks increased brain serotonin levels in rats with drug-induced dementia

Vitamin E

Vitamin E supplementation for 8 weeks increased serotonin in rats suffering from spinal cord injury

Zinc

Zinc can target and activate serotonin receptors
In a meta-analysis of 17 observational studies, blood zinc levels were lower in depressed inpiduals compared to non-depressed inpiduals
In a study (DB-RCT), 25 mg of elemental zinc supplements daily for 12 weeks reduced depressive symptoms in a study of 37 patients with major depressive disorder
Zinc can be increased through diet in foods such as red meat, oysters, and whole grains

Magnesium

Magnesium supplements increase serotonin levels by increasing its availability (reducing reuptake) in the brain. In a (DB-RCT) study, 500 mg of magnesium per day for 8 weeks significantly improved symptoms in 60 patients diagnosed with mild to moderate depression
Magnesium is found in green leafy vegetables, nuts, and legumes

Inositol

Inositol increases the sensitivity of serotonin receptors
In one study of 30 women with a PMS mood disorder, myo-inositol reduced symptoms and improved mood given over 6 menstrual cycles
Inositol decreases depression in rats by binding serotonin receptors

Turmeric

Curcumin is the active component of turmeric. In stressed rats, curcumin extended the length of time serotonin stays active in the brain (by blocking the reuptake of serotonin). It also improved cognition and reduced serum corticosterone, a cortisol equivalent, in rats
In mice, a single dose of curcumin (10 – 80 mg/kg) increased serotonin levels

Velvet Bean

Mucuna pruriens, known as the velvet bean, combats Parkinson’s disease better than the standard treatment (levodopa) in rats. In addition to being a source of dopamine, the long-term use of the powder form of Mucuna pruriens also restored serotonin levels in rat brains

L-Theanine

L-theanine, an amino acid found in tea leaves (e.g. green, black, or oolong tea) and Bay Bolete mushrooms, has relaxing effects on the mind. Green tea has the highest concentration of L-theanine
In a cohort study of over 42K Japanese inpiduals, those who consumed at least 5 cups of green tea a day experiences less psychological distress that is often associated with reduced serotonin
In rat studies, L-theanine raised serotonin levels in the brain

Rhodiola

Rhodiola rosea is a flowering plant that may help improve anxiety and depression. In a (DB-RCT) clinical trial of 89 patients with mild to moderate depression and low serotonin, Rhodiola rosea extracts (340 mg/day and 680 mg/day) for 42 days improved overall depression, including insomnia and emotional instability
In 70 depressive rats suffering from chronic mild stress and serotonin deficiency, Rhodiola extract (1.5, 3, or 6g/kg) for 3 weeks restored normal levels of serotonin

Saffron

Safranal, one of the main active components of saffron (Crocus sativus), increases serotonin availability in the brain (by blocking reuptake)
A meta-analysis (5 RCTs) of 177 participants concluded that 30 mg per day of saffron capsules can improve symptoms of depression in adults with major depressive disorder within 6 to 8 weeks

Psychedelics

Psychedelics are hallucinogenic drugs such as lysergic acid diethylamide (LSD) and psilocybin mushrooms. Psychedelics can stimulate serotonin activity (by directly binding to serotonergic receptors and also increasing their number), raise serotonin levels, and reduce its breakdown
In a recent pilot study (DB-RCT) of 12 patients with anxiety, 200 μg of LSD significantly reduced self-reported anxiety. LSD was given in a safe psychotherapeutic environment with medical supervision to avoid side effects
In a (DB-RCT) study of 17 healthy inpiduals, psilocybin (215 micrograms/kg) enhanced mood, increased goal-directed behavior and decreased recognition of negative facial expressions
Though psychedelics can activate serotonin signaling, unsupervised use may lead to serious psychological consequences. Certain plant hallucinogens, as well as synthetic hallucinogens, can be especially toxic. Using this substance should be under professional supervision.

Magnolia Tree

The bark and seed cones of the Magnolia tree (Magnolia officinalis) appear to have anti-stress, anti-anxiety, and antidepressant effects
20 and 40 mg/kg of honokiol and magnolol, the main components of Magnolia officinalis, restored low levels of serotonin in rats with chronic mild stress
Magnolia bark and ginger rhizome are commonly used to treat mental disorders in traditional Chinese medicine (TCM). 30 mg/kg of a magnolia bark and ginger rhizome mixture increased serotonin in the brains of depressed mice

Essential Oils

Essential oils are commonly used to reduce anxiety, stress, low mood, and other mental health disorders. Smelling the essential oils (inhalation) can activate pathways in the brain to boost serotonin and dopamine production
In a study of aromatherapy in 60 elderly patients with depression (RCT), 5 ml of essential oil mixture (containing lavender, sweet orange, bergamot, and almond oil) increased serotonin levels after application two times a week for 8 weeks
Ylang-ylang essential oils increased serotonin levels in mice brains (hippocampus)
Bitter orange is an essential oil that reduced anxiety and improved mood by boosting serotonin activity in mice after 14 days of use
Lavender oil blocked the breakdown/reuptake of serotonin in cell studies

Valerian

The root of the Valerian plant increases serotonin levels and activity (by decreasing its turnover)
Valerian may help with irritable bowel syndrome. In a rat study, components of the Valeriani root balanced overactive serotonin in the gut (colon) and serum
Valeriana officinalis root extract prevented the breakdown of serotonin in mice exposed to stress

Apigenin

Apigenin is a nutrient in citrus fruits that may improve cognition and behavior as well as symptoms of depression and stress
In mouse models, 20-day treatment with apigenin (10 and 20 mg/kg) increased serotonin levels, and decreased anxious behavior
Apigenin was able to reduce the impact of chronic mild stress in rats by increasing serotonin availability and reducing its breakdown

Berberine

Berberine is a salt derived from plants in the Berberis family (the roots, rhizomes, stems, and barks), including barberry, tree turmeric, Oregon-grape, and others. It blocks the enzyme MAO-A, which breaks down serotonin, thereby raising serotonin levels
A single berberine dose increased levels of serotonin by 47% in the brains of depressed mice. Long-term treatment with berberine (5 mg/kg for 15 days) increased serotonin by 19%
Mice given berberine in a different study had increased serotonin levels in regions of the brain (hippocampus and frontal cortex) important for memory and mood

Acetyl-L-Carnitine

Carnitine may increase serotonin in the cerebral cortex, a region of the brain involved in cognition and memory
Acetyl-L-carnitine (ALCAR) is a modified form of carnitine, a common dietary supplement sold in health food stores. ALCAR protects the brain and may help with depression. In mice, it increased levels of serotonin in the brain when given daily for 25 days

Lithium

Lithium has long been used in the treatment of mental disorders such as bipolar disorder. It works by increasing serotonin activity in the brain

Physical Treatments that Increase Serotonin

Neurofeedback

Neurofeedback allows inpiduals to consciously change their brain activity (EEG waves) and therefore modify their behavior and cognition. Some of its clinical uses are for migraines, ADHD, and PTSD
In a study (RCT), neurofeedback (30 minutes, 5 sessions weekly, 4 weeks) was applied to 40 patients with fibromyalgia syndrome (FMS). FMS patients have lower serotonin and widespread pain in their muscles and bones. After 2 weeks, patients experienced less pain, fatigue, anxiety, and depression

Massage

Massage therapy decreased cortisol and raised serotonin and dopamine in a broad population with stress-related health problems in 3 studies
In one (RCT) study, 24 adults with low back pain were either given two 30 minute massages per week or subjected to standard relaxation procedures over the span of 5 weeks. Urine serotonin levels were higher in inpiduals who received massage therapy

Acupuncture

In a randomized clinical trial, 75 women with fibromyalgia, acupuncture increased levels of serotonin in the serum, compared to placebo
In rats, acupuncture-like stimulation increased serotonin activity in certain regions of the brain

Light Therapy

When sun exposure is not possible, bright light therapy can help increase serotonin levels
Bright light therapy (photobiomodulation) shows promising results for depression based on clinical trials
In a study of 10 women with chronic headaches (observational), 34 seconds daily use of low-level laser therapy (LLLT) significantly increased serotonin levels after just 3 days
In a study of 25 drug-free hospitalized veterans with depression or bipolar disorder, bright white light improved depressive symptoms. However, further testing needs to be done on the negative consequences of long-term light treatment

Vagus Nerve Stimulation

Long-term vagus nerve stimulation (14 days) increased serotonin levels in rat brains
In rats, sustained vagus nerve stimulation for 14 days also increased the action of serotonin

Testing Serotonin

Serotonin that gets released into the blood gets rapidly broken down in the liver and lungs, to inactive metabolites (such as 5-HIAA) that are excreted in urine . That is why normally, blood and urine contain very small amounts of serotonin. Larger quantities of serotonin in the blood/urine can be found in people with serotonin-producing tumors (carcinoid tumors).
Beware of the use of urine serotonin levels to check for “neurotransmitter imbalances”. While the companies providing these tests state that the levels in urine correspond to brain neurotransmitter levels, science has repeatedly shown that this is not the case
Serotonin doesn’t cross the blood-brain barrier. Even if it did, it is released intermittently and influenced by many different stimuli. Furthermore, levels differ within different parts of the brain. And finally, values differ for the same person from one day to another
In addition, companies have been known to intentionally use extremely narrow ranges, without any scientific support whatsoever, in order to sell supplements to their clients
If you do have neurotransmitter imbalances in the brain, more reliable tests of serotonin levels are cerebrospinal fluid tests or measurements of serotonin in blood platelets
A PET scan is the only direct way to detect changes of serotonin production in specific areas of the brain
Serotonin Risks and Safety
Excess serotonin may result in serotonin syndrome, which can be fatal. Usually, though, serotonin syndrome is a result of drug interactions. No cases have been observed just from safe, natural approaches
MDMA, LSD, and other synthetic drugs may cause serotonin syndrome, and should not be taken without medical supervision or outside a psychotherapeutic environment
Most of the studies mentioned above were performed on adults. More research involving children is needed in order to determine safety.
Abnormally heightened levels of serotonin (hyperserotonemia) is a consistent finding in inpiduals with autism. Pregnant women with hyperserotonemia are more likely to give birth to children with autism

Drug Interactions

The use of St. John’s Wort, SAMe, or lithium simultaneously with serotonergic drugs like selective serotonin reuptake inhibitors (SSRI), monoamine oxidase inhibitors (MAO-I), and triptans, can increase the risk of serotonin syndrome, a life-threatening and potentially fatal condition

Limitations and Caveats

Some of these studies have fairly small sample sizes. Additionally, many of these natural methods of increasing serotonin in the body have only been tested in animals and need further research in humans through clinical trials.
In addition to the concentration of serotonin, both the number of serotonin receptors and their sensitivity may also play an integral role in determining serotonin activity.
Though serotonin is mostly made, stored, and released in the gut, serotonin acts as an important neurotransmitter in the brain. Some of these natural remedies and supplements need further testing to determine if they are able to cross the blood-brain barrier. Long-term application of these remedies should also be further studied.

firstly thnx really for all doctors here who is helping people and answer their questions, My message is a bit long, but I wanted to mention all the details. My problem is in the specialty of urology. I'm an athletic young man with no health problems, age 34, single, never had sex before, I masturbat for a few times a weekly, About five months ago, I suddenly and without warning, and immediately after I got out of the shower, experienced severe pain in the left testicle, abnormal pain, to the point that I could not walk or stand due to the severity of the pain. At the same time, I felt pain in my bladder, like a rupture, and I began to urinate a lot. An entire night like this, I used a pain killer that I had, and then the testicle pain began to ease and return until the morning. The second day the pain returned, I went to a nearby hospital, but there was no doctor whose specialty was urology, so they gave Ciprofloxacin 500 and a painkille- diclofenac potassium 50. I used these pills for the next days, The result was the disappearance of the left testicle pain, but a constant feeling of mild pain in the bladder, frequent urination, a constant feeling of the presence of light urine in the urethra, and really strong weakness in the bladder muscles, and I feel when I squeeze the bladder to expel urine that it comes out weakly, and when I squeeze the bladder muscles I do not feel strong control on it as before. The most important thing is a feeling of lack of sexual desire, the absence of a morning erection, and the difficulty of maintaining an erection. I felt that the desire was 90% absent. I stayed like this for a week and I was surprised because usually my desire is strong and I always have a morning erection. Even after that I tried masturbating, but the erection was weak, the desire diminished. To a very large extent, ejaculation was rapid and at an unusual time, and there was no ejaculation, only fluid came out. Unlike my normal condition, the ejaculation was strong and the erection took a long time to disappear, and even after ejaculation the erection remained.
I stayed like this for a while, taking ciprofloxacin, and the symptoms were the same. In fact, I thought I had an enlarged prostate. After two weeks, I visited a urologist in my area, after examining and taking an ultrasound of the area of ​​the ureters, kidneys, and prostate. The doctor did not order a urine analysis or anything, and he said that there is nothing wrong with you and the prostate is fine. Your problem is simple, and it is bloating in the colon that has affected the bladder, and it goes away with time and you will return to your normal condition as soon as possible. He prescribed me Ciprofloxacin 500 two pills a day, and he said take the medicine until you return to normal and there is no need to review, and this has been going on for 4 months and a little, and now I am taking two pills in the morning and evening. If I quit the medication, I feel worse. My current situation: - Urinate quickly after drinking fluids - A feeling of heat in the body in general and constant heat in the genital area after every morning awakening - A feeling of coldness in the head of the penis always - Almost complete absence of sexual desire (and I was usually very active, meaning that I had an erection in the morning and thought less about topics of desire, as there was a response from my body) - Erection is very weak, ejaculation is rapid and small in quantity and comes out without ejaculation. (I tried masturbating several times during this period to see if my condition was normal or not.)

• After ejaculation, sexual pleasure disappeared by 80 percent compared to my previous normal state.
• The external area of ​​the penis began to feel that its response to the sense of touch had diminished by 50 percent or more, to the point that sometimes I pinched it forcefully and did not feel anything. Unlike before, the penis was sensitive to any touch.
  My psychological condition has worsened for these reasons, and I want to visit a good doctor later im looking for a new one in my area,cuz i live in a place wich doesn't have the good doctors. In general, what do the specialists think about this case, Will I remain like this, because I really feel that I have become sexually impotent?
  

*sorry for my english, it not my native language

Our sweet 9 year old female cat has been acting strange the past month like she's in heat. She's was spayed when she was very young (blue dot on tummy to confirm), and has never acted like this before. We thought it was due to tooth pain (resorption) but she's still having these symtptoms after the extraction.
Symptoms: - urinating outside of the box (mostly walls, not an accidental miss), which she's never done before. We keep the litter boxes clean and have multiple. - howling loudly, quite frequently - squatting with butt in the air - grumbling - some clear liquid from her rear when squatting - rubbing face on things more often than usual
She's strictly an indoor cat. We have another indoor only spayed female cat and she hasn't had any issues.
We thought maybe it was a UTI and she was just straining to pee, but multiple vet visits have not found anything with a physical exam, bladder ultrasound, blood work (protein / blood counts) or urine analysis.
Has anyone else experienced this? Or have ideas of what may be going on?
We're planning to do a follow up visit with our vet but wanted to see if we could get a better idea of what to look out for or check.

It started with a UTI 3 weeks ago when I started experiencing pain/urgency in the bladder. Consistently the pain has been a feeling of urgency and burning sensation with some relief during urination but the symptoms get worse after urination (within 15-minutes) and the pain gets much worse at night. There has never been blood, though I have noticed some sediment in my urine and stuff in my urine. Sometimes there is cloudiness in the last few drops after I pee
I first went to urgent care and the PA said the rapid test did not show a positive results but I had the symptoms of a UTI, so she prescribed me Macrobid for 5 days and in parallel ran a cell culture test. The symptoms got better for the next day or so, but came back towards the end of the treatment. The cell culture results came back as "mixed urogenital flora" which was puzzling considering the extent of the pain. I went to a different GP and they also did not find anything in the rapid test and they said the urine analysis didn't indicate any infection or kidney disease. They suggested IC and referred me to a urologist but it would take at least 2 weeks to get an appointment! The next week was hell with managing the pain. I ended up in the ER where they ran blood tests, urine tests, and CT scan and found nothing. Finally about a week later, reached out to me saying that they found a bacteria called klebsiella aerogenes (I guess they had been running the cell culture all along and did not tell me). They prescribed Bactrim for 2 weeks since Macrobid is not as effective in treating this strain. Immediately after starting the Bactrim I started feeling better but 5 days in it took a turn for the worse and the pain came back with a vengeance. At that point I also started getting a fever, GI symptoms, chills, achy and just feeling really sick. My GP agreed that it was not normal and expedited my visit with the urologist. The urologist ran another cell culture to rule out the possibility of another infection. The results were negative and they said the infection was gone, so to stop the Bactrim at 7 days. The fever, chills, and achiness went away after 2 days of stopping the antibiotic.
However, the pain/urgency have not gone away after 3 weeks. The urologist said that in some people with OAB (overactive bladder), there can be residual inflammation after an infection which can cause pain, so in the meantime he prescribed me Oxybutin to treat the urgency. However, this broke me out into a rash. After 2 days of being off the Oxybutin, I am starting Myrbetriq today. Yesterday the symptoms were much more manageable even at night, but today they have come back throughout the day so I am really worried about tonight.
The things that have helped me find some relief are walking, yoga but the pain always comes back. It's really hard to tell what triggers the pain and to manage it. I'm avoiding doing a lot of things that will trigger the pain and I'm not sure what triggers it or if it's really IC or another infection or what is happening. I have been in agony and just need some relief. Please if anyone has any suggestions of things to try that have worked for you in a similar situation? I am also just really scared that this is never going to go away. I am so afraid of spending even another week with this pain and need to find some relief while we figure out what is going on. I hope the Mytrebiq will work temporarily but need a back up in case it doesn't. Thank you!
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If this is real I’ll change the title and the post flair to evidence. If it’s real it shows us that the Arvizos were gone most of the day for Gavin’s kidney and urine analysis and did not get to back to Neverland for a long time.

Disclaimer:

Despite how the title and intro may look, I am not here to dunk on feminism. If you came looking for a post that said, "Feminist Soy! Am i rite?" Sorry, got to disappoint. Conversely, this isn't a sermon about why you should convert. Believe whatever you want to believe bro. Also, Not a Christian, but I do like Wendigoon talking about it. Finally, Mods plz don't nuke my post this isn't about religion but about the mythology around the figure.

Why Post This Here:

Lilith has been involved in literary discourse for a while as well as being seen as a Feminist Icon in literature. This post is meant to debunk these claims and misreading of the Abrahamic Myths.

Intro:

This really isn't a specific work of fiction, but rather, a general fictional trope I guess., Ever since the release of Hazbin Hotel, discussion has increased on Lilith being a sympathetic/feminist icon, and this is the most laughable idea to me as a guy who is currently studying Christian Mythology for a project. Today, I am going to debunk this claim of Lilith being sympathetic or any sort of feminist girlboss or even being anyway relevant to the Abrahamic Mythos. I'll try source all my arguments, so it doesn't look like I am talk out of my ass.

In The Bible:

Ah, the Bible. It is amazing how such a small book can cause so much violence, but we are not here for a religious debate (well not really). We are here to discuss Lilith. For context, I am going to be used the New Revised Standard Version (NRSV) & English Standard Version (ESV). This is because NSRV and ESV and considered the most popular when it comes to the Bible Versions.
Let's start with NRSV, and Lilith shows up...once? Hell, she doesn't even show up. She's just mentioned.

Isaiah 34:14: "Wildcats shall meet with hyenas, goat-demons shall call to each other; there too Lilith shall repose,"

You can read the full chapter here, but the full chapter really doesn't change much. From what I could gleam (admittedly I ain't a theologian so I could be missing stuff), the dude in this chapter is talking about God's Judgment and is more focused on the natural disasters that would happen. Lilith isn't even really that important. She seems to be at best a higher demon with some power, but this same chapter says an undead apocalypse will happen. She is a footnote at best.
Okay what about ESV? It is even worse there. She doesn't even show up.

Isaiah 34:14: "And wild animals shall meet with hyenas; the wild goat shall cry to his fellow; indeed, there the night bird settles and finds for herself a resting place" (Source)

Okay, but I am clearly cherry-picking though right? What about the other versions? Well, it get even more nebulous. In certain version, it isn't even Lilith but an unnamed night-demon (Source). In others, it isn't even a demon but just a creature of the night/ animals of the night (Source). Hell one of them there are no demons instead an unnamed ogress (Source).
You'd think that Lilith, being the first woman and rebelling against Big G himself, should get more than one very sketchy mention. I mean Eve the mother of humanity is mentioned between 2,000 -2,500 times (Source), Mary the mother of Jesus Motherfucking Christ himself gets around 40 times (Source), hell Queen Sheba, whose existence I only know because a sword in KCD is name after her, is mentioned nearly 70 times (Source)(obviously this varies on which version you take as some books are just removed but the point stands). You mean to tell me a fucking side character is mentioned more than literally Female Satan. Funnily enough, Satan is only mention like 30 times in the Bible (Source).
Okay, so already the foundations of Lilith are shaky, but what do the other Abrahamic Religions say?

In The Quran/The Tanakh (IMPORTANT):

The Quran. She never shows up. Weird since both Eve and Mary get mentioned.
Okay, but what about The Tanakh? (For those who don't know the Tanakh is the "Hebrew Bible". A lot of people say that's the Torah, but the Torah is just the compilation of the first five books of the Tanakh.) Well, yes.

Otzar Midrashim, The Aleph Bet of ben Sira, The Alphabet of ben Sira, (alternative version) 34 - He said to him, "The angels appointed for healing: Sanoy, Sansanoy, Semangalof. When the Holy Blessed One created the first Adam alone, They said, (Genesis 2:18) 'It is not good for this Adam to be alone.' They created for him a wife out of the Earth like he had been, and called her Lilith. Immediately they began to challenge each other. She said, 'I will not lie below,' and he said, 'I will not lie beneath you, but only on top. For you are fit only to be in the bottom position, while I am to be the superior one…

So case closed - STOP. I ain't done cooking yet. See, I got to apologize a bit to you reader. I kind of lied, but to understand how I lied. You got to understand the Jewish Faith first, specifically their holy texts.
Okay, all Holy Jewish Texts fall under Sifrei Kodesh (aka Holy Books). . Within the Siferi Kodesh, there are two main categories texts fall into Tankah and Rabbinic. The Tankah is The Hebrew Bible. It is the considered the canonical collection of Hebrew scriptures and is comprisied of the Torah, the Nevi'im, and the Ketuvim. (Source and Source). Meanwhile, the Rabbinic is Jewish Rabbis studying and interpreting the Tankah (Source, Source, Source). The Alphabet of Ben Sira is squarely in the Rabbinic.
Most of you have already seen a problem, but for those of who didn't, let me spell it out. When you are quoting this passage, you are not quoting from the Tankah. You are quoting a Rabbi's interpretation of the Tankah. This would be equivalent to me using My Immortal to critique Harry Potter (No offense to any Jewish Rabbis. This comparison is meant to be extreme).
Ah, but ain't done yet reader, I have saved the biggest bombshell for last.
The Alphabet of Ben Sira is a shitpost. It a satire. It isn't real.
The reasoning is several. This reddit comment sums it up. And This. Also This
From The Jewish Virtual Library:

There is no reason to doubt the unity of the work as a whole, despite the fragmentary character of the different versions. All the versions share a special, satirical, and even heretical, character, and this indicates that they all were written by a single hand. They seem to reflect varying degrees of censorship on the part of editors and copyists. The complete work contains four parts. The first part is the biography of Ben Sira from his conception until the age of one year. This story, omitted in many editions, explains how Jeremiah, the prophet, was simultaneously Ben Sira's father (the numerical value of Ben Sira's name equals that of Jeremiah), and grandfather. Ben Sira's mother was Jeremiah's daughter. The old prophet was forced to an act of onanism by wicked men, and his daughter conceived from his emissions when she came to bathe. The form of this story is based on a biblical verse that tells the glories and wonders of God's deeds; thus the story satirizes not only Jeremiah, but God's deeds as well.
The second part is more sophisticated in form. It tells how Ben Sira, now one year old, meets with his teacher, who tries to teach him the alphabet. Instead of repeating each letter of the alphabet after his teacher, Ben Sira responds with an epigram beginning with that letter. The epigrams lead the teacher to tell the story of his life. It may be assumed that the original structure of this part was 22 + 12 paragraphs, each containing a letter, an epigram, and a part of the story.
The third part is the longest and contains most of the narrative material in this work. It recounts the story of Ben Sira's life and adventures in the court of Nebuchadnezzar, king of Babylonia. It also includes stories told by Ben Sira himself as answers to the king's questions. These stories often include pornographic elements, as well as derogatory descriptions of biblical figures, like King Solomon or Joshua. Some of the stories in this section contain motifs from international folklore and may be based on folktales, but they were adapted to the special framework of the work and satirical elements were added to them. Examination of the various versions indicates that here, too, there were 22 stories, arranged according to the letters of the alphabet, to which 12 other stories were added.
The fourth part, which is found in most versions and gave the work its name, contains 22 alphabetically arranged epigrams attributed to Ben Sira that serve as material for discussion and interpretation by Ben Sira's son, Uzziel, and his grandson, Joseph b. Uzziel. The contents are satirical and even heretical. It may be assumed that this part was constructed in the same manner as the two previous ones – 22 + 12 sections. The work, therefore, displays elements of unity both in structure and in its ideological aims. It is all but impossible, however, to discover the background upon which such a work could have been written. Some scholars (L. Ginzberg and others) believe that it aimed at ridiculing the story of Jesus' birth; but the basis for such a conclusion may be found only in the first part, and even this is not very clear, for the irony seems to be directed more against God than against Jesus. It is hardly possible that the author was a Karaite, as some of the abusive stories are directed against biblical figures, and not only against the Talmud and Midrash. It seems likely that the author did not belong to any organized group or definable ideological movement, but was merely a writer with an anarchistic tendency who used satire to ridicule all the institutions of established religion in his day.
Another difficult problem is the relationship between this pseudepigraphal work and the original proverbs of Ben Sira. Some of the proverbs and epigrams included in the work are originally in the work of Ben Sira, but many such proverbs are found in talmudic literature, and the author probably took them from there. The author of the pseudepigraphal work did not even know Ben Sira's first name. There is only one slight connection that might be accidental: the Wisdom of *Ben Sira has a preface written by the author's grandson, who edited the work, and in the pseudepigraphal work the figure of a grandson is also present.

Buh buh But thats just a reddit comment and some random websites. Whu Whu What are you gonna do OP? Analyze the entire text to prove its a shitpost.
Yes.
Mods turn the music on.

Analysis Of Alphabet of Sirach/The Alphabet Of Ben Sira:

The text we will be using.
We are going to skip most of it and just jump straight into the section with Lilith, but if you do chose to read it, have a good time. Shit is funny as hell. Let's start of with Lillith's Birth. Many like to potray Adam and Lilith's first interaction like this.
1, 2, 3
It is often either stated or implied Adam either tried to force Lilith into a s*x position she didn't want or that he he stated that she was inferior to him and she spit back. While this nicely fits into the "yas Queen SLAYYY" interpretation, its not the truth...mostly.
Here is the actual text:

When the Holy Blessed One created the first Adam alone, They said, (Genesis 2:18) 'It is not good for this Adam to be alone.' They created for him a wife out of the Earth like he had been, and called her Lilith. Immediately they began to challenge each other. She said, 'I will not lie below,' and he said, 'I will not lie beneath you, but only on top. For you are fit only to be in the bottom position, while I am to be the superior one.' Lilith responded, 'We are equal to each other inasmuch as we were both created from the Earth.' But they would not listen to one another. When Lilith saw this, she pronounced the Ineffable Name and flew away into the world's air.

So first, no she wasn't going to be sexually assaulted. Secondly, it was just a couple arguing with each other. Yes, Adam shouldn't have said that about Lilith, but we shouldn't take a statement said by an angry man as gospel for the religion. Plus, how on earth is blaspheming your Father and then running away from an argument an appropriate reaction to the situation? God didn't do anything wrong. Why you picking a fight with him? We will discuss this more, but lets continue.

The Holy Blessed One said to Adam, 'If she agrees to come back, good. If not, she must permit one hundred of her children to die every day.' They departed and pursued her, and overtook her in the midst of the sea, in the mighty waters wherein the Egyptians would ultimately drown. They told her God's word, but she did not wish to return. The angels said, 'We shall drown you in the sea.' She said to them, 'Let me be. I was created only to cause illness to infants. I have dominion over them for eight days after birth if they are male, and if female, after birth for twenty days.' When the angels heard Lilith's words, they insisted on taking her. But she swore to them by the name of the living and eternal God, 'Whenever I see you or your names or your forms in an amulet, I will have no power over that infant.' She also agreed to have one hundred of her children die every day.

There is much to go over here. First, WHERE ARE THE HUNDRED CHILDREN COMING FROM! These are the first man and woman. THERE ARE NO CHILDREN. Who is he talking about? And don't give me that bullshit that he mad a mistake. HE IS GOD. IN THE TORAH, HE IS OMNISCIENT. This makes no sense.
"I was created only to cause illness to infants. I have dominion over them for eight days after birth if they are male, and if female, after birth for twenty days." I am sorry fucking what? Who said that? God? No. Adam? No. The Angels? Definitely not. No one told Lilith she had to cause illness. She is just being a toxic bitch and offloading her problems. What the fuck?
Finally, "She also agreed to have one hundred of her children die every day." At this point, who has sympathy for Lilith? Lets objectively look at Adam's sin. Yes, he was sexist. Yes, that was wrong. Can't Lilith convince him to change? We know it is possible for a woman to convince Adam because EVE CONVINCED HIM TO EAT THE APPLE. So, clearly the man can develop his thoughts. Instead, Lilith just runs away from her problem, knowing that a hundred innocent children (HER CHILDREN BY THE WAY- hang on does that mean she fucked Adam and Eve's Sons. Isn't she like their aunt? I am pretty sure that's still incest) will die. Yes, God is partly to blame as well, but if I had to choose between a Misandrist Wife or dead innocents, I will go with the Misandrist Wife. Nothing shows Adam as violent just a dick, and she clearly has access to powers he doesn't cuz he can't fly.

Accordingly, every day one hundred demons perish, and for the same reason, we write their names on the amulets of young children, and she sees them, she remembers her oath, and the child is healed

I guess that's nice? But does she even really heal them? She just takes away an illness she caused. This is like saying I put out the fire, but I am the arsonist who started it. There wouldn't be a problem if I didn't create one. And that's how the story ends. Seriously.
There is more, but it doesn't really matter. Ben Sira cures a girl of farting everywhere, talks about hair follicles, slanders David, explains why Donkey Urine is important, and ends with a raven cucking an eagle. Its pretty funny.

In Conclusion:

So, TL;DR: Lilith's entire existence is based on a shitpost. In said shitpost, she isn't even that great of a person and isn't even a feminist.
So yeah, that's all I got. There is more to this Rabbit Hole if you are willing to go down, but that is the gist of it. I don't see how a woman who runs away from responsibilities, blames others for her failures, and would rather kill babies than do something hard is a feminist icon, but here we are. I don't really know how to end this. Uh, were you entertained?
Addendum: If you are of the Christian, Muslim, or Jewish Faith please comment below and clear up any misconceptions I wrote in this post. I will try to edit it to make it better. Feminists please try to be respectful in the comments. Sup Mods. Uh yeah, cool.

Addendum #2 - Mesopotamian Lilith:

Some people have been saying that I should analyze Lilith from Mesopotamian Origins as this would give her a more sympathetic view. Very well. There are three main sources: Tablet XII of the Epic of Gilgamesh, a Burney Relief, Arslan Tash amulets
Tablet XII of the Epic of Gilgamesh (Text we'll use): Lilith, a snake, and a bird steal a tree from a goddess and squat in it. Gilgamesh comes around kills the snake. The Bird flees. Lilith chimps out, destroys her home, and runs. Tbf, this is Gilgamesh, so I guess Lillith W?

The dyer (?) had not dyed his leather with it (?)
At its root the serpent, 'that knew not silence (?)' had made its nest
At its top the storm-bird (Zû) had put his young
In its midst Lilith had built a house
The shrieking maid the joyful
The bright Queen of Heaven tears for them (?) wept
His lady said a word to him
'Warrior Gilgamesh, its .... will thee'
The ibbaru garment that was of 50 minas from his loins he removed
What was 50 minas 30 ... . he made
His (?) brazen axe a road (?) his ....
1 talent 50 minas his in his hand he seized
At its root the serpent ' that knew not silence (?) ' he slew
At its top the storm-bird (Zû)
took his young (and) went away to the mountain
In its midst Lilith destroys (her) house

Burney Relief (Source): Yeah no

Even so, the possibility that the Queen of the Night plaque, with its high degree of skill in craftsmanship and attention to detail would be a representation of a lilitu is highly unlikely. According to the Hebrew tradition, Lilith was the first woman made by God who refused to submit to Adam's sexual demands and flew away, thus rebelling against God and his plans for human beings. She was thought to have then occupied the wastelands and, like the lilitu, to have preyed on unsuspecting men ever since. In either tradition, the lilitu was not a popular enough figure to have been portrayed on a plaque such as the Queen of the Night. Dr. Black notes, “Evil gods and demons are only very rarely depicted in art, perhaps because it was thought that their images might endanger people” (62). The mountain range depicted at the bottom of the relief is also thought to suggest lilitu identification in representing the wilderness the spirit inhabits but the headdress, the necklace, the rod-and-ring symbols and the significance of the plaque all go to argue against Lilith as a possibility.

Arslan Tash amulet (Source):

Whispering-incantation against the Flying-one, the oath of Sasam, son of Pidrišiša, god, and against the Strangler of the lamb: “The house I enter, you shall not enter And the court I tread, you shall not tread!He has made an eternal contract with us. Assur made a pact with us, all the sons of El,, and the great council of all the holy ones,With the oath of heaven and earth With the oath of Baal, lord of the earth With the oath of Horon, whose utterance is true,His seven concubines and the eight wives of Baal Qudš”[Written around and between the images] Oh Flying one, from the dark room pass away!Now! Now, night demons! [Written on the Sphinx figure] From my house, O crushers, go away! [Written on the wolf-like figure] Oh Sasam, let it not be opened for him And let him not come down to the door-posts The sun is rising for Sasam. Disappear, and fly away home.[Written on the axe-wielding figure](modified from Cross and Saley 1970 and Berlejung 2010).

So where the fuck is Lilith? Well the text in its original language features lly- which if you add a "t" could be llyt [Lilith], but it also can be ll wyn which means "night and day." So, yeah not exactly a Lilith W. And that's it. I don't know how this makes her sympathetic, but to each their own.

Addendum #3 - Lilith R*ped Adam?

u/howhow326 said that there was a tale about Lilith raping Adam and being thrown out of Eden. This intrigued me to search for it, but unfortunately, I can't find a source for this anywhere. The closest I get is this Blogpost, but this seems to be more of a hypothetical than anything. Frankly, I don't think this should be part of the debate.
Edit 1: Originally, there was a line that said : "Hell fucking Jesus gets mentioned the prophet of the ENEMY, but not Lilith." I have since been informed that this is a gross misrepresentation of the Muslim Faith, and it has been removed.
Edit 2: Spelling and Formatting Errors Corrected
Edit 3: Mesopotamian Lilith added. Lilith's Rape Accusations.

Hello,
I'm asking for any advice an what other tests and analysis to do for my dogs urinary inconsistencies. He's a mix breed, sorta looks like a black lab, but both his parents were strays (mother still alive), large (~45kg), 8 years old, neutered. Has a few kilos to lose to be ideal (around 40 would be great).
Issues started couple of months ago. He has trouble controling his bladder. First diagnosis was infection, but antibiotics did nothing, and his urine was sterile. On ultrasound it looked like he had a thickening of one bladder wall, so thats why they thought he had it at some point. We checked him for tumors, nothing on radigraphy scans (x-ray) up as suspicious.
He got testosterone shots as other diagnosis was weakening of the bladder muscles due to age and sterilisation. It sort of help but really short term, couple of days, when that dosage should last longer than 5 days. He also got medication for osteoarthritis (librela) with next shot of testosterone, and he was okay for a while, but we also apply almost daily the testosterone gel topically as advised by our vet. But again, he can't control his bladder.
He has no noticeable hair loss, but does seem less active, and often would prefer to just lie down and be petted rather than play actively as before, and looks like his hind legs are weaker. He doesn't like his diet food, but appears to not have increased or decreased appetite.
Might be time for next librela shot, but we also want to see if there is more to check that might also be cause of this. He drinks water, and then has to go in less than 10 minutes or he will have an accident. His kidney function appeared okay based on blood markers. Maybe we should check him for diabetes insipidus, or Cushing's? Anything else that might be a cause? Any advice will be helpful really.

I want to preface this post by saying if you are recently dealing with STD symptoms please do not panic when you read posts like this. The vast majority of cases are easily treatable and do not create long term issues.
That being said I'm one of the unlucky people that have been dealing with symptoms for over 5 months now. Negative tests for all the usual suspects in addition to some of the less common ones, with many doctors not having answers. Like many of you here, I've had a lot of time to read through hundreds of posts and I wanted to get an aggregate of success stories after months of struggle.
The idea of this post is to help bring awareness to some of the edge cases that are usually unlikely but still exist. If you are struggling to find your own diagnosis maybe one of these stories help you and your doctor find the right treatment. Do not go trying to treat yourself with this information, but instead use it to make sure you are doing the right testing to figure out your issue. Misuse of antibiotics will only make it more difficult for you to solve your problem and can create resistances to those treatments.
If you have a success story to share, or remember one shared by others please tell us about it here.
Here are some that stuck out to me the most:
-Patient misdiagnosed with herpes. Negative test for many other things. Spent 8 months trying to treat herpes with antivirals only for it to actually be trichomonas found by a swab test. Patient was immediately cured after being prescribed the correct antibiotics.
-Countless people with Mycoplasma or Ureaplasma. Unfortunately these are rarely tested for and many doctors aren't even aware that they have now become a more common STD. Once you test negative for gonorrhea and chlamydia and you still have symptoms, you need to start testing for things like trichomonas, mycoplasma, and ureaplasma.
-UTI's are also not always considered during an STD test but sometimes our issue is a simple urinary tract infection. Any competent doctor should be doing a urine culture in addition to a urine analysis. I've read too many posts where the doctor doesn't do a standard checkup.
-Herpes is always a possibility. Unfortunately it may not be the easiest to test for. The most reliable way to test for herpes is to swab the active sores as soon as possible. Waiting too long to be tested can result in a false negative on a swab. HSV blood testing will only tell you that you have had exposure in the past. It will not tell you if those active legions are indeed herpes.

Hi, I’m 24 I’ve been having some of these symptoms for the past 4 years maybe. I have pelvic pain that comes and goes and it’s only on the right side but I have a cyst on my left ovary. Sometimes I wake up with lower back pain it comes and goes but sometimes I don’t feel it for months. My periods aren’t super painful it’s rare that I have an excruciating period. My flow changes sometimes it’ll be heavy and sometimes it’s normal. My period is sometimes regular for a couple of months and sometimes it’s late almost 2 weeks. I just ordered a CA-125 test from my doctor for next week. I also have a trace of blood in my urine and this has been happening since then as well. I can’t see it but my tests show it and I had a normal cystoscopy I’ve had multiple blood tests which have been normal. I did have fluid in my pelvic area from a ruptured cyst is what they told me. My Transvaginal Ultrasound findings are below:
FINDINGS: Transabdominal ultrasound was performed. Uterus measures 7 x 4.1 x 2.8 cm. Normal echotexture is noted. Endometrial echo complex measures 6 mm. No cul-de-sac fluid is seen.. No uterine mass identified. Right ovary measures 3.8 x 2.3 x 1.9 cm. Left ovary measures 5.1 x 4.2 x 2.7 cm. Normal echotexture is noted. 4.4 x 3.9 x 2.4 cm left ovary and cyst is seen. Duplex ultrasound was performed, including grayscale imaging, color Doppler flow, and spectral analysis. Bladder appear unremarkable.
IMPRESSION: Left ovarian cyst.
I’m just wondering if there’s any other tests I can take or advice anyone else might have? I’m afraid of cancer and I had a pap when this all started which was normal. Thank you!

how the hell is one supposed to extract ephedrine from bronkaid tablets with ephedrine base being so damn inconveniently soluble in water? (btw ephedrine in bronkaid is the sulfate incase anyone didn’t know)
“Ephedrine hydrochloride: Freely sol in water; sol in alcohol. Practically insol in ether (Merck Index, 13th ed). Soluble 1 in 3 to 1 in 4 of water and 1 in 7 to 1 in 14 of ethanol; very slightly soluble in chloroform, practically insoluble in ether (Clarke's Analysis of Drugs and Poisons, 3rd ed).
Ephedrine sulfate: Freely sol in water, sparingly sol in alcohol (Merck). Soluble 1 in 1.3 of water and 1 in 90 of ethanol (Clarke).
Ephedrine base, hemihydrate: Sol in water, alcohol, chloroform, ether (Merck). Soluble 1 in 20 of water and 1 in less than 1 of ethanol; soluble in chloroform with turbidity owing to separation of water; soluble in ether (Clarke).
Ephedrine base, anhydrous: Soluble 1 in 20 of water; very soluble in ethanol; soluble in chloroform; freely soluble in ether (Clarke).”