#non-alcoholic liver disease treatment

[kaizengastrocare]

If you are experiencing signs of NAFLD or are at risk? If you are concerned about fatty liver disease or need expert care for NAFLD, Dr. Vikrant Kale at Kaizen Gastro Care is here to provide you with the best liver care in Pune. With a focus on early detection, prevention, and treatment, Dr. Kale and his team are dedicated to helping patients achieve optimal liver health.

[anandkhakar]

Types of Liver Damage - best liver transplant hospitals

The liver is a vital organ that conducts hundreds of functions including metabolism, energy storage, and detoxification. best liver transplant hospitals

[expert-ayurveda]

Non-Alcoholic Fatty Liver Ayurvedic Treatment in India

Reclaim Your Liver Health with  Ayurvedic Treatment for Non-Alcoholic Fatty Liver Disease (NAFLD) in India.

The liver is an extraordinary organ, responsible for a myriad of vital functions within the human body. It plays a central role in detoxification, metabolism, and the production of essential proteins. However, an alarming health issue has emerged in recent years, affecting millions across the globe—Non-Alcoholic Fatty Liver Disease (NAFLD). In India, Expert Ayurveda offers a beacon of hope through their specialized Ayurvedic Treatment  for NAFLD, focusing on the complexities of fatty liver.

Understanding NAFLD and Its Prevalence in India

Non-Alcoholic Fatty Liver Disease, often referred to as NAFLD, is a condition characterized by the accumulation of excess fat in the liver. Remarkably, it occurs in individuals who do not consume excessive amounts of alcohol. NAFLD is closely associated with modern lifestyles, poor dietary choices, lack of physical activity, and metabolic syndrome. It encompasses a spectrum of liver conditions, ranging from the relatively benign accumulation of fat (steatosis) to more severe inflammation and liver damage (non-alcoholic steatohepatitis or NASH). Left untreated, NAFLDcan progress to advanced liver diseases such as cirrhosis and even liver cancer.

The Ayurvedic Approach to fatty liver Treatment in India

India's rich heritage of Ayurveda provides a holistic approach to health and wellness, including the treatment of liver diseases like NAFLD. Ayurvedic Treatment focuses on harmonizing the body's energies (doshas), bolstering digestion, detoxifying the liver, and promoting overall vitality.

Expert Ayurveda: Your Trusted Partner in NAFLD Treatment

Expert Ayurveda stands at the forefront in India, specializing inAyurvedic Treatment for NAFLD, with an emphasis on addressing the intricacies of fatty liver. Here's why they are the preferred choice for individuals seeking natural and effective remedies:

Ayurvedic Mastery: Expert Ayurveda boasts a team of highly accomplished Ayurvedic doctors and practitioners who possess profound knowledge of NAFLD and its Ayurvedic Treatment. Their expertise ensures that patients receive the highest standard of care.

Personalized fatty liver Solutions: Understanding that NAFLD varies from person to person, Expert Ayurveda provides customized treatment plans tailored to the unique needs and constitution of each individual, putting a spotlight on the management of fatty liver

Holistic Healing: Ayurveda's philosophy is deeply rooted in treating the root causes of ailments, rather than merely alleviating symptoms. Expert Ayurveda's approach is holistic, focusing not only on liver health but also on overall well-being.

Natural Remedies: Expert Ayurveda harnesses the power of natural herbs, dietary recommendations, lifestyle modifications, and detoxification therapies to treat NAFLD. These natural remedies are safe, time-tested, and have minimal side effects, making them particularly apt for addressing fatty liver.

Preventive Measures: In addition to treatment, Expert Ayurveda emphasizes preventive measures and long-term management of NAFLD. They offer guidance on dietary choices, physical activity, and lifestyle changes to help patients maintain optimal liver health, with a keen focus on the fatty liveraspect.

Patient-Centric Approach: At Expert Ayurveda, patient-centered care is paramount. They ensure that patients are well-informed, comfortable, and empowered throughout their NAFLD treatment journey, with a deep understanding of the fatty liver intricacies.

The Ayurvedic fatty liver Treatment Process

Your journey towards liver health with Expert Ayurveda typically involves the following steps, with a strong emphasis on fatty liver:

Comprehensive Consultation: The process commences with a thorough consultation where Ayurvedic doctors assess your condition, medical history, and individual constitution (prakriti), paying particular attention to the presence of fatty liver.

Accurate Diagnosis: Based on the consultation and diagnostic tests, the severity and nature of your NAFLD, including fatty liver characterization, are determined.

Tailored Treatment Plan: An individualized treatment plan is meticulously crafted, incorporating Ayurvedic herbs, dietary recommendations, lifestyle modifications, and detoxification therapies, all designed to specifically target fatty liver issues.

Treatment Phase: You embark on a structured treatment phase, during which you'll receive Ayurvedic remedies and therapies customized to address the fatty liver aspect of your condition.

Regular Monitoring: Regular follow-up consultations and assessments ensure that your progress, especially concerning fatty liver, is closely tracked. Adjustments are made to the treatment plan as necessary.

Lifestyle Guidance: Expert Ayurveda provides detailed guidance on maintaining a healthy lifestyle, including dietary choices and exercise routines. This comprehensive approach is key to preventing the recurrence of fatty liver

Sustained Support: Even after the successful completion of treatment, Expert Ayurveda remains your partner in long-term liver health, offering ongoing support, particularly for managing fatty liver concerns.

Choose Ayurveda for fatty liver Treatment in India

If you're in search of a natural, holistic, and effective treatment for NNon-Alcoholic Fatty Liver Disease, especially focusing on the complexities of fatty liver, Expert Ayurveda is your unwavering ally. Their Ayurvedic prowess, personalized treatment plans, and patient-centric philosophy offer a pathway to healing for individuals grappling with liver health challenges. Take the first step towards revitalizing your liver health by scheduling an appointment with Expert Ayurveda, and embark on a transformative journey towards a healthier and more vibrant life.

For More Information

Dr. Paresh J Thakkar, 32,Raj ami complex, Amin Society,Near swastik school, Sardar patel colony, Narayanpura, Ahmedabad.

+91 9924184234

drpjthakkar@gmail.com

[lifeandstylexyz]

Non-alcoholic fatty liver disease: Research identifies potential new targets

Non-alcoholic fatty liver disease: Research identifies potential new targets

Non-alcoholic fatty liver disease. Researchers have uncovered novel candidate drug targets for non-alcoholic fatty liver disease (NAFLD) by using the latest technologies, including both single-nuclear sequencing of mice and human liver tissue and advanced 3D glass imaging of mice to characterize key scar-producing liver cells. The research was led by investigators at the Icahn School of Medicine…

[marshemillow]

You know what? I'm talking about "phone addiction" again because I'm not done.

Do you know what an addiction is? Addiction isn't "you do it just out of habit because you don't think about it" addiction is "if you stop you will literally be in agony and that's why you keep turning to the thing."

We have this baked-in idea that addiction is a moral failing, that if you have a phone addiction, it really just means you need to get off your phone. Yeah, addicted to alcohol? Just stop! Don't drink it anymore! Withdrawl? What's that? If you drink alcohol, it obviously means you just don't have enough willpower! If you can't stop drinking alcohol, it means you're a bad person. You basically deserve to have liver failure at that point!

Yes some people actually believe this! They don't know that paramedics carry alcohol with them specifically because it saves the lives of people going through alcohol withdrawl, they don't care! It's something they cheer themselves up with because they aren't addicted to alcohol, and that means they're a good person.

I am so sick and fucking tired of people pathologizing and moralizing non-moral issues. Addiction, or Substance Abuse Disorder, is an actual physical health condition. It's a disease. You can't stop it with enough willpower, it's something that needs actual medical treatment. Just looking at coping mechanisms or even just things that make you feel good because they release dopamine in your brain and calling that an "addiction" does so much damage to people's understanding of real addiction and makes addicts look like evil weak cowards instead of people with a disease that needs treatment. That's fucking evil. Imagine telling someone with cancer that they just didn't have enough willpower to stop it. Disgusting.

And it's extra ironic coming from these people who think they're addicted to their phone saying "you just need to stop" and then not stopping, meanwhile I have often just forgotten I don't have my phone with me and then get confused when I don't have it. Shouldn't it be the other way around? Why is the person who "knows" it's an "addiction" (in the moral failing way) still not have enough willpower to stop whereas I have to consciously remind myself to go find my phone because I just forget it exists when I don't believe in phone addiction? Literally half the time I take my phone out of my pocket, it's just to check the time.

It's almost like "phone addiction" is just another way to make people feel guilty for doing things they like doing. It doesn't make them stop, they just feel worse about it. They don't think about it as a coping strategy that fades as their life circumstances get better.

And every single time, when you find these people who feel bad for doing things that make them happy, they grew up christian. Every fucking time. "Struggle with addiction" and it's just guilt applied to something normal.

STOP MAKING YOUR CATHOLIC GUILT EVERYONE ELSE'S PROBLEM!!! IF YOU CARED ABOUT "PHONE ADDICTION" YOU WOULD BE TAKING ACTUAL STEPS TO MINIMIZE HARM, NOT THROWING GUILT AT PEOPLE JUST FOR ITS OWN SAKE!!!

[helen0086]

Progress in the Study of the Protective Effect and Mechanism of C-phycocyanin on Liver Injury

Abstract: C-phycocyanin (C-phycocyanin) is a pigment-containing protein from marine algae that has shown promising results in the treatment of many inflammatory diseases and tumors. C-alpha-cyanobilin is a pigment-containing protein from marine algae that has been shown to be effective in the treatment of various inflammatory diseases and tumors. C-alpha-cyanobilin has a protective effect on various liver diseases, such as drug-induced or toxic substance-induced liver damage, non-alcoholic fatty liver disease, hepatic fibrosis, and hepatic ischemia-reperfusion injury. The protective effect of C-alginin on liver injury is mainly realized through the regulation of signaling pathways such as nuclear factor (NF)-κB, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and AMP-dependent protein kinase (AMPK), and the inhibition of oxidative stress, etc., and is not toxic to normal cells. Therefore, C-alginin has a broad application prospect as a potential natural hepatoprotective marine active substance. In recent years, the research progress of the protective effect of C-alginin on liver injury and its mechanism is summarized.

 C-phycocyanin (C-phycocyanin) is a complex protein of cyanobacteria and a natural food protein pigment with pharmacological effects such as antioxidant, anti-inflammatory and anti-tumor effects, as well as fast-acting and low-toxicity, it can be used as a functional food [1-2]. C-Alginin can also enhance immunity and is safe, without causing acute and subacute toxic reactions [3]. Selenium-enriched PC has been shown to have stronger pharmacological effects [4]. Therefore, C-alginate has important research value both as a drug and a functional food, and has become a hot spot in the field of pharmaceutical research [5]. In this paper, we summarize the progress of research on the application and mechanism of C-alginin in liver diseases.

1 Ameliorative effect of C-phycocyanin on liver injury caused by drugs and toxic substances

The liver is the metabolic center of drugs and exogenous toxic substances, and metabolites are prone to liver injury. C-PC can inhibit the synthesis and release of inflammatory factors such as tumor necrosis factor (TNF)-α and interferon-γ, and increase the activities of catalase and superoxide dismutase (SOD), which can inhibit hepatic inflammation and alleviate hepatic injury [3]. It has been found that C-PC can significantly prevent thioacetamide-induced liver injury, significantly reduce the levels of alanine aminotransferase (ALT) and aliquot aminotransferase (AST), shorten the prothrombin time and reduce the hepatic histopathological damage, and improve the survival rate of rats with fulminant hepatic failure [6]. C-alginin also has a good effect on thioacetamide-induced hepatic encephalopathy, which can be seen in the reduction of tryptophan and lipid peroxidation indexes in different regions of the brain, and the enhancement of catalase and glutathione peroxidase activities in rats with fulminant hepatic failure [6].

Another study found that C-alginin not only attenuates the oxidative stress induced by 2-acetylaminofluorene and reduces the generation of reactive oxygen species (ROS) radicals, but also inhibits the phosphorylation of protein kinase B (Akt) and the nuclear translocation of nuclear factor (NF)-κB induced by 2-acetylaminofluorene, thus inhibiting the expression of multidrug resistance genes [7]. Osman et al. [8] also showed that C-alginin could normalize the levels of ALT, AST, catalase, urea, creatinine, SOD and glutathione-s-transferase in the livers of rats poisoned with carbon tetrachloride (CCl4). This result was also verified in human liver cell line (L02) [9]. C-phycocyanin can effectively scavenge ROS and inhibit CCl4-induced lipid peroxidation in rat liver [10], and C-PC can improve the antioxidant defense system and restore the structure of hepatocytes and hepatic enzymes in the liver of gibberellic acid-poisoned albino rats [11]. As a PC chromophore, phycocyanin can also significantly inhibit ROS generation and improve liver injury induced by a variety of drugs and toxic substances [10]. Liu et al. [12] found that phycocyanin showed strong anti-inflammatory effects in a CCl4-induced hepatic injury model in mice, which could significantly reduce the levels of ALT, AST, the expression of TNF-α and cytochrome C, increase the levels of albumin and SOD, and proliferate cytosolic nuclei. It can significantly reduce ALT and AST levels and the expression of TNF-α and cytochrome C, increase albumin levels and the expression of SOD and proliferating cell nuclear antigen, promote hepatocyte regeneration and improve the survival rate of mice with acute liver failure.

Gammoudi et al [13] used response surface method to optimize the extraction process of C-phycocyanin, and obtained high extraction recovery. C-phycocyanin extracted by the optimized method has the ability of scavenging hydroxyl, superoxide anion and nitric oxide radicals as well as the ability of metal chelating, and it has stronger antioxidant effect; C-PC significantly increased the activity of SOD and inhibited the increase of ALT, AST, and bilirubin in cadmium-poisoned rats. C-PC significantly increased the activity of SOD and inhibited the increase of ALT, AST and bilirubin in rats with cadmium poisoning. The above studies show that C-phycocyanin can effectively protect liver injury caused by drugs and toxic substances, and has the efficacy as the basis for drug development.

2 Preventive effect of C-alginin on hepatic fibrosis

Liver fibrosis is an inevitable process in the development of various chronic liver diseases and may be reversed with early and timely treatment. The key to liver fibrosis is the activation of hepatic stellate cells. Previous studies have found that low-dose C-alginin combined with soy isoflavones can inhibit hepatic stellate cell activation by inhibiting the activity of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase［14］, but it is not clear whether C-alginin alone can inhibit the activity of NADPH oxidase. Therefore, the combination of C-algin and soy isoflavones at appropriate doses may have a preventive effect on liver fibrosis in high-risk groups. C-alginin may inhibit the progression of NADPH by suppressing oxidative damage, thereby inhibiting the development of hepatic fibrosis [15].

Epithelial mesenchymal transition (EMT) is one of the key mechanisms contributing to the development of fibrotic diseases. C-alginin inhibits transforming growth factor β1 (TGF-β1)-induced human EMT [16]. Although the effect of C-alginin on EMT in hepatic fibrosis has not been reported, it has been found that C-alginin can reduce pulmonary fibrosis by inhibiting epithelial mesenchymal transition [17]. Another study found that C-alginin could reduce the expression of α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF) mRNA in human dermal fibroblasts and alleviate fibrous contracture [18]. The results of these studies also have significance for the inhibition of hepatic fibrosis, and provide a theoretical basis for the further study of C-PC as a potential antifibrotic drug.

3 Protective effect of C-alginin on hepatic ischemia-reperfusion injury

Liver ischemia/reperfusion injury is an important clinicopathophysiological phenomenon. It was found that the addition of two different doses (0.1 g/L and 0.2 g/L) of C-alginin to the Krebs Henseleit preservation solution significantly decreased hepatic ALT, AST and alkaline phosphatase activities, and reduced the rate of lipid peroxidation and malondialdehyde content in an isolated perfused rat liver model, and increased the activities of hepatic glutathione-s-transferase and glutathione peroxidase, as well as sulfhydryl groups in hepatic tissue. On the other hand, it can increase the activities of hepatic glutathione-s-transferase and glutathione peroxidase and the content of sulfhydryl groups in liver tissues, therefore, C-alginin can significantly reduce hepatic ischemia/reperfusion injury as an antioxidant [19]. In isolated perfused mouse livers, it was found that C-alginin significantly reduced the phagocytosis and respiratory burst activity of hepatic macrophages (Kupffer cells), attenuated cytotoxicity and inflammation induced by highly active Kupffer cells, and dose-dependently inhibited carbon phagocytosis and carbon-induced oxygen uptake by perfused livers, and then inhibited the increase of hepatic nitric oxide synthase activity induced by gonadotropins [20]. and thus inhibit the thyroid hormone-induced elevation of hepatic nitric oxide synthase activity [20].

However, C-alginin has a very short half-life in vivo, which limits its application in vivo. It was found that the use of polyethylene glycol-b-(polyglutamic acid-g-polyethyleneimine), a macromolecular material with good drug-carrying capacity and slow-release properties, as a nanocarrier of C-alginin could solve this problem, and the release of C-alginin could be delayed by subcutaneous injection into the abdominal region of rats, which could attenuate islet damage caused by hepatic ischemia/reperfusion and enhance the function of the islets [21]. This study broadens the scope of application of C-alginin in vivo and improves the therapeutic effect of C-alginin.

4 Inhibitory effect of C-alginin on hepatocellular carcinoma

It was found that C-alginin significantly reduced the expression of matrix metalloproteinase (MMP)-2 and MMP-9 and the expression of tissue inhibitor of metalloproteinase 2 (TIMP2) mRNA in human hepatocellular carcinoma cells (HepG2 cells) [22]. C-alginin is a natural photosensitizer, and photodynamic therapy (PDT) mediated by alginin microcystin induced a large accumulation of ROS in HepG2 cells, which promoted mitochondrial damage and cytochrome C release, and led to apoptosis of hepatocellular carcinoma cells [23].

Liu et al. [24] used nanoscale C-alginate particles prepared by lactobionic acid grafting and adriamycin loading to enhance the growth inhibition of HepG2 cells when combined with chemo-PDT, and the C-alginate particles could effectively accumulate and diffuse in tumor multicellular spheres. In vitro and in vivo studies on the effects of selenium-enriched PCs on PDT in hepatocellular carcinoma showed that selenium-enriched PCs could migrate from lysosomes to mitochondria in a time-dependent manner, and that selenium-enriched PCs could induce the death of tumor cells through the generation of free radicals in vivo, increase the activities of antioxidant enzymes in vivo, induce mitochondria-mediated apoptosis, and inhibit autophagy, thus offering a relatively safe pathway to tumor treatment and showing new development perspectives [4]. It can provide a relatively safe way to treat tumors and shows a new development prospect [4].

Lin et al. [25] combined C-phycocyanin with single-walled carbon nanohorns and prepared phycocyanin-functionalized single-walled carbon nanohorn hybrids, which enhanced the photostability of C-phycocyanin and protected the single-walled carbon nanohorns from adsorption of plasma proteins, and synergistically used with PDT and photothermal therapy (PTT) to treat tumors. C-phycocyanin covalently coupled with biosilica and PDT or non-covalently coupled with indocyanine green and PTT on tumor-associated macrophages can also increase the apoptosis rate of tumor cells [26-27]. The development of PDT and PTT synergistic methods for the treatment of cancer has broadened the application of C-PC and enhanced its value in the treatment of hepatocellular carcinoma.

In addition, C-phycocyanin can inhibit the expression of multidrug-resistant genes in HepG2 cells through NF-κB and activated protein-1 (AP-1)-mediated pathways, and C-phycocyanin increases the accumulation of adriamycin in HepG2 cells in a dose-dependent manner, which results in a 5-fold increase in the susceptibility of cells to adriamycin [28]. Even in adriamycin-resistant HepG2 cells, C-PC induced the activation of apoptotic pathways such as cytochrome C and caspase-3 [29], and the results of Prabakaran et al. [30] also confirmed the inhibitory effect of C-PC on the proliferation of HepG2 cells, mediated by the inactivation of BCR-ABL signaling and the downstream PI3K/Akt pathway. mediated by BCR-ABL signaling and inactivation of downstream PI3K/Akt pathway. In addition, C-phycocyanin modifies the mitochondrial membrane potential and promotes apoptosis in cancer cells [30]. Currently, C-phycocyanin is a synergistic molecule with other drugs that have been widely used in the treatment of cancer [31]. The above studies demonstrate that C-phycocyanin has good therapeutic potential in the field of hepatocellular carcinoma.

5 Amelioration of metabolic syndrome and non-alcoholic fatty liver disease by C-phycocyanin

It has been found that C-alginin can reduce ALT and AST levels, decrease ROS production and NF-κB activation, and attenuate hepatic fibrosis in rats induced by high-fat choline-deficient diets, and thus C-alginin has a protective effect on NAFLD rats through anti-inflammatory and antioxidant mechanisms [15].

Another study on the effects of aqueous extract of Spirulina (mainly C-alginin) on NAFLD induced by a high-calorie/high-fat Western diet in C57Bl/6J mice showed that aqueous extract of Spirulina significantly improved glucose tolerance, lowered plasma cholesterol, and increased ursodeoxycholic acid in bile in mice [32]. Kaspi-Chadli et al. Kasbi-Chadli et al. [33] showed that aqueous extract of Spirulina could reduce cholesterol and sphingolipid levels in the liver and aortic cholesterol levels in hamsters fed a high-fat diet by significantly decreasing the expression of hydroxy-3-methylglutaryl-coenzyme A reductase (HMG CoA) gene, a limiting enzyme for cholesterol synthesis, and TGF-β1 gene, and that ursodeoxycholic acid levels in the feces of hamsters fed high-fat diets were increased in the high Spirulina aqueous extract treatment group.

A daily dose of C-alginin-enriched Spirulina can reduce the harmful effects of oxidative stress induced by a diet rich in lipid peroxides [34]. Ma et al. [35] found that C-alginin promoted the phosphorylation of hepatocyte AMP-dependent protein kinase (AMPK) in vivo and ex vivo, and increased the phosphorylation of acetyl coenzyme A carboxylase. In the treatment of NAFLD in mice, C-alginin can improve liver inflammation by up-regulating the expression of phosphorylated AMPK and AMPK-regulated transcription factor peroxisome proliferator-activated receptor α (PPAR-α) and its target gene, CPT1, and by down-regulating the expression of pro-inflammatory factors such as TNF-α and CD36 [35]. This suggests that C-phycocyanin can also improve lipid deposition in the liver through the AMPK pathway.

Endothelial dysfunction is associated with hypertension, atherosclerosis and metabolic syndrome. Studies in animal models of spontaneous hypertension have shown that long-term administration of C-alginin may improve systemic blood pressure in rats by increasing aortic endothelial nitric oxide synthase levels, with a dose-dependent decrease in blood pressure, and thus C-alginin may be useful in preventing endothelial dysfunction-related diseases in the metabolic syndrome [36]. In the offspring of ApoE-deficient mice fed C-alginate during gestation and lactation, male littermates had an elevated hepatic reduced/oxidized glutathione ratio and significantly lower hepatic SOD and glutathione peroxidase gene expression.

C-PC is effective in preventing atherosclerosis in adult hereditary hypercholesterolemic mice [37]. In vitro, C-phycocyanin also improved glucose production and expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase) in high-glucose-induced insulin-resistant HepG2 cells [38]. C-alginin also increases glucose uptake in high glucose-induced insulin-resistant HepG2 cells through the insulin receptor substrate (IRS)/PI3K/Akt and Sirtuin-1 (SIRT1)/liver kinase B1 (LKB1)/AMPK signaling pathways, activates glycogen synthase, and increases the amount of glycogen [38]. C-phycocyanin can improve blood glucose and fasting serum insulin levels in tetracycline-induced diabetic mice [39]. Therefore, C-phycocyanin can maintain cellular glucose homeostasis by improving insulin resistance in hepatocytes.

6 Hepatoprotective role of C-phycocyanin in other liver diseases

Studies have shown that C-alginin can inhibit total serum cholesterol, triacylglycerol, LDL, ALT, AST, and malondialdehyde levels in mice modeled with alcoholic liver injury, significantly increase SOD levels in the liver, and promote the activation and proliferation of CD4+ T cells, which can have an ameliorative effect on alcoholic liver injury [40]. In addition, C-phycocyanin may enhance the intestinal barrier function, regulate the intestinal flora, reduce the translocation of bacteria and metabolites to the liver, and inhibit the activity of the Toll-like receptor 4 (TLR4)/NF-κB pathway, which may reduce the inflammation of the liver and prevent the occurrence of hepatic fibrosis in mice [41]. In mice with X-ray radiation-induced liver injury, C-phycocyanin can reduce radiation-induced DNA damage and oxidative stress injury by up-regulating the expression of nuclear factor (NF)-E2-related factor 2 (Nrf2) and downstream genes, such as HO-1, and play a hepatoprotective role by enhancing the activities of SOD and glutathione peroxidase [42].

7 Outlook

Liver fibrosis is the common final process of chronic liver diseases, and there is no effective therapeutic drug at present. Although some research progress has been made in the field of traditional Chinese medicine (TCM) on the reversal of liver fibrosis [43], its toxicological effects have not yet been clarified. Although the incidence of viral hepatitis has gradually decreased with the development and popularization of vaccines and antiviral drugs, the incidence of drug-induced liver injury (DILI) and liver diseases such as NAFLD has been increasing year by year with the improvement of people's living conditions [44]. Therefore, there is an urgent need to find drugs or nutrients that can help maintain normal hepatocyte function and effectively inhibit liver inflammation and fibrosis. C-alginin, with its anti-inflammatory, antioxidant, and antitumor effects, as well as good food coloring, has a wide range of applications in both the pharmaceutical and food industries.

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[20] REMIREZ D, FERNÁNDEZ V, TAPIA G, et al. Influence of C- phycocyanin on hepatocellular parameters related to liver oxidative stress and kupffer cell functioning[J]. Inflamm Res, 2002, 51(7): 351-356. doi: 10. 1007/pl00000314.

[21] TONG F, TANG X, LIU D. Phycocyanin/PEG-b-(PG-g-PEI) attenuated hepatic ischemia/reperfusion-induced pancreatic islet injury and enlarged islet functionality [J]. Int J Nanomedicine, 2019, 14: 339-351. doi: 10.2147/IJN.S190938.

［22］KUNTE M, DESAI K. The inhibitory effect of C-phycocyanin containing protein extract on human matrix metalloproteinases (MMP-2) and MMP-9 in hepatocellular cancer cell line (HepG2)［J］. and MMP-9) in hepatocellular cancer cell line (HepG2) [J].  Protein J, 2017, 36(3): 186-195. doi: 10. 1007/s10930-017-9707-0.

［23］WANG C Y, WANG X, WANG Y, et al. Photosensitization of phycocyanin extracted from microcystis in human hepatocellular carcinoma cells: implication of mitochondria-dependent apoptosis ［J］. J Photochem Photobiol B, 2012, 117: 70-79. doi: 10. 1016/j.  jphotobiol.2012.09.001.

［24］LIU X, DU J, XIE Z, et al. Lactobionic acid-modified phycocyanin nanoparticles loaded with doxorubicin for synergistic chemo- photodynamic therapy［J］. therapy[J]. Int J Biol Macromol, 2021, 186: 206- 217. doi: 10. 1016/j.ijbiomac.2021.07.047.

［25］LIN Z, JIANG B P, LIANG J, et al. Phycocyanin functionalized single-walled carbon nanohorns hybrid for near-infrared light- mediated cancer phototheranostics [J].  Carbon, 2019, 143: 814- 827. doi: 10. 1016/j.carbon.2018.12.011.

[26] PU Y, WEI M, WITKOWSKI A, et al. A hybrid biomaterial of biosilica and C-phycocyanin for enhanced photodynamic effect  towards tumor cells[J]. Biochem Biophys Res Commun, 2020, 533 (3): 573-579. doi: 10. 1016/j.bbrc.2020.09.049.

[27] WAN D H, MA X Y, LIN C, et al. Noncovalent indocyanine green conjugate of C-phycocyanin: preparation and tumor-associated macrophages-targeted photothermal therapeutics[J].   Bioconjug Chem, 2020, 31(5): 1438-1448. doi: 10. 1021/acs. bioconjchem. 0c00139.

［28］NISHANTH R P, RAMAKRISHNA B S, JYOTSNA R G, et al. C- phycocyanin inhibits MDR1 through reactive oxygen species and cyclooxygenase-2 mediated pathways in human hepatocellular carcinoma cell line[J]. Eur J Pharmacol, 2010, 649(1/3):74-83. doi: 10. 1016/j.ejphar.2010.09.011.

[29] ROY K R, ARUNASREE K M, REDDY N P, et al. Alteration of mitochondrial membrane potential by spirulina platensis C- phycocyanin induces apoptosis in the doxorubicinresistant human hepatocellular-carcinoma cell line HepG2[J].  Biotechnol Appl Biochem, 2007, 47 (Pt 3): 159-167. doi: 10. 1042/BA20060206.

[30] PRABAKARAN G, SAMPATHKUMAR P, KAVISRI M, et al. Extraction and characterization of phycocyanin from spirulina platensis and evaluation of its anticancer , antidiabetic and antiinflammatory effect[J]. Int J Biol Macromol, 2020, 153: 256- 263. doi: 10. 1016/j.ijbiomac.2020.03.009.

[31] SILVA M R O B D, M DA SILVA G, SILVA A L F D, et al. Bioactive compounds of Arthrospira spp. (spirulina) with potential anticancer activities: a systematic review[J].  ACS Chem Biol, 2021, 16 (11): 2057-2067. doi: 10. 1021/acschembio.1c00568.

[32] COUÉ M, TESSE A, FALEWÉE J, et al. Spirulina liquid extract protects against fibrosis related to non-alcoholic steatohepatitis and increases ursodeoxycholic acid [J]. Nutrients, 2019, 11 (1): 194. doi:10.3390/nu11010194.

[33] KASBI-CHADLI F, COUÉ M, AGUESSE A, et al. Spirulina liquid extract prevents metabolic disturbances and improves liver sphingolipids profile in hamster fed a high-fat diet[J]. Eur J Nutr, 2021, 60(8):4483-4494. doi: 10. 1007/s00394-021-02589-x.

[34] OULD AMARA-LEFFAD L, RAMDANE H, NEKHOUL K, et al. Spirulina effect on modulation of toxins provided by food, impact on hepatic and renal functions [J] . . Arch Physiol Biochem, 2019, 125 (2): 184-194. doi: 10. 1080/13813455.2018.1444059.

[35] MA P, HUANG R, JIANG J, et al. Potential use of C-phycocyanin in non-alcoholic fatty liver disease [J].  Biochem Biophys Res Commun, 2020, 526(4):906-912. doi: 10. 1016/j.bbrc.2020.04.001.

［36］ICHIMURA M, KATO S, TSUNEYAMA K, et al. Phycocyanin prevents hypertension and low serum adiponectin level in a rat model of metabolic syndrome［J］. Nutr Res, 2013, 33(5): 397-405. doi: 10. 1016/j.nutres.2013.03.006.

[37] COUÉ M, CROYAL M, HABIB M, et al. Perinatal administration of C-phycocyanin protects against atherosclerosis in apoE-deficient mice by modulating cholesterol and trimethylamine-N-oxide metabolisms[J]. Arterioscler Thromb Vasc Biol, 2021, 41(12): e512-e523. doi: 10. 1161/ATVBAHA.121.316848.

［38］REN Z, XIE Z, CAO D, et al. C-phycocyanin inhibits hepatic gluconeogenesis and increases glycogen synthesis via activating Akt and AMPK in insulin resistant hepatocytes [J]. Food Funct, 2018, 9(5): 2829-2839. doi: 10. 1039/c8fo00257f.

［39］OU Y, REN Z, WANG J, et al. Phycocyanin ameliorates alloxan- induced diabetes mellitus in mice ：involved in insulin signaling pathway and GK expression [J]. Chem Biol Interact, 2016, 247: 49- 54. doi: 10. 1016/j.cbi.2016.01.018.

[40] XIA D, LIU B, XIN W, et al. Protective effects of C-phycocyanin on alcohol-induced subacute liver injury in mice [J].  Journal of Applied Phycology, 2015, 28(2):765-772. doi: 10. 1007/s10811- 015-0677-3.

[41] XIE Y, LI W, ZHU L, et al. Effects of phycocyanin in modulating  the intestinal microbiota of mice [J].  Microbiologyopen, 2019, 8 (9): e00825. doi: 10. 1002/mbo3.825.

［42］LIU Q, LI W, QIN S. Therapeutic effect of phycocyanin on acute liver oxidative damage caused by X-ray［J］. Biomed Pharmacother, 2020, 130: 110553. doi: 10. 1016/j.biopha.2020.110553.

［43］SONG Y N, CHEN J, CAI F F, et al. A metabolic mechanism analysis of fuzheng-huayu formula for improving liver cirrhosis with traditional chinese medicine syndromes [J]. Acta Pharmacol Sin, 2018, 39(6): 942-951. doi: 10. 1038/aps.2017.101.

［44］XIAO J, WANG F, WONG N K, et al. Global liver disease burdens and research trends : analysis from a chinese perspective［J］. J Hepatol, 2019, 71(1):212-221. doi: 10. 1016/j.jhep.2019.03.004.

#phycocyanin #cphycocyanin #phycocyaninspirulina

[melodic-melovin]

Mélovin Health Update: What We Know So Far (11/13/2023)

Okay so normally I'd just reblog the last post I made, but after trawling through countless news/tabloids sites, Reddit, and the cesspool that is Twitter and sorting through the various information available, it seemed more important to make a separate post entirely so people could see.

HERE IS WHAT HAS HAPPENED/WHAT WE KNOW:

-Mel has been diagnosed with a serious illness.

-I cannot *personally* confirm for sure what illness, HOWEVER, most sources are reporting that it is steatohepatitis, a liver condition, sometimes also known as "Nonalcoholic Fatty Liver Disease"

-In essence: this is essentially an inflammation of the liver caused by fat cells building up in said liver, not brought on by drinking alcohol.

-It is considered a metabolic disorder. There are several potential causes, most of which are tied to type 2 diabetes and obesity complications, hormone imbalances such as with the thyroid, but it can also just be bad luck of the genetic draw.

-This is NOT the same condition as viral hepatitis (aka Hepatitis C, etc.) I mention this specifically because some sites are incorrectly reporting this claim and people are already using that misinformation as ammo to be homophobic and claim that he got this condition as a result of his "orientation". Do not do this. Do not be these people.

-Is it terminal or is it incurable? Well, that's the muddied part of this. Even Mel used the term 'terminal' in his Instagram post about this, however many sources seem to point to 'incurable' as a more accurate term. It could be that the words are very similar in Ukrainian and thus the confusion there.

-Note that steatohepatitis *is* incurable, however it *may* or *may not* be terminal/fatal. We don't know how long he's had it, if there was liver damage already present before his being officially diagnosed, and to what extent. The main complications that can lead to death if no treatment is administered are cirrhosis and scarring, even liver cancer, which the only treatment at that point would be a full liver transplant. Without treatment, expectancy is anywhere between 3-5 years in severe cases, or 10-15 in lesser ones. Again, this is not proof of anything yet, this is only the general knowledge I have gained from researching this condition.

-This diagnosis came about as a result of bloodwork when he intended to get some kind of cosmetic procedure.

-(Before anyone asks what cosmetic surgery was he getting - that I don't know, and I don't think anyone else does either. He hasn't said, and cosmetic is a very broad term and can range from anything like traditionally thought-of plastic surgeries to something less intensive like a mole removal or getting his teeth worked on. Personally I think he's too young to be getting cosmetic work done, but that's not important right now.)

-He is seeking/undergoing treatment and currently resting and recovering at home with his family.

-His Instagram is currently private to non-followers, probably to prevent harassment. I have downloaded the video regarding this apparent diagnosis announcement and will try to upload it.

-He is still apparently on the longlist for competing in Vidbir, as announced by Suspilne.

-It is not known if this will impact the release of his newest song or further music going forward.

= o = o = o = o = o = o =

If more develops, I will try to let you all know. Right now, please just try to be supportive, don't harass him or his friends/family for more info (he will no doubt tell us when he is ready), and don't spread wild misinformation. We can only imagine what he must be going through right now. Even if this ends up not being nearly as bad as it sounds, getting a lifelong illness diagnosis is not easy for anyone to handle.

[pellaaearien]

🌟

So this has been sitting in my inbox for... Jesus, nearly a month now, but I finally feel like I have something worthwhile to answer. Dealer's choice: I'm going to talk about my headcanons for Hob's immortality.

It had been up to Hob to figure out the limits of it, over the centuries. Injuries that would have killed him, like the broken neck, healed swiftly, and left scars. Non-fatal wounds healed at the same rate as any mortal’s, and rarely left remnants behind. (Another Word for Ache, chapter 12)

There was an excellent post going around a bit ago positing the different options for Hob's healing ability. The one that seems most popular with authors is that Hob heals at a slightly faster rate than most humans, and can heal from just about anything. There's a good reason for this: it keeps the action moving along, and it means that you can be as whumpy as you want and it won't have any lasting effects.

Other potential options include things like super fast healing, where he heals as you put the bullets in him, or taking the wording of "can't die" to the logical conclusion where Hob has "super luck" instead -- anything that would have killed him simply misses him.

What I've chosen to go with is a bit of a middle ground, and it's one that feels true to me. Hob can't die, so any fatal wounds are not fatal. In chapter 10 of my fic, the Corinthian breaks Hob's neck, and he wakes up after 42 minutes, resets his neck, and he's back in business. (As a side note, I do kind of wish circumstances were such that ALL his wounds would have to heal at a normal rate; like yeah, a broken neck won't be FATAL but you're going to be in traction for however long it takes for it to heal naturally. I don't know how long it would take a broken neck to heal naturally, because the lack of oxygen to the brain tends to be fatal long before healing can occur, but I know it's certainly longer than the Corinthian wanted to hang out in Hob's office with an unconscious Hob so concessions had to be made, hence the 42 minutes (I think Death would be a Douglas Adams fan)).

BUT, that doesn't mean that non-fatal wounds magically heal faster. When the Corinthian stabs him in the liver, that will heal on its own but it means Hob's off the alcohol for a solid month until it does.

I don't think it'll come up in my fic, but I thought a LOT about additional implications. What about illness? Same thing: if the illness would be fatal, Hob won't die, but if it's just a cold, he's gotta suffer through it like the rest of us. However, I had a lot of fun thinking about all the antibodies Hob probably has bouncing around inside him thanks to building up immunity to all kinds of diseases over the years (note I am not a doctor and I don't know if this is how it works, but again, we don't exactly have a bevy of immortals to test it on.)

Then I got to thinking about other non-fatal injuries. Losing a limb, for instance, isn't necessarily fatal if you can access the proper treatment in time. Would Hob's arm grow back? I have to assume that it wouldn't. Lacking an arm is not a fatal condition. Even if he did die from blood loss, I'm assuming the arm isn't going to grow back or reattach. Hob had better be careful to keep all his bits! (And frankly this is the most surprising element given all the soldiering he did early on.)

Anyway, a fun thought experiment, and by a certain definition, the best of all worlds. Hob still gets some sexy scars, he's not going to be laid up long enough to derail the action scenes, and sick fics are still a go! But it can be fascinating to speculate about the implications of a single small decision either way.

Ask away!

[akashbajaj123]

Effective Non-Alcoholic Steatohepatitis Treatment in Pune

Non-Alcoholic Steatohepatitis (NASH), a severe kind of non-alcoholic fatty liver disease, necessitates prompt and specialist care. Pune provides quality medical care with knowledgeable physicians who focus on individualized treatment approaches. Obesity, diabetes, or metabolic syndrome are common causes of NASH, and addressing these underlying factors is key to managing it.

Non alcoholic steatohepatitis treatment in Pune often entails lifestyle changes such as eating a balanced diet, exercising regularly, and addressing underlying problems such as high cholesterol or diabetes. Expert hepatologists in Pune also offer medication treatments to minimize liver inflammation and slow disease progression.

Leading hospitals in Pune are equipped with state-of-the-art diagnostic tools, enabling accurate assessments of liver health. Regular monitoring and early intervention play a crucial role in managing NASH effectively. Specialists work closely with dietitians and fitness experts to ensure a comprehensive approach to improving liver function and overall well-being.

If you’re seeking non-alcoholic steatohepatitis treatment in Pune, look for hospitals and clinics with a proven track record in liver care. Patient reviews, doctor credentials, and accessibility are key factors to consider when choosing the right healthcare provider. Early diagnosis and expert care can significantly improve outcomes for NASH patients.

[kaizengastrocare]

If you are experiencing signs of NAFLD or are at risk? If you are concerned about fatty liver disease or need expert care for NAFLD, Dr. Vikrant Kale at Kaizen Gastro Care is here to provide you with the best liver care in Pune. With a focus on early detection, prevention, and treatment, Dr. Kale and his team are dedicated to helping patients achieve optimal liver health.

[anandkhakar]

The Impact of Sugar on Your Liver and the Role of Liver Transplant Surgeons in Gujarat

Liver transplant is a replacement of diseased liver in a patient with end-stage liver failure with a healthy organ. Liver transplant surgery in India

[openintegrative]

Gout: Symptoms & Natural Treatment

Gout results from the accumulation of uric acid crystals in the joints, causing severe pain and inflammation.

High uric acid levels are often linked to metabolic issues and excessive fructose consumption.

Fructose, not red meat, is a primary contributor to elevated uric acid and gout development.

Proper management of gout involves reducing sugar intake and optimizing nutrient balance.

Addressing underlying metabolic dysfunctions is essential for long-term gout relief.

Introduction

Gout is a form of arthritis characterized by sudden and severe pain, swelling, and redness in the joints, most often in the big toe.

It occurs when uric acid crystals accumulate in the joints, causing inflammation and pain.

Gout is closely related to high levels of uric acid in the blood, but several factors influence its development, including diet, metabolic health, and lifestyle.

Causes and Risk Factors

Uric Acid and Gout

Uric acid is a natural waste product formed when the body breaks down purines. Normally, uric acid is dissolved in the blood and eliminated through the kidneys.

However, when uric acid levels become too high, it can crystallize and settle in the joints, leading to gout.

The main drivers of elevated uric acid include metabolic issues, fructose consumption, and impaired kidney function.

The Role of Fructose in Gout

Fructose, found in sugary drinks and processed foods, is a major contributor to high uric acid levels.

Unlike glucose, fructose metabolism rapidly generates uric acid, particularly in the liver. Excessive fructose consumption has been linked to metabolic disorders such as insulin resistance, non-alcoholic fatty liver disease (NAFLD), and gout.

Reducing fructose intake is key to preventing gout flares and managing uric acid levels.

Common Triggers for Gout Attacks

Gout attacks can be triggered by various factors, including:

High consumption of fructose or sugar-laden foods

Alcohol intake, especially beer

Dehydration

Sudden increases in physical activity or stress

Certain medications that raise uric acid levels, like diuretics

Symptoms and Diagnosis

Common Symptoms

The most common symptom of gout is intense joint pain, often starting in the big toe, though other joints can be affected. Additional symptoms include:

Swelling and redness in the affected joint

Warmth and tenderness around the joint

Limited joint movement due to pain

Gout attacks, which can occur suddenly and last several days

Diagnosing Gout

Gout is typically diagnosed through physical examinations, blood tests to check uric acid levels, and imaging studies like ultrasounds or X-rays to detect uric acid crystals in the joints.

Joint fluid tests can also confirm the presence of uric acid crystals.

Treatment and Management

Dietary Adjustments

Managing gout involves making key dietary changes to reduce uric acid levels and prevent gout flares. Prioritizing nutrient-dense, low-sugar foods while reducing fructose intake is needed.

Contrary to popular belief, red meat is not a major cause of gout and provides essential nutrients like iron, zinc, and B vitamins.

Instead, eliminating sugary foods and drinks, especially those containing high-fructose corn syrup, is essential for reducing gout risk.

Medication Options

Medications are often prescribed to manage gout, especially during acute flare-ups. These include:

Nonsteroidal anti-inflammatory drugs (NSAIDs): Used to reduce pain and inflammation.

Colchicine: Helps reduce inflammation during a gout attack.

Allopurinol: Lowers uric acid levels by reducing its production in the body.

Probenecid: Increases uric acid excretion through the kidneys.

While medications are effective, long-term management should focus on lifestyle changes that address the underlying causes of high uric acid.

Long-Term Management Strategies

In addition to dietary changes and medications, managing gout involves other lifestyle adjustments:

Stay hydrated to support kidney function and uric acid excretion.

Maintain a healthy weight to reduce the metabolic stress associated with high uric acid levels.

Limit alcohol consumption, as it can interfere with uric acid excretion and trigger gout attacks.

Preventing Gout Flares

Reducing Fructose Intake

As fructose significantly contributes to elevated uric acid levels, cutting back on sugary drinks and processed foods is vital.

A diet rich in whole, low-carbohydrate foods supports metabolic health and prevents gout flares.

Optimizing Nutrient Intake

Eating a bioavailable nutrient-rich diet ensures the body gets essential nutrients like copper, which plays a key role in managing oxidative stress and iron regulation.

Proper nutrient balance helps the body manage uric acid more effectively.

Beta-hydroxybutyrate (BHB)

Beta-hydroxybutyrate (BHB) is one of the main ketone bodies produced by the liver during fat metabolism.

BHB is produced through a process called ketogenesis, where fats are broken down into ketones in the liver.

This occurs during times of carbohydrate restriction, fasting, or prolonged exercise. The body converts stored fat into ketones, with BHB being the primary ketone that circulates in the bloodstream and provides energy.

Beta-hydroxybutyrate (BHB) has shown promising effects in reducing inflammation related to gout. Research indicates that BHB inhibits the NLRP3 inflammasome, a key driver in gout’s inflammatory response, particularly in neutrophils.

This inhibition reduces the production of IL-1β, a pro-inflammatory cytokine involved in gouty flares.

The anti-inflammatory properties of BHB offer a potential therapeutic avenue for treating gout, providing relief from the intense joint pain and inflammation associated with the condition.

Exercise and Weight Management

Regular physical activity and maintaining a healthy weight help improve insulin sensitivity, reduce inflammation, and lower the risk of metabolic conditions that contribute to gout.

However, sudden intense physical activity may trigger gout attacks, so exercise should be moderate and consistent.

Conclusion

Gout is a painful condition rooted in metabolic imbalances and high uric acid levels. While often misunderstood, the primary contributors to gout are fructose consumption and metabolic dysfunction, not red meat. Managing gout requires a combination of dietary changes, medication when needed, and long-term lifestyle adjustments that target the root causes of elevated uric acid. By focusing on reducing fructose intake and optimizing metabolic health, individuals can effectively manage and prevent gout flare-ups.

FAQs

What causes gout?

Gout is caused by the accumulation of uric acid crystals in the joints, often triggered by metabolic issues, fructose consumption, and impaired kidney function.

Is red meat a cause of gout?

No, red meat is not a primary cause of gout. The real culprit is excessive fructose consumption, which raises uric acid levels.

How can I prevent gout flare-ups?

Prevent gout flare-ups by reducing sugar and fructose intake, staying hydrated, maintaining a healthy weight, and following a nutrient-dense diet.

What is the role of fructose in gout?

Fructose is metabolized into uric acid, which contributes to gout development. Limiting sugary drinks and processed foods helps manage uric acid levels.

Can gout be cured?

While there is no cure for gout, it can be effectively managed through lifestyle changes, proper diet, and medications that reduce uric acid levels

Research

Ayoub-Charette S, Liu Q, Khan TA, Au-Yeung F, Blanco Mejia S, de Souza RJ, Wolever TM, Leiter LA, Kendall C, Sievenpiper JL. Important food sources of fructose-containing sugars and incident gout: a systematic review and meta-analysis of prospective cohort studies. BMJ Open. 2019 May 5;9(5):e024171. doi: 10.1136/bmjopen-2018-024171. PMID: 31061018; PMCID: PMC6502023.

Bai, L., Zhou, J.-B., Zhou, T., Newson, R.B. and Cardoso, M.A., 2021. Incident gout and weight change patterns: a retrospective cohort study of US adults. Arthritis Research & Therapy, [online] 23(1). https://doi.org/10.1186/s13075-021-02461-7.

Basaranoglu, M., Basaranoglu, G., & Bugianesi, E. (2015). Carbohydrate intake and nonalcoholic fatty liver disease: Fructose as a weapon of mass destruction. Hepatobiliary Surgery and Nutrition, 4(2), 109-116. https://doi.org/10.3978/j.issn.2304-3881.2014.11.05

Cristina, M. (2023). Insulin and the kidneys: A contemporary view on the molecular basis. Frontiers in Nephrology, 3, 1133352. https://doi.org/10.3389/fneph.2023.1133352

Ghio, A.J., Ford, E.S., Kennedy, T.P. and Hoidal, J.R., 2005. The association between serum ferritin and uric acid in humans. Free Radical Research, [online] 39(3), pp.337–342. https://doi.org/10.1080/10715760400026088.

Goldberg, E. L., Asher, J. L., Molony, R. D., Shaw, A. C., Zeiss, C. J., Wang, C., Morozova-Roche, L. A., Herzog, R. I., Iwasaki, A., & Dixit, V. D. (2017). β-hydroxybutyrate deactivates neutrophil NLRP3 inflammasome to relieve gout flares. Cell Reports, 18(9), 2077. https://doi.org/10.1016/j.celrep.2017.02.004

Jamnik, J., Rehman, S., Blanco Mejia, S., de Souza, R.J., Khan, T.A., Leiter, L.A., Wolever, T.M.S., Kendall, C.W.C., Jenkins, D.J.A. and Sievenpiper, J.L., 2016. Fructose intake and risk of gout and hyperuricemia: a systematic review and meta-analysis of prospective cohort studies. BMJ Open, [online] 6(10), p.e013191. https://doi.org/10.1136/bmjopen-2016-013191.

Lanaspa, M.A., Sanchez-Lozada, L.G., Cicerchi, C., Li, N., Roncal-Jimenez, C.A., Ishimoto, T., Le, M., Garcia, G.E., Thomas, J.B., Rivard, C.J., Andres-Hernando, A., Hunter, B., Schreiner, G., Rodriguez-Iturbe, B., Sautin, Y.Y. and Johnson, R.J., 2012. Uric Acid Stimulates Fructokinase and Accelerates Fructose Metabolism in the Development of Fatty Liver. PLoS ONE, [online] 7(10), p.e47948. https://doi.org/10.1371/journal.pone.0047948.

Lanaspa, M.A., Tapia, E., Soto, V., Sautin, Y. and Sánchez-Lozada, L.G., 2011. Uric Acid and Fructose: Potential Biological Mechanisms. Seminars in Nephrology, [online] 31(5), pp.426–432. https://doi.org/10.1016/j.semnephrol.2011.08.006.

Maiuolo, J., Oppedisano, F., Gratteri, S., Muscoli, C. and Mollace, V., 2016. Regulation of uric acid metabolism and excretion. International Journal of Cardiology, [online] 213, pp.8–14. https://doi.org/10.1016/j.ijcard.2015.08.109.

Mainous, A.G., Knoll, M.E., Everett, C.J., Matheson, E.M., Hulihan, M.M. and Grant, A.M., 2011. Uric Acid as a Potential Cue to Screen for Iron Overload. The Journal of the American Board of Family Medicine, [online] 24(4), pp.415–421. https://doi.org/10.3122/jabfm.2011.04.110015.

Muscelli, E., 1996. Effect of insulin on renal sodium and uric acid handling in essential hypertension. American Journal of Hypertension, [online] 9(8), pp.746–752. https://doi.org/10.1016/0895-7061(96)00098-2.

Nakagawa, T., Lanaspa, M. A., & Johnson, R. J. (2019). The effects of fruit consumption in patients with hyperuricaemia or gout. Rheumatology, 58(7), 1133-1141. https://doi.org/10.1093/rheumatology/kez128

Pina, A.F., Borges, D.O., Meneses, M.J., Branco, P., Birne, R., Vilasi, A. and Macedo, M.P., 2020. Insulin: Trigger and Target of Renal Functions. Frontiers in Cell and Developmental Biology, [online] 8. https://doi.org/10.3389/fcell.2020.00519.

Rasool, M., Malik, A., Jabbar, U., Begum, I., Qazi, M.H., Asif, M., Naseer, M.I., Ansari, S.A., Jarullah, J., Haque, A. and Jamal, M.S., 2016. Effect of iron overload on renal functions and oxidative stress in beta thalassemia patients. Saudi Medical Journal, [online] 37(11), pp.1239–1242. https://doi.org/10.15537/smj.2016.11.16242.

Rho, Y.H., Zhu, Y. and Choi, H.K., 2011. The Epidemiology of Uric Acid and Fructose. Seminars in Nephrology, [online] 31(5), pp.410–419. https://doi.org/10.1016/j.semnephrol.2011.08.004.

Singh, J.A., Reddy, S.G. and Kundukulam, J., 2011. Risk factors for gout and prevention: a systematic review of the literature. Current Opinion in Rheumatology, [online] 23(2), pp.192–202. https://doi.org/10.1097/bor.0b013e3283438e13.

Skøtt, P., Hother-Nielsen, O., Bruun, N.E., Giese, J., Nielsen, M.D., Beck-Nielsen, H. and Parving, H.-H., 1989. Effects of insulin on kidney function and sodium excretion in healthy subjects. Diabetologia, [online] 32(9). https://doi.org/10.1007/bf00274259.

Wang, Y., Yang, Z., Wu, J., Xie, D., Yang, T., Li, H. and Xiong, Y., 2020. Associations of serum iron and ferritin with hyperuricemia and serum uric acid. Clinical Rheumatology, [online] 39(12), pp.3777–3785. https://doi.org/10.1007/s10067-020-05164-7.

Yamanaka H. [Alcohol ingestion and hyperuricemia]. Nihon Rinsho. 1996 Dec;54(12):3369-73. Japanese. PMID: 8976122.

[iqbalnabi]

The Link Between Jaundice and Liver Health: What You Should Know

Jaundice is a medical condition characterized by a yellowish tint to the skin, sclera (the white part of the eyes), and mucous membranes. While jaundice itself is not a disease, it is often a sign of an underlying issue, typically related to liver health. Understanding the connection between jaundice and liver function is crucial, as it can provide valuable insight into the state of one's overall health.

What is Jaundice?

Jaundice occurs when there is an excess of bilirubin in the bloodstream. Bilirubin is a yellow compound that results from the breakdown of hemoglobin in red blood cells. The liver typically processes bilirubin, converting it into a form that can be excreted in bile. However, when the liver is compromised, its ability to process and eliminate bilirubin may be impaired, leading to its accumulation in the body, causing the yellowish discoloration of the skin and eyes.

Jaundice can also result from issues outside the liver, such as hemolysis (increased breakdown of red blood cells) or bile duct obstruction. However, when jaundice is associated with liver dysfunction, it usually points to problems affecting the liver's ability to metabolize or excrete bilirubin. If you're in need of jaundice treatment in Indore, consulting with a specialist can help identify the root cause and recommend the appropriate course of action.

How the Liver Functions in Bilirubin Processing

The liver plays a central role in the processing of bilirubin. The lifecycle of bilirubin begins with the breakdown of red blood cells in the spleen and bone marrow. The hemoglobin from these cells is broken down into heme and globin. The heme is then converted intounconjugated (indirect) bilirubin, which is transported to the liver bound to albumin (a protein in the blood).

Once in the liver, the unconjugated bilirubin is processed by liver cells called hepatocytes. These cells convert unconjugated bilirubin into conjugated (direct) bilirubin by attaching it to a sugar molecule. The conjugated bilirubin is water-soluble and can be excreted into bile, which is stored in the gallbladder or released into the intestines. In the intestines, bilirubin is eventually excreted from the body through feces, giving stool its brown color.

Causes of Jaundice Linked to Liver Health

Several liver-related conditions can cause jaundice by impairing the organ's ability to process and excrete bilirubin. These include:

1. Hepatitis

Hepatitis is inflammation of the liver, often caused by viral infections (e.g., hepatitis A, B, or C). The inflammation disrupts the liver’s ability to function properly, including its role in bilirubin processing. Chronic hepatitis can lead to cirrhosis and liver failure, both of which significantly impair bilirubin metabolism.

2. Cirrhosis

Cirrhosis is the scarring of liver tissue due to long-term damage, often from chronic alcohol use, viral hepatitis, or fatty liver disease. As liver cells are destroyed and replaced by scar tissue, the liver's capacity to filter toxins, process bilirubin, and produce bile becomes compromised. This can lead to jaundice, along with other complications such as ascites and encephalopathy.

3. Liver Cancer

Cancer in the liver, whether primary (originating in the liver) or metastatic (spreading from other organs), can obstruct bile ducts or directly affect the liver’s ability to process bilirubin. This blockage can result in elevated bilirubin levels and jaundice.

4. Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is characterized by an accumulation of fat in liver cells, which can impair liver function. In its advanced stages (non-alcoholic steatohepatitis, or NASH), fatty liver disease can cause inflammation, fibrosis, and cirrhosis, all of which increase the risk of jaundice.

5. Gilbert’s Syndrome

Gilbert's syndrome is a genetic condition that affects the liver's ability to process unconjugated bilirubin. Although typically mild and not life-threatening, people with Gilbert's syndrome may experience intermittent jaundice, particularly during periods of stress, fasting, or illness.

Other Causes of Jaundice Linked to Liver Health

Jaundice can also result from blockages in the bile ducts or conditions affecting the blood. For instance:

Bile Duct Obstruction: Gallstones, tumors, or strictures (narrowing) of the bile ducts can block the flow of bile, causing a buildup of bilirubin in the bloodstream.

Hemolytic Anemia: When red blood cells are destroyed more rapidly than normal, the liver may be overwhelmed by the excess bilirubin. This type of jaundice is typically unrelated to liver function, but it can complicate underlying liver issues.

Liver Infections: Bacterial or parasitic infections in the liver, such as liver abscesses or schistosomiasis, can lead to liver damage and jaundice.

Symptoms of Jaundice Related to Liver Health

In addition to the characteristic yellowing of the skin and eyes, jaundice related to liver problems may be accompanied by other symptoms, including:

Fatigue: A common symptom of liver disease due to the organ's reduced ability to filter toxins and produce energy.

Abdominal Pain: Particularly in the upper right side of the abdomen, where the liver is located.

Swelling: In the abdomen (ascites) or legs (edema), often associated with cirrhosis or liver failure.

Dark Urine: Due to excess bilirubin being excreted through the kidneys.

Pale Stools: As bilirubin isn't being excreted properly through the intestines, stools may become lighter or clay-colored.

Given the range of liver-related conditions that can cause jaundice, it is important to seek medical attention if you or someone you know develops yellowing of the skin or eyes, especially if accompanied by other symptoms such as pain or swelling. Early diagnosis and treatment of liver issues can significantly improve outcomes and prevent serious complications. For the best jaundice treatment in Indore, consulting with a skilled healthcare provider will help identify the cause and determine the most effective treatment plan.

[cmcshealth]

Liver Transplant in India

The Liver is one of the five Vital Organs in the human body. The Liver performs many important functions for the proper functioning of the Human Body. Any changes or abnormalities in liver tissues can affect the quality of life and may need medical treatments. Certain Medical Conditions like Cirrhosis of the Liver, primary Liver cancer, or an ill-functioning Liver may require a Liver Transplant to save the life of the patient.

What is a Liver Transplant Surgery?

A liver Transplant is a life-saving Surgery performed by a specially trained gastroenterology surgeon to replace the damaged or faulty liver in a patient with a healthy liver either from a deceased donor liver or the portion of the Liver obtained from a living liver donor. Liver Transplant Surgery is a complicated surgery and requires great expertise from gastroenterology surgeons and a proper hospital setup.

Why a Liver transplant is needed?

A liver transplant is needed when the liver tissues are damaged and the Liver is unable to perform its functions. An end-stage liver disease patient requires a Liver Transplant for survival. A liver Transplant is also indicated for the treatment of primary Liver Cancer when the cancer is localized and the tumor size is smaller. Following medical conditions may make a Gastroenterologist or Hepatologist recommend a Liver Transplant for a patient:

Liver Cirrhosis

Alcohol-induced liver damage due to chronic alcoholism

Non-alcoholic fatty liver disease

Hemochromatosis

Wilson's disease

Primary biliary Cholangitis (PBC)

Primary sclerosing cholangitis (PSC)

Biliary atresia (generally for pediatric liver patients)

Autoimmune hepatitis

Acute Liver failure

Primary Liver cancer

Types of Liver Transplants

Liver Transplants are done either with a deceased liver donor or a healthy liver donor.

Deceased Donor Liver Transplant

Orthotopic liver transplant is replacing the damaged liver in an end-stage liver disease patient with a healthy liver procured from a deceased donor.

Split liver transplants are also orthotopic liver transplants where the deceased donor's liver is split into two and transplanted into two end-stage liver disease patients. In Split liver transplant surgery, the left lateral cadaveric liver is transplanted into a child, and the right extended liver is transplanted into an adult patient.

Living Donor Liver Transplants

Living donor liver transplants are done by taking a portion of the liver from an HLA matching Liver Donor. The Donor reverts to the full functionality of the Liver within 6 weeks of liver donation and lives a perfectly normal life.

CMCS Health is a leading medical tourism company in India. We offer medical tourism services such as finding the right doctor, the right hospital, and cost estimation for medical treatment in India for foreign patients. Some of the main countries are Bangladesh, South Africa, Egypt, Kenya, Saudi Arabia, Ethiopia, Nigeria, Uganda, Zambia, Sudan, Dubai, Namibia, Iraq, and so on. We provide free medical assistance aplastic anemia treatment cost, stomach cancer treatment, sickle cell treatment cost, the best hospital for heart valve replacement, heart valve surgery, arthroscopic surgery, bone marrow transplant cost, best liver transplant hospital, brain tumor surgery cost, cosmetic andplastic surgery, heart surgery, kidney transplant cost, spine tumor surgery,cancer treatment cost, lung transplant,liver transplant cost, top knee replacement surgeons, knee replacement surgery cost, top shoulder replacement surgeons, hip replacement surgery cost, best bone marrow hospital, etc.  If you are searching for free medical and healthcare consulting to find the best hospitals and top doctors and surgeons in India for any treatment then contact us- Cmcshealth.com.

Source: https://cmcshealth1.blogspot.com/2024/11/liver-transplant-in-india.html

[docganeshnagaranjan]

How Can Liver Cancer Treatment in Mumbai Help Improve Patient Outcomes?

Liver cancer treatment in Mumbai offers advanced care options for patients diagnosed with this serious condition. The city is home to a range of renowned hospitals and specialized oncologists who employ cutting-edge techniques for the diagnosis and treatment of liver cancer. These treatments include surgical options like liver resection and liver transplant, which are often recommended based on the stage of cancer and the overall health of the patient.

In addition to surgery, Mumbai offers various non-surgical treatments such as chemotherapy, targeted therapy, and immunotherapy. These methods aim to shrink tumors, control the spread of cancer, and improve quality of life. Interventional radiology procedures like radiofrequency ablation (RFA) and transarterial chemoembolization (TACE) are also available for patients who are not candidates for surgery.

The comprehensive liver cancer care in Mumbai is further enhanced by a multidisciplinary approach, with teams of specialists from oncology, radiology, surgery, and palliative care working together. Many of the leading medical centers in Mumbai also offer personalized treatment plans, taking into account the individual needs and health conditions of the patient. With world-class healthcare infrastructure, expert doctors, and the latest treatment options, Mumbai has become a leading destination for liver cancer treatment in India.

Liver cancer is typically classified into four stages based on the extent of the tumor and its spread. The treatment options in Mumbai are tailored according to these stages:

Stage 1 (Early Stage):

The cancer is confined to a single tumor in the liver and has not spread to nearby blood vessels or other organs.

Treatment: Surgical removal of the tumor (liver resection) or liver transplant may be possible.

Stage 2 (Localized Advanced):

The cancer may have spread to nearby blood vessels but is still localized to the liver.

Treatment: Surgery, liver transplant, or interventional procedures like radiofrequency ablation (RFA) or transarterial chemoembolization (TACE).

Stage 3 (Advanced):

Cancer has spread to nearby lymph nodes or organs outside the liver, but not to distant parts of the body.

Treatment: A combination of surgery, radiation therapy, chemotherapy, targeted therapy, or immunotherapy may be recommended.

Stage 4 (Metastatic):

Cancer has spread to distant parts of the body, including other organs like the lungs or bones.

Treatment: Palliative care, chemotherapy, targeted therapy, and immunotherapy to manage symptoms and slow the progression.

Treatment options vary and are based on the patient's overall health, liver function, and the cancer's extent, with expert oncologists in Mumbai providing personalized care at each stage.

Dr. Ganesh Nagarajan, a highly experienced specialist in gastrointestinal, hepatobiliary, and pancreatic cancers, offers several precautions and lifestyle recommendations for those undergoing liver cancer treatment in Mumbai. His suggestions include:

Healthy Lifestyle: Maintaining a balanced diet, regular exercise, and avoiding excessive alcohol consumption are crucial for liver health. A high-carbohydrate diet, particularly refined sugars, can worsen liver conditions, so a diet rich in vegetables, fruits, and lean proteins is recommended​..

Managing Risk Factors: He emphasizes managing conditions like diabetes, as it increases the risk of liver cancer. Monitoring blood sugar levels and adopting a healthy diet to prevent fatty liver disease are key preventive strategies​.

Early Detection: Regular check-ups and liver function tests are essential for early diagnosis. If liver abnormalities are detected early, they can be treated before progressing to cancer​ Cancer Surgery Clinic.

Surgical Treatment: For patients in the early stages of liver cancer, surgical intervention such as liver resection or a liver transplant may offer the best outcomes. Dr. Nagarajan specializes in such procedures​.

These lifestyle and medical approaches play a significant role in enhancing liver health and improving the chances of successful cancer treatment. For more personalized advice, it's essential to consult directly with Dr. Nagarajan.

For more detailed insights on liver cancer treatment in Mumbai with Dr. Ganesh Nagarajan, you can watch this informative YouTube video: Liver Cancer Treatment with Dr. Ganesh Nagarajan. It covers essential aspects of liver cancer, treatment options, and the approach taken by Dr. Nagarajan in managing liver cancer.

The Cancer Surgery Clinic, led by Dr. Ganesh Nagarajan, is located at Sanskruti by Sugee, 202, 2nd Floor, Lady Jamshedji Road, opposite Kohinoor Tower, Dadar West, Shivaji Park, Mumbai – 400028. You can view the clinic location directly on Google Maps.

How to Reach the Clinic:

From the Western Line (Mumbai Local):

Dadar Station is the closest on the Western Line. Once you exit the station, it’s about a 10-minute walk or a short cab/auto rickshaw ride to the clinic. You can take the Lady Jamshedji Road toward Kohinoor Tower.

From the Central Line (Mumbai Local):

Dadar Station is also the closest on the Central Line. After exiting, follow the same route as above via Lady Jamshedji Road. Alternatively, you can take a cab or auto from the station.

For Patients Coming from Outside Mumbai:

By Train: You can arrive at Dadar Railway Station by any major train from your city. From there, follow the walking directions or take a cab/auto to the clinic.

By Flight: The nearest airport is Chhatrapati Shivaji Maharaj International Airport (BOM). You can take a cab or an Ola/Uber directly to the clinic, which is around 30-40 minutes away from the airport depending on traffic.

This convenient location and the well-connected transport options make it easy for patients from Mumbai and beyond to reach Dr. Ganesh Nagarajan’s clinic.

[ellabdiagnosticcenter]

Liver Function Tests in Nigeria: Key to Early Detection and Better Liver Health

Liver Function Tests in Nigeria are essential diagnostic tools widely used in Nigeria to evaluate liver health and diagnose liver-related diseases. These tests measure specific enzymes, proteins, and other substances in the blood that reflect liver function or potential damage. Given the rising prevalence of liver diseases such as hepatitis, fatty liver disease, and liver cirrhosis in Nigeria, access to LFTs has become increasingly important.

Common Liver Function Tests

LFTs include several different tests that collectively provide insights into liver health:

Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST): These enzymes are released into the bloodstream when liver cells are damaged. Elevated levels indicate liver cell injury, which can be caused by hepatitis, fatty liver, or excessive alcohol use.

Alkaline Phosphatase (ALP): This enzyme is present in the liver, bile ducts, and bones. High ALP levels may signal blockages in the bile ducts or liver diseases like hepatitis.

Bilirubin: This pigment is produced from the breakdown of red blood cells and is processed by the liver. High bilirubin levels because jaundice and may indicate liver dysfunction or bile duct obstruction.

Albumin and Total Protein: The liver produces albumin and other proteins essential for various bodily functions. Low levels can indicate chronic liver disease or malnutrition.

Gamma-glutamyltransferase (GGT): GGT levels increase in liver and bile duct disorders. It’s often used alongside other tests to diagnose bile duct problems or excessive alcohol use.

Importance of LFTs in Nigeria

In Nigeria, liver diseases are a major public health concern, with hepatitis B and C being particularly prevalent. According to the World Health Organization (WHO), Nigeria has one of the highest rates of hepatitis B infection in the world, which significantly contributes to the burden of liver diseases. LFTs play a crucial role in the early detection of liver diseases, enabling timely treatment and potentially preventing progression to more severe conditions like cirrhosis or liver cancer.

Nigeria also has a growing issue with non-alcoholic fatty liver disease (NAFLD), partly due to changes in diet, lifestyle, and an increase in obesity rates. LFTs can help diagnose NAFLD in its early stages, encouraging lifestyle changes or medical interventions to prevent further complications.

Accessibility and Challenges

Despite the importance of LFTs, access to these tests remains a challenge in many parts of Nigeria, especially in rural areas. While urban centers and private healthcare facilities generally have the necessary equipment and trained personnel, rural clinics often lack these resources. Additionally, the cost of LFTs can be prohibitive for many Nigerians, as they are often not covered by insurance.

The Role of Health Education

Raising awareness about the importance of LFTs is crucial in Nigeria. Many people are unaware of liver disease risks or may not seek testing until symptoms are severe. Public health campaigns and community education can emphasize the importance of regular liver function monitoring, especially for high-risk groups.

In conclusion, liver function tests are vital in Diagnostics services in Nigeria for diagnosing and managing liver diseases. Increased accessibility, along with public awareness, could significantly improve early diagnosis and reduce the burden of liver disease in Nigeria.

Source & Reference: https://sites.google.com/view/ellabdiagnosticcenter/liver-function-tests-in-nigeria-key-to-early-detection-and-better-liverhe