#interferon-alpha

[medicomunicare]

All hands on DECs: lift your skin up 'cause immunity won't TLR8 further X-age-rated IFNrence

Scleroderma or systemic sclerosis (SYS) affects approximately 300,000 people in the U.S., with about one-third developing systemic disease, which can affect major organs such as the lungs, kidneys or heart. Women are four times more likely than men to be diagnosed with the disease, but until now, the underlying reason for this gender disparity had remained elusive. Two new studies led by…

[anmapvnn]

GLUKAFERON

Interferon

[darkmaga-returns]

By Nicolas Hulscher, MPH

The study titled, Altered Circulating Cytokine Profile Among mRNA‐Vaccinated Young Adults: A Year‐Long Follow‐Up Study, was just published in the journal Immunity, Inflammation and Disease:

Objectives This longitudinal study aimed to assess the impact of COVID-19 vaccination on cytokine profile. Methods A total of 84 Saudi subjects (57.1% females) with mean age of 27.2 ± 12.3 participated in this longitudinal study. Anthropometric data and fasting blood samples were obtained at baseline and after final vaccination, with an average follow-up duration of 14.1 ± 3.6 months for adolescents and 13.3 ± 3.0 months for adults, calculated from the first dose of vaccination. Assessment of cytokine profiles was done using commercially available assays. Results After follow-up, a significant increase in weight and body mass index was observed overall (p = 0.003 and p = 0.002, respectively). Postvaccination, significant increases were observed in several cytokines, including basic fibroblast growth factor 2 (p < 0.001), interferon gamma (IFNγ) (p��= 0.005), interleukin-1 beta (IL1β) (p < 0.001), IL4 (p < 0.001), IL6 (p = 0.003), IL7 (p = 0.001), IL17E (p < 0.001), monocyte chemoattractant protein-1 (MCP1) (p = 0.03), MCP3 (p = 0.001), tumor necrosis factor alpha (TNFα) (p < 0.001), and VEGFA (p < 0.001). A significant reduction was observed only in macrophage colony-stimulating factor (p < 0.001). When adjusted for age, epidermal growth factor (EGF), IL4, IL6, MCP3, TNFα, and vascular endothelial growth factor (VEGFA) remained statistically significant. Gender-based analysis revealed that men experienced greater increases in IL6 (p = 0.008), IL4 (p = 0.04), and TNFα (p = 0.015) compared to women. Age-based analysis showed that older participants had more pronounced increases in EGF (p = 0.011), IL6 (p = 0.029), MCP1 (p = 0.042), and TNFα (p = 0.017), while younger participants had a greater increase in VEGFA (p = 0.025). Conclusions The findings of this study indicated that COVID-19 vaccination resulted in an increase in cytokine levels, which signifies the persistence of the humoral immune response to messenger RNA (mRNA) vaccines. This effect may be attributed to the persistent production of spike protein and highly inflammatory nature of mRNA–lipid nanoparticle. Additionally, the results suggested differences in cytokine levels based on gender and age. Notably, the cytokine profile remains favorably altered in young adults who received mRNA vaccinations, even after 1 year.

[covid-safer-hotties]

Reference saved in our archive (Daily updates!)

Covid has not and *does* not magically evolve to be more mild: It evolves to survive and reproduce. Mask up. Stay safe.

Abstract SARS-CoV-2 variants of concern (VOC) have been associated with increased viral transmission and disease severity. We investigated the mechanisms of pathogenesis caused by variants using a host blood transcriptome profiling approach. We analysed transcriptional signatures of COVID-19 patients comparing those infected with wildtype (wt), alpha, delta or omicron strains seeking insights into infection in Asymptomatic cases.

Comparison of transcriptional profiles of Symptomatic and Asymptomatic COVID-19 cases showed increased differentially regulated gene (DEGs) of inflammatory, apoptosis and blood coagulation pathways, with decreased T cell and Interferon stimulated genes (ISG) activation. Between SARS-CoV-2 strains, an increasing number of DEGs occurred in comparisons between wt and alpha (196), delta (1425) or, omicron (2313) infections. COVID-19 cases with alpha or, delta variants demonstrated suppression transcripts of innate immune pathways. EGR1 and CXCL8 were highly upregulated in those infected with VOC; heme biosynthetic pathway genes (ALAS2, HBB, HBG1, HBD9) and ISGs were downregulated. Delta and omicron infections upregulated ribosomal pathways, reflecting increased viral RNA translation. Asymptomatic COVID-19 cases infected with delta infections showed increased cytokines and ISGs expression. Overall, increased inflammation, with reduced host heme synthesis was associated with infections caused by VOC infections, with raised type I interferon in cases with less severe disease.

[maaarine]

The Cause of Depression Is Probably Not What You Think (Joanna Thompson, Quanta Magazine, Jan 26 2023)

"A literature review that appeared in Molecular Psychiatry in July was the latest and perhaps loudest death knell for the serotonin hypothesis, at least in its simplest form.

An international team of scientists led by Joanna Moncrieff of University College London screened 361 papers from six areas of research and carefully evaluated 17 of them.

They found no convincing evidence that lower levels of serotonin caused or were even associated with depression.

People with depression didn’t reliably seem to have less serotonin activity than people without the disorder.

Experiments in which researchers artificially lowered the serotonin levels of volunteers didn’t consistently cause depression. (…)

Although serotonin levels don’t seem to be the primary driver of depression, SSRIs show a modest improvement over placebos in clinical trials.

But the mechanism behind that improvement remains elusive.

“Just because aspirin relieves a headache, [it] doesn’t mean that aspirin deficits in the body are causing headaches,” said John Krystal, a neuropharmacologist and chair of the psychiatry department at Yale University.

“Fully understanding how SSRIs produce clinical change is still a work in progress.”

Speculation about the source of that benefit has spawned alternative theories about the origins of depression. (…)

Repple warns, however, that another explanation for the effects his team observed is also possible: Perhaps the depressed patients’ brain connections were impaired by inflammation.

Chronic inflammation impedes the body’s ability to heal, and in neural tissue it can gradually degrade synaptic connections.

The loss of such connections is thought to contribute to mood disorders.

Good evidence supports this theory.

When psychiatrists have evaluated populations of patients who have chronic inflammatory diseases like lupus and rheumatoid arthritis, they’ve found that “all of them have higher-than-average rates of depression,” said Charles Nemeroff, a neuropsychiatrist at the University of Texas, Austin.

Of course, knowing that they have an incurable, degenerative condition may contribute to a patient’s depressed feelings, but the researchers suspect that the inflammation itself is also a factor.

Medical researchers have found that inducing inflammation in certain patients can trigger depression.

Interferon alpha, which is sometimes used to treat chronic hepatitis C and other conditions, causes a major inflammatory response throughout the body by flooding the immune system with proteins known as cytokines — molecules that facilitate reactions ranging from mild swelling to septic shock.

The sudden influx of inflammatory cytokines leads to appetite loss, fatigue and a slowdown in mental and physical activity — all symptoms of major depression.

Patients taking interferon often report feeling suddenly, sometimes severely, depressed.

If overlooked chronic inflammation is causing many people’s depression, researchers still need to determine the source of that inflammation.

Autoimmune disorders, bacterial infections, high stress and certain viruses, including the virus that causes Covid-19, can all induce persistent inflammatory responses.

Viral inflammation can extend directly to tissues in the brain. Devising an effective anti-inflammatory treatment for depression may depend on knowing which of these causes is at work.

It’s also unclear whether simply treating inflammation could be enough to alleviate depression.

Clinicians are still trying to parse whether depression causes inflammation or inflammation leads to depression. “It’s a sort of chicken-and-egg phenomenon,” Nemeroff said.

Increasingly, some scientists are pushing to reframe “depression” as an umbrella term for a suite of related conditions, much as oncologists now think of “cancer” as referring to a legion of distinct but similar malignancies.

"And just as each cancer needs to be prevented or treated in ways relevant to its origin, treatments for depression may need to be tailored to the individual."

[mleprae]

Cytokines are so cute, you know those weird numbers you see in medical text? The one you'll likely see around is Interleukin, shortned to IL. The name literally means 'Cell communication', they're chemicals that cells release to speak to one another, depending what interleukin you find in a test, you can deduce what these little guys are planning and doing at the moment

The most common ones are TNF-a (tumor necrosis alpha) and IL-6, both stimulate inflammation in damaged area. Inflammation is just the cells setting up the battlefield, the redness is due to bloodflow in the area bringing more immune cells in, the pain is that sometimes the area increases, pressing onto nerves. It's your body telling you that you need to stop using that part.

IL-6 and TNF-a are the cytokines that the cells use to call one another, kind of a "I need backup here" signal. Some of these cytokines are pyrogenic, which is what we call the ones that go to the brain and tell it to raise body temperature!

You also have interferons (shortned to IFN), those are what cells produce to warn others in a "I'm infected with something, stay away" kind of way, this tells the other cells that they need to protect themselves, it also calls some cells responsible to kill infected cells to do their jobs

[didanawisgi]

How the innate immune system manages to cope with antibody resistant SARS2 varieties

December 17, 2024 Radagast 

"So, as I have been documenting over the past few years now, we’ve seen a situation in which the new coronavirus, SARS-COV-2, become forced to evolve first into increasingly infectious variants (Alpha, Delta) with higher ACE2 affinity and then into highly antibody evasive variants (the Omicron variants). This then results in a population that has a relatively wide range of antibodies, to a wide range of Spike epitopes.

That results in a situation, where SARS-COV-2 becomes increasingly forced to increase its inherent antibody resistance. That involves the accumulation of sugar molecules (glycans) on the N-Terminal Domain, that prohibit the antibodies from binding that are now necessary for neutralization. This interplay between the vaccine, the immune system and the virus, is a process that takes many years to unfold. 

What critical thinkers would ask themselves, is why we don’t just see every virus that regularly reinfects humans develop a bunch of glycans on its surface, if that allows viruses to render an antibody response useless. Logic would suggest there has to be some sort of cost involved for a virus, in covering a viral protein in these glycans that prohibit antibodies from binding to the protein.

This is a correct assessment. The innate immune system evolved various mechanisms to recognize basic patterns that pathogens and misbehaving cells in our bodies tend to display. As one example, our cells are forced to display small bits of proteins they’re producing in their MHC molecule on their surface. This allows your T cells to inspect whether they’re producing the right proteins, or whether their protein factory was hijacked by a virus.

Many viruses thus evolved mechanisms to interfere in this phenomenon, by stopping cells from displaying the MHC molecule on their surface altogether, so that the T cells can’t inspect what’s going on. The human immune system of course has to have ways to deal with that behavior of viruses. So what you see is that our Natural Killer cells, a population part of the innate immune system, treat it as suspicious when a cell fails to produce the MHC molecule, and weigh it as a factor part of their complex calculation on whether a cell should be killed or not.

The innate immune system has various other such clever mechanisms. There are specific molecules it produces, that allow it to recognize proteins that are unusually densely covered in these antibody-blocking glycans. These molecules are called Lectins. Lectins are what we call carbohydrate binding proteins that seek out sugar groups part of bigger molecules.

When it comes to the immune system, C-type Lectins appear to be the most relevant in our defense. These are proteins expressed by most cells part of the innate immune system. There are many different types of C-type Lectins and they tend to look specifically for proteins that have a high density of glycans. 

That is, the recognition is density dependent. A normal protein part of our body may have some glycans, but a very high density of glycans on a protein reveals to the innate immune system that something weird may be going on that requires intervention.

As I have explained a few times before, natural immunity results in the expansion of the population of plasmacytoid dendritic cells, which recognize viral RNA and/or DNA. This is only possible when the first exposure occurs in the absence of an adaptive immune response induced by previous vaccination, as otherwise the B cells will just deal with an infection, before the plasmacytoid dendritic cells ever get to see the virus and proliferate in response.

When the plasmacytoid dendritic cells detect viral RNA/DNA, through their toll like receptors, they start to produce large amounts of Interferon alpha, which is a molecule that evolved to interfere in just about every step of the viral reproductive cycle. However, how much Interferon alpha they produce, is also dependent on secondary factors.

One of these factors, is whether their own specialized C-type lectin receptors like CLEC4C, recognized some protein that’s densely covered in glycans. If that is the case, they boost their interferon alpha production. For the plasmacytoid dendritic cells it becomes easier to realize it’s time to do their job, when the glycan density on the Spike protein starts to increase.

Another place where you see the innate immune system respond differently in breakthrough infections versus natural immunity, is in the brain. What you see here is that a population of monocytes gets to enter the brain upon infection, that does not get to enter the brain if someone was vaccinated before being infected. You also see an increase in Natural Killer cells and Dendritic cells in the brain.

The natural killer cells recognize whether a cell is infected by the virus and then decide whether the infected cells should be killed or not. But the monocytes and the dendritic cells also have an important job: Their job is to “eat” viral particles.

The dendritic cells try to capture viral particles, so that they can then degrade the viral particles with their lysosomes. But how do the denritic cells capture viral particles? They use their C-type lectin receptors for that!

In other words, what you would expect to see, is that as the dendritic cells now become faced with variants of SARS-COV-2 with more glycans on the Spike protein, they start to be able to do their job more effectively.

In essence, what’s currently happening is that SARS-COV-2 is being forced by the mass vaccination experiment, to evolve in a direction that makes it easier for the innate immune system to recognize the virus.

This is good for young people, as their innate immune system tends to be strong and capable. After all, it has to be able to protect them against all sorts of pathogens, as they normally don’t have any adaptive immunity yet against most of the pathogens that circulate (except for the passive adaptive immunity from breastfeeding).

You would expect this to cause problems however, for people whose adaptive immune system is mainly responsible for suppressing this virus. After vaccination, antibody concentration are about fifty times higher than normally seen after infection. 

Constant breakthrough infections have not stimulated innate immunity. Rather, they just recall and broaden the adaptive immune response developed as a consequence of vaccination with non-live vaccines. 

Once antibodies against the Receptor Binding Domain became unable to solve the problem, the immune system developed a type of antibody that targets part of the Receptor Binding Domain and part of the N-Terminal Domain (the N1 loop), to which the virus then responded with BA.2.86, which has a unique insertion mutation exactly in the part where these antibodies bind. 

This BA.2.86 lineage wiped out all other lineages, revealing that most of the world’s population depends very strongly on the antibody response to keep the virus under control. The body then developed antibodies to this new version of the N1 loop, to which the virus then began to respond by putting the glycans on the N1 loop.

This is why you’re dealing with a situation where everyone keeps catching SARS-COV-2 and getting sick as a result. 

All these elegant receptors our innate immune cells have to recognize glycoproteins like the Spike protein, like the C type lectin receptors, tend to depend on the Spike protein not being covered by antibodies. If there are antibodies on the Spike protein, those receptors bump into the antibodies, rather than managing to bind the Spike protein.

This is important to understand: If the antibodies are already on the job, they have to solve the job. And so when the virus has mutated to make the antibodies that bind to it of poor quality and to mainly keep around enhancing antibodies, that bind in places where they won’t stop the Spike protein from correctly binding to the ACE2 receptor, the immune system is forced to start targeting more and more regions of the Spike protein (immune refocusing).

Worst of all perhaps, some of these antibodies directed against SARS-COV-2, seem to cross-react with other respiratory viruses, like Influenza, where they bind to the glycans, but don’t neutralize the protein. So, these antibodies against SARS-COV-2, seem to be making it more difficult for the immune system to deal with other respiratory viruses too, because it’s just much harder for the C-type lectin receptors of the innate immune cells to bind to a protein when it already has these antibodies on it, particularly on its glycans.

You see an epidemic of various respiratory viruses around the world right now, sickening people at abnormally high levels. You need to be asking yourself, what the cause of that is. Some of it may be damage to the immune system, some of it may be due to antibodies against SARS-COV-2 interfering in the innate immune system’s ability to deal with those viruses. I already warned about this long ago.

The point I wish to make clear however with this post, is that it’s inappropriate to expect that the evolution of SARS-COV-2 towards a glycan-covered antibody resistant virus would increase its inherent virulence for everyone.

Instead, what you would expect to see, is that as these glycans accumulate on the Spike protein, the virus will increasingly begin to sicken people who depend on an adaptive immune response against it, whereas when the innate immune system handles the response to this virus, the impact on people’s health will start to decline.

Who cares about any of these details? Well, I’m explaining this for a reason. Immunologists are currently in the process of developing new types of SARS-COV-2 vaccines, that manage to evade recalling the original antigenic sin antibodies and encourage the development of new antibodies instead.

BUT THIS IS THE WRONG APPROACH!

You are very clearly dealing with a virus, that is increasing its glycan density!

And when a virus is rapidly increasing its glycan density, the immune system becomes increasingly dependent on the innate immune response to deal with it, as it just becomes easier to recognize it through the C-type lectins, while the most important parts of the virus for antibody mediated neutralization become inaccessible due to the glycans!

You have to figure out how to suppress the adaptive immune response, allowing the innate immune system to take over and do its job. I have seen just one approach that looks viable to me: Cannabinoids like CBD can suppress adaptive immunity, while encouraging NK cell activity. 

It’s not coincidence, that you see better immunological functioning in HIV infected people with strong cannabis use. You see a DECREASED VIRAL RESERVOIR, in cannabis using HIV infected people. Because HIV rapidly mutates and establishes persistent infections, an antibody response is the wrong tool for the job. HIV already covers itself in a dense glycan shield.

Heavy cannabis use has the effect in HIV infected people of shifting their immune response to HIV more towards dependence on the innate immune system. For a respiratory virus like SARS-COV-2, which is still mostly targeting the lungs of vaccinated people, vaporized cannabis would seem like a proper candidate to me, to reduce the immunological abnormalities that were induced by vaccination. The terpenes are also known to have beneficial stimulating effects on the innate immune system.

Look, I understand this is just a weird blog, but look around you. People are coughing everywhere. They’re collapsing on stage. The hospitals are overwhelmed, there’s an epidemic of “walking pneumonia”, at record levels that have never been seen before since we started measuring in the 90’s. People don’t have to believe me, you can just connect the dots yourself.

This is not just some inherent trait of SARS-COV-2, it is mostly a consequence of provoking an inappropriate immune response towards SARS-COV-2. It really doesn’t have to be like this."

[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.

References:

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#phycocyanin #cphycocyanin #phycocyaninspirulina

[drvikeshshahsblog]

What is Cancer Immunotherapy Treatment in India? A Comprehensive Guide

Cancer has been one of the biggest health challenges for decades. Traditional treatments like chemotherapy, radiation, and surgery have helped many people. But now, there’s a new way to fight cancer: cancer immunotherapy. This treatment is becoming more popular in India, offering new hope to patients. This guide explains what cancer immunotherapy is, how it works, the different types, and how experts like Dr. Vikesh Shah are leading its use in India.

What is Cancer Immunotherapy?

Cancer immunotherapy helps your body’s own immune system find and destroy cancer cells. Normally, your immune system can detect and kill abnormal cells. But sometimes, cancer cells hide or block the immune response. Immunotherapy boosts or changes how your immune system works so it can find and attack cancer cells more effectively.

One big advantage is that it targets only cancer cells, so healthy cells around them are mostly unharmed. This is especially helpful for patients who don’t respond well to traditional treatments or whose cancer has come back.

How Does It Work?

Your immune system is built to fight off infections, viruses, and abnormal cells. But cancer cells often escape this defense. Immunotherapy gives the immune system extra tools like special proteins or immune cells to better find and fight cancer.

Some cancer cells produce “brake” proteins (called checkpoints) that stop the immune system from attacking them. New drugs remove these brakes, letting the immune system do its job. This is one of the most exciting areas of cancer research today.

Types of Cancer Immunotherapy

Here are the most common types:

1. Checkpoint Inhibitors

These drugs block the “brake” proteins on cancer or immune cells. This helps the immune system recognize and attack cancer.

Some examples:

Pembrolizumab (Keytruda)

Nivolumab (Opdivo)

Ipilimumab (Yervoy)

They are used for cancers like melanoma, lung cancer, head and neck cancer, and more.

2. Monoclonal Antibodies

These are lab-made proteins that act like the immune system. They stick to cancer cells and either:

Mark them for destruction

Or block signals that help them grow

Example: Trastuzumab (Herceptin), used for breast cancer.

Some monoclonal antibodies even carry chemo or radiation directly to the cancer cells.

3. CAR T-Cell Therapy

In this treatment, doctors take out a patient’s T-cells (a type of white blood cell), change them in a lab to recognize cancer cells, and put them back into the body. These modified cells then hunt down and kill cancer.

It has shown great success in blood cancers like leukemia and lymphoma, and research is ongoing for its use in solid tumors.

4. Cytokine Therapy

Cytokines are proteins that help control the immune system. Man-made versions, like IL-2 and interferon-alpha, are used to boost the immune system.

This therapy works best for certain cancers like melanoma and kidney cancer.

5. Cancer Vaccines

Unlike vaccines that prevent diseases, these are made to treat cancer. They help the immune system recognize and destroy cancer cells.

Example: BCG vaccine is used for bladder cancer, and research is being done on its use in melanoma, lung, and prostate cancer.

Dr. Vikesh Shah’s Role in Cancer Immunotherapy

Dr. Vikesh Shah is a leading oncologist in India with deep knowledge of immunotherapy. He creates personalized treatment plans based on each patient’s needs and type of cancer. His work with advanced immunotherapies has helped many patients who had limited options before.

Through his clinical work and research, he is giving new hope to people fighting cancer.

What’s Next for Immunotherapy in India?

The future of immunotherapy in India is promising. As research grows, it may become the first line of treatment for many types of cancer not just a backup.

India’s partnerships with global research centers and pharma companies are helping speed up the development of these treatments. With doctors like Dr. Vikesh Shah at the forefront, India is becoming a key player in the global fight against cancer.

Conclusion

Cancer immunotherapy is changing the way we fight cancer in India. From checkpoint inhibitors to CAR T-cell therapy, it gives new hope to many patients. Thanks to experts like Dr. Vikesh Shah, India is leading the way in using the body’s immune system to fight cancer.

With ongoing research and better access to advanced care, the future looks bright. Cancer may no longer be seen as a death sentence but a disease that can be managed, and in many cases, overcome.

[twinkl22004]

“Immune Interferon Receptor”, Victor McKusick, Mendelian Inheritance in Man, 1966. (IFNGR1) 免疫干扰素受体。idc10=R76.12

  Here I present: “Immune Interferon Receptor”, Victor McKusick, Mendelian Inheritance in Man’, 1966. (IFNGR1) 免疫干扰素受体。idc10=R76.12 INTRODUCTION. Interferons may be regarded as polypeptide hormones because of their role in communicating from cell to cell a specific set of instructions that lead to a wide variety of effects. Viruses induce type I interferon, subdivided into alpha-interferon…

[medicomunicare]

Le tante facce dell'interferone: il responsabile del lupus, non importa se diretto o provocato dai virus

Il lupus eritematoso sistemico (LES) è il prototipo della malattia autoimmune guidata da interazioni patologiche tra cellule T e cellule B. L’espansione delle cellule T helper follicolari (TFH) e delle cellule T helper periferiche (TPH), due popolazioni di cellule T che forniscono aiuto alle cellule B, è una caratteristica importante del LES. Le cellule TFH e TPH umane producono tipicamente alti…

[moleculardepot]

Interferon-α A Protein, Recombinant (Human)

Interferon-α A Protein, Recombinant (Human) Catalog number: B2022463 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: ≥5000000 units Molecular Weight or Concentration: N/A Supplied as: Solution Applications: a molecular tool for various biochemical applications Storage: −70°C Keywords: Interferon alpha-2 Grade: Biotechnology grade. All products are highly pure. All solutions…

[bcisurat]

High Platelet Count (Thrombocytosis): Symptoms, Causes, and Treatment

Platelets are essential blood components responsible for clotting and wound healing. However, an abnormally high platelet count, known as thrombocytosis, can lead to severe health complications, including excessive clotting or, in some cases, bleeding disorders. While many people may have a slightly elevated platelet count without noticeable symptoms, it is important to understand the underlying causes, symptoms, and available treatments from our blood cancer specialists in Surat at BCI- Blood and Cancer Institute.

Understanding Thrombocytosis

A normal platelet count ranges between 150,000 to 450,000 platelets per microliter of blood. When the count exceeds this range, a person is diagnosed with thrombocytosis. This condition is broadly categorized into two types:

● Primary (Essential) Thrombocythemia — A disorder in which the bone marrow produces too many platelets without an identifiable cause.

● Secondary (Reactive) Thrombocytosis — A condition resulting from underlying factors such as infections, inflammation, or other medical conditions.

Symptoms of High Platelet Count

Many individuals with thrombocytosis do not experience symptoms, and the condition is often discovered incidentally during routine blood tests. However, in cases where symptoms do appear, they may include:

● Frequent headaches or dizziness

● Numbness or tingling in hands and feet

● Unexplained bruising or excessive bleeding

● Vision disturbances

● Chest pain or shortness of breath

● Blood clots in veins or arteries (deep vein thrombosis, pulmonary embolism, or stroke)

Severe complications, such as stroke or heart attack, may occur if blood clots form and block vital arteries, warn expert blood cancer specialists in Surat.

Causes of Thrombocytosis

The cause of thrombocytosis determines whether it is primary or secondary:

Primary Thrombocythemia Causes

● Genetic mutations (such as JAK2, CALR, or MPL gene mutations) that affect bone marrow cell production.

● Bone marrow disorders, including myeloproliferative neoplasms.

Secondary Thrombocytosis Causes

● Infections — Bacterial, viral, or fungal infections can trigger an increase in platelets.

● Chronic inflammatory conditions — Diseases like rheumatoid arthritis or inflammatory bowel disease can stimulate excessive platelet production.

● Iron deficiency anemia — A lack of iron in the body can lead to a compensatory increase in platelet count.

● Surgery or trauma — Recent operations, significant injuries, or post-surgical recovery may temporarily elevate platelet levels.

● Cancer — Certain types of cancer, including lung, gastrointestinal, and ovarian cancer, can lead to thrombocytosis, says our cancer specialist in Surat at BCI-Blood and Cancer Institute.

● Splenectomy (surgical removal of the spleen) — The spleen helps regulate platelets; its removal can result in higher platelet levels.

Diagnosis of Thrombocytosis

A hemato-oncologist in Surat may diagnose thrombocytosis through the following tests:

Complete Blood Count (CBC) — Measures platelet levels.

Blood Smear — Examines the shape and size of platelets under a microscope.

Bone Marrow Biopsy — Determines abnormalities in platelet production.

Genetic Testing — Checks for gene mutations linked to essential thrombocythemia.

Additional Tests — To identify underlying conditions causing secondary thrombocytosis.

Treatment Options for High Platelet Count

Treatment depends on whether thrombocytosis is primary or secondary, as well as the patient’s overall risk of developing complications such as blood clots.

Treatment for Primary (Essential) Thrombocythemia

● Aspirin Therapy — Low-dose aspirin is often prescribed to reduce the risk of blood clots.

● Platelet-Lowering Medications — For high-risk individuals, drugs like hydroxyurea, anagrelide, or interferon-alpha may be recommended to suppress platelet production.

● Plateletpheresis — In rare cases, a procedure to remove excess platelets directly from the blood is performed in emergencies.

Treatment for Secondary (Reactive) Thrombocytosis

● Addressing the underlying cause — Managing infections, inflammation, or other medical conditions typically resolves secondary thrombocytosis.

● Iron Supplements — If caused by iron deficiency anemia, increasing iron intake can help regulate platelet levels.

● Surgery Follow-Up — If thrombocytosis occurs after spleen removal, doctors monitor the patient and recommend lifestyle adjustments as part of treatment.

Managing Thrombocytosis: Lifestyle and Prevention

While some cases of thrombocytosis cannot be prevented, healthy lifestyle choices can help minimize complications:

● Stay Hydrated — Drinking enough water improves blood circulation and prevents clotting.

● Maintain a Balanced Diet — Eating foods rich in omega-3 fatty acids (fish, flaxseeds), leafy greens, and whole grains can support heart and blood vessel health.

● Exercise Regularly — Physical activity reduces the risk of blood clots and promotes overall well-being.

● Avoid Smoking and Limit Alcohol — These habits can negatively affect blood vessel function and increase clotting risks.

● Routine Health Checkups — Regular screenings can detect abnormalities early and prevent severe complications.

Final Thoughts

Thrombocytosis may seem like a silent condition, but its potential complications can be severe. Recognizing the symptoms, understanding the causes, and seeking timely medical intervention from an experienced hematologist in Surat are key to managing a high platelet count effectively. If you or someone you know experiences symptoms associated with thrombocytosis, consulting a healthcare provider can help ensure proper diagnosis and treatment, ultimately reducing health risks and improving quality of life.

[nursingwriter]

Hypothyroidism is a fairly common disorder that patients are diagnosed with and it can have wide ranging effects. While hyperthyroidism is when the thyroid is excreting too much into the bloodstream, hypothyroidism is the opposite. If untreated, the effects on the body are numerous and substantial with the most prominent affected area being the body's metabolism rate and quality. Even with these risks, there is absolutely treatment available for the disorder once it is identified with certainty. This report will cover, after a more detailed description of hypothyroidism, the pharmacological and non-pharmacological methods that are used to address the disorder. As indicated in the introduction, the main effect that hypothyroidism has on the human body is a slower and more sluggish metabolism. However, to say it is just that is less than accurate. As described by WebMD, the thyroid is in charge on controlling how one's body uses energy from food. This is precisely what metabolism is. The metabolism and how well it performs is no small thing as it affects body temperature, heartbeat, how well calories are burned and so forth. If a person's thyroid is not active as it should be, all of these processes slow down and become more inefficient than they could or should be. This means less energy for the body and a lower burn rate of calories. This means less energy is consumed when the body is at rest and this makes it easier to gain and keep on body weight. The implications for obesity and the associated disorders that come with it such as diabetes, heart disease and so forth are quite obvious to see (WebMD, 2016). The most common cause of hypothyroidism is what is known as Hashimoto's thyroiditis. This is a fancy way of saying that the thyroid is inflamed. This problem actually falls under the category of autoimmune disorders. When this disorder happens, the thyroid is inflamed because it is being attacked by antibodies. There may or may not be a viral infection in play as this is going on. There are other causes that can rear their head, though. Just a few examples can include a side effect of radiation therapy (e.g. for cancer treatment), radioactive iodine treatment, use of certain medications, surgery on the thyroid and too little iodine in one's diet. The medications that can cause an issue include Cordarone (amiodarone), lithium, interferon alpha an interleukin-2. Other potential causes or aggravating factors of hypothyroidism include pregnancy (the reason is unknown), thyroid problems at birth, pituitary dysfunction or problems with the hypothalamus, an area of the brain. Hypothyroidism manifests in one of two ways, those being primary hypothyroidism and secondary hypothyroidism. Primary is when the gland itself has a problem. Secondary is when another problem exterior of the thyroid is causing problems with the secretion levels of the thyroid. The pituitary dysfunction catalyst mentioned earlier would be an example of a secondary cause of hypothyroidism (WebMD, 2016). People that are at risk of hypothyroidism include white and Asian people, older people, people that have graying hair at an early age, people with any sort of autoimmune disorder such as diabetes or celiac disease, people with bipolar disorder (since the aforementioned lithium is a commonly prescribed medication for that disorder), people with Down syndrome and people with Turner syndrome. Symptoms of hypothyroidism include changes in menstrual cycle (women, of course), constipation, dry hair, hair loss, dry skin, fatigue, sensitivity to col, slower heart rate, swelling of the thyroid, unexplained weight gain or a general inability to lose weight even with great effort and carpal tunnel syndrome. Other symptoms include cold hands or feet, extreme sleepiness, hoarse cries, little or no growth, very low muscle tone (especially in infants), persistent jaundice (yellowing in the skin or eyes), poor feeding habits, puffy face, bloating of the stomach and swollen tongue. The presence of hypothyroidism is done via blood tests. The two commonly used ones are the thyroid-stimulating hormone (TSH) and T4 (thyroxine). When it comes to the latter, a lot T4 level means that hypothyroidism is present. TSH test can be useful because moderate levels of TSH means that the hypothyroidism case is milder rather than more severe (WebMD, 2016). The primary treatment for hypothyroidism is pretty basic and that would be the taking of synthetic (man-made) T4 hormone so as to boost the presence of thyroid in the system. It is not unlike a type I or II diabetic that takes insulin because the body is not producing enough of it. Leaving hypothyroidism untreated is less than wise as it can lead to heart problems, infertility, joint pain and obesity, just to name a few. Women who have hypothyroidism and are pregnant need to know that the disorder can and will affect their unborn child. As one might expect, a baby needs thyroid as well and that would come from no place other than the mother herself. If this is not address in utero, there can be mental development issues with the child when it is born. Further, extremely low levels of thyroid can lead to a condition that is known as myxedema. This is far and away the most severe form of hypothyroidism. Someone that gets bad enough can lose consciousness (faint) or even slip into a coma. There can also be a body temperature drop that can be fatal if it is not addressed (WebMD, 2016). All of the above information came from the WebMD website. However, there are other sources and websites out there that have great information on how to prevent and treat hypothyroidism when it is identified and diagnosed. One important aspect that is not fleshed out above is that there are a number of different drugs and dosages that are used when it comes to the use of synthetic T4. Just a few drugs that can be used are Synthroid, levothyroxine, Armour Thyroid, Levoxyl, Cytomel, Tirosint and Thyrolar. The vast majority of thyroid treatment drugs are oral. However, the Mayo Clinic has a write-up on treating hypothyroidism and they are very cautioning when it comes to starting or adjusting a thyroid medication. They note that taking too much T4 can cause its own problem including increased appetite, insomnia, heart palpitations and shakiness. Mayo is highly regarding of levothyroxine. The cost of levothyroxine varies based on dosage. However, it is relatively cheap. Thirty tablets of fifty milligrams costs about fourteen dollars even without insurance and two hundred milligrams is about twenty-two dollars without insurance. However, they do note that starting at a low dose and gradually raising it is perhaps the best way to go sometimes. One potential complicating factor is if a person is taking iron supplements, Cholestyramine, aluminum hydroxide (found in antacids) and calcium supplements. There are alternative medicines out there such as synthetic thyroxine that is derived from pigs. However, those products are not regulated by the Food and Drug Administration and should be used with caution (Mayo, 2016). Not all of the touted treatments for hypothyroidism involve prescription drugs. Indeed, there are other ways to help mitigate or even eliminate hypothyroidism even if the prescription drug route is the obvious and perhaps easier path. Things that can be done include the cutting of caffeine, the cutting of sugar (including any refined carbohydrates), taking in more protein, taking more nutrients such as vitamin D, iron, omega-3 fatty acids, selenium, zinc, copper, vitamin A, vitamin B (all of them) and iodine. Other suggestions include removing gluten (wheat) from one's diet and being mindful of goitrogens. These are foods that potentially or definitely interfere with the thyroid. They include broccoli, Brussels sprouts, cabbage, cauliflower, kale, kohlrabi, rutabaga, turnips, millet, spinach, strawberries, peaches, watercress, peanuts, radishes and soybeans. This does not mean those foods can never be eaten. In fact, cooking those items will eliminate the problem most of the time. Regardless, eating them in moderation is a minimum. Beyond the above, a hypothyroid patient can also address underlying food sensitivities (if any), the use of probiotics (to boost good bacteria in the gut), the addressing of silent inflammation, the addressing of adrenal fatigue, the reduction of stressors and/or addition of relaxation techniques and the use of a "thyroid collar" to wear when getting x-rays so that the gland is not aggravated by the rays of the machine (MBG, 2011). Another website that has a litany of non-drug tips is HealthWyze. They suggest a number of things that include the discarding and non-use of non-stick cookware, the eliminate of soy, an adherence to an alkaline diet, the balancing of estrogen levels in women, exercise, hemp fiber (as a laxative and supplement), the use of L-Tyrosine (an amino acid), the use of L-Arginine, the use of iodine, the avoidance of fluoride, eating a natural diet, eating more chlorophyll, a focus on eating pears or apples, taking zinc/selenium supplements, the use of coconut oil and the avoidance of canola oil. To come back to one point made, many SSRI anti-depressant drugs have fluoride in the contents of the pill and fluoride and the thyroid do not get along well. Indeed, the thyroid and its behavior react very negatively to what it deems to be bad substances and fluoride is apparently one of those substances (Corriher, 2013). When it comes to the epidemiology of hypothyroidism, there are a few important things to take note of. Primary data sources are from the population samples in the United States and Europe. Thyroid disorders in general, including hypothyroidism, are prevalent in all areas and their manifestations are determined by the availability and consumption of dietary iodine. There are some areas of controversy surrounding the study of hypothyroidism including what hypothyroidism actually is, the selection criteria used, the influence of age and/or sex, environmental factors involved and the different techniques used to measure thyroid function. However, areas of agreement include that iodine deficiency is the main source of the problem and this leads to goiter formation. In areas of the world where iodine is not widely available, many to most people with hypothyroidism or other thyroid disease have autoimmune issues. Developing research is centering on cancer relating to the thyroid, the use of supplements to address iodine deficiency and screening of adults for hypothyroidism and other thyroid dysfunction (Vanderpump, 2016). Conclusion If there are a few takeaways from the above, they would be the following. First of all, the diagnosis of hypothyroidism is fairly straight forward and easy to pull off once it is suspected. At the very least, it can be easily ruled out and whatever is indeed ailing the patient can be found if TSH and T4 levels are fine. Second, the standard synthetic T4 drugs are the obvious and first-line treatment methods to use. While "going natural" or alternative may be possible or practical in certain situations, the standard treatments that exist for hypothyroidism are typically very effective and there is really no reason to eschew them unless the drug causes new problems or enhances new ones. Generally speaking, healthy living and careful attention are the best practice. Just like a diabetic should keep an eagle eye on their blood sugar and A1C, a hypothyroidism patient should do the same thing with their TSH and T4. References Corriher, S. (2013). How to Cure Hypothyroidism Naturally. Healthwyze. Mayo. (2016). Treatment - Hypothyroidism - Mayo Clinic. Mayoclinic.org. Retrieved 7 June 2016, from http://www.mayoclinic.org/diseases-conditions/hypothyroidism/diagnosis-treatment/treatment/txc-20155362 MBG. (2011). 13 Ways to Treat Hypothyroidism Naturally. mindbodygreen. Retrieved 7 June 2016, from http://www.mindbodygreen.com/0-3139/13-Ways-to-Treat-Hypothyroidism-Naturally.html Vanderpump, M. (2016). The epidemiology of thyroid disease. - PubMed - NCBI. Ncbi.nlm.nih.gov. Retrieved 11 June 2016, from http://www.ncbi.nlm.nih.gov/pubmed/21893493 WebMD. (2016). Common Drugs and Medications to Treat Underactive Thyroid. Webmd.com. Retrieved 7 June 2016, from http://www.webmd.com/drugs/condition-584-Underactive+Thyroid.aspx?names-dropdown= WebMD. (2016). Hypothyroidism (Underactive Thyroid): Symptoms, Causes, and Treatments. WebMD. Retrieved 7 June 2016, from http://www.webmd.com/women/hypothyroidism-underactive-thyroid-symptoms-causes-treatments Read the full article