#ferroportin

[etlu-yume]

Trying to make notes from the articles about estradiol and 4th generation progestins affecting iron metabolism and finding MORE bullshit that has me going "oh god did I read that right?"

Choice findings:

• Short term effects of hepcidin changes could lead to an uneven iron distribution between serum (blood) and tissues.

• Estradiol found not to alter serum iron but induced a low iron status in bone marrow, an important target of iron controlled by the hepcidin-ferroportin axis

me, sitting here remembering being on the pill and having a ferritin of 600+: me reading these, about how the estradiol component could cause uneven iron distribution and ??? if I'm reading right ??? a decrease in bone marrow iron?? Which... (sorry science/biomed twitter I'm spitballing from my very headachey, visual artist brain here) if I'm putting two and two together and getting four - does that mean that there's potentially more shit stored in tissues that we can't/don't regularly test for? (that super form of ferritin, for example? Which usually stores in tissues and causes damage to organs?)

I hate how complicated this becomes when trying to weigh up options. Because these mood swings are ridiculous and unsustainable, and while I can cope with a little bit of "hey monitor the iron closely 'cause it could be wilding", if it's wilding in all the untestable directions* that's not very helpful.

* afaik there's no easy way to test for things like NTBI (Non-Transferrin Bound Iron) or Hemosiderin (all I can imagine, based on what I've read in some articles, is that this is like Ferritin molecules doing a fusion dance, DBZ style. Super Ferritin) which are like. All the things that do the nasty stuff.

[schlauemaus]

Eisen

Resorption im Darm -> Bindung an Transferrin -> Transport zu Organen -> wenn kein Bedarf -> Bindung an Ferritin -> Speichern in Makrophagen (=Siderophagen) in Leber, Milz u. Knochenmark -> kein Eisenmangel bei akuten Blutverlusten (dann werden Speicher geleert)

Bestimmung dient der (Pseudo)Eisenmangelanämiediagnose

-> chron. Blutung -> Hämoglobin (Eisen ist Bestandteil) geht verloren -> hypochrome Erys -> später auch Mikrozyten, weil nicht genug Hämoglobin vorhanden, welches physiologischerweise Signal zum Zellteilungsstop gibt (fehlt aber, somit kommt es zu zu vielen Teilungen -> kleinere Zellen)

Pseudoeisenmangelanämie

bei chron. Entzündungen, weniger stark ausgeprägte nicht regenerative Anämie wg. Entzündung vermehrte Produktion v. Hepcidin in Leber -> hemmt Ferroportin-Rez. in Darm u. Makrophagen -> verminderte Eisenaufnahme aus Darm, Heraustransport aus Makrophagen -> Bindung an Ferritin (=Speicherprotein) -> Eisen kann nicht zur bakteriellen Vermehrung genutzt werden, aber auch nicht mehr zur Hämoglobinsynthese

Differenzierung Pseudoeisenmangel od. Eisenmangelanämie über Siderophagen -> wenn erhöht= Pseudoeisenmangelanämie

Erniedrigt:

-> chron. Blutung -> blutsaugende Parasiten -> portokavaler Shunt -> dysfunktionale Leber -> verminderte Transferrinproduktion -> Proteinverluste (wg. zB Nephropathie) -> erniedrigte Transferrinkonz. -> Akute-Phase-Reaktion -> Hepcidinproduktion -> verminderte enterale Aufnahme -> Bindung an Ferritin wg. Entzündung (=Pseudoeisenmangel)

Steigt:

-> Hd.: durch Kortikoide -> zu hohe Gabe/Aufnahme= Eisenüberladung -> toxische Oxidationsprodukte -> Leberschädigung -> erbliche Eisenspeicherkrankheit (Hyperferrämie) -> Leberzellzerstörung -> Eisenaustritt

[mcatmemoranda]

Looking at this makes more sense to me than just reading about it. Now I understand why a high transferrin saturation would prompt you to think about hereditary hemochromatosis. Basically, if the transferrin is more saturated with iron than normal, it's because excessive amounts of iron are being absorbed and transported in the blood.

[innovationshealthwellness]

10 Signs You Have An Iron Deficiency

https://s-media-cache-ak0.pinimg.com/564x/2b/40/62/2b406272f541c013343fdcff89c64061.jp gPosted by Crisha Alyziah Miller -When you have iron-deficiency, your cells can’t get enough oxygen. How can you tell if your levels are a little low? Be on the lookout for these 10 warning signs.

Iron is crucial to biologic functions, including respiration, energy production, DNA synthesis, and cell proliferation. Although the prevalence of iron-deficiency anemia has declined somewhat recently, iron deficiency continues to be the top-ranking cause of anemia worldwide.

The human body has evolved to conserve iron in several ways, including the recycling of iron after the breakdown of red cells and the retention of iron in the absence of an excretion mechanism.

However, since excess levels of iron can be toxic, its absorption is limited to 1 to 2 mg daily, and most of the iron in the body (about 25 mg per day) is recycled by macrophages that phagocytose senescent erythrocytes. The latter two mechanisms are controlled by the hormone hepcidin, which maintains total-body iron within normal range, avoiding both iron deficiency and excess.

Hepcidin is a peptide hormone that is synthesized primarily in the liver. It functions as an acute-phase reactant that adjusts fluctuations in plasma iron levels by binding to and inducing the degradation of ferroportin, which exports iron from cells. In iron deficiency, the transcription of hepcidin is suppressed. This adaptive mechanism facilitates the absorption of iron and the release of iron from body stores.

In most cases, iron resistance is due to disorders of the gastrointestinal tract. Partial or total gastrectomy or any surgical procedure that bypasses the duodenum can cause resistance to oral iron. Laparoscopic Roux-en-Y gastric bypass, which is performed in selected obese patients to reduce caloric intake and to correct diabetes, is an emerging cause of iron deficiency and anemia because the procedure effectively removes an active iron absorption site from the digestive process and increases gastric pH. Helicobacter pylori infection decreases iron absorption because the microorganism competes with its human host for available iron, reduces the bioavailability of vitamin C, and may lead to microerosions that cause bleeding. Since it is estimated that half the world’s population is infected with H. pylori, clinicians should be aware of the possibility of infection and provide treatment in order to eradicate this source of iron-resistant iron-deficiency anemia.

Patients with malabsorption and genetic iron-refractory iron-deficiency anemia may require intravenous iron. Intravenous administration is also preferred when a rapid increase in hemoglobin level is required or when iron-deficiency anemia caused by chronic blood loss cannot be controlled with the use of oral iron, as is the case in patients with hereditary hemorrhagic telangiectasia. Active inflammatory bowel disease is an emerging indication for the use of intravenous iron; oral iron is not only ineffective but may also increase local inflammation. Intravenous iron is essential in the management of anemia in patients with chronic kidney disease who are receiving dialysis and treatment with erythropoiesis-stimulating agents.

[jurnalnisrina]

Resiko Anemia pada WUS (Wanita Usia Subur) yang Mengalami Obesitas

Dari Hasil penelitian Status Besi dan Kualitas Diet berdasarkan Status Obesitas pada Wanita Usia Subur di Semarang pada tahun 2019, menunjukan bahwa 20% WUS yang obesitas memiliki status FE yang rendah sebanyak 94%, yang akan berdampak ganda pada kesehatan WUS diantaranya ; dapat mengakibatkan terjadinya anemia, kematian pada ibu pada saat melahirkan, kematian janin, bayi berat lahir rendah (BBLR), kelahiran prematur, lahir cacat hingga kematian pada bayi. Sementara dari segi Obesitas maka akan berdampak kepada siklus reproduksi wanita yaitu menimbulkan infertilitas pada wanita akibat anovulasi, siklus menstruasi yang tidak teratur, Polycystic Ovary Syndrome (PCOS), meningkatknya risiko keguguran, bahkan kematian janin, resiko bayi halir dengan hipoglikemia, bayi makrosemia hingga kemungkinan persalinan secara Caesar.

Obesitas terkait anemia salah satunya dipicu oleh adipositas yang mengakibatkan inflamasi tingkat rendah dengan mengaktifkan Interleukin-6 untuk menginduksi produksi hepsidin.11 Peningkatan hepsidin menghambat kerja ferroportin sehingga besi tertahan di dalam makrofag dan hepatosit dan menghambat pelepasan besi ke plasma. Selain itu, absorbsi besi di enterosit juga terhambat sehingga penurunan jumlah besi dalam plasma menurun (hipoferremia). Hal ini dapat menurunkan potensi produksi hemoglobin sehingga mengarah pada kejadian anemia akibat inflamasi (Anemia Chronic Disease).

angka kejadian obesitas mengalami peningkatan yang dihimpun dari Riskesdas 2018 yaitu pada 2007 (10,5 %), 2013 (14,8 %), dan 2018 (21,8 %). Wanita Usia Subur dengan Obesitas akan berdampak pada siklus reproduksi wanita yaitu menimbulkan infertilitas pada wanita akibat anovulasi, siklus menstruasi yang tidak teratur, Polycystic Ovary Syndrome (PCOS), meningkatknya risiko keguguran, bahkan kematian janin. WUS berada dalam masa prakonsepsi yaitu periode kritis yang berpengaruh pada anak atau keturunan saat dilahirkan dan di kehidupan setelahnya.

Dapat disimpulkan bahwa, Status besi WUS obesitas signifikan lebih rendah dibandingkan WUS non-obesitas. Kelompok WUS obesitas dengan status besi rendah memiliki kualitas diet yang rendah dibandingkan kelompok lainnya. Sebaiknya WUS pranikah terutama sebagai calon ibu menyadari pentingnya mempersiapkan periode 1000 HPK dengan cara mencapai status gizi yang optimal melalui kontrol berat badan secara teratur, memperbaiki gaya hidup dan kualitas diet.

[aalt-ctrl-del]

The “I’m doing my own research” crowd, trying to convince people they can pull sources and site them.

Half of my research is me seeking references for all the technical doctor bullshit from these high level research sites. It’s material meant for doctors in the field, open for public viewing. National Center for Biotechnology Information is a good source, I think it is more up to date than the CDC website, but the CDC.gov site is more general information for the public, condensed down. But the two sites are run by difference parties, and that’s a factor to consider.

But the “I’ll do my own research” crowd is trying to convince you they can read this bullshit 

“Hepcidin, an oligopeptide, has two major functions in mammals. Hepcidin regulates iron homeostasis by controlling iron export from absorptive enterocytes, hepatocytes, and macrophages into the circulation via ferroportin inactivation.“

I can maybe get bits and pieces from this jargon, because I’ve done checks on the info already. I have no idea what it’s telling me, aside from Hepcidin is in warm blooded animals and regulates balance in the body by controlling iron absorption to whatever this enterocytes is. I know what macrophage is, and it has something to do with circulation.

Enterocytes is a cell of the intestinal lining source. So my guess is iron absorbed from nutrients in the intestines, into the blood. The blood and plasma takes nutrients from the intestines, and takes it through the body to the organs. Especially the brain - a big chonk of cholesterol. It’s a big hunky of fat full of oils.

Macrophage is hungry white blood cells source. Monocytes are the evolved form of macrophages. Neat.

Right now I’m trying to figure out more details on what covid does to red blood cells. In the past, doctors believed it stole hemoglobin from the red blood cells, rendering them incapable of carrying the O to the capillaries among tissues. I believe that is still being explored at this time, in that the doctors believe the covid cells when hijacking the red blood cell, use hemoglobin for something regarding replication, but I haven’t found information regarding this. But like I said, browsing these sites is tedious due to the language used.

There’s also the iron content of red blood cells, the loss of it and what covid does to the iron levels. Like, does covid do something with the iron or does the cell and its destruction just sort of lose it in the process of hijacking.

Okay, here’s a good article about the hemoglobin issue source.

“ These three domains were highly overlapping so that ORF3a could dissociate the iron of heme to form porphyrin. Heme linked sites of E protein may be relevant to the high infectivity, and the role of heme linked sites of N protein may be related to the virus replication. The docking results showed that orf1ab, ORF10, and ORF3a proteins coordinated to attack the 1-beta chain of hemoglobin, and some structural and non-structural viral proteins could bind porphyrin. Deoxyhemoglobin was more vulnerable to virus attacks than oxidized hemoglobin. But ORF3a was specific and would not attack blue blood protein, normal cytochrome C, and peroxidase. As for the attack, it would cause increasingly less hemoglobin that could carry oxygen and carbon dioxide, thus producing symptoms of respiratory distress and coagulation reaction, damaging many organs and tissues.“

The bolded text highlights that red blood cells without O were more vulnerable to viral attack, rather than red blood cells carrying the unhelpful CO2. I find that interesting, because I site that the covid virus loves areas where there is a lot of oxygen and iron, such as the lung tissue, liver, and kidneys. But the alveoli (lung cells) is the initial infection site when someone gathers too many covid cells, then the cells replicate and pass into the blood stream. But infection and destruction does not cease in the lungs, its a deriving, duplicating attack.

Some bacterial pathogens and G-tract viral pathogens can pass from within the intestinal tract, and into the enterocytes cells (we learned a new word), and from there pass into the blood stream - often this is fatal to the infected, because that shit should not be in the blood. Because once a virus or bacteria goes from the G-tract into the blood, it gets into the brain and mingles into other tissues, and then systemic death begins to occur, and these affects are often fatal EVEN WITH MEDICAL INTERVENTION.

That stated, you can see why I hate the covid virus, and why I site it as the deadliest pathogen of our timeline. It is a respiratory borne infection which is highly contagious through free floating aerosol droplets, and it very easily breaches into the blood stream. The level of attack and death to red blood cells is wholly dependent to the immune response of the recipient of the virus - i.e, an immune system that is primed to deal with this virus, let alone any pathogen before it multiplies beyond control. I.e, i.e, before symptoms PRESENT.

When symptoms present, that is an indication that the immune system has failed, and now the body has to mount an attack on the invading cells, to mitigate the spread and damage the viral cells might cause. While at the same time, the body can fly out of control with an aggressive viral attack, and begin attacking its own cells. This is the case in most infections, as the body cannot distinguish which cells are compromised, or which ones are healthy. The body homeostasis simply nukes them all.

If the “I’ll do my own research” crowd actually did their own research, this stuff would be common knowledge. They wouldn’t be out here throwing a bitch fit about mask mandates.

ACtually, they would still be throwing bitch fits. Because they say, “Some will die, but survival of the fittest.” Or, “I don’t care if I live or die.” Or some bull.

In retrospect, the polio virus was a less successful spreader than the covid virus. But people were very afraid of it, because it really only infected the precious children. But polio would have been less capable of spreading, if children practiced better hygiene techniques, and the people back then had the cleaning products we have today, which are specifically engineered to kill G-tract viral pathogens. Not all, but 99.9% of pathogens.

However, it is difficult to disinfect the air, without harming people or causing respiratory issues. Aside from the addition to adequate and routine filtration maintenance. 

But “doing your own research” requires a lot of free time, hours spent just trying to grasp the most rudimentary terminology. But along the way, you can focus less on that and more on filtering through sources that are fresh and new, because a lot of these articles are repeats on different sites. It’s exhausting, it proves that covid is capable of becoming much worse than it is now. But a lot of these articles imply covid has a very effortless capacity for mutating very quickly, and I would wager based on “doing my own research” it is not a complicated virus. It’s simply very good at its job, very basic and simple, and you don’t need to outclass the body to get the job done. It just has to endure outlast. 

[indianfitnesscare]

Iron Supplements can Worsen Malaria Infection

Iron Supplements can Worsen Malaria Infection

They also found that a mutant form of ferroportin that occurs in African populations appears to . These basic findings may help researchers and healthcare officials develop strategies to prevent and treat malaria infections, which numbered nearly 216 million worldwide in 2016.. “Our study helps solve a long-standing mystery,” said Tracey Rouault, M.D., the study’s senior author and a senior…

[martz2-blog]

Saison 1 Episode 9

ITEM 158 : IST 

La syphilis est un du à Treponema pallidum = un spirochète (bactérie hélicoïdale Gram négatif) : c’est une IST non immunisante, très contagieuse . - Seul les lésions muqueuses sont contagieuses uniquement (chancre et syphilide érosive) : transmission surtout sexuelle (après rapport non protégé, dont oro-génital), rarement maternofœtale (4-5 mois de grossesse), post-transfusionnelle ou greffe d’organe.                                                                                              En recrudescence depuis quelques années en France, surtout chez l’homosexuel masculin et les sujets VIH.                                                                   - Dépistage sérologique : sujet à risque (homo-, bi- ou hétérosexuel à partenaires multiples) et patient VIH

/!/ Le tréponème ne se cultive pas in vitro : aucune culture possible, aucun antibiogramme !!! 

Le diagnostique se fait grâce :

- Microscope sur fond noire :  Pratiqué sur des lésions érosives : chancre d’inoculation ou syphilide érosive muqueuse , la Sensibilité est de 50% au niveau du chancre, sans valeur au niveau buccal (spirochètes saprophytes).

- Sérologie :  Examen standardisé, peu coûteux, fiable : généralement seulement TPHA-VDRL  (FTA en plus si nouveau né ou syphilis précoce)                                                                                                    /!/  Ne différencie pas une syphilis et une tréponématose endémique non vénérienne (pian, béjel, pinta)

Traitement selon le stade : 

ITEM 215 : Hémochromatose

- mutation homozygote du gène HFE : mutation C282Y (90%) ou mutation H63D, S65C...

- Maladie génétique la plus fréquente en France (prévalence = 1/300), pénétrance incomplète (10-50%), d’expression variable                                           - Mécanisme : disparition de l’hepcidine -> absence d’inhibition de la ferroportine -> absorption duodénale excessive de fer - Autres facteurs influençant : sexe, génétique, vitamine C, virus à tropisme hépatique, alcool, autres facteurs génétiques

-> Manifestation chez l’homme entre 40 et 50 ans et chez la femme ménopausée (retardées par les règles)

Clinique : 

[sbgridconsortium]

Structural basis of physiologic iron regulation

Serum iron levels are tightly controlled in humans through the action of hepcidin, a peptide hormone, on ferroportin, an iron efflux transporter. While iron is essential for life, this control is particularly important because iron in the free ferrous state is toxic. Ferroportin is expressed on enterocytes, allowing absorption of dietary iron from the intestine, and it also enables iron recycling in hepatocytes and macrophages. In states of high serum iron levels, hepcidin levels increase and negatively regulate the expression of ferroportin on the cell surface. While it is known that the amount of ferroportin controls the magnitude of iron efflux, the molecular-level regulation of hepcidin on ferroportin remained unclear. 

SBGrid members Yifan Cheng and Aashish Manglik and other researchers have been working to elucidate this regulation. The authors determined the cryo-electron microscopy structures of ferroportin in lipid nanodiscs and completed molecular dynamics simulations. 

Using this, they determined that hepcidin regulates ferroportin by binding the transporter and occluding the iron efflux pathway. Interestingly, they found that hepcidin binding to ferroportin results in an 80-fold increase in hepcidin affinity in the presence of iron. This suggests that ferroportin loaded with iron is the target for degradation by hepcidin. 

Read more about this research in Nature.

[healthtimetaylor]

Gastrodin can inhibit H2O2-induced ferroptosis through its antioxidative effect in C6 cells.

PMID:  Biol Pharm Bull. 2020 ;43(3):480-487. PMID: 32115506 Abstract Title:  Gastrodin Inhibits HO-Induced Ferroptosis through Its Antioxidative Effect in Rat Glioma Cell Line C6. Abstract:  Ferroptosis is a form of necrosis caused by iron-induced accumulation of lipid hydroperoxide, involving several molecular events, and has been implicated in Parkinson's disease. Gastrodin is a component of Gastrodia elata Blume with strong antioxidant activity. We examined whether gastrodin can prevent HO-induced cytotoxicity in rat glioma cell line C6. For this purpose, C6 cells were pretreated with gastrodin (1, 5, 25 µM) and then exposed to 100 µM HO. Results showed that pretreatment of C6 cells with gastrodin decreased HO-induced lactate dehydrogenase (LDH) release and cell death. Moreover, gastrodin decreased intracellular malondialdehyde (MDA) level, whereas increased glutathione peroxidase (GPX) activity and glutathione (GSH) level after HOtreatment. In addition, treatment of deferoxamine (DFO), ferrostatin-1, and liproxstatin-1 abolished ferroptosis induced by HOor erastin pretreatment. Treatment with gastrodin attenuated HO-induced ferroptosis and decreased lipid reactive oxygen species (ROS) (C11-BODIPY) production in C6 cells. Moreover, gastrodin increased the protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2), GPX4, ferroportin-1 (FPN1), and heme oxygenase-1 (HO-1) in C6 cells treated with HO. RSL3, a GPX4 inhibitor, inhibited GPX4 protein level in cells co-treated with gastrodin and 100 µM HO. These findings indicate that gastrodin can inhibit HO-induced ferroptosis through its antioxidative effect in C6 cells.

read more

[mcatmemoranda]

Hepcidin regulates iron absorption by degrading ferroportin 1 when there is high serum iron so that less iron will be absorbed into the bloodstream. When the serum iron is low, hepcidin decreases, so there is more ferroportin 1 and thus more Fe is absorbed.

Haptoglobin is a protein that binds hemoglobin in the plasma. Free Hb is toxic, so haptoglobin binds to it to make it less toxic. If you have hemolytic anemia, there's more Hb, so all available haptoglobin is used up to bind to the Hb.

[innovationshealthwellness]

10 Signs You Have An Iron Deficiency

https://s-media-cache-ak0.pinimg.com/564x/2b/40/62/2b406272f541c013343fdcff89c64061.jp gPosted by Crisha Alyziah Miller -When you have iron-deficiency, your cells can’t get enough oxygen. How can you tell if your levels are a little low? Be on the lookout for these 10 warning signs.

Iron is crucial to biologic functions, including respiration, energy production, DNA synthesis, and cell proliferation. Although the prevalence of iron-deficiency anemia has declined somewhat recently, iron deficiency continues to be the top-ranking cause of anemia worldwide.

The human body has evolved to conserve iron in several ways, including the recycling of iron after the breakdown of red cells and the retention of iron in the absence of an excretion mechanism.

However, since excess levels of iron can be toxic, its absorption is limited to 1 to 2 mg daily, and most of the iron in the body (about 25 mg per day) is recycled by macrophages that phagocytose senescent erythrocytes. The latter two mechanisms are controlled by the hormone hepcidin, which maintains total-body iron within normal range, avoiding both iron deficiency and excess.

Hepcidin is a peptide hormone that is synthesized primarily in the liver. It functions as an acute-phase reactant that adjusts fluctuations in plasma iron levels by binding to and inducing the degradation of ferroportin, which exports iron from cells. In iron deficiency, the transcription of hepcidin is suppressed. This adaptive mechanism facilitates the absorption of iron and the release of iron from body stores.

In most cases, iron resistance is due to disorders of the gastrointestinal tract. Partial or total gastrectomy or any surgical procedure that bypasses the duodenum can cause resistance to oral iron. Laparoscopic Roux-en-Y gastric bypass, which is performed in selected obese patients to reduce caloric intake and to correct diabetes, is an emerging cause of iron deficiency and anemia because the procedure effectively removes an active iron absorption site from the digestive process and increases gastric pH. Helicobacter pylori infection decreases iron absorption because the microorganism competes with its human host for available iron, reduces the bioavailability of vitamin C, and may lead to microerosions that cause bleeding. Since it is estimated that half the world’s population is infected with H. pylori, clinicians should be aware of the possibility of infection and provide treatment in order to eradicate this source of iron-resistant iron-deficiency anemia.

Patients with malabsorption and genetic iron-refractory iron-deficiency anemia may require intravenous iron. Intravenous administration is also preferred when a rapid increase in hemoglobin level is required or when iron-deficiency anemia caused by chronic blood loss cannot be controlled with the use of oral iron, as is the case in patients with hereditary hemorrhagic telangiectasia. Active inflammatory bowel disease is an emerging indication for the use of intravenous iron; oral iron is not only ineffective but may also increase local inflammation. Intravenous iron is essential in the management of anemia in patients with chronic kidney disease who are receiving dialysis and treatment with erythropoiesis-stimulating agents.

[plxyboi-blog]

Health Benefits of Garlic – Version Weekly

New Post has been published on https://healthy4lives.com/health-benefits-of-garlic-version-weekly/

Health Benefits of Garlic – Version Weekly

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The Medicinal Attributes Of Garlic

Scientifically acknowledged as allium sativum, garlic is utilized mostly as a flavouring agent broadly close to the globe. Garlic also has several medicinal homes that support reduce many overall health relevant challenges. This pungent herb has been utilised by people today for countless numbers of many years for equally therapeutic and culinary functions as very well.

Garlic plays a essential job in dealing with cardiovascular challenges like amplified blood stress, substantial cholesterol and atherosclerosis. It helps reduce liver challenges, flatulence, intestinal worms, rheumatism, controls blood sugar and fever and also fights from respiratory challenges. It is also utilized to establish immunity and handle bacterial and fungal bacterial infections.

Garlic gets its pungent smell thanks to the existence of a amount of sulphur abundant compounds. The compound allicin has many anti viral, anti-bacterial, antioxidant and anti-fungal homes. Gurus feel that it is most effective to try to eat garlic right after chopping or mincing it and letting it rest for a although.

Nutrition Garlic is a small calorie food stuff packed with valuable nutritional vitamins and minerals. It is abundant In vitamin B6, vitamin C, manganese and other minerals in trace quantities.

Wellbeing Benefits

Encourages Coronary heart Wellbeing Consuming garlic regularly for two months helps in decreasing LDL by 3-one 5mg/dl and total cholesterol by eleven-23mg/dl in older people with dyslipedemia. The anti-clotting homes of ajoene, a compound present in garlic, helps reduce the formation of clots inside the blood vessels. The sulphur abundant compounds of garlic also reduce the blood vessels from receiving blocked and gradual the progress of atherosclerosis (hardening of the arteries). Garlic also helps protect the heart from the harming results of no cost radicals. With age, the arteries are inclined to lose their potential to extend and garlic can support sustain this elasticity.

Anti-Cancer Attributes Garlic minimizes the risk of distinctive types of cancer. Garlic’s anti cancer homes are thanks to the existence of allyl sulphides which inhibit the transformation of PhlP (a type of compound that has been involved with amplified incidence of breast cancer) into carcinogens.

Combats Allergy symptoms Garlic is full of important compounds that support reduce viral and bacterial bacterial infections. Consuming raw garlic is also said to kill bacteria like e-coli and other people that trigger food stuff poisoning in people today. It is also wonderful In dealing with pores and skin bacterial infections as it incorporates antiviral and antibacterial homes. Ajoene, the compound present in garlic, is also said to treatment several pores and skin bacterial infections.

Maintains Blood Force The polysulphides present in garlic are converted into hydrogen sulphide by the pink blood cells that helps dilate the blood vessels and helps manage blood stress. If your blood stress levels are of issue, there are pure alternate options to manage it as a substitute of employing blood stress medicine that a single can test right after a consultation with a health practitioner. Allicin in garlic blocks the action of angiotensin li (a protein that is accountable for an improve in blood stress) and helps in decreasing blood stress levels.

Garlic is utilized to establish immunity and handle bacterial and fungal bacterial infections

Superior For The Respiratory Procedure Garlic may well also minimize the severity of upper respiratory tract bacterial infections. Its potential to endorse expectoration can make it irreplaceable in continual bronchitis. The day by day use of garlic may minimize the frequency of colds. Also, its antibacterial homes support in dealing with throat irritations.

Controls Blood Sugar Concentrations This herb will increase the levels of insulin and regulates blood sugar levels in the entire body, specially in diabetics.

Beats Anaemia Diallyl sulphides present in garlic improve the generation of ferroportin (a protein that helps in the absorption and release of iron) and enhances iron metabolic rate that is helpful in preventing iron deficiency and involved ailments like anaemia.

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[beautytshirts]

Labrador Labveners Shirt

Iron is subject to tight homeostatic control in mammals. At the systemic level, iron homeostasis is controlled by the liver-derived hormone hepcidin acting on its target ferroportin in the gut, spleen, and liver, which form the sites of iron uptake, recycling, and storage, respectively. At the cellular level, iron Labrador Labveners Shirt homeostasis is dependent on the iron regulatory proteins…

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Best 15 Amazing Benefits of Garlic https://www.youtube.com/watch?v=lHxNJhZLEQs We are focusing on best 15 amazing benefits of garlic among all other benefits. In the well-known natural remedy, garlic has several health benefits and has been used to treat many health problems. Here you will find some of the best 15 amazing benefits of garlic. So lets begin! 00:28 Benefit no. 1: Fight bacteria and viruses Antibacterial and antiviral properties of garlic are well known. They can help prevent food poisoning when they kill bacteria, like E. coli and salmonella. Garlic also helps with bacterial, fungal, worm, yeast and viral infections. 00:50 Benefit no. 2: Improve metabolism Diallyl sulfides in garlic increase Ferroportin in the body, and it helps to improve the metabolism of iron. 01:03 Benefit no. 3: Relieve toothache Antibacterial and analgesic powers in garlic can help reduce the pain of toothache. 01:13 Benefit no. 4: Reduce weight Garlic helps to slow down the formation of fat cells in the body. Anti-inflammatory factor of garlic, which slows down the formation of fat. 01:26 Benefit no. 5: Treat skin infections Chemical called ajoene helps treat skin infections caused by fungus, such as ringworm and athlete's foot. 01:38 Benefit no. 6: Thin blood The same chemical works in the prevention of blood clots. This can be dangerous if you are having surgery. 01:49 Benefit no. 7: Regulate blood sugar Another property of garlic is to increase the release of insulin and help regulate blood sugar levels in diabetics. 02:00 Benefit no. 8: Low blood pressure Allicin in garlic helps to lower the blood pressure and polysulfides are converted to hydrogen sulfide. This sulfide also helps to control the blood pressure. 02:15 Benefit no. 9: Lower cholesterol Able to reduce the level of cholesterol is another feature of garlic. It also helps to reduce the formation of plaque. 02:27 Benefit no. 10: Improving allergy symptoms Juice of raw garlic can be used to stop the itching from rashes and bug bites. Garlic can also improve airway issues due to allergic reactions. 02:41 Benefit no. 11: Protect the Heart Its sulfides protect heart health. Garlic helps prevent artery hardening. Blood thinning properties of garlic also helps to prevent clots in blood vessels. 02:55 Benefit no. 12: Prevent cancer The use of garlic every day is the way to reduce the risk of some cancers. Allyl sulfides in garlic prevents forming of cancer cells. 03:09 Benefit no. 13: To treat respiratory conditions The antibacterial properties of garlic can reduce the number of colds you get. It can also help in the treatment of upper respiratory tract infections, asthma and shortness of breath. Garlic may also be used as an expectorant, to help in loosening phlegm body. 03:32 Benefit no. 14: Martial warts and calluses When the garlic is put on the warts and calluses, it is believed to help with these conditions. 03:42 Benefit no. 15: Fan the flame Garlic can increase circulation in the body that increases the body's ability to feel passionate. So start eating 2 to 3 cloves of garlic everyday and have a healthy happy life. Recommended Video: https://www.youtube.com/watch?v=yEUv8l59ETA DISCLAIMER: This video is purely informative. Do not self-medicate and in any case, consult a qualified medical professional before applying any information presented in the video. We do not guarantee any results and does not bear any responsibility for the harm that can be caused by using the information stated in the video. ------------------------------------------------- Health Apt Channel https://www.youtube.com/healthaptgala Facebook Page: http://bit.ly/2j1w04r Google+ Page http://bit.ly/2jNsQVU Video: https://www.youtube.com/watch?v=lHxNJhZLEQs by Health Apt

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Dear Mark: Iron Followup

Last week’s post on iron levels got a big response and garnered a ton of questions from you guys. Today, I’m going to clarify a few things and answer as many questions as I can. First, do iron and ferritin levels mean different things for men and women? If so, how do those differences manifest? What about premenopausal women vs postmenopausal women? Second, what do we make of the fact that ferritin is also increased in times of inflammation? Is there a way to distinguish between elevated ferritin caused by inflammation and elevated ferritin caused by high iron? Third, is desiccated liver a good option for liver haters? And finally, I share some exciting plague news.

Let’s go:

Emma wrote:

I’d love to see more info on iron levels as they relate to men and women differently. I recently had an iron infusion for low ferretin, not thinking much would change I actually experienced so many positive effects I didn’t even know were coming my way. I’m less cold, no more afternoon fatigue, less hair falling out, no more random palpitations, improved restless leg syndrome and the number one big change is it improved anxiety levels – in fact my anxiety is now gone. The last two are due to a connection between iron and dopamine. I learnt that children with mental health issues are often treated for low ferretin where possible, elevating levels to around 100 showing positive results (would love to see literature on this), for me my ferretin went from 20 to 130 and its changed my life, at 31 I haven’t felt this good in years. Yay iron!

That’s awesome to hear. Yes, it’s important to stress the very basic essentiality of iron. Without it, we truly cannot produce energy. And since energy is the currency for everything that happens in the body, an iron deficiency makes everything start to fall apart.

As for gender and iron, there’s a lot to discuss.

A good portion of women with hemochromatosis never actually express it phenotypically, meaning their lab tests don’t show evidence of dysregulated iron metabolism or storage. According to one study of hemochromatosis homozygotes (people who inherited the mutation from both of their parents), being a woman makes it 16x more likely that your hereditary hemochromatosis won’t actually present as iron overload.

Another study found that among mostly-age-matched men (42 years) and women (39 years) with hemochromatosis, 78% of the men had iron overload while just 36% of the women had it. Iron overload was defined as transferrin saturation over 52% combined with ferritin levels of 300 ng/mL for men and 200 ng/mL for women.

High iron levels are more of an issue for postmenopausal women than premenopausal women. The latter group regularly sheds blood through menstruation, and if anything, they’re at a higher risk of low iron. Plus, estrogen is a key regulator of iron metabolism. As menopause sets in and estrogen diminishes, that regulation suffers.

For instance:

In postmenopausal Korean women, high ferritin levels predict metabolic syndrome and subclinical atherosclerosis.

High ferritin predicts metabolic syndrome in postmenopausal but not premenopausal women.

In premenopausal Korean women, higher ferritin levels predict better bone mineral density; menopause nullifies this relationship.

Remember that ferritin is actually a measurable protein bound to iron, so testing a ferritin level is technically an indirect way to measure iron. Why is this important? Another characteristic of ferritin (the protein) is that it is an ACUTE PHASE REACTANT. This means that ferritin levels can fluctuate with illnesses and other inflammatory states in the body that drive up a ferritin value that is not related to an actual iron level fluctuation. Don’t get ferritin checked when you are sick with a cold or other illness.

This is a great point.

Ferritin is marker of long term iron storage, but it’s also an acute phase reactant that up regulates in response to inflammation or oxidative stress.

If you want to be really careful, you should get a HS-CRP test—that measures your overall inflammatory status. If CRP is elevated, ferritin can be elevated without saying anything about your iron status.

Come to think of it, if elevated ferritin can be a marker of inflammation and oxidative stress, the inflammation could be responsible for some of the negative health effects linked to high ferritin. Or, if having too much iron in the body can increase oxidative damage, it may be that high iron levels are increasing inflammation which in turn increases ferritin even further. Biology gets messy. Lots of feedback loops. However, the fact that many studies cited in the previous iron post that use blood donation to treat high ferritin have positive results indicates that for most people, ferritin can be, in most situations, an accurate estimation of your iron status.

To make sure it’s an iron problem, get a transferrin saturation test as well. That indicates the amount of iron you’re absorbing, with below 20% being low and over 45% being high. People with high ferritin and high transferrin saturation do have high iron levels. People whose ferritin is artificially enhanced by inflammation will have normal transferrin saturation levels.

I have one last question on this. You say “Don’t stop eating liver every week.” If you can’t stand the taste of liver, what do you think about taking liver capsules made from grass-fed New Zealand beef every day instead?

That’s a great option. Go for it.

People should generally aim for 4-8 ounces of fresh liver a week. Note the amount of desiccated liver in your capsules and multiply by 3 to get the fresh liver equivalent, then take enough each day (or all at once) to hit 4-8 ounces over the week. I hear good things about this one.

Mark, Thank you for your article on HH. I carry the gene but have been managing my iron levels through phlebotomies. I am full Keto, meat and all and have found my iron levels have not been effected by going Keto. Early detection is the key and ongoing monitoring. Bring on the plague!!!

You joke about that now, but there’s a startup that’s breeding heritage rat fleas that produce a mild strain of the plague that evades the attention of the immune system and proliferates throughout the body to keep iron levels in check without killing you. I’m an early investor, have a couple swarms installed in my condo, and (knock on wood) so far have avoided anything worse than a sore throat and maybe a mild open sore or two. There’s actually a big rift forming between the techs who want to keep the fleas heritage and those who want to go ahead with CRISPR and engineer them. One variant has had a deer tick gene inserted that adds an anesthetic compound to the flea’s saliva. That way you can have a personal swarm on you and never feel any bites or itches.

I’m not sure about CRISPR just yet, but I gotta say it’s pretty nice to be covered in fleas and not feel the bites. Time will tell.

Ok, I’m joking.

That’s it for today, folks. I hope I’ve answered some of your concerns, and if not, let me know down below. Thanks for reading!

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References:

Lainé F, Jouannolle AM, Morcet J, et al. Phenotypic expression in detected C282Y homozygous women depends on body mass index. J Hepatol. 2005;43(6):1055-9.

Qian Y, Yin C, Chen Y, et al. Estrogen contributes to regulating iron metabolism through governing ferroportin signaling via an estrogen response element. Cell Signal. 2015;27(5):934-42.

Seo SK, Yun BH, Chon SJ, et al. Association of serum ferritin levels with metabolic syndrome and subclinical coronary atherosclerosis in postmenopausal Korean women. Clin Chim Acta. 2015;438:62-6.

Cho GJ, Shin JH, Yi KW, et al. Serum ferritin levels are associated with metabolic syndrome in postmenopausal women but not in premenopausal women. Menopause. 2011;18(10):1120-4.

Chon SJ, Choi YR, Roh YH, et al. Association between levels of serum ferritin and bone mineral density in Korean premenopausal and postmenopausal women: KNHANES 2008-2010. PLoS ONE. 2014;9(12):e114972.

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