I am a double BK amputee who wears prosthetic legs daily. The fit of the prosthetics and thereby my activity level is obviously hugely dependent on weight. After an accident last year I've gained 40+ lbs and am really struggling. I've struggled with my weight most of my life, tried every diet etc. I also work in a medical adjacent field and I know the efficacy of the GLP1 weightloss meds. I even tried paying out of pocket for Saxenda for a month last year, which worked very well, but now of course it's out of stock. It's not covered by my Cigna plan.
My Cigna plan refuses to cover any of the GLP1s, just denied me for Mounjaro too after denying Saxenda. They won't cover Zepbound even though it's been approved by the FDA specifically for weightloss. I can't afford to pay out of pocket. To reiterate, I am overweight BMI of 39, have high cholesterol, and take Losartan for hypertension. I don't see why a double amputee with all these comorbidities would be denied these life-changing medications, particularly considering the bill Cigna has to continue to foot as I have issues, falls, etc because of my weight. It's infinitely cheaper for them in the long run to approve me for one of these and help me get active again.
Does anyone have any thoughts, experience with appeals, etc, given my unique case as an amputee with these comorbidities? I am very desperate to get help and my general doctor and an endocrinologist seem clueless. Thank you.

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A couple of ideal scenarios. If you've read any of my posts, you know I consider the timing of the lift of the hold as Imminent. "Imminent" means that it can happen at any time. However, we now know that the "Final Submission" remains outstanding and is requisite for the lifting of the hold but we understand that it should be ready sometime in mid to late September, 2023. So then, the lift of the hold has as its pre-requisite that the Final Submission be made first. In order to make the Final Submission, CytoDyn must initially make a decision or selection on which one select HIV -subpopulation it is which they feel would still benefit by the use of LL despite all the recent HIV drug approvals within the same indication or -subpopulation.
I have speculated here that HIV-MDR shall be the selected HIV -subpopulation which CytoDyn chooses to base their "Final Submission" masterpiece on. If -MDR does turn out to be the HIV -subpopulation, then all the work which CytoDyn has done thus far over the past year and all the submissions that CytoDyn has made in all of their efforts to get the hold lifted, would not have been executed in vain. That is because, all of those prior submissions shall eventually be incorporated into a new, revised BLA for HIV-MDR which won't be difficult to assemble. The FDA did request that CytoDyn does produce a new HIV Trial protocol and this trial shall require completion to validate safety and efficacy in the same chosen HIV -subpopulation which will likely be -MDR.
Up until the day he left, CA never once expressed any doubt in the work which he did, or CytoDyn had done and CA always felt that all of his efforts to get the hold lifted would eventually become successful. He only exuded confidence in his submissions and he was willing to wait it out. "The FDA then responded back with a 3rd further written communication to us, again relating to the Benefit / Risk Assessment as well as requesting submission of a new Protocol for HIV indication to be studied once the Partial Hold is lifted or some clarification that CytoDyn may not continue to develop Leronlimab in that indication.
09:24: So, at the end of March 2023, just last month, we had, an informal meeting with the FDA, where the agency clarified some of our more specific questions with respect to the information that we would like to see addressed. The Risk / Benefit Assessment portion, of the clinical hold and work on finalizing the supplemental submissions to address the items that we discussed with the agency during that informal meeting and we remain fully committed to the submission of the complete response to lift the partial clinical hold for that indication."
What else may be Imminent? We know that SA made request on July 10, 2023 for a "Final Hearing date". Amarex and the Arbiter had 28 days to provide that date. 28 days from that formal request will be this coming Monday, August 7, 2023. Once the requested date is provided by the Arbiter, Amarex then enters into a period where they should determine to offer up proposals of lesser settlements made significantly sooner such that SA/CytoDyn possibly might accept the reduced offer being sufficiently sooner than the date given, otherwise, Amarex would opt to allow the full binding judgement of the Arbiter to determine the final award, knowing that if Amarex delays too long, then, SA/CytoDyn will simply refuse Amarex's offer and decide to wait for the Arbiter's binding decision. Amarex/NSF shall keep in mind the recent regulatory action taken against them by the FDA. Tick tock, Tick tock.
Minimum $100 million. That gives CytoDyn options. That gives CytoDyn value. This award shall be considered in buy out / partnership negotiations. This is what the R & D Update of 12/7/22 was pointing to. Value creation through a chain of events. Cyrus mentioned that funding is expected when the hold is lifted. He also said NASH would be monotherapy and that CytoDyn would do NASH alone. What is certain is that the award shall be used to increase CytoDyn's value. But what is also certain, is that the outcome of the Amarex award is only a small part of the opening act. The ball is now rolling but it is picking up steam.
Following the Final Submission, it won't be longer than 30 days before CytoDyn hears that the hold on LL is lifted. The FDA is expecting this, to insure that all which was discussed in their meetings together with CytoDyn is properly documented and in order. The hold will then be lifted and subsequently, both Celebrations and parties commence while CytoDyn promptly gets down to business. The NDAs in Oncology are revealed and those partnerships are triggered. 3rd party AI is revealed and how their work will benefit all indications. It becomes another All Hands On Deck Effort. All hands together. But, this time another CEO leads the show and the identity of this individual will bring it all home.
CytoDyn is entering a precipice now. Taken from the R & D Update, most shareholders were thinking that by about Valentine's Day or a little bit thereafter, the hold was supposed to lift. But that didn't happen. Instead, what did happen on that day was that CA bought $100k worth of stock. 7 months following that day is somewhere around mid - September 14, 2023. We are not clear why CA is no longer President, nor why he didn't become CEO. All we really know is that one day, Cyrus got sick and then, after he had healed, he returned back to work again, but, he was demoted and brought back as a Senior VP. However, we also know, that when he came back, that the company accelerated his full vesting cycle to be achieved within 6 months starting from July 7, 2023. Therefore, by January 7, 2024, CA shall be fully vested. Therefore, instead of having to wait 4 years to be fully vested, Cyrus may have reluctantly settled or agreed to take the Senior VP position because as a result of the agreement, his full vesting occurs much sooner, by 1st month of New Year instead of 4 years from now. That's my take at least.
Why did CytoDyn want CA to step down? It is kind of strange I think. What we do know is that another CEO shall be coming on board. Cyrus never was brought on a CEO, but had he fulfilled certain milestones, he would have. But, they were not fulfilled and his sickness interfered with the process at exactly the right time to make this smooth transition. Right now, CytoDyn is searching and is hopeful that a new CEO comes on board within 6 months and by then, CA is by then fully vested and therefore, he could be let go, but he would own all his shares as per his new vesting agreement. The other reason is that CytoDyn/CA may be aware of the possibility that a buy-out may be happening within a year or two and CA/CytoDyn wanted to insure that he be fully vested within only 6 months, so that he would benefit fully by the time of the possible buy out if he were already fully vested.
According to Tanya Urbach, "The board has recently begun its efforts to recruit, interview and retain, a highly qualified CEO to guide the company. To that end, we are engaged with an executive search firm and have leveraged corporate partners and board members in our effort to identify exceptional CEO candidates. I have great confidence in our ability to successfully retain a seasoned executive with the right mix of ethical leadership scientific knowhow and financial backing to drive CytoDyn forward. In the interim, I am gratified to note that with recent additions, CytoDyn has, without a doubt, the strongest mix of just these attributes that it has had through my entire tenure on the board of directors. As such, the company is well positioned to effectively advance corporate objectives during the CEO search period. And, we expect to announce several positive developments in the coming months."
The new CEO brings with him/her ethical leadership, scientific knowhow and financial backing. Financial backing, to me, sounds like a buy out or a partnership. CA as President, gets sick, gets demoted to Senior VP, but also receives an accelerated full vesting with in 6 months and a search for a new CEO with Financial Backing is initiated. We also have the Amarex Arbitration Award and the lift of the hold all going on simultaneously. The Chain of Events takes place with a great multitude of shareholders watching all the events as they unfold. On the message boards, some shareholders now express their desire to participate in the shareholder meetings. CytoDyn won't have a greater time of strength than when the hold is lifted. At that time, all the shareholders realize, that their molecule is no longer shunned, no longer hand cuffed, but rather, that it is now accepted. They will understand, that their molecule went through the ringer and has passed the test of the Grim Reaper and now, they realize, that there is nothing standing in its way. Celebration and festivity spontaneously erupt. Patients again are benefited by the subsequent treatment with the drug.
Now, we have been recently told that NASH is no longer monotherapy, but shall be combination therapy. Was this recommendation made by AI? It may have been, but, I am of the opinion that it was made by Salah Kivlighn, PhD Clinical and Strategic Advisor . "Dr. Kivlighn began his career at Merck & Co. (“Merck”) where he held positions of increasing responsibility during his 15-year tenure. While at Merck, Dr. Kivlighn was the lead scientist for the discovery and development of Cozaar® (losartan), and later helped to lead the massive growth of Cozaar® to $3.5B in worldwide revenue. As a scientist and marketer, Dr. Kivlighn contributed to the successful launch of a number of trials. At Merck, he also co-led the development and commercialization of RotaTeq® leading to an $800M franchise; RotaTeq® was awarded universal recommendation by the Advisory Committee on Immunization Practices. Among Dr. Kivlighn’s many accolades, his team earned the prestigious Prix Galien Award for Best Biotechnology Product for RotaTeq®." Do I have to say it again? Salah Kivlighn is a Merck guy. We also know that Merck uses AI to help in the work of getting drugs approved much quicker.
The Last Friday in September is 9/29/23. Could we be getting our new CEO as soon as this date? New CEO, Amarex Award, Final Submission?
The Last Friday in October is 10/27/23. Same questions. I believe the new CEO will be tied in somehow, to Amarex Award and to the Final Submission or the lift of the hold.
Things should fall into place in the fall because of what the R & D Update communicated. Although things did not occur as we originally envisioned it, those same things still may come to pass, but played out in an entirely different manner. The R & D Update does come to pass, one way or another. It doesn't dwindle away or fade away into nothing. The R & D Update delivers on its promises. It put CytoDyn on the clock and the clock is still ticking. When SA requested the "Final Hearing Date", that started one of the timers. That request for the Final Hearing Date was a partial fulfillment of some of the promises made in the Update. That request won't end up in embarrassment but rather in fulfillment. It comes together in a sense of urgency. It doesn't just linger on and on and on. No, it happens in a rapid, but orderly manner. The date should be decided by Monday 8/7/23 or 28 days from when it was requested on 7/10/23. This does come to fruition and CytoDyn shareholders won't look like jackasses standing around waiting for something to happen.
According to CA, what was the most important part of the R & D Update? I'll give it to you right here. "1:31: 40: So in terms of what potential time lines can look like, I think it's really important to highlight that from a value-creation standpoint, and I've mentioned this before, we truly do need to generate a large robust and what I call unequivocal data set that will leave no questions left on the table, right? And that a strategic partner would find attractive and attractive enough to do a real value-accretive deal with the company." In a few words, "A large, robust, unequivocal data set that will leave no questions on the table." So that a strategic partner would find attractive enough to do a real value-accretive deal wtih CytoDyn. We already have an aggregated and validated data set. In short time, CytoDyn will be obtaining even more data in a new, small HIV trial with a new protocol. Another pre-clinical trial in NASH is under development and is slated to be initiated subsequent to the hold being lifted. We have the MD Anderson Top Line Data. It has to be out. It has been over 2 years since. The study is not still happening, so the data is being used SOMEWHERE. But where? My answer: AI. AI can mix and match. It can mesh and unite. It can take what was done separately and determine what happens if you combine. It can look at xenograft models and extrapolate into human beings. It can combine known drugs and their effects into what has only been partially studied. AI is taking as input the existing data plus the data that will be soon coming and will extrapolate it in combination with known outcomes of key drugs like Keytruda. We already know the synergistic effects of combining LL with Keytruda. That AI generated data set is currently in the making using AI and that data set will be unequivocal.
The R & D Update yet has time to be fulfilled. Seems like this coming fall, September, October and November shall be very interesting and exciting for CytoDyn shareholders. The timer counts down now. We all have placed our bets. The prime peak period is being broached right about now. Things are right about to start and they will happen imminently. There will be no degradation of the R & D Update. It will happen. Buckle Up.

Hi all, the next month of AE results are coming out tomorrow, so I've been reading Novavax's briefing document to the FDA for their meeting as I'm waiting (thanks to u/SandhillCrane5 for the link). Here are some of my notes that I thought worthy of attention. NVX = Novavax, PBO = Placebo, pre = pre-crossover, post = post-crossover, part's = participants.
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In the Phase 3 study with 30k people and crossover (301: US/MEX), the median follow up post-dose 4 was 4.4 months, 99% of people were followed for at least 2 months after dose 4. At FDA's request, median post crossover follow up duration was 8.4 months after 2-dose crossover series.
This US/MEX Phase 3 (301) was manufactured by Par Sterile Products, international studies 302 (UK Phase 3), 501 (South Africa Phase 2), and 101 (Phase 1/2 AUS) were manufactured by Emergent BioSolutions. Due to the difference in manufacturing processes, these studies cannot be used to review.
Obesity is defined as having a BMI of >= 30 (keep in mind as a co-morbidity).
2 NVX vs 1 PBO events of thrombocytopenia. Of that, 1 of the NVX thrombo's was hospitalized for fracture surgery, looks like everything was normal 45 mins after abnormal platelet count found? 1 NVX on losartan, losartan discontinued so was probably caused by that (investigator thinks NVX, FDA thinks losartan plausible).
3 vs 3 peripheral neuropathy (numbness/weakness in nerves, including paresthesia). 2 NVX thought related, 1 of which had no details
2 vs 2 uveitis. 1 NVX probably pre-existing and from herpes
NVX's explanation of why myocarditis cases happen in mRNA or NVX: the spike protein antigen can induce antibodies to covid spike glycoproteins that cross-react with myocardial contractile proteins […] It has been postulated that the effect of these antibodies, influenced by hormonal differences, immune-genetic background, age, and sex are potential mechanisms of myocardial injury associated with covid infection or vaccination. 6 vs 1 myocarditis:

Trial	Age/Sex	Preferred Term	Dose/Days	Comments	Outcome	FDA Opinion
US/MEX	16/M	Myo	Dose 2, 2 days	Preceding viral illness + ADD meds use	Resolved, 4 days in hospital	Temporally related, lack of other possibility
UK	19/M	Myo	Dose 2, 2 days		Resolved after 1 month, hospitalized 5 days	Temporally related, lack of other possibility, event of special interest
US/MEX	28/M	Atypical chest pain	Booster, 3 days		Resolved, hospitalized 2 days	Temporally related, lack of other possibility
UK	60/F	Peri	Dose 2, 8 days		Resolved, hospitalized 2 days	Temporally related, lack of other possibility
US/MEX	20/M	Peri + myo	Dose 1, 10 days	Had strep throat 8 days prior	Non-serious, not hospitalized	Strep and ARF possible cause
US/MEX	67/M	Myo	Dose 1, 28 days	Concomitant covid + kidney injury	Resolved with sequelae, hospitalized 5 days	Longer temporal relation but can't exclude
US/MEX	31/F	Myo	Placebo, Dose 2, 72 days		Resolved, hospitalized 2 days	Temporally distant, unrelated

Cardiac events were similar in proportion. Total was 76 vs 34, half of each being serious. On a general level, the events were comparable, but were sometimes worse in NVX when looking at specifics.

• 6 vs 4 fatal cardiac events (cardiac arrest + myocardial infarction).
• 3 vs 2 fatal events considered related by investigator (arrhythmia + tachycardia + sinus bradycardia for NVX, myocarditis + myocardial infarction for PBO).
• Cases of ischemic heart disease were 16 vs 8.
• Cases of cardiomyopathy or cardiac failure was 9 vs 2, but none were considered related and all of the NVX except 1 had history of cardiac disease, obesity, or other (the 1 exception had a non-serious event of stress cardiomyopathy).
• Cases of cardiac failure was 8 vs 2, but none were considered related, all had co-morbidities (including obesity), and 6 had a history of congestive heart failure.
• Cases of arrhythmia were the same, though slightly higher for atrial fibrillation in NVX.
• Although it is possible that some cardiac events, including fatal events, were severe manifestations of undiagnosed myocarditis, there is comparability across treatment arms in aggregate analyses of the type, severity, and temporality of cardiac events. Additionally, attribution of causality in many of the cardiac events is confounded by the presence of pre-existing conditions and risk factors.

Hypertension (high blood pressure) was proportional in pre at 0.6%. 5 vs 1 serious, 9 (all non-serious) vs 3 considered related. The majority with new onset hypertension were older and/or had obesity
Biliary events (gallbladder) in pre was 0.08% vs 0.04%. Cholecystitis was 10 vs 1. None were considered related, all were serious except 1 NVX, most were female, obese, and/or had history of cholelithiasis. Through 2/17/22 (pre and post), 38 NVX had reports consistent with cholelithiasis and cholecystitis, 24 were cholecystitis. "there is no clear biologically plausible mechanism to support a causal association." Some clustering of events in part's with risk for gallstones.
Neurovascular events were comparable in pre. Strokes were 11 vs 2. For NVX: 7 CVA, 1 ischemic stroke, 1 cerebral infarction, 2 transient ischemic attack, in individuals aged 49-74, 1 event from someone who withdrew from study, 1 was fatal. 2 had potential alternative etiologies (1 with atrial fibrillation and CTA, 1 had stroke-like symptoms but discharged as a "pinched nerve"), all except 1 had co-morbidities that increased risk (hypertension, obesity). For PBO, included 1 cerebellar infarction and transient ischemic attack in part's aged 61 and 58. In post, higher in crossover to PBO (3 TIA, 1 IS, 1 CVA, in 35-79, most with co-morbidities of elderly, obesity, etc.). Additional data by 2/17/22 showed 19 total in pre/post, 2 fatal. confounded by the presence of risk factors in the individual participants, the observation of events in close temporal relationship to vaccination in both treatment arms, and no clear pattern in the time to onset of events to suggest a specific pathophysiologic mechanism for a causal relationship to NVXCoV2373. It is notable that several neurovascular events were associated with arterial wall defects.
1 female UK NVX age 65 with Guillain Barre Syndrome, considered related.
Embolic and thrombotic events were comparable (embolisms and thrombo stuff). 11 vs 6 pre. 9 vs 4 post. Through 2/17/22, 83 part's who had NVX either pre or post had an event, but this is including other things like the strokes and cardiac stuff mentioned above. Attribution of causality is confounded by the presence of the pre-existing conditions and risk factors.
Deaths were 11 vs 5 in pre, none considered related except 1 PBO. For NVX included 5 cardiac arrest (4 with co-morbidities and histories of substance use, no medical history for fifth), myocardial infarction (79 year old female with many co-morbidities, considered unrelated), toxicity to agent (drugs), accidental overdose, CVA (75 year old female with history of hypertension and concomitant pneumonia), gunshot wound, and septic shock (strep). For PBO included 3 cardiac arrest, myocardial infarction, and covid. For post, it was 6 vs 10. NVX: 2 motor vehicle accidents, toxicity to fentanyl, septic shock from esophageal cancer, aneurysm rupture (35 year old female, multiple co-morbidities, post Dose 2, considered by FDA as unrelated), and fatal cardiac arrest (47 year old male with obesity and concomitant use of quetiapine and Adderall, post Dose 2). For PBO: suicide, respiratory failure, pulmonary disease, toxicity to agents, alcoholic liver cirrhosis, alcoholic cardiomyopathy, ischemic stroke, myocardial infarction, and 2 unknown deaths. In follow up, 4 vs 13 deaths, none considered related.
5 vs 3 serious AE's considered related in pre. For NVX: headache, angioedema, Basedow's disease, thrombocytopenia, and nervous system disorder (neuropathy). For PBO: myocarditis, pneumonia/septic shock/kidney injury, myocardial infection. Almost all had co-morbidities. For post, it was 2 vs 3. NVX: pulmonary embolism (39 year old female with co-morbidities, risk factors, and concomitant estradiol use), chronic cholecystitis (25 year old male with pathologic changes suggestive of a chronic condition). PBO: lymphoma, CVA, pancreatitis.
NVX submitted their 3rd monthly safety monitoring report covering cumulative results for April 2022. 744,235 doses administered cumulatively, with 923 cumulative safety reports representing 3,859 AE's (86% non-serious), NO DEATHS reported. 37 reports of myo/peri (2 reports were duplicates, 29 peri/4 myo/2 myoperi/1 carditis, only 14 medically confirmed, majority from Australia), 6 of the reports were recurrent peri (for 5 of which the previous episode of peri was after an mRNA covid vaccination). A query of VigiBase showed 1,677 reports: 90% were from AUS (43.3%), Germany (42.3%), and Italy (7.3%), with 84.1% non-serious, 46 reports related to myo/peri (37 peri, 6 myo, 4 myoperi, 1 carditis, 89.1% of these reports being from AUS).
The analyses have a limited length of follow up, therefore, it is not currently possible to assess sustained efficacy over a period longer than 2 months.
Relevant data [vs] Omicron [& sons] […] are currently unavailable; however, based on the efficacy estimate in the clinical trial of this vaccine, it is more likely than not that the vaccine will provide some meaningful level of protection against COVID-19 due to Omicron, in particular against more severe disease.
Observational data with other COVID-19 vaccines have demonstrated an added benefit of vaccination to protection conferred by natural immunity (Plumb et al, 2022). Additionally, for individuals previously infected with the Omicron variant of SARS-CoV-2, a vaccine based on the ancestral strain S protein could provide a greater breadth of protection against SARS-CoV-2 variants.

If you are considering requesting a “religious” exemption to the COVID-19 vaccination there are a number of things you should know about and consider beforehand.
NORMAL VACCINE DEVELOPMENT TIMELINE 1. Development timeline – the normal vaccine undergoes multiple stages of development a. Phase 1 – Clinical trials to assess safety, dosing and immune response – can be anything from 2 months (required minimum) to a few years b. Phase 2 – Clinical trials to assess safety and immune response – can be anything from 3 months (required minimum) to a few years c. Phase 3 – Clinical trials to assess safety and efficacy – can be anything from 6 months (required minimum) to a few years d. Regulatory Approval Process – US FDA may (when there is good scientific reason to believe a vaccine is safe & likely to prevent disease) authorize use through an Emergency Use Authorization (EAU) even if definitive proof of the efficacy of the vaccine is not yet know…especially in diseases with high mortality rates. e. Scaling up Vaccine manufacturing – the FDA inspects manufacturing facilities as part of the late phase of the regulatory process f. Post-licensure vaccine safety monitoring – required and tracked to monitor development of rare side effects only detectable after large groups of people have been vaccinated…safety concerns at this stage can result in withdrawal from use but is very rarely required.
COVID-19 VACCINE DEVELOPMENT TIMELINE 1. Research on Coronavirus vaccines have been underway for decades so the work to develop a vaccine for COVID-19 didn’t begin from the same place as a viral disease we’d never experienced before 2. The mRNA vaccine development process was explored during the SARS and MERS viral outbreaks and so wasn’t actually a “new” technology and HAS been used to develop medications for humans 3. The typical timeline for a vaccine development (see paragraph above) is approximately 7 years but that is when each phase in the process uses the full period and they only occur consecutively instead of concurrently like the COVID-19 vaccine 4. All FDA required testing was conducted on the COVID-19 vaccine – 74,000 people received one or two of the vaccines and the people tested covered the full range of ages, genders, ethnicities and races. There were no reports of serious side effects. 5. The FDA and two Independent Advisory Committees reviewed the vaccine data and clinical trial results before the EUA was authorized.
REPORTED ADVERSE EVENTS FROM COVID-19 VACCINATION 1. Anaphylaxis – Under 5 people per million vaccinated 2. Thrombosis – under 3 people per million vaccinated 3. Guillain-Barre Syndrome – under 14 people per million vaccinated (most recover fully) 4. Myocarditis and pericarditis – under 60 people per million vaccinated (investigation underway to determine relationship to the COVID-19 vaccine) 5. DEATH – FDA requires that if someone dies FOR ANY REASON after being vaccinated then that must be reported. Determining the impact of the vaccination on the death of the person requires in depth review of the clinical information, death certificate, autopsies and medical records. So while under 530 people per million have been reported as having died after the COVID-19 vaccine, the causal relationship has not been determined.
USE OF HUMAN EMBRYONIC KIDNEY 293 CELLS

1. Origin – the actual origin of the fetal kidney cells used to generate the HEK 293 line of cells is NOT documented. Many people state they are from an aborted fetus; however, this cannot be proven nor disproven. They could just as easily have been from the body of a fetus that didn’t survive and was donated “to science”. https://en.wikipedia.org/wiki/HEK_293_cells (and yea, it’s Wikipedia but it lists all of the sources for the article)
2. The HEK 293 line of cells was NOT used to create or manufacture the vaccine and there are absolutely no cells IN the vaccine. https://www.health.nd.gov/sites/www/files/documents/COVID%20Vaccine%20Page/COVID-19_Vaccine_Fetal_Cell_Handout.pdf
3. The HEK 293 cell line was used in early development of the mRNA vaccine technology (NOT the vaccine itself) to test the ability of the new technology to react with the SARS-CoV-2 spike protein which indicated if the new technology would be effective in combatting the virus

4.  Finally, if you don’t want to use any medication which was tested using the HEK 293 line……you need to quit taking pretty much 90% of all medications currently available. At the bottom of this is a list which is just a VERY SMALL portion of the complete list of medications which were tested using the HEK 293 cell line but the items of most interest might be: a. The medical alternatives to the Covid Vaccine (Hydroxychloroquine and Remdesivir) were both tested using the HEK 293 line, just like the vaccine was SO…..if you refuse the vaccine and get sick then you probably won’t be taking the other meds to treat it either I guess? b. If you have EVER taken a med for a headache or body ache…..it was tested using HEK 293, just like the vaccine c. If you have EVER taken an OTC or prescription med for upset stomach or gas….it was tested using HEK 293, just like the vaccine d. If you have EVER taken a cold/cough/flu medicine….it was tested using HEK 293, just like the vaccine e. If you are diabetic, hypertensive, asthmatic, suffer allergies or have high cholesterol….your medicines were mostly all tested using HEK 

OTC medicines testing on HEK 293 or derivitate lines
Tylenol/Acetaminophen
Advil/ Motrin/ Ibuprofen
Aleve/ Naproxen
Pseudoephedrine/ Sudafed/ SudoGest, Suphedrine
Diphenhydramine/ Benadryl
Loratadine/ Claritin
Dextromethorphan/ Delsym/ Robafen Cough/ Robitussin
Guaifenesin/ Mucinex
Tuns/ Calcium Carbonate
Maalox/ Aluminum Hydroxide/ Magnesium Hydroxide
Docusate/ Colace/ Ex-Las Stool Softener
Senna Glycoside/ Sennoside/ Senna/ Ex-Lax/ Senokot
Pepto-Bismol/ Bismuth Subsalicylate
Phenylephrine/ Preparation H/ Vazculep/ Suphedrine PE
Mepyramine/ Pyrilamine
Lidocaine/ Lidode Recticare
Prescription drugs tested on HEK 293 or derivitate lines
Levothyroxine/ Synthroid/ Tirosint/ Levoxyl Atorvastatin/ Lipitor
Amlodipine/ Norvasc
Metropolol/ Toprol XL/ Lopressor
Omeprazole/ Prilosec OTC/ Zegerid OTC/ OmePPi Losartan/ Cozaar
Albuterol/ Salbutamol/ ProAi Ventolin
Sacubitril/ Valsartan/ Entresto
Tenapano Ibsrela
Enbrel/ Etanercept
Azithromycin/ Zithromax
Hydroxychloroquine/ Plaquenil
Remdesivi Veklury
Dapagliflozin/ Farxiga/ Ipragliflozin/ Suglat/
Enavogliflozin/ Jardiance
Ivermectin/ Stromectol
Canagliflozin/ Invokana/ Sulisent/ Prominad
Metformin/ Glucophage/ Riomet/ Glumetza
Cerivastatin/ Baycol/ Lipobay/ Fluvastatin/ Lescol/
Pitavastatin/ Livalo/ Pravastatin/ Pravachol/
Rosuvastatin/ Crestor
Simvastatin/ FloLipid/ Zocor
Oxbryta/ Voxelotor
Lisinopril/ Qbrelis/ Zestril/ Prinivil

32 Male 6'2" 225 lbs Caucasian Eastern US Currently on a tumor reduction chemotherapy of Avastin(Bevacizumab) for vestibular schwannomas that I have had for around a decade with no major symptoms, apparently it is not immuno-compromising whatsoever according to the Oncologist. Currently on Losartan as the chemo has raised my blood pressure a bit.
I work in a hospital in the US, not directly with patients, but I often am in and out of the ICU and ER, etc. I was vaccinated back in January with the Pfizer variety.
I am going on vacation to the Caribbean October 2, that will put me at about 9 months after my second dose. Everywhere I have read that I should be vaccinated before traveling and even moreso internationally. Therein lies my dilemma, if everywhere says I should be vaccinated but many doctors agree that the vaccine loses efficacy after6 or 7 months, then won't it just be as though I am traveling unvaccinated at the 9 month mark? Kinda worried.

The spike protein binds to human ACE2 receptors and also causes cellular damage. This has an effect on what’s known as the renin-angiotensin system. This system plays a role in many important biological functions. I think they are hiding the long term effects of COVID as well as the long term effects of the vaccine.
I’m going to make an educated guess based on all the data cited below about delayed symptoms of COVID as well as the vaccine which we could see in the future.

Possible delayed effects of COVID infection as well as vaccination

Blindness
Diabetes
Erectile dysfunction
Mental health disorders caused directly by the spike protein
Menstrual irregularities
Malformed and damaged ovum
Lack of strength, lack of body building muscle in response to exercise
Premature aging
Kidney fibrosis
Issues with T-cell differentiation (AIDS symptoms)
Central nervous system disorders caused by inflammation
This is not the whole list, just a start!
Below are the titles and links to scientific articles which back up my assumptions. They are all credible sources of information.

Proof the mRNA travels through your whole body

No company has publicly published their biodistribution studies, however we have the below.
This is the EMA (European Medical Association) review of the company data they had access to for "Comirnaty" (Covid-19 mRNA vaccine) which included animal biodistribution studies
https://www.ema.europa.eu/en/documents/assessment-report/comirnaty-epar-public-assessment-report_en.pdf
(The biodistribution was also studied in rats using radiolabeled LNP and luciferase modRNA (study 185350). The radiolabeling data, measuring distribution to blood, plasma and selected tissues, of IM injection of a single dose of 50 μg mRNA over a 48-hour period is considered more sensitive than the bioluminescence method and indicate a broader biodistribution pattern than was observed with bioluminescence. Over 48 hours, distribution from the injection site to most tissues occurred, with the majority of tissues exhibiting low levels of radioactivity.)
So, basically, they made the mRNA radioactive so they could detect it and checked where they could find it 48 hours after vaccinating rats. They gave the rats an intramuscular injection which is the same type of injection they are giving people now. It ended up in almost all of their tissues.
This proves that, contrary to popular belief and what the media is spouting, the mRNA does not stay in the muscle and travels throughout the whole body!
This also proves the mRNA will create spike proteins anywhere ACE2 receptors exist in the entire body, which is how it could potentially effect all the systems mentioned below.
The problem with this is that once a spike protein binds to an ACE2 expressing cell (angiotensin converting enzyme II receptor) it prevents the angiotensin circulating from being picked up by the receptor. There are trillions of mRNA fragments in a single dose of vaccine. This can cause a disruption to your renin-angiotensin system.

Proof the spike proteins the vaccine creates actually detach and free-float in your body after they are produced and thus cause some of the same issues as the actual virus itself

SARS-CoV-2 vaccines: Lights and shadows
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8084611/
(The resulting pathological features may resemble those of active coronavirus disease. The free-floating Spike proteins synthetized by cells targeted by vaccine and destroyed by the immune response circulate in the blood and systematically interact with angiotensin converting enzyme 2 (ACE2) receptors expressed by a variety of cells including platelets, thereby promoting ACE2 internalization and degradation.)
The above also states that when a vaccinated cell dies or is destroyed by the immune system, the debris may release a large amount of Spike proteins and protein fragments (free-floating Spike proteins). Which can then bind to ACE2 expressing cells.

Renin-angiotensin system and mental health

Estradiol modulation of the renin-angiotensin system and the regulation of fear extinction
https://pubmed.ncbi.nlm.nih.gov/30696810/
(Giving rats drugs that altered the renin-angiotensin system helped de-condition them from previously taught triggers, essentially the equivalent of helping them get over PTSD)
The renin-angiotensin system: a possible new target for depression
https://pubmed.ncbi.nlm.nih.gov/28760142/
(Drugs blocking the angiotensin system have efficacy in several animal models of depression.)
The effect of combined treatment with SSRIs and renin-angiotensin system (RAS) drugs: A propensity score matched cohort study
https://pubmed.ncbi.nlm.nih.gov/32001138/
(Drugs acting on the renin-angiotensin system (RAS) may have beneficial effects on mental health.)
Linking Meditation with Improved Mental Health
I included this article because it ties in the importance of the RAS system and mental wellbeing.
https://www.womenmeanbusiness.com/2020/02/linking-meditation-with-improved-mental-health/
(Although the scope of research is currently limited, it seems that meditation may also influence the RAA system, corresponding with improved well-being and changes in hormonal stress.”)
High blood pressure drugs impact depression, bipolar disorder
https://www.medicalnewstoday.com/articles/313380
(In contrast, patients prescribed angiotensin antagonists had the lowest risk for hospitalization with mood disorders, compared with patients taking other blood pressure drugs)
Exploring the Evidence Implicating the Renin-Angiotensin System (RAS) in the Physiopathology of Mood Disorders
https://www.eurekaselect.com/177717/article
(“Low levels of RAS components (renin activity or aldosterone) and mood symptoms improvement with ACE inhibitors or AT1 blockers were also observed in mood disorders. Overall, this review reiterates the strong and under-researched connection between RAS and mood disorders.”)
Associations of trauma exposure and post-traumatic stress disorder with the activity of the renin–angiotensin–aldosterone-system in the general population
https://www.cambridge.org/core/journals/psychological-medicine/article/abs/associations-of-trauma-exposure-and-posttraumatic-stress-disorder-with-the-activity-of-the-reninangiotensinaldosteronesystem-in-the-general-population/68719C08146981C29782F25440857591
(Finding elevated renin levels in PTSD independent from trauma load supports the concept of PTSD as a disorder with specific neuroendocrine characteristics.)
Association between anxiety and hypertension: a systematic review and meta-analysis of epidemiological studies
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4411016/
(Second, anxiety has a close relationship with the renin angiotensin system and increases the level of angiotensin II)

Renin-angiotensin system and strength and endurance

System That Regulates Blood Pressure May Also Affect Aging
https://www.sciencedaily.com/releases/2004/11/041122095829.htm
(At the end of the program, however, participants with the combination associated with highest ACE production showed a 75 percent improvement in knee strength – compared to a 23 percent improvement in participants who had the combination associated with lowest ACE production)

Renin-angiotensin system and diabetes

An Interview with Björn Folkow, M.D., Ph.D.
https://www.stress.org/stress-hypertension-and-the-metabolic-syndrome
(These and other drugs like ACE inhibitors that inhibit the renin-angiotensin system have also been shown to significantly reduce the incidence of Type 2 diabetes in patients with hypertension and congestive failure.)
Role of ACE inhibitors in patients with diabetes mellitus
https://pubmed.ncbi.nlm.nih.gov/11708761/
(Finally, there are a growing number of arguments favouring the use of ACE inhibitors very early in patients with diabetes mellitus.)

Renin-angiotensin system and male reproductive health

Diminazene protects corpus cavernosum against hypercholesterolemia-induced injury
https://pubmed.ncbi.nlm.nih.gov/25411084/
(ACE2 is expressed in erectile tissue and its reduction is associated with hypercholesterolemia-induced ED)

Renin-angiotensin system and female reproductive health

Research sheds light on the role of ACE2 in ovulation
https://www.bionews.org.uk/page_158735
(This research suggests the potential involvement of ACE2 as a critical enzyme for the LH surge-induced cyclic events of ovulation.)

Renin-angiotensin system and eyesight

The retinal renin-angiotensin system: roles of angiotensin II and aldosterone
https://pubmed.ncbi.nlm.nih.gov/22537944/
(The therapeutic utility of inhibiting key components of the renin-angiotensin system is complex, but may hold promise for the prevention and improvement of vision threatening diseases.)
The renin-angiotensin system and the retinal neurovascular unit: A role in vascular regulation and disease
https://pubmed.ncbi.nlm.nih.gov/31408629/
(The retina is known to have a local renin-angiotensin system (RAS) and dysfunction in the RAS is often associated with diseases of the retinal vasculature that cause irreversible vision loss.)

Renin-angiotensin system and immune system

Role of the renin-angiotensin system in autoimmune inflammation of the central nervous system
https://pubmed.ncbi.nlm.nih.gov/19706425/
(Treatment with the renin inhibitor aliskiren, the angiotensin II converting-enzyme inhibitor enalapril, as well as preventive or therapeutic application of the AT1R antagonist losartan, resulted in a significantly ameliorated course of MOG-EAE)
Role of renin-angiotensin system in inflammation, immunity and aging
https://pubmed.ncbi.nlm.nih.gov/22283774/
(Classic RAS blockers have been proposed as anti-inflammatory and immunomodulatory agents and some studies suggest a new potential application of RAS blockers in autoimmune diseases.)
Angiotensin II Regulates Th1 T Cell Differentiation Through Angiotensin II Type 1 Receptor-PKA-Mediated Activation of Proteasome
https://pubmed.ncbi.nlm.nih.gov/29462804/
(This study for the first time demonstrates that Ang II activates AT1R-PKA-proteasome pathway, which promotes degradation of IκBα and MKP-1 and activation of STAT1 and NF-κB thereby leading to Th1 differentiation. Thus, inhibition of proteasome activation might be a potential therapeutic target for Th1-mediated diseases.)
The above issue of a lack of T-cell differentiation is also a result of AIDS as seen in this next link.
T cell selection and differentiation in AIDS disease: the model of HIV-discordant monozygotic twins
https://pubmed.ncbi.nlm.nih.gov/18088551/
(In our HIV-discordant monozygotic twins, a significant reduction of naive T cells and a parallel accumulation of effectomemory T cells was induced by HIV infection)

Renin-angiotensin system and kidneys

The renin-angiotensin system: an old, newly discovered player in immunoregulation
https://pubmed.ncbi.nlm.nih.gov/19539879/
(Of special clinical interest is the ability of the RAS to activate the transforming growth factor beta(1) and the Smad pathways leading to fibrinogenesis)

24F, 125 lbs, white, c3 glomerulonephritis (dormant 9 years) , unspecified autoimmune disease, unexplained hypertension for 4 years. I have the vaccine and for the record, tested negative for COVID 3 times. Was taking 50mg Losartan when this started, stopped working so started taking 75 and then 100mg, still still not working and now am on 100-25mg Losartan-HCTZ which has my bp down to 140's. On Friday 8/13, I was eating dinner outside in a quiet backyard. Somehow beer ended up coming out through my nose, only drank less than half the beer total. When I came inside I had muffled hearing from my right ear, and it was kind of ringing and felt slightly off balance. Tried to remain calm that its just a normal ring that everyone gets, but the muffled hearing persisted and has lasted since. I wasn't overly stressed and didn't feel any weird symptoms so I don't think it was a sudden BP spike, the only weird thing that happened from when I went outside to when I came back in was the beer coming out my nose. I didn't feel anything with my ears at the moment, but obviously it did hurt my sinuses.
I tried to remain calm because I do suffer from chronic sinus congestion and my ears (the side that I sleep on) do get clogged sometimes, but a week later not only was it still muffled, but I had horrible ear pain and my throat felt like someone was taking a razor to it. My kinesiologist looked in my ear on Monday and said it was red. Went to urgent care Wednesday, they told me they saw fluid behind my ear and that it was red but didn't see an infection, but my blood pressure was so high they told me to go to the ER. My blood pressure spiked because 1. I had only slept 2 hours and 2. was studying for a final exam, but since then I haven't been able to get my blood pressure under control. I didn't go to ER because last time I went for my BP and i had lost feeling in all my limbs and face they told me there was nothing they could do and just to relax, lol. Went to an ENT the next day who barely looked in my ear (didn't look nearly as deep as the Urgent Care), told me he didn't see fluid, didn't want to give me steroids or have me take Sudafed because of the BP, and instead gave me a z-pack for its anti-inflammatory properties and told me to take regular Mucinex. The z-pack cleared up the throat pain and ear pain, but left the muffled ear.
I went on a plane and both my ears, but especially my right (bad) ear were horrible. When I went in elevators my right ear would refuse to pop for 30+ minutes (if I was lucky), sometimes it would take hours. I spent days opening and closing my mouth to try and get it to pop but barely had luck. When it does pop it feels good for a couple seconds (still only about 75%+ clear) and then immediately re-muffles. I also have a rocking sensation for about a week. I first noticed it while standing I felt like I was at an amusement park and the ground would suddenly shake, then I noticed it on the toilet it felt like I was going around in a circle. Its not that the room is spinning, its that I'm rotating. I have doubled my Losartan dose from 50mg-100mg which is when I noticed this dizziness starting, but my blood pressure is still on the higher end.
Last but not least, what I mean by chronic congestion is that one side of my nose - usually my left is ALWAYS clogged. Once it a while it would switch to my right, but always on my left. I couldn't blow any mucus out of it, it was just as if it was swollen. And as I briefly mentioned - whatever side I slept on I'd wake up with that ear clogged. Since this started, my right side of my nose is clogged majority of the time, but again no mucus comes out. I've tried the Navage, Flonase daily, and when I don't feel symptomatic from BP I've even tried the steroid nose spray but while it helps the nose congestion for a bit, it does nothing for the ears.
​
With all of this said, is it likely my muffled hearing is from persistent congestion/allergies of some sort/ What can I do to fix this once and for all? Is it possible I had an ear infection/strep throat that the z-pack knocked out but I still have damage/inflammation? (I did have about 1 drink or less on the days that I was taking a z-pack, I don't know if that reduced the efficacy, completely forgot you're not supposed to drink on antibiotics). Is it possible that I had a blood pressure spike and it caused me to lose hearing? Is it possible the Losartan could have caused something? Thanks.

We all got high blood pressure genes. Dad’s BP is controlled with losartan but Mom’s was still uncontrolled despite being on 2 medicines. I was recently diagnosed with hypertension as my BP was averaging 150/ 90 . Before starting the medicine, I wanted to try supplement to bring it down.I started with Kayolic aged garlic which brought down my BP to 120/85 while my mom’s uncontrolled BP was brought down to 115/75 . There are various double blind randomized tests vouching for its efficacy.

Male59 1,70 (5"5') 75kg (165lb) aprox. european ascendency renal insufficience transplanted, taking immunosuppresants never smoked Mycophelonate sodium, tamsulosin, aspirin, Tacrolimus, Losartan.
​
Asking for my father. He was a healthy man (never smoked, excersiced daily, little to no alcohol, normal diet) and was diagnosed with renal insufficence in 2009. He was on hemodyalisis and then peritonneal dyalisis until he received a kidney in late 2015. The transplant was exceptionally succesful, and he didn't even catch a cold ever since. He's very diligent in taking his medication and following his doctors instructions. He's under immunosuppressants.
​
Today, he received a call from the clinic/doctors who treat him, who made the trasplant, saying he will be getting the Covid-19 vaccine tomorrow. I don't know which one, my mother didn't ask and she couldn't tell me, but the ones in my country are Sputnik-V, Sinopharm, and Covishield.
​
I went to the official information source and it says that immunocompromised patients shouldn't be getting the vaccine. Yet, their doctors said he should. I find it odd the clinic and the Ministry don't align here.
​
Official source (google translate):

Q. Will people with some degree of immunocompromise be vaccinated?
A. As of the date of this document, there are no efficacy and safety studies related to the administration of the vaccine in this population, so the vaccine should not be indicated or applied to people with primary or secondary immunodeficiencies, with any level of immunosuppression.

https://www.argentina.gob.acoronavirus/vacuna/preguntas-frecuentes
Updated 4/13/21. consulted 4/14/21.
​
I know that "not indicated" don't necesarily mean "not safe", just that there's not enough information. And there is not enough studies in my country (I'm writing from Argentina, by the way). So I would like to ask what do we know about the effects of the vaccine in solid organ transplant patients in other countries? Are there any studies? Statistics? Case studies? Be honest, what are some contraindications or complications we shall encounter?
Sorry if I seem anxious, I'm not against the vaccine itself, I just want to know more about the effects in this specific population (transplant patients).

Cancer‐associated fibroblasts‐responsive honeycomb‐like nanoassemblies of carbon dots are fabricated to program the sequential and spatiotemporal release of multiple therapeutic agents for synergetic chemoimmunotherapy of cancer.

Abstract

Tumor fibrotic stroma forms complex barriers for therapeutic nanomedicine. Although nanoparticle vehicles are promising in overcoming biological barriers for drug delivery, fibrosis causes hypoxia, immunosuppression and limited immunocytes infiltration, and thus reduces antitumor efficacy of nanosystems. Herein, we report the development of cancer‐associated fibroblasts (CAFs) responsive honeycomb‐like nanoassemblies of carbon dots (CDs) to spatially program the delivery of multiple therapeutics for enhanced antitumor chemoimmunotherapy. Doxorubicin (DOX) and immunotherapeutic enhancer (Fe ions) are immobilized on the surface of CDs, whereas tumor microenvironment modifier (losartan, LOS) is encapsulated within the mesopores. The drugs‐loaded nanoassemblies disassociate into individual CDs to release LOS to mitigate stroma and hypoxia in response to CAFs. The individual CDs carrying DOX and Fe ion efficiently penetrate deep into tumor to trigger intensified immune responses. Our in vitro and in vivo studies show that the nanoassemblies exhibit effective T cells infiltration, tumor growth inhibition and lung metastasis prevention, thereby providing a therapeutic platform for desmoplasia solid tumor.
https://ift.tt/37aeEPd

Tumor fibrotic stroma forms complex barriers for therapeutic nanomedicine. Although nanoparticle vehicles are promising in overcoming biological barriers for drug delivery, fibrosis causes hypoxia, immunosuppression and limited immunocytes infiltration, and thus reduces antitumor efficacy of nanosystems. Herein, we report the development of cancer‐associated fibroblasts (CAFs) responsive honeycomb‐like nanoassemblies of carbon dots (CDs) to spatially program the delivery of multiple therapeutics for enhanced antitumor chemoimmunotherapy. Doxorubicin (DOX) and immunotherapeutic enhancer (Fe ions) are immobilized on the surface of CDs, whereas tumor microenvironment modifier (losartan, LOS) is encapsulated within the mesopores. The drugs‐loaded nanoassemblies disassociate into individual CDs to release LOS to mitigate stroma and hypoxia in response to CAFs. The individual CDs carrying DOX and Fe ion efficiently penetrate deep into tumor to trigger intensified immune responses. Our in vitro and in vivo studies show that the nanoassemblies exhibit effective T cells infiltration, tumor growth inhibition and lung metastasis prevention, thereby providing a therapeutic platform for desmoplasia solid tumor.
https://ift.tt/37aeEPd

We manufactures Fimasartan Trihydrate Potassium. It is a pyrimidine-4(3H)-one derivative of losartan. It is provides a higher potency and stronger efficacy. Call us +91-11-4706 3600. Fimasartan Trihydrate Potassium

I) In Health News, an article by Shawn Radcliffe on March 1, 2019, talked about “Blood Pressure Medication Recall and What You Need to Know”. Numerous blood pressure drugs are now involved in the recall that began in late July over a suspected cancer-causing compound.
The article focused on Losartan tablets because the company has detected in the products trace amounts of N-Nitroso N-Methyl 4-amino butyric acid (NMBA), which has been classified as a potential cancer-causing substance
According to Wikipedia, Losartan (Cozaar) belongs to a group of drugs called angiotensin II receptor antagonists. It keeps blood vessels from narrowing, which lowers blood pressure and improves blood flow. Losartan is used to treat high blood pressure(hypertension).
A study by Boonbaichaiyapruck et. al. in Thailand in 2015 looked at the efficacy of Losartan. With 24 patients recruited for the study, and after 6 to 12 weeks on the study, their systolic blood pressure has been reduced, on average, by almost 30 mmHg (27 and 28 respectively). The average BP (Blood Pressure) dropped from 161/93 to 133/83 at the end of week 6 of the study and was maintained at 120/80mmHg at week 12. WOW!
We wanted to verify their results regarding the efficacy of Losartan so we recruited our own hypothetical patients. The SBP data are as follows.
Use the Sign Test to test the claim at 95% confidence that Losartan is indeed effective in reducing the systolic blood pressure of identified patients who present with high blood pressure.

1. State the Null and Alternative Hypotheses (1)
2. Determine the Critical Value and if appropriate, construct the Probability Density Function (PDF) and state the Decision Rule. (2)
3. Perform the test; state the test value.(1,1)
4. What is the Decision? (1)

Hey all,
I was diagnosed a week and a half ago and am in the middle of learning how to effectively advocate for myself with EDS and dysautonomia, as I'm in the middle of relative nowhere and need to be ready to present what's going on with some manner of accuracy or I'm not going to be taken seriously. I'm looking at medications first, then I plan on addressing physical therapy.
So, my understanding of EDS so far is a genetic abnormality that causes collagen production to not happen right. There are a few different parts that it's messed up - coming from the nucleus of the cell (this is DNA and cannot be addressed), and in a finalization step before it leaves the fibroblast.
This finalization step is what we can medicate. To my understanding, there are a few medications that can address this.
 
Profibrosing effect of angiotensin converting enzyme inhibitors in human lung fibroblasts TL;DR the conclusion is "Results show that ACEis and losartan could play a profibrosing role by inducing the overexpression of molecules such TGF-β1 and Collagen."
Then there's research showing Losartan inhibits collagen synthesis/has antifibrotic activity, Losartan inhibits collagen I synthesis and improves the distribution and efficacy of nanotherapeutics in tumors.
So, I'm not sure if Losartan hurts or helps re: joints. I've not gone through the research papers, yet. I've heard that it can help re: dysautonomia, which I'm dealing with, too. Edit 3/11/2019, I've decided not to take Losartan.
 
Next, estrogen, progesterone, androgen, and testosterone. I've been told to get on testosterone supplementation and that male sex hormones cause the production of more functional collagen in people with EDS. I don't know what I'm looking at, here. The doctor that diagnosed me said, as an example, that he had seen significant improvement in EDS-related symptoms in individuals transitioning from female to male. I have decided not to take DHEA at this point.
 
I've been told to look at beta blockers for dysautonomia. I don't know what else to consider for it. I'm supplementing salt, L-methylfolate, vitamin D, omega 3 fish oil, and am looking at a vitamin C supplement as well.
I'm considering NSAIDs, but don't like the interaction with Losartan/other ACEs.
I'm considering turmeric, but am not 100% sold on it.
 
Lastly, I have a question on Wellbutrin. I know that fibroblast collagen quality significantly degrades when the nicotinic acetylcholine receptors are activated by nicotine, which is a nicotinic agonist. I also know that Wellbutrin is a nicotinic antagonist.
As an aside, Wellbutrin's been the only antidepressant to have any effect on me, SSRIs send me into serotonin syndrome or set me up for really weird episodes I can only describe as dissociative. Trintellix knocked my vision around, tricyclics were overly sedating, etc.
Also, on that vein, I've had moderate success with Xanax taken at bedtime, no success with Buspar during the day (paradoxical effect, actually). Antipsychotics were incredibly sedating and flattening with little to no therapeutic benefit.
Vyvanse helped with a significant issue with 'depression' that was likely complete exhaustion due to being in senior year of collage. I still didn't have the energy to leave my apartment, but I managed to barely scrape by my classes by missing most of them so that my body wasn't completely exhausted - I don't recommend it.
You can PM me with questions as to my medication regiment and my experiences after this thread is archived, this is a permanent/long-term Reddit account. If you have new or revelatory information I am happy to edit this thread so that it's a good resource for future Googlers!
 
3/11/2019: Saw my primary care today. He looked up EDS on the Mayo Clinic website. Turns out they've not updated that site to be current in awhile. He was kind of blown away and is wanting to send me to Mayo Clinic and to a geneticist. Thankfully I brought my mom - who has EDS and a lot of paperwork to back it up - in or I think my PC may not have talked with me about it.
I have NOT started Losartan nor have I started DHEA. I do not trust the doctor that put me on a blood pressure medication after I nearly passed out in his office to medicate me, particularly after not seeing anyone else on this after searching this subreddit and a few other places. I do not believe Losartan will help me with dysautonomia, either. I DO believe the L-methylfolate is a good idea. This may be interesting to skim, page 27 particularly, for other people considering supplementing testosterone and so may this thread though this thread suggests that supplementing testosterone may be detrimental, but it's anecdotal. Stuff that has a more authoritative voice like this is exploratory, this flies over my head in its mention of EDS (Ctrl+F Ehlers), "...Besides these observations, patients with Ehlers-Danlos syndrome (an inherited connective tissue disorder), treated with 1 mg of IGF-1 injected in the patellar tendon, showed an increase in the protein synthesis rate in comparison with the controlateral tendon used as control35.".
As such, I'm going to hold off on things for a bit until I get more advice.

It seems that people with allergies can have T regulatory cells that produce IL-13, which doesn't happen in normal people. This may be genetic due to TGF beta subunit mutations. Losartan interferes with TGF beta signalling.
https://www.hopkinsmedicine.org/news/media/releases/johns_hopkins_researchers_reveal_genetic_glitch_at_the_root_of_allergies
The paper this press release was talking about:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3905327/
"Losartan is a U.S. Food and Drug Administration–approved drug, which has known efficacy in reducing excessive TGFβ signaling in several disorders (33, 34). Studies in mice with Marfan syndrome, an aortic aneurysm syndrome closely related mechanistically and phenotypically to LDS, have revealed a remarkable ability of this drug to prevent the major cardiovascular complications associated with this disease (35). Whether losartan can modify allergic disease remains to be tested, but our finding that losartan mitigates TGFβ signaling alterations in lymphocytes of LDS patients suggests that this or related treatment approaches may hold promise."