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A human body consists of two kidneys that are shaped like beans; however, a kidney transplant is done when the person both kidneys are damaged due to end-stage disease. One of the kidneys is replaced with a healthy kidney so that the patient can live a better quality of life with the new kidney. Kidney transplants can be done with the deceased donor or from the living donor. Kidney transplants depend on factors like blood type and it should be a perfect match, hence most of the time kidney donor comes from the patient's family as if become a good match for the patient. A person can live a better and normal life with one kidney with certain restrictions which are minimal in day-to-day life be it a donor who donates the kidney or the patient whose kidney is replaced with a healthy kidney. A kidney donor should range between 18 to 60 years of age with no long-term health issues or any disease like cancer, diabetes, etc. A donor should be healthy to donate the kidney to the needy. The donor and the patient both recover within 6 to 8 weeks after the surgery and can resume light work.
Kidney Transplant Cost in India
The cost of kidney transplantation surgery depends on the type of transplant, whether it is done with the deceased donor or living donor. Package includes of the medication used, hospital room for the patient and the donor (in case of living donor), different types of blood tests before and after the surgery, tissue type, cross-matching the kidney, post-surgery follow-ups, and extended stay in the hospital if required. The average cost is between 577000 to 769000 INR approximately.
Kidney transplant Hospitals in India
India has the best hospitals for kidney transplants with all the modern techniques and medication that make the surgery successful. It has all the multi-special facilities for the patients to recover at the best possible time with qualified and friendly staff to take care of the patient to feel better after the treatment so that the patient doesn’t feel depressed.
Kidney Transplant surgeons in India
There are well-known and expert surgeons who hold many years of experience in kidney transplantation. They are trained especially in kidney transplantation surgery. There is a team of expert doctors who perform the surgery. Hence it makes India known for its treatments
Al AfiyaMedi Tour is a leading medical tourism company in India. We offer medical tourism services such as finding the right doctor, the right hospital, and cost estimation etc. Some of the main countries are Bangladesh, South Africa, Egypt, Uganda, Zambia, Sudan, Dubai, Namibia, Iraq, Kenya, Saudi Arabia, Ethiopia, Nigeria, and so on. We provide free medical assistance for TURP surgery cost, lung cancer treatment, bone marrow transplant cost, best liver transplant hospital, cosmetic andplastic surgery, heart surgery, liver transplant cost, top knee replacement surgeons, top shoulder replacement surgeons, hip replacement surgery, leukemia treatment cost, best bone marrow hospital, etc.
Source: https://alafiyameditour1.blogspot.com/2024/04/kidney-transplant-in-india-for.html

Hello all, If I'm posting in the wrong sub, please forgive me, I'm not sure where else to go.
tl;dr - Brother was diagnosed with a stage 3 glioblastoma brain tumor in 2016. They removed a cancerous tumor the size of a golfball and while he is alive his life has been completely ruined and it is now beginning to destroy my parent's life. We are running out of options for care and something doesn't happen so he will end up on the street or dead.
The above sums it up. My family needs help and they're running out of options. Up until recently, our 77 year old dad was taking on as much of the caretaking of my brother as he could even though his energy and ability were severely lacking for my brother's needs. He's on Medicare and disability but it's not enough to cover his needs where we live in San Diego, CA. Two weeks ago dad was diagnosed with colon cancer. The doctors went in to place a stent to strengthen his heart and turned out he had four completely blocked arteries. He had to be rushed to the hospital for an emergency heart bypass surgery and is recovering as I type this while we await his treatment plan for the cancer.
As you can imagine this has put the care for my brother into sharp focus. He does not live with my parents but in his own apartment a few minutes away. They tried to have him live with them when his wife finally kicked him out a few years ago and it was a disaster. He was ornery, obstinate, angry, sullen, disgusting, dirty and otherwise a menace to my elderly parents. It was like having a 300 pound, 48 year old 15 year old around the house and it nearly broke my parents. Obviously, he is not himself and they tried for as long as they could but eventually they were forced to find him his own apartment.
The thing is, if you met my brother today, you'd never know that he had a chunk of his brain removed and that he is essentially disabled. He can function somewhat and comes across as a weird, detached, quirky but otherwise normal-ish person. Until it is that you require him to do anything, particularly with self care. He doesn't bathe, refuses to take medication, and makes impulsive and nonsensical decisions like going on a drive in his gas guzzling truck when the meter reads empty and gets stranded on the freeway when his car runs out of gas.
With dad now completely unable to support, and the rest of the family either unable or unwilling to pitch in, we're running out of options and something has to give. He needs resources, trained professionals, and care that none of us are qualified for regarding his specific injury and needs.
I don't know what else to do so I'm coming to you here. Any help, support, guidance or resources would be an incredible boon.
Some additional details:
He lives in San Diego, CA
He is on SSDI disability, Medicare and -cal
He is on medication for seizures, depression and diabetes (which he does not take consistently or at all)

Hello all,
tl;dr - Brother was diagnosed with a stage 3 glioblastoma brain tumor in 2016. They removed a cancerous tumor the size of a golf ball and while he is alive his life has been completely ruined and it is now beginning to destroy my parent's life. We are running out of options for care and if something doesn't happen soon he will end up on the street or dead.
The above sums it up. My family needs help and they're running out of options. Up until recently, our 77 year old dad was taking on as much of the caretaking of my brother as he could even though his energy and ability were severely lacking for my brother's needs. He's on Medicare and disability but it's not enough to cover his needs where we live in San Diego, CA. Two weeks ago dad was diagnosed with colon cancer. The doctors went in to place a stent to strengthen his heart and turned out he had four completely blocked arteries. He had to be rushed to the hospital for an emergency heart bypass surgery and is recovering as I type this while we await his treatment plan for the cancer.
As you can imagine this has put the care for my brother into sharp focus. He does not live with my parents but in his own apartment a few minutes away. They tried to have him live with them when his wife finally kicked him out a few years ago and it was a disaster. He was ornery, obstinate, angry, sullen, disgusting, dirty and otherwise a menace to my elderly parents. It was like having a 300 pound, 48 year old 15 year old around the house and it nearly broke my parents. Obviously, he is not himself and they tried for as long as they could but eventually, they were forced to find him his apartment.
The thing is, if you met my brother today, you'd never know that he had a chunk of his brain removed and that he is essentially disabled. He can function somewhat and comes across as a weird, detached, quirky but otherwise normal-ish person. Until it is that you require him to do anything, particularly with self care. He doesn't bathe, refuses to take medication, and makes impulsive and nonsensical decisions like going on a drive in his gas-guzzling truck when the meter reads empty and gets stranded on the freeway when his car runs out of gas.
With dad now completely unable to support, and the rest of the family either unable or unwilling to pitch in, we're running out of options and something has to give. He needs resources, trained professionals, and care that none of us are qualified for regarding his specific injury and needs.
I don't know what else to do so I'm coming to you here. Any help, support, guidance or resources would be an incredible boon.
Some additional details:
He lives in San Diego, CA
He is on SSDI disability, Medicare and -cal
He is on medication for seizures, depression and diabetes (which he does not take consistently or at all)

Hello all,
tl;dr - Brother was diagnosed with a stage 3 glialblastoma brain tumor in 2016. They removed a cancerous tumor the size of a golfball and while he is alive his life has been completely ruined and it is now beginning to destroy my parent's life. We are running out of options for care and something doesn't happen so he will end up on the street or dead.
The above sums it up. My family needs help and they're running out of options. Up until recently, our 77 year old dad was taking on as much of the caretaking of my brother as he could even though his energy and ability were severely lacking for my brother's needs. He's on Medicare and disability but it's not enough to cover his needs where we live in San Diego, CA. Two weeks ago dad was diagnosed with colon cancer. The doctors went in to place a stent to strengthen his heart and turned out he had four completely blocked arteries. He had to be rushed to the hospital for an emergency heart bypass surgery and is recovering as I type this while we await his treatment plan for the cancer.
As you can imagine this has put the care for my brother into sharp focus. He does not live with my parents but in his own apartment a few minutes away. They tried to have him live with them when his wife finally kicked him out a few years ago and it was a disaster. He was ornery, obstinate, angry, sullen, disgusting, dirty and otherwise a menace to my elderly parents. It was like having a 300 pound, 48 year old 15 year old around the house and it nearly broke my parents. Obviously, he is not himself and they tried for as long as they could but eventually they were forced to find him his own apartment.
The thing is, if you met my brother today, you'd never know that he had a chunk of his brain removed and that he is essentially disabled. He can function somewhat and comes across as a weird, detached, quirky but otherwise normal-ish person. Until it is that you require him to do anything, particularly with self care. He doesn't bathe, refuses to take medication, and makes impulsive and nonsensical decisions like going on a drive in his gas guzzling truck when the meter reads empty and gets stranded on the freeway when his car runs out of gas.
With dad now completely unable to support, and the rest of the family either unable or unwilling to pitch in, we're running out of options and something has to give. He needs resources, trained professionals, and care that none of us are qualified for regarding his specific injury and needs.
I don't know what else to do so I'm coming to you here. Any help, support, guidance or resources would be an incredible boon.
Some additional details:
He lives in San Diego, CA
He is on SSDI disability, Medicare and -cal
He is on medication for seizures, depression and diabetes (which he does not take consistently or at all)

Kidney Failure is a Life Threat, Start Living “Right” Today!
Kidney failure, also known as renal failure, is a critical medical condition characterized by the loss of kidney function. It is a life-threatening condition that demands immediate attention and comprehensive lifestyle changes to manage effectively. With the prevalence of kidney failure on the rise globally, understanding its causes, symptoms, and preventative measures is crucial. This essay delves into the significance of kidney health, the causes of kidney failure, its impact on individuals and society, and most importantly, how adopting a healthy lifestyle can mitigate the risk of kidney failure and improve overall well-being.
Understanding Kidney Function and Failure:
The kidneys play a vital role in maintaining the body's internal balance by filtering waste products and excess fluids from the blood, regulating electrolyte levels, and producing
hormones that regulate blood pressure and red blood cell production. When the kidneys fail to perform these functions adequately, waste products and fluid accumulate in the body, leading to a cascade of health complications. Kidney failure can manifest as acute or chronic. Acute kidney failure occurs suddenly, often as a result of injury, infection, or medication, and requires immediate medical intervention. Chronic kidney failure develops gradually over time, usually due to underlying health conditions such as diabetes, hypertension, or autoimmune diseases.
Regardless of the type, untreated kidney failure can lead to severe complications, including cardiovascular disease, anemia, bone disease, and ultimately, death.
Avoid Kidney Disease
The Growing Epidemic:
Kidney failure is a global health concern, with incidence rates steadily increasing over the past few decades. According to the World Health Organization (WHO), an estimated 850 million people worldwide are affected by kidney diseases, and millions die each year due to lack of access to affordable treatment. The rise in risk factors such as obesity, diabetes, and hypertension, coupled with an aging population, exacerbates the prevalence of kidney failure.
Impact on Individuals and Society:
The consequences of kidney failure extend beyond individual health, impacting families, communities, and healthcare systems. Individuals with kidney failure often experience reduced
quality of life, requiring frequent dialysis treatments or kidney transplantation to survive. These treatments are not only physically demanding but also financially burdensome, placing strain on healthcare resources and affecting productivity and economic stability. Furthermore, disparities in access to kidney care exacerbate health inequities, disproportionately affecting marginalized communities and underserved populations. Addressing the societal impact of kidney failure requires a multifaceted approach that encompasses preventive strategies, early detection, access to affordable treatment, and patient education.
Prevention through Lifestyle Modification:
While certain risk factors for kidney failure, such as age and genetics, are beyond individual control, adopting a healthy lifestyle can significantly reduce the risk of developing kidney disease. Key lifestyle modifications include:

1. Balanced Diet: Consuming a diet rich in fruits, vegetables, whole grains, and lean proteins while limiting salt, sugar, and saturated fats can help maintain kidney health and prevent conditions like diabetes and hypertension.
   
2. Hydration: Staying adequately hydrated by drinking plenty of water throughout the day promotes kidney function and prevents the formation of kidney stones.
   
3. Regular Exercise: Engaging in regular physical activity helps control weight, lower blood pressure, and reduce the risk of chronic diseases associated with kidney failure.
   
4. Avoiding Tobacco and Excessive Alcohol Consumption: Smoking and heavy alcohol use can damage blood vessels and impair kidney function, making individuals more susceptible to kidney disease.
   
5. Monitoring Medications: Certain medications, including over-the-counter pain relievers and prescription drugs, can harm the kidneys if used excessively or inappropriately. Consulting with healthcare professionals and following prescribed dosages is essential.
   

Conclusion:
Kidney failure poses a significant threat to public health, with far-reaching consequences for
individuals and society as a whole. While the prevalence of kidney disease continues to rise, adopting a proactive approach to kidney health through lifestyle modification is key to prevention. By making informed choices regarding diet, exercise, hydration, and medication management, individuals can reduce their risk of developing kidney failure and improve their overall quality of life. Empowering individuals with knowledge and resources to prioritize kidney health is essential in combating this silent epidemic and promoting well-being for generations to come. Remember, kidney failure is a life threat, but by starting to live "right" today, we can safeguard our most vital organs and enjoy a healthier future.
Avoid Kidney Disease

The Janumet 1000mg /50mg Tab is a mixture product that that has the dual in managing high blood sugar in those with the type 2 diabetes mellitus.
It decreases the tendency to have critical side effects of diabetes such achieving ketotarus and blindness and results to lowering your chances of developing cardiac arrest and stroke.
The usage of 1000mg/50mg tablet membrane of Janumet either individually or with the combination of other drugs for diabetes is made frequent in the treatment of it.
Its effectiveness optimises when applied in cohesion with a balanced nutrition and an appropriate physical activity.
Wegovy 2.4 Mg Saxenda Liraglutide 6 Mg

Is racial discrimination in healthcare still a thing?
By: Jatarra Banks
Period 3
My intended audience
My purpose for writing
My stance toward my topic
Seniors interested in learning about racial discrimination in healthcare.
To inform my reader about racial discrimination in health care and how it affects minorities.
I keep a neutral stance throughout my essay.
Racial discrimination is a big problem in America and unfortunately has been present in healthcare for many people. Many people don’t want to discuss or make a big deal out of it because they think it’s not worth solving. But it is difficult for people to agree whether racial discrimination is an actual problem in healthcare. Minorities have experienced being misdiagnosed and treated poorly because of their race. In addition, they are often stereotyped by doctors, and have higher death rates compared to other races. Fortunately for me, I have never experienced any of these things even though I am a minority. But people I know have always complained and would tell stories about their experiences when going to the hospital to see any kind of doctor. The issue should be talked about more but is a sensitive topic and has been avoided by many people because they feel discomfort or denial.
One aspect that both parties can contest to is that racism is present in healthcare. One side believes that it is not an issue for minority patients but is just an excuse they use to get attention. They also think that politicians use it as a scapegoat to get voters on their side but do not fix the problem. In the article, “Liberal lies on ‘racist’ doctors and nurses threaten everyone’s health”, a former lieutenant governor Betty McCaughey, says, “But many activists would rather exploit the race card for political gain than deal with the causes of these deaths. Mary Bassett, a New York state health commissioner until last month, is one of them. Urging support for national reparations, Basset argues they “can bring us closer” to “end[ing] racial health inequities.” That’s ridiculous.” The other side believes that racism is the problem for their health and blames the healthcare system and their doctors. There have been many studies to prove that racism is the problem and has cost many lives. Many minorities can speak about their experiences with racism and how it is hard to find doctors who actually care about their health. According to “Implicit Bias and Racial Disparities in Health Care.”, “NAM [National Academy of Medicine] reported that minority persons are less likely than white persons to be given appropriate cardiac care, to receive kidney dialysis or transplants, and to receive the best treatments for stroke, cancer, or AIDS. It concluded by describing an ‘uncomfortable reality’: ‘some people in the United States were more likely to die from cancer, heart disease, and diabetes simply because of their race or ethnicity, not just because they lack access to health care.’” NAM has many studies that prove how minorities get unfair treatment and diagnosis that leads to death. The evidence shows that there are hidden biases and problems in the healthcare system that affect minority groups more than others. This leads to worse health outcomes for them. It suggests that the healthcare system needs to change to fix these issues and ensure everyone gets fair and equal care.
In order to understand racial discrimination in healthcare, my readers would need to know how it affects black people and even the healthcare workers for many years. Understanding these things informs people of the presents of racial discrimination in healthcare. Readers should also understand the view of black people and how they feel about the topic. They would also need to understand healthcare policies involving race. There are many people sharing their experiences in or working in the hospital. In a reddit post by Sheimonya titled “Discrimination in the hospital – examples.” it states, "Had a black women leave AMA because she could hear the nurses and resp therapist calling her a “he-she” right outside the door. Came back a day later requiring a permanent trach. Could have helped her not get to that point if she were treated like a human being.” This goes to show how doctors can make black people feel uncomfortable and not even want any help from doctors because of being talked about behind their back. Moreover, another post states, “I’m a perinatal nurse. Black women are 3x more likely to die in childbirth than white women. In my field, black women are considered high risk because they typically have a higher rate of developing high risk conditions in pregnancy like preeclampsia, diabetes, IUGR, etc. They are also often labeled as ‘difficult’ ‘diva’. This causes nurses to often pass bias in their care and also turn to NOT listening to them because they are ‘being dramatic’. These women die because of being overlooked, not listened to or ignored. I see this when getting report at change of shift from the previous shift. They seem to have the need to let me know that the patient is black as if alluding that they are going to be or are ‘difficult’. I never get reported ethnicity on white, Asian, Latinx patients. Nurses have bias too. This causes racial and ethnic disparities in healthcare.” These personal experiences shed light on the healthcare system and the racial biases that people go through and witness all the time. Also these things contribute to how black people lives are being impacted and changed over these racial biases.
Theories of racism in healthcare. Many people have their own theories when it comes to racism in healthcare. Many people believe that racism should be addressed more than it is now. But people in higher up positions might not like that as much. For example, there was a time when an editor wouldn't publish an article because the title had “Racism” in it because it was a sensitive topic to readers. They would ask him to comprise, in an article “The health-care industry doesn’t want to talk about this single word” by Ron Wyatt who is the co-chair of the Institute for Healthcare Improvements he says, “Yet, I still sometimes feel that survival mechanism kick in to compromise and veil the truth that structural and systemic racism is a root cause of preventable harm and death across U.S. health care. I have been warned that if I did not continue to compromise, I would be labeled an “angry Black man” and that colleagues would distance themselves from me.” This evidence shows how racism can be a problem because how the system is trying to silence his words and label him an “angry black man” because of his opinions and experiences with the topic. In addition, there are other people who believe that blaming on racism as the main reason for poor healthcare is not effective and will not chance the fact that minorities have poor healthcare. According to “Liberal lies on ‘racist’ doctors and nurses threaten everyone’s health", "This push for anti-racism in medicine will not save the lives of black infants or their mothers” This statement can change your view of racism in healthcare and question if it is used as an escape goat or if it is a real issue. Do you still put attention to it or leave it alone to protect lives? There are many speculations on whether racism should be taken seriously but there are lots of evidence to move that it should. (Figure 1) Shows how healthcare workers suggested five things that would advance health equity for monitories.
Figure 1
📷
Top 5 barriers advancing to health equity collected by the Institute for Healthcare Improvement in 2021
(Source from Commonwealth Fund, October 18,2021)
Minorites are most likely to die from diseases because of racial discrimination in healthcare. Minorities don’t have the same access and resources that whites have because of their different tax bracket, race, and they are in different environments. Minorities don’t have access to the best doctors and services because they can’t afford it and their insurance doesn’t cover it for them. According to editors Bulato Ra and Anderson NB, in a research agenda about racial and ethnic differences, "black-white differences do not appear for the treatment of colored cancer but have shown in the treatment of heart disease, gall-bladder disease and mental health.” This evidence emphasizes the fact that minorities are being misdiagnosed which leads to improper treatment of diseases they may have. In a medical journal, “Racial Inequities Persist in Health Care Despite Expanded Insurance” by Roni Caryn Rabin, a New York Times health writer, says, “Another study in the journal compared health care spending by race and ethnicity, finding that at $8,141 per year, spending for white individuals is higher than for Americans of other races and ethnicities, and the portion of it spent on outpatient care is higher than the average.” This study shows the number difference of how much money is being spent on different races. For minorities to have access to healthcare they need the funding, but it is going to mostly to white Americans. This highlights how disparities in healthcare spending contribute to existing inequalities, further widening the gap in health outcomes between different racial and ethnic groups.
Work Cited
Bridges, Khiara. “Implicit Bias and Racial Disparities in Health Care.” American Bar Association, 2018
Bulatao, RA; Anderson, NB, editors. “Understanding Racial and Ethnic Differences in Health in Late Life: A Research Agenda.” National Academies Press, 2004 https://www.ncbi.nlm.nih.gov/books/NBK24693/
McCaughey, Betsy. “Liberal lies on ‘racist’ doctors and nurses threaten everyone’s health.” New York Post, February 14, 2023
Sheimonya. “Discrimination in the hospital – examples.” Reddit, 2020, https://www.reddit.com/Nurse/comments/hen32t/discrimination_in_the_hospital_examples/
Wyatt, Ron. “The health-care industry doesn’t want to talk about this single word.” The Washington Post, April 5th, 2021

I’ve been having an ongoing sore throat for the last 3 days so I decided to make a teledoc appt for treatment. The appointment started out very normal, and she was asking all the typical questions. She then asked me if I’ve been nauseous, and I go to tell her I’ve felt slightly nauseous but I’m on zepbound and just increased my dose so I’m unsure if it’s because of the zepbound or because I’m ill. This is when things go sideways.
She immediately asks “do you have type 2 diabetes??”
I go “no my endocrinologist recommended it for my pcos, insulin resistance, and excess weight”
She goes “are you obese or what? I’m not understanding why you’re on zepbound”
Tf….. mind you this is a teledoc visit and all she can see is my face.
I go “no. I’m overweight.” She goes “how much do you weigh?” I respond “179.”
She asks “ok….. what’s your goal weight??” At this point I feel defensive and I’m not understanding why this is relevant for a sore throat.
I go “ummm 150.” She’s like “ok. Looking at your face you look fine. But I guess sometimes you can’t tell a persons overweight or obese just by their face” wtf?
She leaves it at that and proceeds to tell me that I should take penicillin even though I explicitly told her I stay away from it due to a family history of highly allergic reactions. Very off putting vibes. I didn’t like her at all lol. Surprising reaction to the use of zepbound coming from a seasoned doctor

In Oct. 23, I got a PSA test w/ a score of 21. I was referred to a urologist and saw him in early Nov. He retested my PSA (now 20.2) and did a biopsy. Results of the biopsy were 3+4 and 4+3 positive for malignant adenocarcinoma. The urologist said that I was “Just over the limit for waiting and seeing, and suggested either surgery + hormone therapy, or radiation + hormone. Referred me for a PET scan.
Between the Imaging folks and Medicaid doing battle it took until Feb 22 to get the scan. The results were positive for cancer with no suggestion of metastasis. “Increased tracer activity throughout the bilateral peripheral zones, left greater than right, more concentrated in the left mid-gland to apex”. No suggestion of lymph node involvement or osseous metastasis. 10mm Kidney stone in the left UVJ and mild kidney and ureter dilation.
It took me until today, 4/30 to get a follow-up with the urologist for an explanation of the results. (Took me 3 weeks just to get hold of his office to make the appointment!) He says “Well no metastasis, what do you want to do”? I told him I wanted the surgery. He says, “Well because you are obese, diabetic, have high BP, and emphysema, surgery is a bad option and I should do radiation. (He knew all my risk factors in Feb. when he said surgery was an option). The radiation requires me to have 4 markers inserted in my prostate, then 45 consecutive days of radiation treatments. I didn’t want radiation because:
1) As I understand it, once you’ve had radiation, surgery becomes impossible. (Is this true? He says it’s not. He actually claimed if we did surgery and need to do radiation later, it would be “horrible”. Again, is this true?)
2) The radiation center is a 45 min. drive and doing that, round trip, for 45 consecutive days would be difficult for me. I have severe arthritis, and back issues, sitting in a car for 20min or more is a pain festival, and just getting prepped to go, etc. takes me a couple hours to go through all the motions.
3) I’m just not wild about that much radiation, because what issue am I going to have next.
I just wanted it out and done with. He essentially refused to consider surgery. I finally said to him, “Well, I guess I don’t really have a choice, you’re not taking no for an answer.” So, he set up a referral for the radiation oncologist. He also set up an appointment to have the gold markers inserted (by him).
Then I asked, “What about the kidney stone and dilation”….. He says, “What Kidney Stone?”. I had to show him on the report from the PET scan I brought with me. He punched around on his computer and said, “OH! I didn’t see that, I’ll need to remove that. What we’ll do is put you under, laser it out via your ureter, and at the same time, insert the markers.” Now wait a minute! He just got done telling me that I was a poor risk for anesthesia/surgery because of all my other problems! I’m OK for his kidney stone procedure, but not the other? Plus the fact that he didn’t even notice the stone in the report, really shocked me. He actually thanked me for pointing it out, and said “Once I saw no metastasis, I stopped reading.”
OK, now I have ZERO confidence in this guy. I Really don’t want the 45 consecutive days of being nuked. He is also insisting that “No matter What”, I need 2 full years of Lupron treatments. (I thought they only did that for cancer that had metastasized, was stage 4, and was super dangerous.) I asked him, and he said, “Oh no, we always do that, we have to be sure to get all the microscopic cancer floating around in you”! That was also the line he used for pushing radiation. “Oh, got to get the lymph nodes too, there may be microscopic cancer there that we can’t see with the PET scan). I also noticed that he kept saying, “You have serious, advanced cancer”. Last time we spoke he was considering Wait & see, cuz I was on the borderline for observation only. Which is it?
Final rub here. If I was still on regular, work provided insurance, I’d just go get another opinion, better yet, go out of state to a better hospital system in general, BUT I’m on our state Medicaid. (Had to stop working 18 months ago for many of these medical issues). So, I’m stuck staying in-state, and using the doctors they say I must, that are part of the state university health/hospital system. (Why the hell couldn’t this crap all happen during the 40 years that I had “normal” insurance!!)
1st, is all the stuff he’s pedaling accurate? Does his prattle make sense?
2nd, Should I fight with Medicaid and try to get another opinion? Do I have a real reason to distrust him?
3rd, Any other helpful input, or Suggestions are appreciated.
Thank you for taking the time to read all this and reply. I wanted to be sure everyone had all the info and context.

Well that was a rough title to type out. She's been pregnant since late January and our baby is due October 5th at the latest. She's diabetic and has a very strict diet and treatment during her pregnancy.
These past couple of weeks I've felt a sudden loss of sex drive, it's not that I don't find her attractive physically, nor am I afraid of hurting the baby with sex (we've had sex multiple times since the positive pregnancy results), but I'm lately feeling more and more tired of her and some of her attitudes and behaviors.
Now, there are a lot of things on my mind such as school (studying a second field) and some debt I'd like paying off this year, I also had some issues at work because of a conflicting boss and haven't been sleeping so well for the past month or so because I am unfortunately an overthinker and because my wife stays up until very late.
The problem I'm having is that my wife won't take care of herself like her doctors have advised her to do multiple times and I don't know if it's the stress and my personal issues combined.. but her complete lack of interest in her own care has been a big turnoff for me. She's not even supposed to do a lot. Take a 15 minute walk every day, try eating her meals at consistent times, and develop healthier sleeping habits. Nevertheless, she doesn't go on walks even when I ask her to do it together, she says she doesn't feel like eating and will skip meals or eat something super unhealthy for dinner, take super long naps in the afternoon instead of going to bed earlier and I guess this is all making me change my mind on whether she'll be able to help raise and take care of our baby together I thought she'd be a good mom, and now I have my doubts.
What I'm finding frustrating is there are things she can do about her own concerns.. like she says she's afraid she'll put up too much weight, but won't go on walks or change her diet, she's saying she never gets enough sleep, yet keeps going to bed at 1am, gets mad because her sugar levels go up, but won't follow her med schedule or drink enough water and it's gotten to where if you complain this much about things and don't do anything about them, it's 100% your fault if you end up being what you were afraid of becoming.
I know pregnancy is a huge change, I know she's going through an extreme physical and emotional/psychological change and I don't want my feelings to contribute more to all the massive changes she's experiencing, but I also can't do a lot of the things she's supposed to do meaning I can't force her, even if I try making the activities about -US-. I don't want her lack of care to end up affecting our baby and her quality of life because my wife would rather sulk than take action.
Am I being an unrealistic self sabotaging idiot here? Should I even bring up these concerns or wait for it to die down and improve while the pregnancy progresses?
TL;DR: Wife sulks, complains and won't take action, and it's making me doubt my feelings towards her right now.

Sole biguanide agent in the US.
Available in short and sustained-release formulations.
Has the best benefit-risk profile for glycemic control, weight loss and safety.
Recommended as initial treatment for type 2 diabetes.
Metformin, compared with lifestyle modification alone, is associated with a 39% reduction in myocardial infarction and a 36% reduction in all-cause mortality in type 2 diabetes.
Works primarily by decreasing hepatic glucose output and a relatively minor effect on increasing insulin sensitivity.
Hepatic gluconeogenesis may be reduced by 75%.
It decreases the amount of blood sugar that the liver produces and that the intestines or stomach absorb.
Its pleitropic affects, include decreased inflammation, increase insulin and leptin sensitivity, and decreased hunger and gherlin levels, especially with twice daily dosing.
Acts in the liver where it inhibits gluconeogenesis by blocking a mitochondrial redox shuttle.
It is an insulin sensitize and likely acts in the lumen through multiple mechanisms.
Metformin, taken with diet and exercise changes to prevent diabetes in people who are at high risk for becoming diabetic.
It is frequently used in patients with pre-diabetes, polycystic, ovary syndrome, and overweight/obesity to mitigate weight gain due to antipsychotic medications.
It increases the effects of insulin, and is termed an “insulin sensitizer”.
A biguanide, is the most widely used oral antidiabetic drug that is generally
Recommended for first-line medical treatment of type 2 diabetes.
Early initiation of metformin at the time of diagnosis, when glycosylated hemoglobin levels are not significantly elevated, has been associated with improved glycemic control over time and decreased long-term complications.
Metformin is believed to activate AMP-activated protein kinase (AMPK), a major cellular regulator of lipid and glucose metabolism.
Metformin has been shown to be highly effective at reducing the onset ofdiabetes by 31% in 3234 prediabetic adults over a period of 2.8 years in the DPP (Diabetes Prevention Program) study 72 and at reducing systemic inflammation.
Also suppresses the endogenous glucose production by the liver, which is mainly due to a reduction in the rate of gluconeogenesis and a small effect on glycogenolysis.
It activates the enzyme adenosine monophosphate kinase (AMPK) inhibiting enzymes involved in gluconeogenesis and glycogen synthesis in the liver while stimulating insulin signaling and glucose transport in muscles.
Metformin is believed to activate AMP-activated protein kinase (AMPK), a major cellular regulator of lipid and glucose metabolism.
Improves glycemic control without inducing hypoglycemia or weight gain.
Metformin has modulating effects on a pathway known to play a major role in lifespan extension.
Metformin also upregulates peroxisome proliferator–activated receptor gamma coactivator 1-alpha, a master regulator of mitochondrial function, and a transcription factor that controls antioxidant programs.
Because these molecules (AMPK, mammalian target of rapamycin, and peroxisome proliferator–activated receptor gamma coactivator 1-alpha) are interconnected through cellular signaling networks implicated in the modulation of the aging process, it has been postulated that metformin could slow aging and age-related diseases.
Metformin is believed to activate AMP-activated protein kinase (AMPK), a major cellular regulator of lipid and glucose metabolism.
Metformin has modulating effects on a pathway known to play a major role in lifespan extension.
Metformin also upregulates peroxisome proliferator–activated receptor gamma coactivator 1-alpha, a master regulator of mitochondrial function, and a transcription factor that controls antioxidant programs.
Observational studies indicate that metformin reduces mortality and frailty.
Use associated with lower rate of atrial fibrillation.
Use associated with lower incidence of atrial fibrillation.
Use associated with lower fasting insulin concentrations.
One of the few drugs that shows a significant reduction of macrovascular events and diabetes related mortality.
Antioxidants have beneficial effects such as anticancer, antidiabetes and antiatherosclerosis properties.
It has been shown to reduce visceral adiposity and insulin resistance after 8 weeks of drug therapy.
Trade name Glucophage.
Use associated with weight loss.
Metformin is associated with approximately 3% weight loss in approximately 25 to 50% of participants achieve at least 5% weight loss.
Long-term use associated with anemia-6% higher risk of anemia for every cumulative yer of metformin exposure (Donnelly L).
Decreases HgbA1C by 1 to 2%.
As much as 88% of weight loss is body fat mass.
Primarily used for the treatment of type 2 diabetes mellitus, particularly in obese.patients.
Reduce diabetes mortality and complications by thirty percent compared to insulin, and chlorpropamide.
Reduces serum glucose level by several different mechanisms, notably through nonpancreatic mechanisms without increasing insulin secretion.
Drug use contraindicated in many patients with impaired kidney function because of concerns of lactic acidosis.
The occurrence of dehydration can increase the risk of lactic acidosis.
The elderly may be at greater risk for hypoglycemia or lactic acidosis.
Its pharmacokinetics are affected by pregnancy, related to the changes in renal filtration and net tubular transport.
A fetus is exposed to variable concentrations of metformin.
Infant exposure to metformin through the breast milk is low.
Has nephroprotective activity against nephrotoxic agents.
Use in patients with diabetes and advanced chronic kidney disease is associated with greater mortality risk.
Side effects include: Nausea, vomiting, stomach upset, diarrhea, weakness, or a metallic taste in the mouth may occur.
It usually does not cause hypoglycemia; however, low blood sugar may occur if this drug is used with other anti-diabetic drugs.
Hypoglycemia is more likely to occur with metforminn with heavy exercise, drinking large amounts of alcohol, or not consuming enough calories from food.
Previous data suggesting it should be contraindicated in patients with impaired kidney function, but more up-to-date information suggests that can be used cautiously in mild to moderate chronic kidney disease.
Use in patients with advanced chronic kidney disease reveals all cause mortality is significantly higher (and is dose-dependent) than in patients with chronic kidney disease in diabetics and non-users of metformin.
Patients with diabetes and reduced kidney function persisting with monotherapy, treatment with metformin compared with a sulfonylurea is associated with a lower risk of major adverse cardiac events.
The presence of hyperinsulinemia has been noted in many patients with cardiac syndrome X, and metformin has been shown to improve vascular function and decrease myocardial ischemia in nondiabetic women with chest pain and angiographically normal coronary arteries.
Although renally cleared drug levels generally remain within the therapeutic range and lactate concentrations are not not substantially increased when used in patients with mild-moderate chronic kidney disease (estimated GFR 30-60 mils per minute per 1.73 m²) (Inzucchi SE et al).
Incidence of lactic acid doses in metformin users is approximately 3 per 100,000-person-years to 10 per 100,000 person years and is indistinguishable from the background rate in th overall population with diabetes.
Lactic acid levels do not increase in patients with normal renal function.
Recent studies suggest no increase in lactic acidosis with mild to moderate chronic kidney disease or congestive heart failure.
Major clinical effect is decreased fasting glucose levels..
Most patients have approximately 1.5 reduction in HbA1C.
Referred to as an antihyperglycemic agent rather than a hypogolycemic drug.
Incidence of associated hypoglycemia is low.
May modestly decrease triglycerides because of decreased very low density lipoprotein production.
Must be stopped 48 hours after intravenous contrast administration and restarted when normal renal function is documented to decrease the chance of lactic acidosis.
Lactic acidosis is the most severe adverse affect and is associated with older age, cardiac disease, the compensated congestive heart failure, renal insufficiency, chronic pulmonary disease, and hypoperfusion.
Can rarely cause lactic acidosis with risk related to sepsis, dehydration, excess alcohol intake liver insufficiency renal impairment and acute congestive heart failure.
Incidence of lactic acidosis very low, approximately 0.03 cases/1,000 patient- years with approximately 0.015 fatal cases/1,000 patient-years.
Lowers blood glucose levels by sensitizing the liver to the effects of insulin, thus suppressing hepatic glucose output.
Decreases the amount of glucose produced by the liver and reduces blood stream level and cellular uptake of insulin.
Improves peripheral insulin sensitivity so that it improves skeletal muscle glucose utilization.
In type 2 diabetics improves both basal and postprandial plasma glucose.
Metformin stimulates AMP-activated protein kinase and reduces hepatic glucose production.
It reduces insulin stimulation resulting in reduced activation of insulin receptors on cell membranes, triggering intracellular molecular effects such as down regulation of the RAS/RAF/MEK/ERK and P13K/AKT/mtor signaling pathways.
Upregulates AMP-activated protein kinase, a key molecule in glucose and insulin regulation and also an inhibitor of mTOR.
Activates AMP-activated protein kinase, a major sensor cellular energy levels and a key enzymes limiting growth during times of cellulitis stress.
Activated AMP protein kinase PX protein, cholesterol, and fatty acids synthesis and inhibits mTOR.
Reverses hyperinsulinemia, leading to the down regulation of insulin-like4 growth factors that can promote tumorogenesis by activating of the phosphatidylinositol 3 kinase/protein kinase B pathway.
Enhances phosphorylation of AMP-activated protein kinase,, inducing changes in the intracellular pathways, ALT is mitochondrial function and may result in improved systolic and diastolic function.
Observation studies of acute myocardial infarction and treatment with metformin is associated with lower peak CK levels, troponins and improve survival after STEMI in patients type 2 diabetes, compared with other anti-glycemic strategies.
Among patients without diabetes and who presented with a STEMI and undergo primary PCI, the use of metformin compared with placebo does not improve left ventricular ejection fraction after 4 months (Lexis CP et al.
Associated with a 31% reduction in diabetes compared to placebo in patients with impaied glucose tolerance (DDP Research Group).
Increases GLP-1 secretion and inhibits GLP-1 degradation.
Among obese adolescents with type one diabetes the addition of metformin to insulin does not improve glycemic control (Libman IM et al).
Lowers cholesterol, triglyceride, and reduces hyperinsulinemeia, improves insulin sensitivity, and assists with weight reduction.
Decreases overall mortality in overweight Type 2 diabetics.
The international Reduction of Atherothrombosis for Continued Health (REACH) Registry indicated that the use of metformin as a means of secondary prevention in diabetes was associated with a 24% reduction in all-cause mortality after two years follow-up.
In obese diabetic patients uses so Siri Siri 2% reduction in the diabetes-related endpoint, 42% reduction in diabetes related death, and 36% reduction in mortality (UKPDS).
In the above study patients receiving metformin had a 39 percent reduction in the risk of nonfatal MI.
Other studies on metformin have not shown improvement in microvascular with macrovascular morbidity or mortality.
Associated with lactic acidosis, anorexia, nausea and diarrhea.
May be associated with metallic taste, nausea, diarrhea, and abdominal pain.
Symptoms can be minimized by starting with a low dose and titrating slowly, dividing doses and taking the drug with food.
Decreased vitamin B12 levels have occurred in patients on long-term treatment and rarely has been associated with anemia.
Metformin, might reduce the absorption of vitamin B12, possibly through alterations in intestinal mobility, increased bacterial overgrowth, or alterations in the calcium-dependent uptake by ileal cells of the vitamin B12-intrinsic factor complex.
10%–30% of patients who take metformin have reduced vitamin B12 absorption.
Contraindicated: in patients older than 80 years unless normal creatinine is present, in patients with abnormal renal or hepatic function and in patients taking medications for congestive heart failure.
Improves ovarian function in polycystic ovarian syndrome.
In women with polycystic ovarian syndrome, it may make menstrual cycles more regular and increase fertility.
In a large review using 27 clinical trials found metformin was not associated with any increase in the number of live births; however, it improved ovulation rates, especially when it was used in combination with clomiphene in polycystic ovarian disease.
With polycystic ovary syndrome, it is a first choice because of positive effects on insulin resistance, hirsutism, anovulation and obesity.
Metformin improves endothelial function in women with PCOS and endothelial dysfunction independent of changes in glucose metabolism metabolism, dyslipidemia or presence of pre-diabetes.
Metformin has a direct effect on endothelial function in PCOS.
In conjunction with clomiphene citrate acts to increased ovulation and pregnancy rates in polycystic ovarian syndrome.
May reduce rate of spontaneous abortion rate.
Decreases free circulating testosterone through an effect on liver sex hormone binding globulin, modulates adrenal androgen production and decreases ovarian androgen production associated well.
Can improve hirsutism.
Crosses the placenta.
Utilization in gestational diabetes alone, or with supplemental insulin, not associated with increased perinatal complications compared to the use of insulin alone.
Metformin
Observational studies indicate the outcomes for individuals with type two diabetes receiving Metformin while undergoing cancer treatment are improved.
Metformin reduces insulin signaling through the PIK3 and RAS pathways and activates AMPK, which inhibits downstream AKT/mTOR, impairing cancer cell growth.
There is strong evidence for a lack of benefit from metformin treatment in metabolically healthy individuals.
Use probably protects against liver cancer, lower risk for oral cancer, improves prognosis of pancreatic cancer in diabetic patients, increases response rate in melanoma treated tumors with BRAF mutations and chemotherapy agents.
The risk of pancreatic cancer in patients taking metformin is a 62% lower than in placebo group who did not use metformin.
While diabetic participants having sulfonylureas or insulin were found to have a 2.5-fold and 5-fold higher risk of pancreatic cancer, respectively, in comparison to placebo group.
Diabetic patients using metformin may have a lower the risk of cancer compared to those using other anti-diabetic drugs.
Has strong antiproliferative effects on colon, pancreatic, breast, ovarian, prostate and lung cancer cells.
Diabetes is a common disease that may occur throughout human life, and can increase the likelihood of the occurrence of various types of cancer, such as colon, rectum, pancreas and liver cancers, compared to non-diabetic patients.
Metformin inhibits mTOR activity by activating ATM (ataxia telangiectasia mutated) and LKB1 (liver kinase B1) and then adenosine monophosphate-activated kinase (AMPK), and thus prevents protein synthesis and cell growth.
mTOR is a protein kinase regulating cell growth, survival, metabolism, and immunity.
metformin can activate p53 by activating AMPK and thereby ultimately stop the cell cycle.
Metformin in nondiabetic, unresectable stage III non-small cell lung cancer (NSCLC) treated with chemoradiation: survival exceeded expectations in both groups, those who received chemoradiation alone vs chemoradiation and metformin: however, the addition of metformin to chemoradiation did not improve overall or progression-free survival.
Addition of metformin to chemoradiotherapy, as a concurrent treatment as well as consolidation therapy, in patients without diabetes who have locally advanced non-small cell lung cancer
addition of metformin to chemoradiotherapy was associated with worse treatment efficacy and increased toxic effects compared with chemoradiotherapy alone.
The proportion of patients who experienced a failure event within 1 year with locoregional disease progression, distant metastases, death, or withdrawal was 69.2% in the metformin arm vs 42.9% in the control arm.
Metformin is not recommended as an adjunct to chemoradiotherapy for the treatment of unresected locally advanced non-small cell lung cancer in patients who do not have diabetes.
Addition of metformin to standard breast cancer treatment
a randomized controlled trial (RCT) found addition of metformin to standard breast cancer treatment did not improve invasive disease free survival vs placebo among patients with high-risk operable disease who did not have diabetes.
Strong evidence for a lack of benefit from metformin treatment in metabolically healthy individuals.
A review found metformin use did not have a significant effect on cancer incidence in subjects with overweight/obesity and/or prediabetes/diabetes.
A clinical trial has demonstrated a beneficial effect in colon and breast cancers.
It possesses antioxidant activity.
Use associated with impaired cognitive performance.
Compared with Sulfonylureas, metformin is associated with reduced risk of major adverse cardiac events among patients with type two diabetes and reduced kidney function.
In non diabetics does not improve carotid intima-media thickness or carotid plaque scores.
May have a Preventative role In peripheral neuropathy induced by diabetes
Treatment with metformin prevents axonal atrophy and fiber degeneration.
Metformin stimulates the expression of neurotrophic and angiogenic factors in the peripheral nerve.
Metformin attenuates inflammation of nerve tissue exposed to chronic hyperglycemia.
Metformin increases the expression of anti-inflammatory markers.
Studies have shown in patients with prostate cancer, colorectal cancer, pancreatic cancer, triple negative breast cancer,, HER2 positive breast cancer, multiple myeloma the median overall survival durations are increased in patients taking metformin than in patients who are not.
Among patients with high-risk operable breast cancer without diabetes, the addition of Met Forman versus placebo to standard breast cancer treatment did not significantly improve invasive disease free survival (Goodwin PJ).
Long-term metformin use is associated with a significantly lower risk of new onset prostate cancer and all cause mortality in patients with type two diabetes than sulfonylureas and more protective against prostate cancer but less protective against all cause mortality in those less than 65 years of age.
Metformin affects multiple key processes related to cell growth, proliferation, and survival.
Epidemiological studies suggest a decreased risk of lung cancer in diabetic patients treated with antidiabetic drugs, including metformin-39-45% decreased risk.
Lung cancer patients treated with first-line chemotherapy and metformin have superior outcomes to those treated with chemotherapy and other diabetic medications.
A study suggests patients using metformin before a diagnosis of COVID-19 only had a third of the mortality risk of their counterparts with no reported use of the drug.
In a study, which included more than 300,000 participants aged 55 or older, the use of low dose metformin was associated with a lower incidence of age-related macular degeneration (AMD).
The use of metformin was associated with a reduction in odds of developing AMD.
The association is dose-dependent, with low to moderate doses of metformin being associated with the greatest benefit.
When assessing doses greater than 1080 g, there was no association with reduced odds of developing AMD at 2 years.
Among patients with diabetes, metformin use was associated with a decreased risk of AMD in patients without existing diabetic retinopathy, but was considered a risk factor for patients with existing diabetic retinopathy.
Metformin use over 2 years in adults aged 55 years and older is associated with 5% to 10% reduced odds ratio of developing AMD.
A dose-dependent association of this potential protective effect is present, with low to moderate doses of metformin being associated with the lowest odds ratio for the development of AMD.
https://standardofcare.com/metformin/
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This is in Arizona. Last month our family dog got very suddenly sick out of nowhere, I don't have a lot of money and she was not my dog, but I loved her dearly so I rushed her to the emergency vet because they were the only ones open during the weekend, and they were an hour away drive.
My aunt who is the owner eventually met with me there. Long story short the dog had diabetes and severe pancreatitis, The initial fee quoted to me included fluids, meds, x-rays, blood work and I was told it would cost about $1200, I used my Care Credit to pay for it because my aunt is unemployed and cannot work or get disability yet, Care Credit is what I use for dental appointments for myself so effectively barring me from that till I get it paid off enough to start using again.
After waiting 3 hours we were finally told what was wrong, I was then shown a tablet with a treatment plan that could consist of 12 or 24 hour care. I looked at the items I was being charged for and a lot of it looked like the same things I had already paid for, meds, insulin, IV, X-ray etc. I told the girl "I already paid for this" she told me "No we haven't charged you anything yet" I pushed again and again she told me no I had not been charged yet. She was making it seem like I had not yet paid for anything and that this new total of $3600 for the 24 care would be the complete total including the initial fee.
So I approved the 24 hour care, but I didn't have the money and neither did my aunt, my aunt and everyone at home refused to let me put her down and were getting actively angry with me (I knew it was bad and unlikely for her to recover) my aunt couldn't get approved for a loan, no one except me could. So I did with Allegro (Synchrony) which was their only option out of two that approved me.
The way this process went was filing out my details on a tablet, name, address, SSN and finding out if I'm approved in seconds, but not being told anything beyond that like interest rate or anything as once I was approved the front desk lady told me to not touch anything, so I couldn't keep reading the tablet. I was approved for up to $5000. I figured this would cover the $3600 I agreed to.
I told them I worked nights and I sleep during the day, so they were given my aunt's phone number as well. They kept calling me several times during the day and waking me up. Giving me updates, most of it consisted of "she's not eating and we want to hold her longer for observation" soon passing "24" hours and into the next day, still telling me the same things and asking if we could bring her food to eat, so my aunt went down there several times at their request because I couldn't make it.
I was not told that if they hold her beyond the 24 hours that it would incurr more charges, I was not given an option to go pick her up, I was just told they wanted to hold her for further observation and maybe in a few more hours she can go home.
Nearly 48 hours pass before they call saying she is ready to be picked up, my aunt goes because again I can't make it becomes of work. My aunt gets there and they ask her to sign For Me to complete the loan. They didn't ask her for ID and they knew she was not me. She put her bank as the one on file, if she refused to do any of this they wouldn't have released the dog and I imagine (now) this would have caused further charges.
I'm at work and I see the email I received from Allegro stating I owe $5000 (the full amount of the loan) plus the interest to the tune of 25% and if I pay the minimum per month of $200, in 32 months I'll have paid $7000, and that the first bill is due on April 11th. I was then also charged $800 on my care credit.
Not only is this WAY beyond what I agreed to, but the loan company I found out after has a 1.5 consumer rating with people having issues paying their bills or getting in contact with the company. I have tried several times to go to their website and switch the payment info to mine instead of my aunt's but the website refuses to update it. I also got a notification in the mail before the due date of the bill, saying they already tried to charge (my aunt's bank) and it was unsuccessful but they are confident it was just a mistake on my end and I'll correct the issue and make payment.
They tried to call me once, and it came up "Scam likely" I only answered because I saw it say Allegro briefly before changing. When I answered it was some Indian lady who sounded like 30 feet away from the phone, she asked me to confirm information about me to make sure it's me she is talking to (SSN, name, address) I had almost been scammed once before from Discover bank until I refused to give my SSN and the guy got angry and hung up (it was a scam I confirmed it) so I was wary, when I told her the call came up as scam likely and I was not comfortable giving her my info, she simply said okay and hung up.
I am still unable to change the bank/payment method, if I call them they do not answer my calls. I'm not comfortable just trying to send them a check in the mail and crossing my fingers it gets there.
I have tried to contact the Vet and medical director to talk about the fees and charges and let them know to probably drop the loan lender because they aren't good, but the medical director emailed me to say she got my complaint and will contact me at Her earliest convenience. I responded to her email and let her know my phone number to call. It has been Nearly a month now of me being unable to pay the loan, I have worked hard to keep my credit score clear of missed payments at all across multiple lines of credit. The single time the medical director did call, she actually called my aunt's number while I was at work and she has not contacted me back since.
I am at a loss of what to do at this point. I don't feel like I should pay this $7000 (ignoring that it's way beyond out of my budget)I did not agree to, along with the $800 on the care credit, it's over double what I agreed to, I couldn't be there to pick up the dog and had I known this if I went, I would have disputed it then. Also they could have charged my care credit more since it has deferred interest and they originally told me $1200 but they put the bulk of it on the loan which has a way higher interest rate. I feel extremely cheated and they didn't even do anything for our dog, we had to put her down the next day, despite all the insulin she was on, nausea medication, appetite stimulate, she still wouldn't eat. So I'm not sure what came out to be over $5000 exactly.
Is there anything I can do, someone I can contact, or a lawyer, would it be a consumer protection lawyer?

What food do you give an over weight cat that’s 12 years old. I just put down my 11 yr old cat last night due to diabetes and was unable to afford treatment he was way too far gone to save. I have a 20 yr old skinny male with arthritis and a 13 year old overweight cat that is probably diabetic as well similar symptoms but not as bad as the cat we lost.

For context. Dad is 70 years old, 144lbs, 5'5, type 2 diabetic on peritoneal dialysis. Earlier this year he began to develop wounds and dry gangrene on his toes and heels. He started going to for wound care treatment but had to get one of his toes amputated due to infection. Now at first while recovering and receiving antibiotics in the hospital he was doing fine for the first few 2 days however he was in an enormous amount of pain. The 3rd day, he began to tell me was starting to forget things. The next day was in a completely vegetative state. That may not be the correct thing to say but it's the best description i can think of. He will face me and the doctors with a blank stare but won't utter a word. On top that, he will not eat anything. That is what worries me the most. The nurses are just as clueless as I am and the doctor says it could be side effects from the antibiotics or he could be depressed. I personally don't think it's depression because he told me he was starting to forget things and he still winces when in pain and adjust himself in his bed. The CT scan came out normal and showed no signs of a stroke so that got ruled out. He will stay in the hospital as the continue his antibiotics so he will be monitored there for a bit. It all seems so bizarre but it reminds of the psych patients that get sedated. I'm open to any and all theories. Thanks.

Intermittent fasting has profound health benefits, and a growing body of research supports its effectiveness in improving metabolic health, boosting weight loss, and promoting longevity.
Here’s a complete guide to 18:6 fasting to get you started and practical tips and tricks to transition smoothly into extended fasting periods.

What is 18:6 fasting?

An 18:6 fast involves alternating between an 18-hour fasting period and a six-hour eating window.
Because of its simplicity, 18:6 fasting is one of the most popular intermittent fasting schedules that has helped many individuals lose weight, improve their metabolic balance, and enhance their overall health.
During fasting periods, the body is forced to utilize stored body fat instead of blood glucose to generate energy. This metabolic switch from using sugar as a fuel source to burning fat triggers ketosis.
Ketosis is a metabolic state that enhances the body’s ability to burn fat. This not only helps weight loss but also has been linked to improved energy levels, mental clarity, and better blood sugar control.
Watch the video below to discover why fasting for 18 hours can dramatically spike brain power.
Dramatically Spike BRAINPOWER with an 18 Hour Fast

Is it safe?

The 18:6 fasting regime has gained widespread popularity due to its impressive health benefits, and research repeatedly confirms the effectiveness and long-term safety of intermittent fasting.
A study published in Diabetes Care evaluated the safety of intermittent fasting in diabetic patients. The authors summarized that adherence to a time-restricted eating pattern is a safe and feasible therapeutic strategy to promote metabolic and hormonal health.
“From an evolutionary point of view, the human body is well adapted to intermittent fasting, which mimics the natural feast-and-famine cycles that our ancestors experienced,” explains Dr. Berg.
Although the 18:6 fast is considered safe for most people, it’s crucial to understand that some people should avoid fasting.

Who shouldn’t do 18:6 fasting

Intermittent fasting can increase the risk of unhealthy eating patterns in individuals with eating disorders.
In addition, those who are underweight or at risk of malnourishment could lose excessive body fat or develop nutrient deficiencies when limiting food intake to restricted time periods.
Pregnancy and breastfeeding are periods of increased caloric needs, and pregnant or breastfeeding mothers shouldn’t practice intermittent, prolonged, or alternate-day fasting.
Fasting can trigger profound metabolic changes, and it’s crucial to consult a healthcare professional if you have underlying medical conditions such as poor liver function, kidney disease, or low blood sugar, also known as hypoglycemia, before starting the 18:6 fasting routine.

Health benefits of 18:6 fasting

Although many individuals start practicing intermittent fasting to achieve a healthy weight, time-restricted eating has various other health benefits beyond weight loss.
Research published in The New England Journal of Medicine investigated the health benefits of the 18:6 fast and concluded, “The 18:6 fasting pattern can trigger a metabolic switch from glucose-based to ketone-based energy, with increased stress resistance, increased longevity, and a decreased incidence of diseases, including cancer and obesity.”
Here are five health benefits of 18:6 fasting.

1. Promotes a healthy body weight

Time-restricted eating patterns naturally limit calorie intake, which helps avoid weight gain and promotes weight loss.
However, the benefits of intermittent fasting for weight management aren’t just linked to calorie restriction during fasting windows.
Fasting stimulates growth hormone production, which can boost muscle mass and enhance the body’s capacity to utilize stored fat as a fuel source, thereby promoting fat-burning and weight loss.

2. May help reverse diabetes

Fasting for 18 hours keeps blood sugar levels balanced, which helps prevent insulin resistance linked to metabolic syndrome, obesity, and diabetes.
Intermittent fasting has been extensively studied as a potential therapeutic tool to prevent, manage, and even reverse diabetes.
A study published in JAMA Network Open found that time-restricted eating improved weight status, long-term blood glucose control, insulin sensitivity, and other metabolic health markers in diabetic individuals.
In fact, 18:6 fasting has such profound benefits for metabolic health that intermittent fasting could replace insulin for diabetes, potentially providing an effective and safe alternative to pharmaceutical diabetes treatments.

3. Boosts brain function

Evidence published in Nutrition Reviews suggests that fasting directly stimulates the release of brain-derived neurotrophic factor (BDNF).
BDNF is a crucial protein supporting neuronal cell growth and functionality. Higher concentrations of BDNF in the central nervous system are associated with improved cognitive function, memory recall, and mood regulation.

4. Triggers autophagy

Fasting for prolonged periods triggers autophagy, a cellular recycling and repair mechanism that removes damaged or dysfunctional cell organelles.
Autophagy is a crucial process that helps maintain cellular health and functionality, which is associated with a lower risk of various chronic diseases, including cancer, atherosclerosis, and neurodegenerative conditions such as Alzheimer's disease and dementia.

5. Supports heart health

Metabolic and cardiovascular health are intricately connected.
Obesity, blood sugar imbalances, and insulin resistance are all established risk factors for heart disease, significantly increasing the chances of cardiovascular issues such as high blood pressure, heart attacks, and strokes.
Intermittent fasting has been shown to restore balanced metabolic functions effectively. This makes time-restricted eating a powerful strategy for promoting a healthy heart and reducing the risk of cardiovascular disease.

How to start an 18:6 fast

The key principle of the 18:6 fast is to avoid food and calorie-containing beverages during an 18-hour fasting period.
While it may be tempting to start with 18-hour fasting periods immediately, it’s crucial to remember that your body needs time to adapt to prolonged caloric restriction.
Fasting for too long too quickly is one of the most common intermittent fasting mistakes and can lead to unpleasant side effects, including headaches, dizziness, irritability, and disrupted sleep.
If you are new to intermittent fasting, it’s recommended to start with a 14-hour fast followed by a ten-hour eating window and gradually prolong your fasting periods until you reach an 18:6 schedule.
How quickly you can achieve a consistent 18:6 fasting routine depends on your metabolic health and overall dietary pattern. While some individuals can fast for 18 hours within a few days, others may require several weeks to comfortably restrict their eating periods to six hours.

What can you drink while fasting?

During the initial stages of adapting to caloric restriction, fasting can lead to temporary fluid loss and disruptions in electrolyte balance.
Adequate fluid intake during fasting periods is crucial to minimize the risk of dehydration. However, it’s vital to consume calorie-free beverages that won’t break your fast.
Here are fasting-friendly drink options:

• Plain water
• Sparkling or carbonated water
• Lemon water
• Black coffee
• Black and green tea
• Herbal tea
• Diluted apple cider vinegar

In addition, replenishing electrolytes during fasting periods with a sugar-free electrolyte powder is an excellent option for maintaining the body’s fluid and electrolyte balance. This supports overall well-being and helps prevent fatigue, dizziness, and muscle cramps.
Many people who practice intermittent fasting drink bulletproof coffee during their fasting period to help curb hunger, boost energy levels, and enhance mental focus.
Although bulletproof coffee does contain calories, it’s considered fasting-friendly as it’s made with black coffee, butter, and coconut oil, none of which interfere with the body’s natural fasting state.

Tips and tricks

While time-restricted eating has various metabolic advantages, it’s equally important to consider what you eat during your eating windows.
Combining an 18:6 fast with a healthy diet can speed up fasting success and help you achieve your health and fitness goals more effectively.
Here are four tips and tricks to smoothly transition into an 18:6 fasting regime.

1. Eat plenty of healthy fats

Consuming plenty of healthy fats during your eating window plays a critical role in providing your body with fuel and can help maintain fat-burning even when you break your fast.
Obtaining the majority of your daily calories from fats while limiting carbohydrate intake keeps blood sugar levels low and forces your body to continue using fat to generate energy.
Limiting carbs keeps your metabolism in ketosis, which explains why a nutritious high-fat diet such as Healthy Keto® is an ideal intermittent fasting diet meal plan.
Combining keto with intermittent fasting is an excellent strategy to maximize the health benefits of ketosis and helps curb hunger and cravings during your 18-hour fasting period.
There are plenty of healthy fat sources on the keto food list to choose from, including olive and coconut oil, full-fat cheese, butter, heavy cream, seeds, and nuts.

2. Focus on nutrient-rich foods

Processed foods can increase the risk of nutritional deficiencies as they typically lack vitamins, minerals, fatty acids, and other vital nutrients necessary for overall health.
It's crucial to prioritize nutritious foods to ensure your body gets the nutrients it needs to function optimally, especially during fasting periods.
Healthy Keto focuses on nutrient-dense organic vegetables, grass-fed meats, wild-caught fish, and pasture-raised eggs, making it a perfect addition to an 18:6 intermittent fasting schedule.

3. Limit carbohydrates

Sugar and carbohydrate-rich foods, such as bread, rice, and pasta, are rapidly broken down and absorbed, which raises blood sugar levels.
Elevated blood sugar will stop ketosis and fat burning, as the liver prioritizes using blood glucose as a fuel source. Consuming carbs and sugars when you break a fast can slow fasting success and hinder weight loss.
In addition, sugar and refined carbs can cause blood sugar imbalances and energy fluctuations. This can trigger hunger and cravings during your fasting window, making it more challenging to achieve an 18-hour fast.

4. Avoid snacking

Breaking a snacking habit is crucial to smoothly transitioning into intermittent fasting and helps prolong fasting periods.
Consuming any foods that raise blood sugar levels, even low-calorie or healthy snacks, can break the fasting state and disrupt ketosis and fat-burning.
Although it might seem challenging to avoid snacking during the initial stages of adapting to intermittent fasting, hunger, and cravings will decrease as your body adjusts to using body fat for fuel.

Are you aware of this: The Treat and Reduce Obesity Act (TROA) is a bipartisan bill that would allow Medicare Part D to cover drugs for weight loss, including obesity screening and treatment. The bill was introduced in the 118th Congress in 2023, and would expand coverage to beneficiaries who are obese or overweight with related comorbidities.
I was not.
Look, the fat shamers have been blaming us forever for rising health care costs. Whenever you see your doctor, they blame every condition under the sun on your weight.
THEN, the insurers say "oh but we won't pay for weight loss therapies." This is an ASBURD and UNFAIR Catch-22. I have to get diabetes or heart disease first before you cover the underlying cause?!
This is ridiculous. If we are insured, we all deserve access to treatment. WL treatment is no different. This act is a start to normalizing coverage, for both retirees on Medicare and hopefully, too, commercial insurers are pressured as well.
Let's organize. Lets go people.

Hey guys and gals. I'm a former analyst at one of the big biotech-specialist hedge funds in Boston. I just left to manage my own investments, and I started a blog because why not? Believe it or not there can be deep value in biotech. I think SPRB is a one of the most compelling risk/reward net-nets I've seen - market cap $28M (85% drop recently due to market overreaction to meaningless data [my opinion]); Ph2 readout in 3Q; validated MoA and good biomarker data; net cash after readout is ~60M (I estimate). I've spoken to management and it's not obvious they'll burn all the cash if Ph2 fails. Pasting the text here but if you like it you should check out my blog for similar content, and subscribe.
https://open.substack.com/pub/vulpescapital/p/spruce-biosciences-upside-from-a?r=3pksaj&utm_campaign=post&utm_medium=web
Standard disclosure stuff: I own a lot of this, not investment advice, do your own research, consult a financial advisor.
An overreaction to negative but largely irrelevant data has created an irrationally attractive opportunity for:

1. High probability of success (PoS) Ph2 readout (validated mechanism [CRF1 inhibition in CAH], comparable biomarker data to nearly approved CRF1 inhibitor crinecerfont)
2. Downside protection: Price to net-cash = 0.36. Price to net cash post-Ph2 readout = ~0.5

Summary
SPRB is developing tildacerfont, a second-generation CRF1 antagonist for the treatment of congenital adrenal hyperplasia (CAH). A discussion of CAH pathology and standard of care follow below. CRF1 is a validated mechanism (first-gen CRF1 antagonist, crinecerfont, will likely be approved in April).
SPRB is a single-asset company, and has everything riding on tildacerfont. In mid-March, tildacerfont failed in a Ph2 CAH trial (study 203). Typically, when single-asset biotechs fail in Ph2, the company is dead. The market has decisively taken this position, and sent shares down ~85% on the news, where they have stayed.
SPRB is not dead. The company will release results from a second, more relevant, Ph2 (study 204) in 3Q24. I would argue that 203’s failure has little impact on the future of the company and that the trial was designed such that it tells us nothing about the prospects of study 204, which are quite positive.
Study 204 is being run in a much more appropriate patient population, and has a good PoS (60%-70% in my opinion).
At present, the market is offering an irrational price at which one can make a bet on 204’s outcome with a reasonable degree of downside protection (cash).

• Market cap = $28M (not fully diluted – warrants priced way OTM)
• Net cash = $81M
• Burn = ~$12M per quarter
• Quarters to data = 2
• Projected net-cash post Ph2 readout = ~$57M

Though I’m typically not inclined to assume downside protection from cash in dev-stage biotechs (and SPRB management is not very invested), the cash here is considerable, and management has few other options to squander the cash.
Though I’m not relying on a short-term price prediction, it wouldn’t shock me if SPRB traded up into data as investors digest the fact the study 203 data weren’t interpretable positively or negatively, and I would consider selling before 204-readout if offered a fair price.
CAH
Patients with classic CAH are unable to make cortisol due to a genetic deficiency in the enzyme (21-hydroxylase) responsible for its production. Cortisol is a negative regulator of a signaling pathway called the hypothalamic-pituitary-axis (HPA). Below, I do my best to explain the HPA’s role in CAH, in plain English:
Androgens are hormones produced by the adrenal gland which have an effect on bone density, muscle mass, and reproductive development among other things. The best known example of an androgen is testosterone.
Androgens are produced in response to a signal from the pituitary gland to the adrenal gland. The signal molecule is called ACTH.
ACTH is produced in response to a signal from the hypothalamus to the pituitary. The signal molecule is called CRH. The pituitary receives the CRH signal through a receptor called CRF1.
The amount of CRH production by the hypothalamus (and thus ACTH and androgen production) is negatively impacted by the presence of cortisol, which is produced by the adrenal gland in response to ACTH. Thus, a hyper-active HPA will produce more cortisol, which puts on the HPA’s brakes and keeps it in check. Conversely, an under-active HPA will produce little cortisol, which can boost it. Lots of signaling pathways maintain homeostasis in a similar way.
Because patients with CAH cannot make cortisol, they have over-active HPA’s, and make way too many androgens. A whole lot of bad things happen when patients produce too many androgens—examples include deformed genitalia, early puberty, shortened stature, and inability to regulate salt concentrations.
Additionally, cortisol absence results in other problems unrelated to androgen production.
CAH treatment
The two main goals of treatment are 1) resupply the body with cortisol, because it needs it, and 2) resupply the body with cortisol to dampen the HPA and reduce excess androgen production.
As such, patients take a glucocorticoid (GC; a steroid; basically cortisol). Since they can’t make cortisol, they’ll have to take a GC for the rest of their lives.
CAH patients need to take very high GC doses to dampen androgen production, which leads to significant side effects such as stunted growth, obesity, increased risk of developing type 2 diabetes, cardiovascular disease, osteoporosis, skin toxicities, gastrointestinal disorders, and reduced lifespan. GC doses also need constant readjustment. Basically, they’re not fun to take.
CRF1 inhibition
If we refer back to the mechanism of CAH pathology, it would seem that if you could block the signal (CRH) from the hypothalamus to the pituitary, that might have the same effect of dampening the HPA as cortisol does. One could achieve this through the design of an antagonist (drug) that binds CRF1, blocking CRH’s access to the receptor.
Does this work? Yes, we already know that it does. Crinecerfont (Neurocrine) is a first-generation CRF1 inhibitor that generated positive Ph3 data in CAH. Patients on crinecerfont were able to reduce GC usage to a stat-sig greater extent than patients on placebo. Moreover, 68% of patients on crinecerfont reduced GC usage to a physiologic level, compared to 18% on placebo. The drug will likely gain FDA approval in the coming weeks (PDUFA date April 30). Estimates of peak sales are in the $1B range).
Tildacerfont
Tildacerfont is a second-generation CRF1 antagonist. Compared to crinecerfont, tildacerfont has better pharmacokinetics and is being dosed once-daily vs. twice-daily.
Does tildacerfont work? It appears to… we have proof of mechanism/target engagement. Here’s what we know:
In patients with poor disease control, tildacerfont (when they take it) significantly reduces elevated ACTH, 17-OHP, and A4 levels (the latter two are downstream markers). Biomarker levels rose again upon termination of treatment (data not shown - can't copy image here).
In patients with good disease-control (patients without severely elevated androgens), tildacerfont didn’t have much of an effect. That’s not such a bad thing— the goal is not to lower androgens (which are already successfully controlled in this population), but to allow these patients to reduce their GC usage.
These biomarker responses were approximately similar to those observed after 2-weeks of treatment with crinecerfont (data not shown - can't copy image here).
All this to say, tildacerfont has a good shot at reading out positive data in study 204, which has the same primary endpoint as crinecerfont’s phase 3, and a similar patient population.
Why this opportunity exists: Phase 2 failure
There are two types of CAH patient:

1. Patients with severe-CAH and poor-disease control. These patients struggle to control their HPA’s despite GC usage. The goal in treating these patients is to bring their androgen levels back towards the upper limit of normal.
2. Patients with good disease-control. These patients, through GC usage have androgen levels close to or within the normal range. The goal in treating these patients is to allow them to reduce their total GC usage.

Spruce decided to run two Ph2 trials–one in each patient group, with the goal of 1) improving disease-control in poorly controlled patients and 2) allowing patients with good control to lower their GC usage. The Ph2 in patients with severe-disease patients (study 203) read out last week. The Ph2 in patients with good disease control (study 204) will read out in 3Q24.
203 did not meet its primary endpoint – a reduction in A4. This looks like a very bad sign and the market reacted mercilessly. There are 40M shares outstanding, and 37M shares traded in the three days following data read-out.
Why did this trial fail and what does this mean for the next one?
The company is blaming their Ph2 failure on poor patient compliance, and I find this to be a reasonable explanation—only 50% of patients were >80% compliant.
The low compliance is cause for concern because a safety/tolerability issue could derail the drug. The company is making the argument that low compliance is an attribute of the poorly-controlled-CAH patient population. I don’t like to blindly trust management teams when they make statements like this, but take comfort in their disclosure that compliance is much higher in study 204. Moreover, discontinuations were quite low at 10% (typically you’d expect around 20%) and there were no safety issues.
The company found a KOL to attend their post-data investor call and say that “The CAHmelia-203 results underscore the complexities inherent in managing a patient group with challenges related to androgenic control and GC compliance. Based on my clinical experience, patients within this group may face difficulties adhering to any therapeutic interventions, potentially impacting treatment outcomes…”
When pressed on the call as to the reason for the low compliance in the 203 population, she insinuated that these patients are often poorly-controlled as a result of their low adherence to medication. This sounds reasonable, but again, what’s important is that we already know compliance is much higher in study 204.
The KOL added that the population in the ongoing Ph2 is more indicative of the patients that are seen in the clinic.
In sum, given the validated mechanism, observed biomarker data, and improved compliance, I give the ongoing Ph2 a 60%-70% PoS.
Valuation
The valuation range post-positive data is wide, but I’m not concerned with precision since the value is most assuredly multiples of $29M.
Sell-side analysts are projecting $500M peak sales (could be higher, as they project crinecerfont peak sales of $1B). At 2X peak sales, accounting for exercise of options/warrants plus 30% dilution on top, I arrive at $13/sh on approval. Discounted back two years and adjusted for PoS, I arrive at $7.5/sh of fair value today. It sounds a little crazy to say that the FV today is 10X the current price given study 204 data is on its way in two quarters, but I would consider that a month-and-a-half ago the stock was trading in the $5 range and, in my opinion, the prospects of the drug haven’t changed at all. Though I can’t predict short-term price action, I would not be surprised to see this trade up into data and would consider getting out before 204 read-out if given a fair price.
Disclaimer: The views and opinions expressed in this blog post are solely those of the author and should not be construed as investment advice. The author owns shares in the company discussed in this post. Please be aware that all investments involve varying degrees of risk, including the potential loss of principal, and there are no assurances that any investment will match or outperform any particular benchmarks or indices. As always, it is important to conduct your own research and consult with a qualified investment professional before making any investment decisions.

F 29, 5'4", 190 lbs
I take ozempic for T2 diabetes and weight loss, but I was on autopilot on Sunday and took it (0.5mg) even though I'm scheduled for endometriosis excision surgery tomorrow. What do I do? I'm scared if I tell them they'll make me reschedule. I've been waiting three months for this surgery. I have severe mental health issues but I can't get into residential treatment until after surgery since I need opioids (oxycodone 10 mg every 8 hrs as needed). My last self harm relapse needed surgery. I need residential. I need this surgery. I can't wait another three months. Can I do a colon cleanse? I haven't eaten since 6:30 pm yesterday. My surgery check in is 1 pm tomorrow. I can take my vyvanse to decrease my appetite.
I take a lot of medications and have a lot of mental health and chronic physical health conditions. It's a long list. Let me know if you need it.

Eli Lilly raised its annual revenue forecast by $2 billion on Tuesday due to strong demand and plans to increase production of its weight-loss treatment Zepbound and related diabetes drug Mounjaro, lifting its shares about 7% premarket.
Sky-rocketing demand for Mounjaro and Zepbound, both chemically known as tirzepatide, has propelled the drugmaker's market value above $700 billion - surpassing both Tesla and Walmart.
However, supply for the drugs remains constrained. Most doses of Mounjaro and Zepbound are expected to be available in limited amounts through the second quarter, according to the U.S. Food and Drug Administration's website.
Lilly said its raised forecast reflects "greater clarity about the company's production expansion for the remainder of the year".
The company continues to expand manufacturing capacity for the drugs, with the most significant production increases expected in the second half of the year. It had earlier said demand would outpace supply this year despite the increased capacity.

The generic injectables market is a crucial segment of the pharmaceutical industry, encompassing a wide range of injectable drugs that are bioequivalent to branded drugs but typically cost less. These drugs are essential for treating various medical conditions and are widely used in hospitals, clinics, and other healthcare settings.

Market Size and Growth

In 2023, the generic injectables market was valued at USD 114.47 billion. The market is expected to grow at a compound annual growth rate (CAGR) of 13% during the forecast period of 2024-2032, reaching a value of USD 343.87 billion by 2032. This growth is driven by several factors, including the increasing prevalence of chronic diseases such as cancer and diabetes, as well as the rising demand for cost-effective treatment options.

Market Drivers

One of the key drivers of the generic injectables market is the growing prevalence of cancer worldwide. Chemotherapy, which is a common treatment for cancer, often requires the use of injectable drugs to manage side effects and improve patient outcomes. Additionally, the rising demand for injectables in chemotherapy is further fueling market growth, as healthcare providers seek more affordable treatment options for their patients.

Competitive Landscape

The global generic injectables market is highly competitive, with several key players dominating the market. Some of the major players in the market include Fresenius Kabi, Hikma Pharmaceuticals PLC, Sagent Pharmaceuticals, Inc., Sanofi, and Sandoz (Novartis). These companies are constantly innovating and investing in research and development to maintain their competitive edge in the market.

Market Challenges

Despite the growth prospects, the generic injectables market faces several challenges. Regulatory challenges, such as the need for approval from regulatory authorities for the sale and distribution of injectable drugs, can hinder market growth. Pricing pressures and the presence of generic competition also pose challenges for companies operating in this market.

Future Trends

Several trends are expected to shape the future of the generic injectables market. Technological advancements in injectables, such as the development of novel drug delivery systems, are likely to drive market growth. Additionally, the increasing focus on biosimilars – which are generic versions of biologic drugs – is expected to create new opportunities for market expansion.

Regional Analysis

The market size and growth of the generic injectables market vary by region. North America and Europe are the largest markets for generic injectables, driven by factors such as the presence of a well-established healthcare infrastructure and favorable reimbursement policies. In contrast, the Asia Pacific region is expected to witness the fastest growth during the forecast period, fueled by factors such as the growing prevalence of chronic diseases and increasing healthcare expenditure in emerging economies.

Product Segmentation

The generic injectables market can be segmented based on the type of injectable drug. Common segments include oncology, anti-infectives, cardiovascular drugs, and others. Each segment has its own market dynamics and growth prospects, influenced by factors such as disease prevalence and treatment guidelines.

Distribution Channels

Generic injectables are typically distributed through various channels, including hospitals, clinics, retail pharmacies, and online pharmacies. The choice of distribution channel can impact market growth, as each channel has its own advantages and limitations in terms of reach and accessibility.

Regulatory Environment

The regulatory environment for generic injectables varies by country and region. Regulatory authorities such as the FDA in the United States and the EMA in Europe play a key role in ensuring the safety, efficacy, and quality of generic injectables. Compliance with regulatory requirements is essential for market entry and success.

Investment Analysis

Investing in the generic injectables market offers several opportunities for investors. The market is expected to grow significantly in the coming years, driven by factors such as the increasing demand for cost-effective treatment options and the growing prevalence of chronic diseases. However, investors should also be aware of potential risks and challenges, such as regulatory hurdles and pricing pressures.

Impact of COVID-19

The COVID-19 pandemic has had a significant impact on the generic injectables market. The pandemic led to disruptions in the global supply chain, affecting the production and distribution of generic injectables. However, the market has shown resilience, with companies adapting to the new normal and implementing measures to mitigate the impact of the pandemic.

Sustainability and Environmental Impact

There is a growing focus on sustainability and reducing the environmental impact of pharmaceutical manufacturing. Companies in the generic injectables market are increasingly adopting sustainable practices, such as reducing waste and energy consumption, to minimize their environmental footprint. These efforts not only benefit the environment but also contribute to long-term market growth and sustainability.
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