Go Get Yourself A Monkey Kidney
Melinda sends along this nicely depressing news: fat people are screwed when it comes to organ transplants.
Segev’s group found the wait to get a transplant increased along with the patient’s body mass index, a height-weight formula. Non-obese patients waited on average 39 months, the overweight waited 40 months, the obese waited 42 months, and the severely and morbidly obese, waited 51 and 59 months, respectively, the researchers found…
However, Philosophe said he and many doctors “will give them the benefit of the doubt that they will lose the weight and will put them on the list hoping that while they lose that weight they will accumulate waiting time.” Patients who fail to lose weight can be placed on inactive status.
Melinda says:
So wait….if someone has a failing or failed kidney/lung/liver, how the fuck are they supposed to be out there exercising to lose weight? Now here’s the part that pisses me off the most…why are obese patients all being painted with the “more at risk for complications” paintbrush? Does that mean they would give a new kidney to a smoker with a history of alcoholism before an obese patient with no health problems other than kidney disease? A BMI of 40 is only 250 pounds for a woman who’s 5’6″, and we all know that you can be a healthy, athletic person at that size; the idea of being denied a transplant or shoved down on the list in hopes of losing weight is absurd. Fucking crap on a cracker, this one pisses me off.
I mean, I’m an organ donor and I always have been; I really believe in it. How much do you want to bet that they’re going to take my fat organs and happily give them to thin people? AND I’LL BE DEAD! Oh man, I’m depressed now. (At least I was able to use a quote from The Office as the post title. Every cloud…)
Posted by mo pie
Filed under: Fatism, Health, Science, The Office
oh man! now I am totally pissed off too! as an organ donor and a chubby, that makes me mad. rrrrrr!
the quote from the office helps ease the pain though. thanks.
As the article mentions, because these researchers had only limited information about the health of transplant candidates , it’s impossible to say what role anti-fat bias plays in this phenomenon on the basis of this study. It is a harsh reality, but given the shortage of organs available for transplantation, doctors have to make choices about which patients stand to gain the most from transplants. I know this all too well, as my father will likely require a kidney transplant in the near future, but will be unlikely to get it due to his age (he’s in his sixties).
I don’t always love the weight loss recommendations that transplant teams hand out to the dialysis patients I work with, it’s true, but I know that we’ve had plenty of big folks transplant in the 7 years I’ve been around dialysis.
Oh, and they do put people who smoke on substance abuse contracts…if they can’t follow-through and quit, they are put on inactive status, as well (which by the way, still means they are accruing time on the list and making their way to the top).
And folks who are on dialysis can, often, have the energy to do exercise if they want. They have special considerations for types of exercise depending on the type of dialysis they are doing, but many of our folks are very active.
The frightening thing to me is that the average wait for a kidney for a patient with type O blood is 7 years (regardless of conditions of transplant) and statistics say that mortality of people on dialysis increases dramatically after 5 years on treatment. Those aren’t good odds no matter how you stack them.
I’m glad you are a donor – I hope that everyone considers it!
La Wade – age is less of a consideration than it used to be for patients. Your father might be offered an opportunity to be on a wait list for a kidney from someone like me…I have high blood pressure, but my kidneys are working fine. In the past, my kidneys (because of the HTN might have been passed over because there might be some damage to them), but they are now being offered to those who may not be best suited to wait the 7 years due to age or other mitigating factors.
Is it possible that fat patients wait longer because they’re in relatively better health? I know that fatphobia is rampant, but as Sandy has pointed out more than once in her “paradox” posts, maybe fat patients wait longer because they don’t degenerate as quickly.
Not a good thing, but not as black as it might at first appear.
I have a dear friend that we almost lost to Bronchiolitis Obliterans (as a complication of RA). She required a double-lung transplant, and was moderately overweight–about a 16. The transplant team gave her a pretty good amount of shit about it. (Yeah, because it’s so easy to lose weight when you can’t breathe and you’re jacked up on steroidal anti-inflammatories!)
But she got her transplant and came through with flying colors, and is a model of good recovery, six years on. She lectures about transplants and organ donation now. It’s scary to think how close we came to losing her because of the stupid disease–if we’d lost her because of her fricking BMI, I think I’d have burned down the hospital.
It is discrimination no matter how you look at it. If you are simply looking at BMI – that is bullshit. Doesn’t mean a damn thing. I am 5’2″ and 197 pounds. I am so healthy it pisses my doctors off. My cholesterol is 138, my BP is 117/78 – No medicines, no diabetes, no thyroid problems. I eat good solid decent food, very little sugar. I don’t smoke – I have a glass of wine once in a while but that is pretty much it – Healthy. and *gasp* fat! Pisses them off. If something eve happens that I need a transplant – what REAL grounds would they have to deny me? That I am fat? That I don’t fit into their charts??
Sorry – but that is discrimination. And whyme – that would have been justified – to burn it down.
What a sick, nasty world we live in.
As I learned from watching ER, and as La Wade points out, there are always difficult decision to be made around organs and younger, healthier people definitely are prioritized over older people… I guess the cold hard truth is, they’ll get more use out of the organ.
What if someone has destroyed their liver via alcoholism; should they be in line ahead of a teetotaler? (I think that was a discussion when an alcoholic athlete… was it Mickey Mantle? got a liver transplant.) And how do doctors make judgement calls like that?
Anyway, it wouldn’t be an issue if more people donated their organs. There wouldn’t be seven-year-long waiting lists. Thank you, Spins, for reminding everyone how important it is to be a donor.
DaisyBug, how _dare_ you be fat at doctors!? Don’t you know that’s an affront to the whole medical community?!
Good on you, though. I make a habit of avoiding doctors when I can.
I forgot to mention in my earlier post that I think the real black box in this study is diabetes. Diabetes is the number one reason for people needing kidney transplants (because fluctuations in blood sugar slowly destroy your kidneys) and obesity is the number one risk factor for diabetes. It looks like they did control for the presence or absence of diabetes here, but the researchers didn’t have information about whether patients’ diabetes was well controlled or not. Since weight loss can often help to moderate diabetic symptoms, it seems plausible to me that high BMI patients may have been less likely to receive transplants because they were more likely to be in poor health from uncontrolled diabetes. Of course it is also plausible that doctors may have subjectively perceived the high BMI patients to be sicker because of their own bias. Or (most plausible of all, if you ask me) it may be some combination of the two.
Wow. I might be considered an awful person, but even *I* think that’s rather offensive. Then again, I’m not a doctor, so I don’t feel qualified to judge the way they choose who gets an organ.
I always assumed you were put on the list and your organ was available in the order you were in.
I’m also a donor, though who would want my black anger filled organs is up for debate, I suppose ;).
Man, I just hate it that medical journals issue press releases before the articles go live online. Drives me batshit that I can’t read the original source. For example, I would love to know whether the heavier patients were more likely to wait for transplant because they were more likely to need both kidney and pancreas transplants. (I don’t know that they were, but the paper should say one way or the other.)
Daisybug said, “If you are simply looking at BMI – that is bullshit.” According to the United Network for Organ Sharing, under the mandate of the National Organ Transplant Act, a committee is currently working on medical criteria for equitable kidney allocation (http://www.unos.org/kars.asp) and is considering a metric that takes into account “age, diabetes status, BMI, albumin, degree of sensitization (PRA), and degree of HLA mismatch with a potential donor.” BMI is in there because it contributes to years of survival (and I cannot vouch that the actual measure used is BMI per se) but it’s not just BMI.
Some of the reasons that fatter people (not higher-BMI folks) have a higher complication rate with surgery in general are: it’s hard to see when there’s a lot of fat in the surgical area; fat has poor vascularization and thus fatter people are more likely to experience wound dehiscence and/or infection; at the same time, the more fat tissue surgeons have to cut down through to get to their objective, the greater the likelihood of a bleeding event; and if a person has limited mobility before surgery because of his size, then he is at greater risk for post-operative complications of decreased mobility (pneumonia and blood clots) than his more-mobile peers. (That last obviously applies to everyone, not just fat people, and there are plenty of fat people who move around just as well as their thin counterparts. Generally, though, the bigger you are, the more work it is to move around, even when your size isn’t about fat – this is one part of why pituitary giants often die of heart failure.) Obviously, fat people and even morbidly obese people have surgery every day; but taken as a group, fat people are at increased risk from surgery.
All that said, the utility criteria are supposed to be balanced by the justice criteria – it’s not supposed to be a straight-up consideration of who will live longest, but a consideration of fairness of distribution. Even if fatness decreases the lifetime survival benefit, I think it’s unjust to limit access to organs on the basis of fatness (much less BMI, which is not a precise enough measure of fatness for life-and-death.) If two people are otherwise completely equal in their survivor predictors, the organ shouldn’t always go to the one with the lower BMI. That’s nuts.
Ginger, the paper is available on the JASN website if your institution has a subscription, under the “JASN express” section. They don’t say anything about pancreas transplants, although diabetes was a statistically significant covariate, as would be expected. The authors seem to have been pretty limited in terms of the information they had available to them.
Something else interesting not commented on in the paper or mentioned in the article: Hispanics and African-Americans were also less likely to receive transplants and more likely to be passed over for them…their numbers were about the same as the BMI=40-60 group. I don’t know if that has to do at all with available donor haplotype compatibility, or if it’s just bias. You’re also apparently screwed if you need a kidney and you’re on Medicaid.
Thanks, La Wade! I looked up the article, and it does appear they looked only at deceased-donor kidney transplants, not kidney-pancreas transplants. However, the likelihood of bypass (i.e. being skipped over for an organ offer), which we would expect to be lower among the obese if the obese who required both a kidney and a pancreas (i.e. the sicker ones more likely to need transplanting) were pulled out of the study population, rose with BMI. Also, the paper contends that the main criterion for kidney transplantation is date of listing, so this is probably a fairly dependable indication of provider bias.
I would also have liked to know about donor characteristics during this time period, because the blood-type results confused me for a minute: the most likely group to be transplanted was AB, then A, then O, then B. That’s pretty wildly inconsistent with the distribution of blood types in the US overall or among any ethnic group (O is most common, A second, B third, AB least among all the groups, with different proportions among the groups.) The likelihood of bypass rises from B to AB to A to O. I think overall the blood type information suggests that if an opportunity arises to transplant a rare-blood-type organ, even if the patient isn’t especially ready to go at the time, the opportunity is seized. So it’s pretty grim that both BMI and race/ethnicity appear to affect transplant and bypass probability.
(Analytically, it’s a really nice paper.)
obesity is the number one risk factor for diabetes
You mean the other way around, right? Type 2 diabetes causes obesity; being fat doesn’t make you diabetic. (While it’s true that increasing activity and decreasing carb intake, for a person with Type 2, will generally both cause c. 10% weight loss and improve blood glucose control, this doesn’t mean that losing weight cures diabetes. Rather, the things activity and eating that improve blood sugar control also tend to cause weight loss to the bottom of the person’s normal range.)
When discussing these topics, it’s critical to keep the causative chains straight – otherwise people read it carelessly and take away nonsense lessons such as “people make themselves diabetic by eating!” (and therefore denying fat people kidney transplants is justified because they magically gave themselves diabetes in the first place). There’s already enough of that sort of thing going around, I think.
This all sounds more fluid than I’d thought. I know some transplant centers, by fixed policy, simply won’t transplant anyone with a BMI over 35 or 40 (in the US – I’ve heard of lower limits in the UK), and I had sort of gotten the impression that this was more or less universal. I guess I’m less depressed than other commenters about this because I’d thought it was even worse.
Jaed, no, I mean that obesity causes diabetes (type II diabetes, that is, which accounts for more than 90% of all diabetes). Diabetes does not cause obesity…in fact, untreated diabetes results in weight loss.
The main mechanism by which obesity results in diabetes is that fat tissue secretes a number of factors into the blood in rough proportion to the fat’s abundance. These factors, including non-esterified fatty acids, hormones such as leptin and adiponectin, and proinflammatory cytokines, are all supposed to help the body maintain a “normal” weight, but long-term exposure to high levels of these factors can cause insulin resistance, and eventually type II diabetes. Sedentary lifestyle is also a risk factor for both obesity and type II diabetes, but that is an indirect link
Obesity is not the only risk factor for type II diabetes, of course. But it is the one with the strongest association.
Actually, La Wade, you can get a kidney transplant on Medicaid…my patients do it all the time. It’s simple economics, the transplant pays for itself within three years.
Spins, I was just referring to the fact that in the study, they found that Medicaid recipients were only 71% as likely to be chosen for a transplant compared to people with private insurance (whereas people on Medicare were 99% as likely). You’re right that these people aren’t precluded from getting transplants, but that’s about the same level of disadvantage as being black or obese.
Not that I’m obsessed with this study or anything, but I wonder what an examination of the likelihood of getting on the transplant list would say about the same variables. I don’t think there is a dataset available for that – by definition, you’re just another guy with a kidney-related discharge code, among millions of other discharge codes, until you’re on the list – but that doesn’t make the bias issue go away.
It’s nice how humanity can be rounded up into scientific studies, isn’t it?
jaed, you forget the #1 rule!
Fat = bad and unhealthy! All the scientific studies point that way!
Since weight loss can often help to moderate diabetic symptoms, it seems plausible to me that high BMI patients may have been less likely to receive transplants because they were more likely to be in poor health from uncontrolled diabetes. Of course it is also
Weight loss might, in some cases help insulin resistance to some extent, but carbohydrate restriction has a larger effect on blood glucose levels and blood pressure, even in the absence of weight loss.
Diabetes does not cause obesity…in fact, untreated diabetes results in weight loss.
Eh? Certainly insulin resistance causes obesity. It’s one of the most visible symptoms if not the most visible. Insulin resistance promotes glucose uptake and conversion by fat cells (since the insulin resistance keeps serum glucose elevated for extended periods of time), and the chronic hyperinsulinemia that goes along with it inhibits fat tissue loss (because fat cannot be metabolized in the presence of insulin). The mechanisms are well understood and have been for decades.
When you say “untreated diabetes results in weight loss”, I think you’re thinking of Type 1 diabetes. Type 1 has a completely different etiology and yes, unexplained weight loss is often a symptom (because the lack of insulin in Type 1, as opposed to the overabundance in Type 2, causes wasting). Although such wasting may occur in patients with “double diabetes” (Type 1 occurring along with usually longterm untreated Type 2), it is not a symptom of Type 2 diabetes per se.
Insulin resistance does cause a mild deficit in utilization of fat as an energy source, but a more prevalent effect of insulin resistance is that you’re not able to utilize the glucose you consume, so there is a net loss of weight. Type I diabetes also causes weight loss because the absence of insulin has the same effect as insulin resistance.
Luckily, most people get treatment for their type II diabetes before it becomes severe, but in animal models I work with in the lab, untreated diabetes results in significant wasting.
Insulin resistance does cause a mild deficit in utilization of fat as an energy source, but a more prevalent effect of insulin resistance is that you’re not able to utilize the glucose you consume, so there is a net loss of weight.
Insulin resistance does not cause weight loss it causes fat storage. You aren’t able to utilize the glucose in muscle cells because they are more resistant than fat cells. Most of the carb you consume in the presence of insulin resistance (and because of hyperinsulinemia, also the protein and fat,) goes to storage in the fat cells. This is the reason people are more sedentary when they are insulin resistant, muscle recovery of glycogen after exercise is inhibited. There is little energy available for exercise or anything else. Hyperinsulinemia causes insulin resistance to increase in a vicious cycle, it leads to wide fluctuations in blood glucose levels that can cause extreme hunger, and it inhibits the use of energy stored in the fat cells. The amount of added resistance due to weight gain is trivial compared to the amount of resistance added by increasing levels of insulin in the blood. It’s a miracle when insulin resistance doesn’t lead to weight gain. Diabetes will only result when a defect of insulin production in the pancreas means it is unable to continue increasing production of enough insulin to overcome the resistance. There are more fat people who will not get diabetes than will because they do not have this pancreatic defect. All along, during this process insulin resistance in the liver complicates the whole scenario by again, increasing glucose levels in the blood which also goes to more fat storage. Even on a WLD, muscle and organ tissue may be broken down by the liver to make more glucose which may still go to fat storage unless insulin levels and resistance can be controlled.
Weight loss from any type of diabetes (muscle wasting mostly) only occurs after blood glucose has risen to a level that causes it to spill into the urine, increasing thirst and again, hunger. This wasting is more dramatic in Type 1 because the people usually start out without resistance, therefore thin, and lose their capacity for insulin production rapidly. A skinny person losing 20 pounds in a couple of weeks is a lot more noticeable than a fat person getting slowly fatter over the course of years and then losing a very small percentage of their weight. A really fat person’s weight can fluctuate that much in a couple of days just from water retention.
Read:
“You Did NOT Eat Your Way to Diabetes!
Don’t fall for the toxic myth that you caused your diabetes by reckless overeating” at
http://www.phlaunt.com/diabetes/14046739.php
Read more about:
“What They Don’t Tell You About Diabetes” at:
http://www.phlaunt.com/diabetes/
Many articles, well documented.
I agree that in the early stages of diabetes, some people experience weight gain as a consequence of increased appetite and promotion of fat storage. But as diabetes progresses, the catabolic side takes over. At any rate, it is exceedingly rare for a lean person to develop type II diabetes and then become obese as a result, which is what Jaed suggested. A majority of type II diabetes patients are obese prior to becoming diabetic, and weight loss has been shown to decrease risk of type II diabetes and weight gain to increase that risk. In addition, many mechanistic studies have been carried out in the last 10 years demonstrating how secreted factors from adipose tissue influence glucose homeostasis.
Before diabetes develops, insulin resistance causes weight gain, sometimes over decades. That is why most types 2s are overweight or obese. Young, thin people without diabetes who are related to diabetics have been shown to already have signs of insulin resistance, ie hyperinsulinemia even without any deterioration in blood sugar control. Read the articles.
Obesity does not cause diabetes, it is ASSOCIATED with diabetes and there is no study anywhere that shows obesity causing diabetes. It is a myth, a dangerous myth that does a disservice to all diabetics, fat diabetics because they are led to believe they caused their disease and the only way to control it is something they have had no long term success at and thin diabetics because they are often misdiagnosed for years because doctors don’t test thin people, even with classic symptoms but slow onset.
The articles you linked claim that diabetes is primarily genetic in origin, which is at odds with the fact that U.S. rates of diabetes have doubled in the last ten years despite a lack of dramatic change in the gene pool. Diabetes certainly has a genetic component, but environmental factors, including obesity, contribute to diabetes, as well. And there are thousands of studies contributing to the body of knowledge that obesity causes diabetes. If you have access to a medical library, a good review article is Kahn et al., Nature 444, 840-846 (14 December 2006).
Furthermore, many patients are obese for 20 or 30 years or more before being diagnosed with type II diabetes. Do you really think it seems plausible that a patient group at high risk for this common disease could routinely go undetected for such a long period of time?
Anyway, I do agree with you about one thing: type II diabetics should not be blamed for their condition. Obviously, nobody deserves to get a disease, and the prevalence of obesity and overweight in our society is a testament to the extreme difficulty most people have in avoiding it.
Not at odds if you believe the huge increase in sugars, other highly refined carbs and vegetable oils in the standard American diet may have a deleterious effect on the expression of our genes. The quality of our food has deteriorated. We may be fat but many of us are also malnourished. It isn’t how much we eat it’s what we aren’t getting from what we eat. We’re also exposed to pollution, plastics and other hydrocarbons, hormone-mimics, other chemicals, etc. Obesity isn’t the biggest change in our environment, it’s actually one of the smallest differences, but all we hear where ever we turn is ‘teh fat’ ‘teh fat!’ The amount of crap we are exposed to from the time we are conceived is vastly different from previous generations, we’re practically on a different planet. Just the amount of (nutritionally bankrupt) sugar we ingest is orders of magnitude higher than the amount our grandparents had. You don’t need a dramatic change in the gene pool to explain an epidemic, if it indeed exists. I suspect that insulin resistance, the resulting obesity and probably the pancreatic defects causing most cases of type 2 diabetes will turn out to be at least partly epigenetic. Someday, almost everything in our environment may be found to have an effect on gene expression. Just the amount of sugar we consume may be enough, by itself, to explain any increase in insulin resistance and obesity.
Also, not at odds if you believe the type 2 diabetes epidemic is as overstated as the obesity epidemic. The average person has only gained a few pounds. The criteria for a diabetes diagnosis seems to have changed as much or more than the BMI chart did a while back. After all, years ago there were no drugs, besides insulin, to treat diabetes, the home blood glucose monitor wasn’t available. The pharmaceutical reps weren’t in the doctors’ offices constantly trying to get them to diagnose it so they could sell more drugs for it. Some doctors once tried to avoid making the diagnosis to spare their patients the social or economic disadvantages. My DH was recently diagnosed as type 2 with the same, supposedly normal, fasting blood glucose that I had at my annual physical for at least 15 years, that I know of, before I was diagnosed. That 15 years began before I gained 80% of my fat. In fact, I may not have been technically overweight then, according to the BMI charts of the time, if they existed.
I never said that decades of weight gain is caused by undiagnosed diabetes, it is caused by insulin resistance. When you get diabetes depends on when (or if) your pancreas finally craps out on you. Many fat people will never get it because they keep making new ß-cells so insulin production increases to keep up with and also exacerbate the insulin resistance, while they keep getting fatter and more resistant. After all, insulin’s job is to stuff glucose into cells. When the liver and peripheral tissues are more resistant than the fat cells, guess where it goes? When a fat person stops gaining weight (gets to their ‘set point’) it usually just means their fat cells have finally become as insulin resistant as their muscle cells.
Insulin resistance causes at least some, probably most, obesity. Insulin resistance and a dysfunctional pancreas causes type 2 diabetes. Correlation is not causation. Don’t stress your pancreas with a lot of carb if you know diabetes is in your family and you may be able to delay developing it. The knowledge is out there but you probably won’t hear it from a doctor and it’s a lead pipe cinch you won’t hear it on the news.
Sorry mo pie, I’ll quit here.
(btw I barely have access to a public library.)