‘Obesity Paradox’ Apparent in Heart Failure
Trigger warning: Discussion of weight, health and weight loss.
Here’s another article for the “No shit, Sherlock” file: “‘Obesity Paradox’ Apparent in Heart Failure” (complete with the requisite headless fatty photo that just has to accompany any article about being fat). That “obesity paradox” they’re talking about is the fact that fat people don’t die as often as their thinner peers when they have heart problems.
“The nicely-designed study by Khalid et al. in this issue of the Journal provides perhaps the best evidence that the obesity paradox is not simply due to cachexia in late-stage [heart failure] or reverse causality,” Thomas J. Wang, MD, of Vanderbilt University Medical Center, in Nashville, Tenn., wrote in an accompanying editorial.
Cachexia /ca·chex·ia/ (kah-kek-se-ah)
1: A profound and marked state of constitutional disorder; general ill health and malnutrition.
2: Weight loss, wasting of muscle, loss of appetite, and general debility that can occur during a chronic disease.
3: A condition of general ill health, malnutrition, undesired weight loss, and physical weakness, often associated with cancer.
These are the first three definitions of cachexia that I found on thefreedictionary.com, under the Medical Dictionary tab.
Again, from the freedictionary.com:
An alternative explanation (“B”) for a particular phenomenon that has traditionally been attributed to sequence or factor “A”.
In other words, correlation is not causation. This study seems to be saying that “obesity” may not be the cause of heart failure in fat people, and that fat people who do have heart failure don’t seem to die from it as often because they don’t lose weight (waste away), don’t lose muscle mass (maybe because their bodies have fat stores from which to draw instead of attacking muscle?), don’t lose their appetites (don’t even go there — it’s not because all fat people are pigs who just can’t put down their forks, even when ill), and aren’t generally debilitated by heart failure.
The Atherosclerosis Risk In Communities (ARCI) study was an ongoing study involving 15,792 men and women who were ages 45 to 64 when they were recruited from 1987 to 1989. Participants came from one of four communities spread across the U.S.
Khalid and colleagues looked at 1,487 patients from the ARCI study who had heart failure. The group was 54% male, 66% white, and had an average age of 67. The researchers measured body mass index (BMI) at least 6 months prior to incident heart failure and again at the time of death.
Seems like a large enough group of participants in the study.
Among the patients, 35% were overweight and 47% were obese. The pre-morbid BMI was measured an average of 4.3 years (±3.1) before the diagnosis of heart failure. Throughout the 10-year follow-up period, 43% of the heart failure patients died.
Adjustments were made for hypertension, history of myocardial infarction, coronary heart disease, diabetes, stroke, and demographics.
On a side note, this is the first time I can recall an article about a study of “obesity” and health risks that actually listed demographics as one of the adjustments made.
Compared with the normal-weight group, and after adjustments, overweight patients had a lower risk of dying (HR 0.72, 95% CI 0.58-0.90, P=0.004), and obese patients had an even lower risk of dying (HR 0.70, 95% CI 0.56-0.87, P=0.001).
The phenomenon of excess weight appearing to protect patients is known as the “obesity paradox,” and in the case of this cohort, the protection did not change significantly based on smoking status, history of cancer, or diabetes status.
For every 0.70 deaths in the “overweight group, there was 1 death in the “normal” weight group (or for every 70 “overweight” deaths, there were 100 “normal weight” deaths). And for every 72 deaths in the “obese” group, there were 100 “normal weight” deaths.
Why this has to be a paradox is beyond me. To me, it just makes sense that someone who has a debilitating disease is going to be better able to survive if they are fat; when you’re ill, you usually lose weight (depending on type and length of illness). If you have fat stores on which to draw, your body uses those to help you survive. If you don’t have fat stores on which to draw, your body uses what fat you do have and then goes on to use muscle (the “wasting” that is seen, especially in cancer patients).
Just a personal example of this “wasting” — in 1972, I weighed 235 lbs. I was crossing the street one night after work and got hit by a car. That accident broke both bones in my lower left leg, fractured my pelvis in three places, and broke three of my upper middle front teeth. I spent two weeks in the hospital, and another six weeks in a nursing home, recuperating.
I was weighed just before I left the nursing home. I still had a plaster cast that ran from my foot to mid-thigh, and with that cast, I weighed 160 lbs. So I lost at least 75 lbs while I was recuperating (this, in spite of the fact that I not only ate all the meals at the nursing home, but that I had one of the aides bring me burgers and fries between meals). Now, if I had weighed what the Air Force recruiter told me was my ideal weight of 140 lbs. (at my then-height of 5’9″), and I lost 75 lbs, I would have weighed 65 lbs with that cast on (and probably would have been dead from muscle loss — remember, your heart is a muscle and it’s not immune to cannibalization by your body). And that’s if I hadn’t been killed by that car in the first place; a car hitting someone who only weighs 140 lbs, doesn’t have near the chance of survival that someone weighing 235 lbs, does.
The authors noted that the “obesity paradox” is not uncommon in heart failure development, and that although several studies have investigated this link, the longitudinal nature of this study allows for an independent association between higher pre-morbid BMI and long-term survival advantage.
Several factors could explain the study results. The investigators suggested that obese patients could have a higher metabolic reserve compared with normal-weight patients and thus have a survival advantage when cardiac cachexia follows the development of heart failure.
Wang agreed that cardiac cachexia and muscle wasting in late-stage heart failure could explain the protective function of excess body weight.
Gee, ya think? How many years of seeing this in practice does it take before you believe the results of a study that tells you the same thing?
Another possible theory the authors posed was that obesity alters the natural history of heart failure through neurohumoral pathways. Also, these results could be a survivor effect, as frailer older adults die sooner.
What? Are you trying to say that older fat people aren’t as frail? Whoever would have thought …
The researchers listed the observational design of the study and its reliance on ICD-9 codes as potential study limitations. Other study limitations, according to Wang, included selection bias, information bias, misclassification bias, and lead-time bias.
If fat people who smoked, had had cancer, or had diabetes survived heart failure, it seems like they’re rather disappointed to find that the “obesity paradox” exists and fat people survive heart failure better than thinner people in spite of having other “obesity-related” diseases (that thinner people get too, but don’t seem to be related to their weight).
The effects of being overweight or obese might have led many of the patients to seek medical care for things like edema, dyspnea, or easy fatigue, leading to an earlier diagnosis of heart failure and therefore earlier treatment, Wang wrote.
Right, because fat people always seek medical care for those symptoms that could lead to an early diagnosis of heart failure and earlier treatment. Because fat people are never shamed at doctor appointments, are never told that their symptoms are caused by being fat, and are never told that losing weight will “cure” all their ills. Nope, that never happens, and so fat people seeking medical care early just has to be the explanation for the “obesity paradox” (/sarcasm).
Wang suggested incorporating more detailed metabolic phenotyping in heart failure studies, such as metabolomics, novel imaging techniques, and dietary interventions, to unravel the mysterious “obesity paradox.”
WT everloving F?! Metabolomics — The systematic study of the unique chemical fingerprints, in the form of small-molecule metabolite profiles, that are left by specific cellular reactions.
And how many years of study is this going to take before researchers can come to a definitive conclusion? Want to bet I won’t see any results in my lifetime (and I’m only 61)? Novel imaging techniques. Okay, what techniques, and what are you going to “image”? Dietary interventions. Again, what dietary interventions are you talking about? Weight loss diets don’t work, remember? And we keep hearing about this, that, and the other new supplement that are “supposed” to help with preventing this, that, and the other disease, only to be told in the next month or next year that it was all a bunch of quackery and we need to follow this, that, or the other supplement instead. Yeah, I’m not buying any of that.
As for the “obesity paradox” being mysterious? Really? Since when is common sense mysterious? And yes, it’s common sense that people with fat reserves would be better able to survive a disease where their body needs fuel, but they just don’t have enough of an appetite to provide that fuel.
I guess when you’re so used to attributing every disease a fat person gets to being “caused” by their fat, there just isn’t any other conclusion you can come to but that it’s a “paradox” for a fat person to survive the same disease their thinner peers get and from which more of them die. Funny (not) how weight isn’t a consideration at all when a thinner person gets a disease …