Now a study by Peter Nordström and colleagues, published in JAMA Internal Medicine, reports that a higher BMI in identical twins is associated with a greater risk for type 2 diabetes but not myocardial infarction or death.
The researchers looked at data from 4,046 monzygous twin pairs with discordant BMIs (difference >0.01 units) from the nationwide Swedish twin registry.
During a mean follow-up of 12 years, the rate of myocardial infarcts and deaths were similar in the twins with lower BMI compared to their higher BMI co-twin (5.0% vs. 5.2% and 13.6% vs. 15.6%, respectively).
This lack of difference remained true even when the researchers compared the extremes of BMI discordance and only considered twins with BMI greater than 30.
In contrast, both higher BMI and greater increase in BMI since 30 years before baseline was associated with greater risk of incident diabetes.
Given that diabetes is such a powerful risk factor for cardiovascular disease, one can only wonder why this did not translate into a higher cardiovascular risk in the higher weight twins.
One possible explanation, offered by the authors is that cardiovascular risk may have been well managed in these individuals thus minimizing any increased risk due to diabetes (or other BMI associated risk factors such as dyslipidemia or hypertension).
Indeed, it would probably have required a far larger group of twins (or much longer follow-up) to fully rule out higher cardiovascular risk in these twins.
Let us also not forget that BMI is a rather lousy measure of overall cardiovascular risk.
Thus, which the study is certainly compatible with the (genetics-independant?) role of higher BMI in the risk for diabetes, it certainly should not be interpreted as demonstrating that this increased risk in benign in terms of cardiovascular disease.
To conclude my miniseries on the recent “Clinical Discussion” on obesity, published in the New England Journal of Medicine, I now turn to the final question – does this relatively healthy 29 year-old woman with a BMI of 32 warrant treatment?
And if yes, what treatment would you recommend.
This question cannot be answered without considering the following:
Often, we tend to focus on potential benefits of treatment, and so most of us would probably approach this question by comparing the potential benefits of treatment vs. the potential risks of not treating this patient – this is often referred to as the benefit-risk ratio.
When this ratio exceeds 1 (i.e. the potential benefits of treatment outweigh the potential risks of treatment), we would recommend treatment.
One could, however, also turn this into a risk-risk ratio.
Both, the decision to treat and the decision to not-treat bear risks.
Given that the woman in this case has Edmonton Obesity Stage 1 at best (borderline hypertension?), her mortality risk over 20 years is rather low.
For one, this means that treating her obesity would likely also have rather modest benefits (if any). In fact, there is currently no proven health benefit of even just modest weight loss in a patient like her.
Thus, we would certainly want to rule out treatments that carry any potential risk.
Clearly, obesity surgery,would not even remotely enter the picture.
Even the risk of medication, although much safer than anything we may have had before, is probably too high. Although the statistical risk for severe side effects (ranging from teratogenicity to pancreatitis – depending on the chosen medication) is rather low, it may still be substantially higher than doing nothing.
This leaves us with behavioural modifications, which would pose the lowest treatment risk (although it is important to remember that the risk of behavioural treatments is not zero: exercise can result in injury, a too restrictive diet could result in nutritional problems or, as some folks fear, trigger an eating disorder).
The most conservative approach would be to reassure her that her mortality risk is indeed rather low (certainly not warranting the risk of medication).
However, treatment decisions are not only guided by mortality risk – we also need to consider quality of life.
Despite being at low medical risk, it may well be that our patient is unhappy with her weight (although we have no information in this regard other than that she has made previous attempts at weight loss).
Exploring this further would certainly require a much deeper dive into how she feels about herself – her weight may not even be the real problem here.
Can she eat better and be more active? Sure, most of us can!
Would I want to see her again, perhaps in a year or so to see how she is doing – sure, even if just to confirm that she still has EOSS 1.
Beyond that, I would be guided by the principle of “first-do-no-harm” and probably leave it at that (at least for now).
Yesterday, I posted about the “Clinical Discussion” of obesity management, presented to us by the venerable New England Journal of Medicine.
I wrote about how the ignorant and moralizing “opinion” of one of the discussants, devoid of even the smallest insight in to the complex sociopsychobiology of this chronic disease, is exactly the kind of “thinking” that is holding back the field (and has been for decades).
But these are not the only problems with the “Clinical Discussion”.
Rather, the problems start with the very choice and description of the “case”.
Indeed, the case warrants a careful line-by-line analysis, to reveal just how the use of the “stereotypical” depiction paints a picture of what (as we will see in a later post), could well turn out to be a much more complicated case than either of the discussants acknowledge.
As we are told,
Ms. Chatham is a 29-year-old woman who recently joined your practice; this is her second visit to your clinic.
In other words, this is a young woman, whose life you know virtually nothing about, not that this should ever stop you from stating your sound medical opinion.
She made today’s appointment to discuss how she can lose weight and whether there are medications that she can take to aid in weight loss.
In other words, a typical “fat” patient looking for a “quick fix” via “diet pills”?
She is relatively healthy, except for a history of childhood asthma.
Did the asthma play any role in her weight gain? Did it limit her physical activity as a kid? Was she on anti-allergic drugs or even systemic steroids that may have led to weight gain? Your guess is as good as mine.
She says that she has been told indirectly, by her friends and family, that she is “overweight.”
Because, obviously, she does not own a mirror, never shops for clothes, and has probably never given her shape or size a second thought, and therefore, needs to be “told” by the good people around her (and perhaps on occasion by perfect strangers she may just happen to meet on the street), that she has a serious health problem and needs to urgently see a doctor.
She has tried several popular diets without success; each time, she has lost 4.5 to 6.8 kg (10 to 15 lb) but has been unable to maintain the weight loss for more than a few months.
Which, I’m guessing, simply goes to prove her lack of motivation and effort. Obviously, like most “fat” people, she is just too weak-willed to maintain weight loss and apparently always gives up far too soon. Never mind, that this is exactly what happens to 95% of people (skinny or fat) who lose weight and never mind, that (as some of us now realise) there is in fact a complex neurohormonal physiology, which tightly regulates body weight and is there solely for the purpose of effectively “defending” against weight loss.
She does not have a history of coronary artery disease or diabetes.
Which would in fact be surprising, given that she is a 29 year-old woman!
She has a regular menstrual cycle.
Which means what exactly? Are we supposed to rule out PCOS or fertility issues based on this clinical “pearl”?
She does not take any medications or nonprescription supplements.
So at least we know that she cannot simply blame her weight gain on any current medications.
She does not smoke but does drink alcohol, occasionally as many as 4 or 5 drinks in a week, when she is out with friends.
Which you could also say about millions of other people (including myself), irrespective of their BMI or health status – it’s what people do!
She tells you that she “watches what she puts in her mouth”…
Which, of course we should have a hard time believing, because as we all know, “fat” people are habitual liars when it comes to what they “tell” us about their diets.
…and reads the nutritional labels on food packaging.
or, at least that’s what she “tells” us – you’re welcome to believe her or not.
However, she enjoys eating out and orders take-out meals 8 to 12 times a week.
Wow! Here we have a “fat” person who actually “enjoys” eating out – as many times as (hold your breath) once or twice a day – and that, despite claiming to read food labels! Never mind that this is exactly how 99.9% of the US population happens to eat (no matter what their size or health status) – clearly, this irresponsible behaviour must change if there is to be any hope for her!
She works as a computer programmer and spends most of her day sitting in an office.
There we have it – typical “sedentariness” a well-known “cause” of obesity (or so we are told), because (as should be obvious to anyone who understands the complexity of energy homeostasis), all people who sit in offices (not to mention the now immortalised 400 lb “hacker”), struggle with their weight.
She belongs to a fitness club and tries to go there about once a week but notes that her attendance is inconsistent.
Because, of course, it’s typically the fat people with gym memberships, who never show up for training. Also relevant, because most of us continue to believe that exercise is the best way to lose weight.
On physical examination, her vital signs are unremarkable except for a blood-pressure measurement of 144/81 mm Hg.
Which we must obviously assume to be reliable, as the docs have certainly ruled out the presence of “White-Coat” hypertension and bothered to ensure that they are indeed using an appropriate cuff size.
She is 1.7 m (5 ft 7 in.) tall and weighs 92 kg (203 lb), and her body-mass index (BMI; the weight in kilograms divided by the square of the height in meters) is 32.
Which contains about as much clinically valuable information as telling us that she is a size 16.
Her waist circumference is 94 cm (37 in.).
Another piece of useless information, especially in an otherwise healthy woman.
There is no peripheral edema.
Which, I guess, clearly tells us that she can forget about using “fluid retention” as an “excuse” for her weight.
The rest of the examination is unremarkable.
There you have it – with this information in hand, we are now clearly poised to give her meaningful clinical advice to help her better manage her weight.
What surprises me about this (apparently “typical”) case history, is that the editors of the New England Journal of Medicine, otherwise so concerned with brevity, did not simply decide to shorten the “case” to the following:
“Ms. Chatham is a pretty healthy 29-year-old working woman, who happens to live in the USA.”
That one line would in fact contain about all of the information we now have about Ms. Chatham, the difference being, that this statement is actually better, in that it is elegantly crafted to avoid the use of “stereotypical” fat-shaming language and imagery.
Furthermore, this sentence, quite like the “case”, is also void of any indication of the actual complexity that even “simple obesity” can present in clinical practice (which, I perhaps mistakenly, assumed would have been the whole point of the Clinical Discussion in the first place).
Is anyone curious as to the information that I would really liked to have about Ms. Chatham to come up with advice that would actual help her?
Then, please stay tuned for tomorrow’s post.
While many folks have no problem seeing how “excess” body fat can often lead to health problems, they may wonder what exactly is meant by “abnormal” body fat and are perhaps unsure as to why this would be included in the definition of obesity.
This is where we need to take a moment to remind ourselves that fat tissue is actually a vital organ, without which, we would experiences all kinds of health problems. Not only, is our ability to store excess calories vital to prepare for the next major illness or famine, it is also a vital organ for reproduction (women stop having periods when their fat stores get too low).
That said, the safest place to store all those excess calories is in your fat tissue, especially the fat tissue directly underneath your skin. This is where the excess calories cause the least trouble, not affecting the functioning of other organs or clogging up your blood stream, and where they can sit for decades, until they are perhaps one-day called upon in a time of need.
It is also “normal” to have a small amount of fat in other depots such as around the gastrointestinal tract, the heart, or the kidneys – here the fat serves both a mechanical and immunological function – again, the fat here generally does not cause any health problems (indeed, lack of fat in these locations may).
All of this is not very interesting from a medical or health perspective, as this kind of fat generally does not cause any real health problems, unless, it perhaps expands to a size that causes mechanical issues simply due to its sheer mass.
In contrast, the term “abnormal” refers to fat accumulation in parts of the body where you would not normally find fat in a “healthy” person. This, is commonly referred to as “ectopic” fat and refers to fat accumulation within organs like the liver, pancreas, heart, skeletal muscle or other organs, where you would rather not have any fat.
These “abnormal” fat accumulations can substantially disrupt organ function, leading to all kinds of metabolic problems.
Interestingly enough, there is not a very strong relationship between the total amount of body fat and the location of that body fat.
The extreme example of this is seen in patients with lipodystrophy, who, being unable to store excess calories in “normal” subcutaneous fat depots, deposit their fat in the liver and other organs, thus presenting with all of the problems generally associated with obesity.
Exactly why some people are more prone to “ectopic” fat deposition that others, who can apparently tuck away all their extra calories underneath their skin with little, if any, impact on their health, remains largely unknown, except that genetics appears to play a very substantial role.
But, whatever the reason, the bottom line remains that even very little extra body fat, if stored in the wrong location, can cause all of the metabolic problems generally associated with obesity.
In contrast, even large amounts of body fat, if safely sequestered away in subcutaneous depots may have little (if any) impact on health.
This is why the WHO included both the presence of “excess” as well “abnormal” body fat in their definition of obesity.
Again, none of this can be measured by stepping on a scale or looking at a BMI chart.
If your excess or abnormal body fat affects your health – you have obesity – if it doesn’t, you don’t.
In all of my interactions with people who believe that the obesity epidemic is vastly overblown and that the links between excess body fat are imagined, I often hear the argument that obesity cannot “cause” [chose your health problem here] because “normal-weight” people can have [same health problem] too!
This is a rather naive argument, pretty much along the lines of, “Tobacco cannot cause lung cancer because non-smokers can get lung cancer too, or alcohol cannot cause liver cirrhosis because teetotalers get cirrhosis too”.
Or, “Drunk driving cannot cause road accidents, because non-drunk drivers get into accidents too”.
Or, “Flu vaccines don’t work, because vaccinated people get the flu too”.
I could go on….
What is missing in this perspective, is a very basic understanding of multiple cause and effect, as well as a fundamental understandings of probability and risk.
Firstly, almost all medical conditions can have more than one cause. Thus, although most lung cancer is by far attributable to smoking, it is also seen with exposure to asbestos, other environmental toxins, and of course sporadic mutagenesis.
Similarly, there are a multitude of reasons why someone may get liver cirrhosis, but, at least in Western societies, alcohol consumption is by far the number one cause of this problem.
And yes, some vaccinated people do catch the flu, but most vaccinated people don’t and when they do, it turns out to be less severe than it would have been without the vaccine.
So, just because “normal-weight” people can also have hypertension, diabetes, fatty liver disease, sleep apnea, osteoarthritis, gastroesophageal reflux, urinary incontinence, plantar fasciitis, and a host of other conditions, does not “prove” that excess weight does not also “cause” all of these conditions.
Yes, skinny people can have sleep apnea too but the overwhelmingly vast majority of sleep apnea is seen in people with excess weight – the same goes for virtually every obesity related health problem.
The other argument I often hear is that obesity cannot be the cause of [chose your health problem here] because not all people with obesity have [same health problem].
This argument is likewise stupid!
The fact that not every smoker dies of lung cancer, in no way “proves” that smoking does not cause cancer.
The fact that not everyone who regularly drinks a lot of alcohol gets a cirrhotic liver, does not disprove the link between alcohol and cirrhosis.
This is where we need to understand the basic concept of risk and probability.
When a certain factor (e.g. excess body fat) increases the risk of a certain condition, it does not mean that everyone exposed to that factor ends up with the condition. It just means that the risk for that condition is vastly higher.
Now let’s add a further level of complexity to the concept of risk, because, as we know, body fat is not body fat is not body fat is not body fat!
Whether or not my body fat actually causes any health problem, depends on a wide range of factors ranging from my underlying genetic predisposition (e.g. for diabetes, hypertension, etc.), my fat location (subcutaneous vs. ectopic), the cellular structure of my fat (hypertrophic vs. hyperplastic), fat-tissue inflammation, and probably countless other factors.
Add to this, that risk for obesity related conditions can be substantially modified by other factors including physical fitness, healthy diets, positive body image, good mental health – it is easy to understand why defining “sick” and “healthy” simply based on a measurement (direct or indirect) of body fat makes no sense.
Thus, we need to ensure that the medical term “obesity” is not used to label everyone above a certain (arbitrary) BMI cutoff.
Rather, we should reserve the medical term “obesity” only for the condition where excess or abnormal body fat directly impairs the health of a given individual (the actual WHO definition of obesity!).
Someone with the exact same amount of body fat (or even more), who does not experience any health impairment should not be referred to as having “obesity” – that person is just “fat” (a word that really needs to be destigmatised!).
Personally, I couldn’t care less about how “fat” anyone is. Only when “fat” becomes “obesity” does it become a medical issue.