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EOSS: Time To Drop Stage 0?

Readers will be well aware of the Edmonton Obesity Staging System (EOSS), which classifies the severity of obesity on a five-point ordinal scale based on presence of medical, mental, and/or functional health issues related to excess weight.

By design, EOSS considers Stage 0 in individuals, who meet the BMI criteria for obesity but do not have any apparent health issues.

However, given the recent change in definition of obesity expressed in the newly released Canadian Adult Obesity Clinical Practice Guidelines, obesity is defined as, “the presence of excess or abnormal body fat that impairs health”, BMI should no longer be used as the defining characteristic of obesity.

Thus, one would not consider someone who has no health impairments, irrespective of BMI, to have obesity.

As a result, the EOSS stage 0 no longer makes sense, as this individual, by definition, would no longer meet the key criterion for obesity, namely an impairment in health (perhaps one may consider the term “pre-obesity” in this context?).

This also means that it is now time to abandon the term “healthy obesity” – either you have obesity, meaning you have a health impairment attributable to excess body fat, or you simply do not have obesity!

In practice, you need to be able to list exactly what weight-related health impairments a given person has before labelling them as having obesity.

If you cannot specifically list the health impairments (at least possibly) attributable to excess body fat, then that individuals, irrespective of BMI, does no longer meets the diagnostic criteria for obesity.

This seismic change in how we apply the term “obesity” to a clinical diagnosis will take time to implement and be adopted. No doubt, many will long back for simpler times, where you could just step on a scale, plug the numbers into a BMI calculator, and make a diagnosis based on tables or charts.

It will be interesting to see how long it will take for this new definition to be widely adopted in policy and practice.

Berlin, D


  1. Good news all around! I imagine arguments being made that zero would be considered pre-morbidity — that it’s at minimum a risk factor for morbidities to develop. Far too often, I continue to hear obesity referred to as a risk factor and not as a disease. I hope for less linear thinking that allows for scales that are more fluid (non-binary perhaps?) where it can be a reminder to block labelling.

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  2. Excellent observation by the creator of the EOSS! The new definition which is supported, does create areas of confusion as identified by Dr Sharma. Pre-obesity as suggested above may also apply to the “Overfat syndrome” (I.e.,TOFI-thin outside- fat inside) in slim individuals with excessive visceral fat & associated metabolic problems.

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    • Yes, if body fat is having a detrimental effect on your health you have obesity – this would also apply to people with low BMI inclduing TOFIs

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  3. How will researchers study the link between fatness and health/disease if they cannot use markers of body fat alone anymore? I mean, that was the whole point of BMI categories, right?

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    • It is probably ok to use BMI and other antrhopometric measures in populations studies. Studies in individuals probably need to use more sophisticated measures of body fat including its location and function.

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  4. Thanks! I agree in both the definition and the proposal to drop stage 0.
    After weight loss when my patients struggle lifetime for mantaining an improved health and a lower weight I consider them living with a cronic disease (and the patients agree..). Some of my colleagues argue in this case that when a few patientes no longer have obesity (if the health improvements are enough after making and upholding changes for a period of time) and therefore the diagnosis should be removed until the criteria for obesity happen to be met again. In a way I agree but it seems to me this is just semantics since there is only a matter of time until my patients meet the criteria again, but later on in life I they might come into a another situation when adipose tissue does not impair their health. Any comments on this?

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    • This problem is similar to that for people living with other chronic diseases. Would a patient with hypertension who is managing his blood pressure with low-salt or the DASH diet, still be considered as a hypertension patient?

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  5. Regarding Stage zero, doesn’t it just depend how close you look for associated health conditions? Are we measuring fasting insulin? Is everyone with excess weight having a sleep study? Is there degenerative joint disease of the knees that is weight related? is there depression secondary to their excess weight? Are we looking at childhood ACE scores? If we could check leptin resistance, would that be obesity? If we start to call excess body weight pre-obesity, do we not treat pre-diabetes? Just looking to give an alternative answer to doing nothing for stage zero.

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  6. Health impairment is related to the amount of polyunsaturated fat in fat stores. Excerpts: “It has been known for a long time that the composition of the fat we store in adipose tissue takes several years to change in response to changes in diet. Dietary habits, that is, the fats we cook in such as butter and different types of oil, as well as the foods we eat, are strongly determined by culture, region, tradition, and what we’re taught is good or bad, though there is little evidence for the latter. In the long term, avoiding high UFA intake may help with future pandemics like COVID-19, and severe pancreatitis or similar disease scenarios.”

    “UFAs also affect obesity, and not all obesity is the same. It is the UFA component in obesity that determines the degree of harm in the event of acute lipolysis as in severe COVID-19 or acute pancreatitis. A larger proportion of UFA accumulation in adipose fat — even when the overall fat amount is lower, as in a leaner person — may be more harmful during acute lipolysis than a greater proportion of saturated fat.”

    “Humans have 1 to 5 kilograms of linoleic acid stored in fat. In this stored form it’s safe, but it’s released by lipases in pancreatitis and in COVID-19. The lethal dose of linoleic acid is 280 milligrams per kilogram — just 23 grams for a person weighing 80 kilos. Similarly, in the case of oleic acid, only very low doses are needed for lethality.”

    “It’s all related to composition based on double bonds in a long fatty acid chain with more than 12 carbons. Linoleic and oleic acid are the two most abundant UFAs in the human body, and linoleic acid has increased to now comprise more than 20% of our stored fat. Commonly consumed vegetable oils such as safflower, sunflower, and corn are all quite high in linoleic acid, while oleic acid makes up a large part of olive, canola, and peanut oil.”

    For at least five decades the American Heart Association has been advising consumers to swap saturated fats for linoleic acid-rich seed oils. While doing so seems to decrease risk for heart attack, one wonders if it does so by shifting cause of death to viral infection, congestive heart failure, bacterial infection, cancer, diabetes complications, etc.

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