In part 1 we looked at the types of fat: subcutaneous; visceral; and ectopic. We observed that, at least in terms of many aspects of health, visceral and ectopic fat are the problem.
We also started looking at the idea that we all have a fat threshold, which when reached results in problems like type 2 diabetes.
We’ll explore this concept in more detail, look at how you might be able to check whether you’ve passed your fat threshold, and if so what you can do about it.
Measuring ectopic fat
So if fat in the organs is such a big problem, why haven’t you heard more about it? One reason is that it’s a slow road going from research to clinical practice.
Count yourself lucky if you have access to a university hospital in which the consultants you see are actively engaged in groundbreaking research.
Even the research sometimes moves slowly. Recognition of non-alcoholic fatty liver disease (NALFD) as a major health problem is new compared to recognition of alcoholic fatty liver for example.
Although recognition of the involvement of the pancreas in diabetes is a nearly century old discovery (1), getting a detailed look at the pancreas in a living person is something we've only recently developed methods for (2,3).
So another key reason for ectopic fat being a ‘new’ topic is the difficulty in measuring it.
Although relatively cheap readily available ultrasound technology gives some indication of liver fat, accurate measurements are really only achieved with magnetic resonance imaging and magnetic resonance spectroscopy (4).
The same is true for the pancreas, as the methods for a accurate assessment have only been developed very recently and also employ magnetic resonance technology (2,3).
We also started looking at the idea that we all have a fat threshold, which when reached results in problems like type 2 diabetes.
We’ll explore this concept in more detail, look at how you might be able to check whether you’ve passed your fat threshold, and if so what you can do about it.
Measuring ectopic fat
So if fat in the organs is such a big problem, why haven’t you heard more about it? One reason is that it’s a slow road going from research to clinical practice.
Count yourself lucky if you have access to a university hospital in which the consultants you see are actively engaged in groundbreaking research.
Even the research sometimes moves slowly. Recognition of non-alcoholic fatty liver disease (NALFD) as a major health problem is new compared to recognition of alcoholic fatty liver for example.
Although recognition of the involvement of the pancreas in diabetes is a nearly century old discovery (1), getting a detailed look at the pancreas in a living person is something we've only recently developed methods for (2,3).
So another key reason for ectopic fat being a ‘new’ topic is the difficulty in measuring it.
Although relatively cheap readily available ultrasound technology gives some indication of liver fat, accurate measurements are really only achieved with magnetic resonance imaging and magnetic resonance spectroscopy (4).
The same is true for the pancreas, as the methods for a accurate assessment have only been developed very recently and also employ magnetic resonance technology (2,3).
Estimating ectopic fat
Most of us don’t have access to ultrasound let alone a magnetic resonance scanner, so we have to rely on things we do have more ready access to.
The easiest is a tape measure because there is usually a moderate relationship between waist circumference and visceral fat (5-7).
Being visibly lean with a flat stomach is obviously a pretty good indicator that visceral fat is low. On the other hand, having a bit of a paunch may not be due to a lot of visceral fat if you have a tendency to be bloated.
Liver and pancreas fat is another matter, although there is some correlation when looking at groups of people, this is unreliable in individuals.
There are also a few routine blood tests that are sometimes used to diagnose fatty liver, namely alanine aminotransferase (ALT), aspartate aminotransferase (AST), and sometimes gamma-glutamyl transferase (GGT), but these mostly indicate general liver injury (8), and are not very good at predicting fatty liver specifically (9-18).
The best way of knowing we don’t have a problem with ectopic fat is not having any signs of insulin resistance, glucose intolerance, or systemic inflammation. That means measures such as fasting insulin, fasting glucose, high-sensitivity C-reactive protein, and the oral glucose tolerance test described earlier in this blog here.
Age is another factor. As we get older, we tend to shift fat into areas where it is more harmful (19). Luckily things don’t have to go this way as these MRI scans of the three peoples' thighs show.
Most of us don’t have access to ultrasound let alone a magnetic resonance scanner, so we have to rely on things we do have more ready access to.
The easiest is a tape measure because there is usually a moderate relationship between waist circumference and visceral fat (5-7).
Being visibly lean with a flat stomach is obviously a pretty good indicator that visceral fat is low. On the other hand, having a bit of a paunch may not be due to a lot of visceral fat if you have a tendency to be bloated.
Liver and pancreas fat is another matter, although there is some correlation when looking at groups of people, this is unreliable in individuals.
There are also a few routine blood tests that are sometimes used to diagnose fatty liver, namely alanine aminotransferase (ALT), aspartate aminotransferase (AST), and sometimes gamma-glutamyl transferase (GGT), but these mostly indicate general liver injury (8), and are not very good at predicting fatty liver specifically (9-18).
The best way of knowing we don’t have a problem with ectopic fat is not having any signs of insulin resistance, glucose intolerance, or systemic inflammation. That means measures such as fasting insulin, fasting glucose, high-sensitivity C-reactive protein, and the oral glucose tolerance test described earlier in this blog here.
Age is another factor. As we get older, we tend to shift fat into areas where it is more harmful (19). Luckily things don’t have to go this way as these MRI scans of the three peoples' thighs show.
You can see from these images that exercise helps to maintain both muscle mass and prevent excessive intermuscular (between muscle) and intramuscular (within muscle) fat (20).
Is there a fat threshold
As mentioned in Part 1, there are those who are obese but have a relatively healthy metabolism (19,21-23), this remains the case even when more accurate measures for body fat than body mass index (BMI) are used to define obesity (24,25).
On the other hand there are people who have a BMI that places them in the normal or just overweight category yet have type 2 diabetes (26). I’m no fan of the BMI, but it is the most commonly reported measure that’s relevant here, and it's also something it only takes scales, a tape measure, and a chart or calculator to work out.
Read the scientific literature from a few decades ago and the association between obesity and type 2 diabetes wasn’t obvious; in fact body mass index wasn’t even found to correlate closely with the development of type 2 diabetes (27).
One large study tracking the development of newly diagnosed type 2 diabetes during the years of 1977 to 1991 showed that 36% of people, so about one in three, were diagnosed at a BMI of less than 25 kg/m2, or what is considered normal weight (26).
Of course type 2 diabetes and obesity were both far less common back in the 1970s and 1980s. Both have become more common over the last decades (28), and this has lead many to conclude there is a causal link.
The nature of that link is where the disagreement starts: does diabetes, or rather ‘pre-diabetes’ make people more prone to putting on excess fat, or does excess fat make people more prone to developing type 2 diabetes?
This is one of those chicken and egg arguments that get people riled up for no good reason. We’ve already discussed that ectopic and visceral fat are bad news for insulin sensitivity (see part 1). The rest I’ll leave for another post, or simply watch my online talks on insulin resistance here.
Beyond the potentially complex and varied beginnings of the road to type 2 diabetes, is the fat threshold hypothesis (26), which basically suggests we each have a certain amount of fat our body can store with no ill-effect, and that when we go above this, we begin to store excess fat in the wrong places discussed last week.
This concept is based on several observations:
1. Insulin resistance in people without type 2 diabetes is lower than insulin resistance in people with type 2 diabetes, and this is consistent among both those classified as obese and those not (29). Also, there is little difference in insulin resistance between obese and non-obese people with type 2 diabetes.
2. Some people with normal BMI can get type 2 diabetes (21,26).
3. Weight reduction in those with type 2 diabetes who are non-obese is as effective at inducing reversal of the condition as weight reduction in those who are classified as obese (30,31). Reversal of type 2 diabetes tended to require greater weight reduction among the obese than the non-obese (26).
4. Being obese but metabolically healthy to begin with is associated with a similar risk of type 2 diabetes in the future as being metabolically unhealthy but normal weight, but more than being metabolically healthy and normal weight (21).
5. Where fat is accumulated, so subcutaneous vs. visceral and ectopic differs in those who go on to develop type 2 diabetes and those who don’t (19,32).
6. Even those considered metabolically healthy but obese sometimes improve insulin sensitivity with lifestyle changes that reduce abdominal fat (33,34).
This hypothesis also offers up an explanation why very low calorie diets (see here), with or without bariatric surgery aren’t always successful, and the effects don’t necessarily last – some of the volunteers simply aren’t dropping or staying below their personal fat threshold.
Physical activity and physical fitness are two potentially major modifiers for this relationship. Being more active and fitter reduces the risk of type 2 diabetes and a host of related conditions even when there is a lot of excess fat (35).
That may well be because the fat is less likely to be visceral or ectopic. I’ll do a series on this in my MOVE blog.
I’d be irresponsible to not note that for many who begin as obese but metabolically healthy, this period of metabolic health only lasts a while before problems begin (32,36-38).
Take homes
Where we store fat matters to our health, so it’s worth focusing on approaches shown to reduce visceral and ectopic fat.
Not everyone who is obese has metabolic problems, but the health outlook for the vast majority of people who would be classified as obese would be improved if they became leaner.
That said, restoring metabolism or maintaining healthy metabolism is the goal for health before above and beyond weight reduction.
Finally, as we get older, the any protection we have from the ill-effects of excess fat goes down, and this trend needs to be actively countered, especially with physical activity/exercise.
In the next and final instalment of this series we’ll delve into the importance of the type of fat and its metabolism. That won’t be for a while though. Next week we finish looking at very low calorie diets; specifically their effects on inflammation, blood pressure, and heart health.
References: click here for a full list of references.
To learn more about type 2 diabetes and what you can do to better manage, and often reverse it, watch my free video education series. If you want one-on-one help dealing with your type 2 diabetes, contact me here to book a consultation.
Is there a fat threshold
As mentioned in Part 1, there are those who are obese but have a relatively healthy metabolism (19,21-23), this remains the case even when more accurate measures for body fat than body mass index (BMI) are used to define obesity (24,25).
On the other hand there are people who have a BMI that places them in the normal or just overweight category yet have type 2 diabetes (26). I’m no fan of the BMI, but it is the most commonly reported measure that’s relevant here, and it's also something it only takes scales, a tape measure, and a chart or calculator to work out.
Read the scientific literature from a few decades ago and the association between obesity and type 2 diabetes wasn’t obvious; in fact body mass index wasn’t even found to correlate closely with the development of type 2 diabetes (27).
One large study tracking the development of newly diagnosed type 2 diabetes during the years of 1977 to 1991 showed that 36% of people, so about one in three, were diagnosed at a BMI of less than 25 kg/m2, or what is considered normal weight (26).
Of course type 2 diabetes and obesity were both far less common back in the 1970s and 1980s. Both have become more common over the last decades (28), and this has lead many to conclude there is a causal link.
The nature of that link is where the disagreement starts: does diabetes, or rather ‘pre-diabetes’ make people more prone to putting on excess fat, or does excess fat make people more prone to developing type 2 diabetes?
This is one of those chicken and egg arguments that get people riled up for no good reason. We’ve already discussed that ectopic and visceral fat are bad news for insulin sensitivity (see part 1). The rest I’ll leave for another post, or simply watch my online talks on insulin resistance here.
Beyond the potentially complex and varied beginnings of the road to type 2 diabetes, is the fat threshold hypothesis (26), which basically suggests we each have a certain amount of fat our body can store with no ill-effect, and that when we go above this, we begin to store excess fat in the wrong places discussed last week.
This concept is based on several observations:
1. Insulin resistance in people without type 2 diabetes is lower than insulin resistance in people with type 2 diabetes, and this is consistent among both those classified as obese and those not (29). Also, there is little difference in insulin resistance between obese and non-obese people with type 2 diabetes.
2. Some people with normal BMI can get type 2 diabetes (21,26).
3. Weight reduction in those with type 2 diabetes who are non-obese is as effective at inducing reversal of the condition as weight reduction in those who are classified as obese (30,31). Reversal of type 2 diabetes tended to require greater weight reduction among the obese than the non-obese (26).
4. Being obese but metabolically healthy to begin with is associated with a similar risk of type 2 diabetes in the future as being metabolically unhealthy but normal weight, but more than being metabolically healthy and normal weight (21).
5. Where fat is accumulated, so subcutaneous vs. visceral and ectopic differs in those who go on to develop type 2 diabetes and those who don’t (19,32).
6. Even those considered metabolically healthy but obese sometimes improve insulin sensitivity with lifestyle changes that reduce abdominal fat (33,34).
This hypothesis also offers up an explanation why very low calorie diets (see here), with or without bariatric surgery aren’t always successful, and the effects don’t necessarily last – some of the volunteers simply aren’t dropping or staying below their personal fat threshold.
Physical activity and physical fitness are two potentially major modifiers for this relationship. Being more active and fitter reduces the risk of type 2 diabetes and a host of related conditions even when there is a lot of excess fat (35).
That may well be because the fat is less likely to be visceral or ectopic. I’ll do a series on this in my MOVE blog.
I’d be irresponsible to not note that for many who begin as obese but metabolically healthy, this period of metabolic health only lasts a while before problems begin (32,36-38).
Take homes
Where we store fat matters to our health, so it’s worth focusing on approaches shown to reduce visceral and ectopic fat.
Not everyone who is obese has metabolic problems, but the health outlook for the vast majority of people who would be classified as obese would be improved if they became leaner.
That said, restoring metabolism or maintaining healthy metabolism is the goal for health before above and beyond weight reduction.
Finally, as we get older, the any protection we have from the ill-effects of excess fat goes down, and this trend needs to be actively countered, especially with physical activity/exercise.
In the next and final instalment of this series we’ll delve into the importance of the type of fat and its metabolism. That won’t be for a while though. Next week we finish looking at very low calorie diets; specifically their effects on inflammation, blood pressure, and heart health.
References: click here for a full list of references.
To learn more about type 2 diabetes and what you can do to better manage, and often reverse it, watch my free video education series. If you want one-on-one help dealing with your type 2 diabetes, contact me here to book a consultation.
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