2

votes

I don't understand this article?

Answered on September 12, 2014
Created August 08, 2012 at 5:52 AM

http://www.reuters.com/article/2012/08/07/us-is-there-an-obesity-paradox-in-diabet-idUSBRE8761AZ20120807

Fat diabetics live longer than skinny ones? I better start eating more paleo food then.

77877f762c40637911396daa19b53094

(78467)

on September 07, 2013
at 01:28 AM

the problem is in asserting that evolution drove the process of diverting glucose to fat synthesis for a protective function rather than an energy storage function, i.e. there are easier ways of disposing of excess glucose

77877f762c40637911396daa19b53094

(78467)

on August 12, 2012
at 01:34 AM

You said, "gaining fat as a metabolic response to developing diabetes is protective". I've taken your usage of the term "protective" to imply an evolutionary adaptation.

Cbb1134f8e93067d1271c97bb2e15ef6

on August 11, 2012
at 10:14 PM

+1 Ambi.I always appreciate your well developed capacity to really think and evaluate.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 11, 2012
at 04:45 PM

I don't understand why you keep repeating that I have made an assertion that I haven't made. I give up.

77877f762c40637911396daa19b53094

(78467)

on August 11, 2012
at 04:56 AM

Precisely, but you miss the point. You need to ask yourself, is it easier for the body to evolve a mechanism as complicated as fat synthesis to address excess glucose or simply to excrete it, or alternatively, the body can increase its insulin sensitivity. In other words, there are many easier mechanisms to develop other than one as complex as adipogenesis. Ergo it is unlikely that the evolution of adipogenesis was driven by the risk of T2D. It's also very unlikely that T2D existed with sufficient frequency in ancestral populations to become a selective factor. Today, it's a different story.

E12ead3bf63c94b5b619b03722ef554f

on August 10, 2012
at 09:42 AM

the problem is that lean diabetics are often misdiagnosed with type 2 diabetes, while they actually have a form of diabetes that is closer to type 1 diabetes where their pancreas fail and they can't produce insulin (which means that they often have a worse blood sugar control)

100fd85230060e754fc13394eee6d6f1

(18696)

on August 10, 2012
at 09:07 AM

What? Excretion of excess glucose in the urine is practically the definition of diabetes.

77877f762c40637911396daa19b53094

(78467)

on August 10, 2012
at 07:53 AM

Storage of the energy in glucose, either through polymerisation into glycogen or synthesis of fatty acids did not evolve to protect from chronic high blood sugar (one can easily excrete it) but to manage homeostasis of energy during times of a deficit in caloric intake.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 10, 2012
at 07:15 AM

(See my update.)

100fd85230060e754fc13394eee6d6f1

(18696)

on August 10, 2012
at 06:46 AM

As to downvotes, I only use them when a post is factually incorrect, misleading, illogical, or offensive. In fact, I ought to upvote you for spurring me to find some articles to support the idea.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 10, 2012
at 06:43 AM

It's not so much a contention as a conjecture, and it's not to protect against t2d, but to protect against the damage from chronic high blood sugar. If 2 people have chronically high BG, and one of them efficiently gets it out of the blood and into the fat tissue, that person is not going to suffer as much damage from it. That's the idea anyway. I'm not saying it's so.

77877f762c40637911396daa19b53094

(78467)

on August 09, 2012
at 02:37 PM

.. but do mark my answer down if it makes you feel better. :)

77877f762c40637911396daa19b53094

(78467)

on August 09, 2012
at 02:34 PM

Your contention is that adipogenesis has evolved as a protective mechanism against type 2 diabetes. This is very unlikely.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 09, 2012
at 02:24 PM

Great! It sounds like you have some scientific data that distinguishes these hypotheses by showing that one direction can't be true. I'm all ears.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 09, 2012
at 02:21 PM

Of course not, Harry. There is a big difference between asserting that a "skinny diabetic" phenotype might get healthier by getting fat (ridiculous) and asserting that the metabolic process that is happening in the "fat diabetic" phenotype serves a protective function (plausible).

77877f762c40637911396daa19b53094

(78467)

on August 09, 2012
at 12:48 AM

Actually, his comments are rather clear: "And no, if you’re a skinny diabetic, this DOESN’T mean gaining weight will make you live longer. it just doesn’t."

77877f762c40637911396daa19b53094

(78467)

on August 09, 2012
at 12:40 AM

That's a long stretch of the bow. If this observation were considered in isolation, your conclusion would be the only reasonable one. However we have a great deal of context to place it in.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 10:28 PM

Exactly. Epidemiology can't give you the direction of causality. At this point it could be either. I only asserted a hypothesis of the direction. I didn't assert that it was so.

81fca18329e68e227cdfef3857bfef96

(1320)

on August 08, 2012
at 08:59 PM

I agree that BMI is not a good measurement of overall health. BF% is a good measurement of overall health.

4b5be253ac1981c690689cab7e4bf06d

(3043)

on August 08, 2012
at 04:32 PM

@Mark, I'm saying that looking at weight, by itself, is not a good marker of health. If we look at fitness, cardiovascular fitness, and eating habits, those items are much more likely to show true health. Studies that look at only BMI (and this one didn't even control for smoking), are basically worthless.

81fca18329e68e227cdfef3857bfef96

(1320)

on August 08, 2012
at 02:47 PM

People who are overweight are less likely to die from 'normal' causes of various diseases because they end dying of heart disease or complications caused by their obesity. That is not a paradox. Consider that overweight populations are much more likely to be sick than non-overweight populations. That is like saying HIV is not deadly because most people who die with HIV die because of the common cold/flu/or some other mundane ailment. Fat stored around the belly region is a great indicator of someone's overall health and susceptibility to disease.

77877f762c40637911396daa19b53094

(78467)

on August 08, 2012
at 09:32 AM

You should reconsider the arrow of causality.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 09:31 AM

To be fair, mine is also a pet idea, but it is not a less valid one at this point, as far as I know. I'd be grateful and even excited to hear about experimental evidence that disproves it.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 09:25 AM

Finally, if that quote from Carthenon was meant to imply anything more than trying to prevent people from making the stupid interpretation that they should gain fat, then it would be completely unsupported. He is an epidemiologist, and this study was epidemiology. It gives no clues to him or to us about the mechanism. So unless he had some other scientific reason to imply that, it would be just a pet idea -- if he had other evidence, I'm sure he would be telling us.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 09:18 AM

And to be more precise, it is the process of fat accumulation, not the "excessive pounds" that is a plausible protection.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 09:15 AM

First of all, that comment was in response to the suggestion that diabetics might try to gain fat to protect themselves, which is obviously stupid. I'm not suggesting that. I'm suggesting that gaining fat as a *metabolic response* to developing diabetes is protective, which is essentially the same as saying that becoming diabetic prior to (or simply without) getting fat is more dangerous.

3cdc762b2ae30b4ca3529f011ccac174

(186)

on August 08, 2012
at 06:27 AM

If you think about why T2Ds get fat, you'll understand why this is true, and even get what the real disorder is.

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4 Answers

4
100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 06:24 AM

Bill Lagakos talks about that a little here: http://caloriesproper.com/?p=1912

My half-baked take on it is in the comments -- essentially that fat is a protective mechanism against an underlying disorder.

ETA: This idea is still just a fancy, but thanks to several challenges from Harry, I was motivated to find some articles that express the same idea (emphasis mine):

Abdominal Subcutaneous Adipose Tissue: A Protective Fat Depot?

In summary, whereas abdominal adiposity is associated with a higher absolute risk of metabolic and cardiovascular disease, subcutaneous abdominal fat is not associated with a linear increase in the prevalence of all risk factors among the obese. Indeed, in the case of high triglycerides, SAT may actually be a protective fat depot in obese individuals.

Abdominal Superficial Subcutaneous Fat A putative distinct protective fat subdepot in type 2 diabetes

We found that abdominal SSAT correlated with improved glycemic control and indicators of cardiovascular risk. The SSAT depot may be less lipolytic than VAT, or even DSAT, and so improved insulin sensitivity of SSAT may favor accumulation of excess energy in this depot. In this regard, higher deposition of excess calories in the SSAT is a consequence, not the cause, of improved metabolic function. Conversely, it is plausible that the abdominal SSAT fat mass may be a unique abdominal fat subdepot that has protective effects on glycemic control and cardiovascular function. This is reminiscent of a finding by some, but not all, studies that suggest peripheral SAT might be less ???pathogenic??? than VAT. Currently, two hypotheses have been put forward to explain the difference between peripheral SAT and VAT: The ???portal theory??? (6,20) implicates a direct mechanism whereby VAT is more pathogenic because its venous blood drainage is directly via the portal vein to the liver. The ???ectopic fat hypothesis??? (6) suggests an indirect mechanism whereby increased energy storage in peripheral SAT exerts a protective effect by decreasing fat deposition in the liver, muscle, and heart. Because abdominal DSAT exhibits an intermediate phenotype between VAT and abdominal SSAT in various functions tested (lipolysis, adipocytokine profile) (4), it is possible that these theories can underlie the unique positive association between abdominal SSAT and cardiovascular and metabolic health. Although it may be possible that peripheral SAT differs significantly from abdominal SAT, and some studies have indicated the potential pathogenic role of increased abdominal (total) SAT as opposed to peripheral SAT (9???11), further studies are required to fully understand the distinct role of the SSAT subdepot. It is tempting to speculate that discrepancies in the literature among studies assessing associations between abdominal SAT and morbidity were confined by differences in the SSAT or SSAT/DSAT distribution.

Low subcutaneous thigh fat is a risk factor for unfavourable glucose and lipid levels, independently of high abdominal fat. The Health ABC Study.

CONCLUSION: Larger subcutaneous thigh fat is independently associated with more favourable glucose (in men) and lipid levels (in both sexes) after accounting for abdominal fat depots, which are associated with unfavourable glucose and lipid levels.

Increased fat intake, impaired fat oxidation, and failure of fat cell proliferation result in ectopic fat storage, insulin resistance, and type 2 diabetes mellitus.

Abstract It is widely accepted that increasing adiposity is associated with insulin resistance and increased risk of type 2 diabetes. The predominant paradigm used to explain this link is the portal/visceral hypothesis. This hypothesis proposes that increased adiposity, particularly in the visceral depots, leads to increased free fatty acid flux and inhibition of insulin action via Randle's effect in insulin-sensitive tissues. Recent data do not entirely support this hypothesis. As such, two new paradigms have emerged that may explain the established links between adiposity and disease. (A) Three lines of evidence support the ectopic fat storage syndrome. First, failure to develop adequate adipose tissue mass in either mice or humans, also known as lipodystrophy, results in severe insulin resistance and diabetes. This is thought to be the result of ectopic storage of lipid into liver, skeletal muscle, and the pancreatic insulin-secreting beta cell. Second, most obese patients also shunt lipid into the skeletal muscle, the liver, and probably the beta cell. The importance of this finding is exemplified by several studies demonstrating that the degree of lipid infiltration into skeletal muscle and liver correlates highly with insulin resistance. Third, increased fat cell size is highly associated with insulin resistance and the development of diabetes. Increased fat cell size may represent the failure of the adipose tissue mass to expand and thus to accommodate an increased energy influx. Taken together, these three observations support the acquired lipodystrophy hypothesis as a link between adiposity and insulin resistance. (B) The endocrine paradigm developed in parallel with the ectopic fat storage syndrome hypothesis. Adipose tissue secretes a variety of endocrine hormones, such as leptin, interleukin-6, angiotensin II, adiponectin (also called ACRP30 and adipoQ), and resistin. From this viewpoint, adipose tissue plays a critical role as an endocrine gland, secreting numerous factors with potent effects on the metabolism of distant tissues. These two new paradigms provide a framework to advance our understanding of the pathophysiology of the insulin-resistance syndrome.

3cdc762b2ae30b4ca3529f011ccac174

(186)

on August 08, 2012
at 06:27 AM

If you think about why T2Ds get fat, you'll understand why this is true, and even get what the real disorder is.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 09, 2012
at 02:21 PM

Of course not, Harry. There is a big difference between asserting that a "skinny diabetic" phenotype might get healthier by getting fat (ridiculous) and asserting that the metabolic process that is happening in the "fat diabetic" phenotype serves a protective function (plausible).

77877f762c40637911396daa19b53094

(78467)

on August 09, 2012
at 12:48 AM

Actually, his comments are rather clear: "And no, if you’re a skinny diabetic, this DOESN’T mean gaining weight will make you live longer. it just doesn’t."

77877f762c40637911396daa19b53094

(78467)

on September 07, 2013
at 01:28 AM

the problem is in asserting that evolution drove the process of diverting glucose to fat synthesis for a protective function rather than an energy storage function, i.e. there are easier ways of disposing of excess glucose

Cbb1134f8e93067d1271c97bb2e15ef6

on August 11, 2012
at 10:14 PM

+1 Ambi.I always appreciate your well developed capacity to really think and evaluate.

1
4b5be253ac1981c690689cab7e4bf06d

(3043)

on August 08, 2012
at 02:37 PM

There is an "obesity paradox" in almost any disease, and in life itself. People in the "overweight" BMI category artless likely to die from all causes than those in the "normal" category.

Until medical science sees people's health outside of weight classes, we will continue to get these "paradoxes.". See http://www.ncbi.nlm.nih.gov/pubmed/21416445

In short: a persons cardiovascular fitness and diet are so much more important than their weight or BMI. unless the studies accounted for these factors, and if the study only looks at weight, I ignore it for being bad science.

81fca18329e68e227cdfef3857bfef96

(1320)

on August 08, 2012
at 08:59 PM

I agree that BMI is not a good measurement of overall health. BF% is a good measurement of overall health.

4b5be253ac1981c690689cab7e4bf06d

(3043)

on August 08, 2012
at 04:32 PM

@Mark, I'm saying that looking at weight, by itself, is not a good marker of health. If we look at fitness, cardiovascular fitness, and eating habits, those items are much more likely to show true health. Studies that look at only BMI (and this one didn't even control for smoking), are basically worthless.

81fca18329e68e227cdfef3857bfef96

(1320)

on August 08, 2012
at 02:47 PM

People who are overweight are less likely to die from 'normal' causes of various diseases because they end dying of heart disease or complications caused by their obesity. That is not a paradox. Consider that overweight populations are much more likely to be sick than non-overweight populations. That is like saying HIV is not deadly because most people who die with HIV die because of the common cold/flu/or some other mundane ailment. Fat stored around the belly region is a great indicator of someone's overall health and susceptibility to disease.

1
77877f762c40637911396daa19b53094

(78467)

on August 08, 2012
at 07:20 AM

This does not mean that getting fat is protective!

It means that if you get diabetes PRIOR to becoming overweight it's even worse for mortality risk.

Article: "In fact, it's probably not that excessive pounds are protective, said Carnethon, but rather that lean people who get diabetes are somehow predisposed to worse health."

It implies that certain people are very sensitive metabolically and must take extra care with managing diabetes risk as they can get diabetes without becoming overweight.

EDIT (supplementary):

There is a hypothesis being put forward that the ability to store fatty acids, i.e. adipogenesis, was driven by adaptations to protect against type 2 diabetes (T2D). This would imply that the frequency of T2D in ancient populations was sufficiently high to drive the selection of this function. Ignoring for a moment that other, simpler adaptations of addressing T2D are conceivable and that fat synthesis is highly conserved in species where T2D does not exist, there is no evidence that T2D was a pathology of any significance in hunter-gatherer food practices.

77877f762c40637911396daa19b53094

(78467)

on August 09, 2012
at 12:40 AM

That's a long stretch of the bow. If this observation were considered in isolation, your conclusion would be the only reasonable one. However we have a great deal of context to place it in.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 09:15 AM

First of all, that comment was in response to the suggestion that diabetics might try to gain fat to protect themselves, which is obviously stupid. I'm not suggesting that. I'm suggesting that gaining fat as a *metabolic response* to developing diabetes is protective, which is essentially the same as saying that becoming diabetic prior to (or simply without) getting fat is more dangerous.

77877f762c40637911396daa19b53094

(78467)

on August 08, 2012
at 09:32 AM

You should reconsider the arrow of causality.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 09:18 AM

And to be more precise, it is the process of fat accumulation, not the "excessive pounds" that is a plausible protection.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 09:31 AM

To be fair, mine is also a pet idea, but it is not a less valid one at this point, as far as I know. I'd be grateful and even excited to hear about experimental evidence that disproves it.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 10, 2012
at 07:15 AM

(See my update.)

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 10:28 PM

Exactly. Epidemiology can't give you the direction of causality. At this point it could be either. I only asserted a hypothesis of the direction. I didn't assert that it was so.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 08, 2012
at 09:25 AM

Finally, if that quote from Carthenon was meant to imply anything more than trying to prevent people from making the stupid interpretation that they should gain fat, then it would be completely unsupported. He is an epidemiologist, and this study was epidemiology. It gives no clues to him or to us about the mechanism. So unless he had some other scientific reason to imply that, it would be just a pet idea -- if he had other evidence, I'm sure he would be telling us.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 10, 2012
at 06:43 AM

It's not so much a contention as a conjecture, and it's not to protect against t2d, but to protect against the damage from chronic high blood sugar. If 2 people have chronically high BG, and one of them efficiently gets it out of the blood and into the fat tissue, that person is not going to suffer as much damage from it. That's the idea anyway. I'm not saying it's so.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 10, 2012
at 06:46 AM

As to downvotes, I only use them when a post is factually incorrect, misleading, illogical, or offensive. In fact, I ought to upvote you for spurring me to find some articles to support the idea.

77877f762c40637911396daa19b53094

(78467)

on August 09, 2012
at 02:37 PM

.. but do mark my answer down if it makes you feel better. :)

100fd85230060e754fc13394eee6d6f1

(18696)

on August 09, 2012
at 02:24 PM

Great! It sounds like you have some scientific data that distinguishes these hypotheses by showing that one direction can't be true. I'm all ears.

77877f762c40637911396daa19b53094

(78467)

on August 09, 2012
at 02:34 PM

Your contention is that adipogenesis has evolved as a protective mechanism against type 2 diabetes. This is very unlikely.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 10, 2012
at 09:07 AM

What? Excretion of excess glucose in the urine is practically the definition of diabetes.

77877f762c40637911396daa19b53094

(78467)

on August 10, 2012
at 07:53 AM

Storage of the energy in glucose, either through polymerisation into glycogen or synthesis of fatty acids did not evolve to protect from chronic high blood sugar (one can easily excrete it) but to manage homeostasis of energy during times of a deficit in caloric intake.

77877f762c40637911396daa19b53094

(78467)

on August 12, 2012
at 01:34 AM

You said, "gaining fat as a metabolic response to developing diabetes is protective". I've taken your usage of the term "protective" to imply an evolutionary adaptation.

77877f762c40637911396daa19b53094

(78467)

on August 11, 2012
at 04:56 AM

Precisely, but you miss the point. You need to ask yourself, is it easier for the body to evolve a mechanism as complicated as fat synthesis to address excess glucose or simply to excrete it, or alternatively, the body can increase its insulin sensitivity. In other words, there are many easier mechanisms to develop other than one as complex as adipogenesis. Ergo it is unlikely that the evolution of adipogenesis was driven by the risk of T2D. It's also very unlikely that T2D existed with sufficient frequency in ancestral populations to become a selective factor. Today, it's a different story.

100fd85230060e754fc13394eee6d6f1

(18696)

on August 11, 2012
at 04:45 PM

I don't understand why you keep repeating that I have made an assertion that I haven't made. I give up.

0
Fbe5ccefbaa491771675404cd766578f

on August 08, 2012
at 10:22 AM

Unfortunately, they don't give much information about the study participants. Individuals are often diabetic for several years before they learn that they have the disease. Depending on their level of insulin production and their ability to utilize insulin, they may go into ketosis even though they are eating lots of carbs and have high blood glucose. Their bodies would be consuming fat for energy because they couldn't fully utilize the glucose. The resulting high blood glucose level would be damaging their bodies while they remained thin.

It would been helpful to know if the levels of insulin production/utilization at diagnosis was also considered in these studies.

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