Obesity is protective? – T2D 14

Obesity is not widely considered a protective mechanism. Quite the opposite. It’s usually considered one of the causal factors of the metabolic syndrome and insulin resistance. I think obesity is a marker of disease, but ultimately it serves to protect the body from the effects of hyperinsulinemia. Let me explain.

Claire Johnson

Gina Kolata, a journalist at the New York Times wrote a recent, very interesting article called ‘Skinny and 119 Pounds but with the health Hallmarks of Obesity‘. In this article, she describes Claire Johnson, a patient with a rare case of lipodystrophy, a genetic disorder characterized by the lack of fat. She was skinny but always ravenously hungry and could never get fat, because she lacked fat cells.

In college, Claire discovered that she had a huge, fatty liver, polycystic ovaries and severely elevated triglycerides – all hallmarks of obesity. Yet she was super skinny. She was finally diagnosed in 1996 with lipodystrophy by Dr. Simeon Taylor, who was chief of diabetes at the National Institute of Diabetes, Digestive and Kidney Diseases. He had several other patients all with the same rare genetic syndrome.  These patients had the most severe insulin resistance he had ever seen, but no fat that he could see (subcutaneous variety). Patients eventually also developed high blood pressure and type 2 diabetes, diseases typically associated with obesity.

In rodent models of lipodystrophy, researchers transplanted a little bit of fat back into the fat-free mice. The metabolic syndrome disappeared! The fat was protective against insulin resistance, not causative! What’s happening here?

We need to understand the new paradigm of insulin resistance to understand how insulin resistance, obesity, fatty liver, and fatty pancreas are actually all the different forms of protection our body uses. But what is the underlying disease? Hyperinsulinemia.

Dr Roger Unger had eludicated the basics of the syndrome a few years ago in this article. We’ll take it one step at a time. As I’ve outlined in my book ‘The Obesity Code’, the basic problem is hyper-insulinemia. There are many possible causes of too-much-insulin, but one of the major ones is excessive dietary intake of refined carbohydrates and particularly sugar. However, this is not the only cause.

Insulin has several roles. One is to allow glucose into cells. Another is to stop glucose production and fat burning in the liver (gluconeogenesis). After this stops, then it stores glycogen in the liver and turns excessive carbohydrates and protein into fat via de novo lipogenesis. Insulin is basically a hormone to signal the body to store some of the incoming food energy, either as glycogen or fat.

When insulin falls, during fasting, the reverse happens. The body releases some of this stored food energy to power the body. That’s why we don’t die during our sleep. If feeding and fasting are relatively balanced, then it all works as planned.

However, if insulin becomes excessive, then the body is always trying to store glycogen and fat. Since there’s not much room for glycogen, it produces fat. (Note – this is normal. This process reverses during fasting) The liver exports this fat out as triglycerides along with very low density lipoprotein (VLDL) to other organs but particularly to fat cells called adipocytes.

Now, adipocytes are specialized cells to store fat. Having more fat cells is not particularly dangerous. That’s what it does. Other than taking up room, it doesn’t really matter. The fat cell is designed to hold fat, so you don’t get sick from from it. Obesity itself is not the cause of the problem. The critical problem occurs when you get fat where it’s not supposed to be.

It’s usually first noticed in the liver. Fat is not supposed to be stored in the liver. But under conditions of hyperinsulinemia and excessive carbohydrates, it can develop. Glucose get turned into fat and too much of it ends up in the liver instead of the fat cells. The fat cells (adipocytes) are trying to protect the body by holding the fat in a safe place. Fat inside the fat cell is OK. Fat inside the liver is not.

The fat cells actually have a secondary protective mechanism. The expansion of the fat cells encourages the release of leptin, which will cause us to stop eating. However, over time chronic excessive release of leptin will create leptin resistance, which is what we find in common obesity.

So the liver tries really, really hard not to get anymore fat. But insulin is pushing really really hard to shove more fat into the liver. In Claire Johnson’s case, there are no adipocytes to hold this excess fat so it must remain in the liver and other organs.So, what’s a liver to do? Develop insulin resistance of course! The liver is yelling ‘Get that glucose out of here! It’s killing me’. So the glucose piles up outside in the blood. The insulin resistance is not a bad thing, it’s a protective mechanism. What’s it protecting us from? The very name tells you. Insulin resistance develops to resist insulin. The problem is too much insulin.

Meanwhile, the liver is busy trying to pump out as much of the fat as it can. It’s pumping out triglycerides like its life depended upon it, which it does. So blood triglyceride levels go up (a classic sign of metabolic syndrome). It’s trying to relieve the fat-engorged liver by exporting it out. So muscles get fat, and you get fatty muscle.

The pancreas also gets some fat and you get fatty pancreas. As the pancreas becomes distended with fat, it produces less insulin. Why? Because it’s trying to protect the body from the effects of too much insulin! The body knows full well the problem is too-much-insulin. So developing fatty pancreas protects us by shutting down production.

Both the fatty liver creating insulin resistance and fatty pancreas, creating lowering insulin levels results in the same thing. Increase glucose in the blood, but organ protection against this excessive insulin. This high blood glucose causes the symptoms of diabetes – excessive thirst, excessive urination and loss of weight. The high blood glucose exceeds the renal threshold of glucose.

The kidneys normally reabsorb all the glucose that passes through. However, when the glucose level exceeds approximately 10 mmol/L, the kidney cannot reabsorb it all. Glucose is excreted in the urine carrying along with it lots of water. Weight is lost as large amounts of glucose are urinated out of the body. Is this bad? No, it’s good!

The precise underlying problem is too much glucose and too much insulin. The body has protected itself by getting rid of all the extra glucose. The lowered blood glucose lowers the insulin, too and creates weight loss. These are all protective mechanisms taken by the body to protect against excessive insulin.

With this new understanding, we can see that obesity, insulin resistance, high triglycerides and beta cell dysfunction are all protective mechanisms against the same problem – HYPERINSULINEMIA.

So, what happens when you present to your doctor? Ignoring the hyperinsulinemia, (s)he decides that the problem instead is hyperglycaemia so he prescribes…. insulin! This neatly destroys the protective mechanisms so carefully put into place by the body. It forces glucose back into the body and crams more fat into the engorged, fatty liver and gagging, fatty pancreas. No more glucose is excreted out of the urine, so it instead all stays inside the body to wreak havoc. Nice. Nice.

This is, by the way, the exact protective mechanism which the SGLT-2 inhibitor class of drugs provides. These drugs lower the renal threshold of glucose so that you urinate out glucose – exactly what happens during uncontrolled type 2 diabetes. What happens if you don’t block the protective effect, but enhance it?

The EMPA-REG study was released last year. Using one of these new drugs reduced the risk of death by 38% and the risk of cardiovascular death by 32%. These sorts of benefits were exactly what we were looking for. Because this drug actually gets to the root problem. There’s too much glucose and too much insulin. This lowers glucose and lowers insulin. Of course, if we didn’t treat the type 2 diabetes at all, we probably would have had the same benefit.

There are two main problems with metabolic syndrome. Glucotoxicity and insulin toxicity. It does no good to trade the increased insulin toxicity to reduce glucotoxicity. That’s what we do when we treat people with insulin or sulphonyureas. Instead, it only makes sense to reduce BOTH glucotoxicity and insulin toxicity. Drugs such as SGLT2 Inhibitors do this, but diet is obviously the best way. Low Carb diets. Intermittent Fasting.

In the end, obesity, fatty liver, and type 2 diabetes and all the manifestations of the metabolic syndrome are caused by the same underlying problem. NOT insulin resistance. The problem is hyperinsulinemia. It’s the insulin, stupid!

The power of framing the problem in this way is that it unveils the solution immediately. The problem is too much insulin and too much glucose? The solution is to lower insulin and lower glucose. How? Nothing simpler. Low Carb, High Fat diets. Intermittent fasting.

2017-10-14T21:55:16+00:0039 Comments

About the Author:

Dr. Fung is a Toronto based kidney specialist, having graduated from the University of Toronto and finishing his medical specialty at the University of California, Los Angeles in 2001. He is the author of the bestsellers ‘The Obesity Code’ and ‘The Complete Guide to Fasting’. He has pioneered the use of therapeutic fasting for weight loss and type 2 diabetes reversal in his IDM clinic.

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Rob Hanna
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As I was reading your descriptions of fatty liver and fatty muscle I couldn’t help but think of corn-fed gauvage done to geese and ducks to create foie gras (fatty liver), as well as grain-fed cattle to create well-marbled (fatty) muscle meat.

In effect, if correct, my assumption reveals our dietary customs, food culture and corporate profits of industrial agriculture are the perfect storm turning all of us consumers into ready for slaughter animals… well, if we were back in the foodchain.

I appreciate your sharing such revealing insights.

Jane
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Jane

Dr. Fung, You have written another beautifully clear and succinct explanation of how people develop obesity, metabolic syndrome, and Type II Diabetes. The verbal and graphic descriptions are so clear. Your explanation of the best type of medication, the SGL2 inhibitors, to target the toxic effects of hyperinsulinemia by lowering the threshold for the kidney to release glucose would help thousands of patients is they could learn about it! I have already wished for a magical ability to transmit your insights about the effectiveness of LCHF eating patterns and Fasting to solve diabesity problems caused by hyperinsulinemia. Now, I wish… Read more »

Wenchypoo
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Wenchypoo

Isn’t he like a teacher up in front of the class? With every article, I feel like I’m getting a medical school education (or what SHOULD be a medical school education) for free. “Professor Fung” has a nice ring to it.

Anthony Williams
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Anthony Williams

I thought I was the only one who felt that way. I’ve learned more from this site that I learned in a general biology class. I believe this should be required coursework for all practicing physicians. Thank you Dr. Fung for your knowledge and insight. With your help and others, I have significantly lowered my blood sugars, lost weight and gained confidence and energy.

Eric Adkins
Guest

How can we measure the insulin in our bodies? Everyone talks about measuring blood glucose. But what about insulin?! I’m dying to know.

Vivien
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Vivien

Its possible to get your insulin levels tested you just need to ask for it. I asked my GP was it possible and what was the cost. And it was possible but pricey

Roger
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Roger

I just got my fasting insulin done. It cost me $49.00. Well worth it. Knowledge is power.

Vivien
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Vivien

Its possible to get your insulin levels tested you just need to ask for it. I asked my GP was it possible and what was the cost. And it was possible but pricey. Its not test you could do at home.

sten bjorsell
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sten bjorsell

In Cork in Ireland I had to go to (Bon’s) Hospital to draw the blood and then it took just over a week for the results to come back. My GP ordered the test after I advised him the tests I wanted. It took him several days first time to find out where and how…, so I respect him for that! Not sure if they have to freeze samples and ship to UK or if they do the lab work in Ireland. Cost around 70 euro, but I took apoA and apoB at same time so not sure what costed… Read more »

jim
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jim

As I am reading the current thoughts on insulin, fasting insulin labs are of low value for measuring diabetes/insulin resistance. Doctor Joseph Kraft has changed the playing field. It is how quickly insulin decays after a rise that is important. IMHO the option that what is available to the vast majority of us is try to keep our level of insulin at the lowest level possible by using fasting and eating practices to modify basal insulin levels. Doctor Ron Rosedale theorizes that insulin is a master hormone for controlling storage in the body, not just fat. Evolutionary basal insulin has… Read more »

Sam
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Sam

Fascinating. But the original problem CAN’T be high carb. Because there have been (and are) dozens of traditional societies around the globe with 60 to 80 and even 90% carbs in their diet. They are perfectly healthy. And the problem CAN’T be “refined carbs” either. See the recent study by Dr. Lustig, who replaced sugary foods with refined carbs (bagels, pizza) and immediately reversed MetS in obese children (within days!). Something is wrecking our carbohydrate metabolism, but it’s not “carbs” (glucose). Perhaps it’s (isolated) fructose (and therefore sugar). Of course, once your carbohydrate metabolism has been wrecked, carbs (glucose) DO… Read more »

Robin
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Robin

I don’t think high carb is usually the problem. Dr. Fung also cites meal frequency and the amount of sugars in our diet. Some people are metabolically able to eat more carbs than others. Much of it is in our genes. I would also suspect environmental contaminants and gut flora play a role.

Robin
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Robin

I had meant to type high carb is not *always* the problem. Dr. Fung has addressed the paradox of the Chinese rice eaters in other blog posts. I read recently that some people of Asian descent have larger pancreases than other ethnicities. How much of this is actually genetics and how much is a response to diet? Who knows? People with Inuit ancestry have a particularly hard time with refined sugars and carbs, and apparently Samoans do not suffer from metabolic syndrome even when they have a high BMI: In Nature Genetics: “Higher BMI and adiposity are usually associated with… Read more »

Jane
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Jane

Thank you!
— for the links to the facinating stories about genetic variants among Arctic peoples and Samoans.

sten bjorsell
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sten bjorsell

To me it seems that as long as no excess food is eaten, there will be no de novo lipogenesis in the liver and no liver fattening, explaining why it is possible to live on carbs as long as they are in short supplies most times of the year. With plenty of very cheap carbs and fructose containing sugar from childhood it becomes however hard to not overeat, mainly because the “natural blood sugar swings” carbs cause make it “NECESSARY” for many that can snack to snack. Carbs naturally become abundant only in the autumn and all animals including ourselves… Read more »

Richard S Stone
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Richard S Stone

Excess carbs as the culprit… Well, I wonder about that statement. First, because “excess” by definition means too much. Otherwise it wouldn’t be “excess.” Instead Dr. Fung generally notes in his blogs that insulin is produced both by carbs and by protein, and to get insulin production under control, to be back to the pulsatile nature of proper insulin production, you can’t snack between meals,etc. Ultimately, what most us would end up with, as adults in his feeding regime would be, I think, at most two meals per day. And at that point the body may be able to manage… Read more »

Walt
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Walt

Maybe but I have one main issue with what you said in response to Sten. Yes, Dr Fung suggests no snacking between meals indicating, as you point out, the pulsatile nature of consuming carbs. However, Dr Fung also refers often to primitive man and I would argue primitive man grazed vs had three square meals per day. I am not sure when, anthropologically, the notion of three, and only three, meals per day arrived on the cultural scene. I would suspect it occurred after agriculture started where stores exceeded requirements such that it became something of a rationing vehicle. Interesting… Read more »

Richard S Stone
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Richard S Stone

Walt: Over about the last six or seven years I have been a voracious reader of many things Paleo. I started with Kurt Harris’ blog, PaNu. And no one has a real understanding of “the” one true primitive diet, exactly, because that diet has always varied depending on the season and the location. We do have some primitive or less developed tribes and people to refer to and consider, and they are not obese and diabetic. And yet, as generally marginalized groups, there is some some doubt about how much they presently, or have ever, reflected ancestral eating patterns. Dr.… Read more »

Walt
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Walt

@Richard, that may well be however, primitive man predates agriculture. I define agriculture as the evolutionary point where a society jointly/cooperatively grew their own crops and hunted their own meat. Not being an anthropologist, I don’t know when the concept of 3 square meals/day came from but I’d guess the second mellenium (>10000AD). Therefore before there were periods of plenty that, over night, turned to famine (aliens stole all the food while the townfolk were asleep), food would gradually become scarce and gradually become plentiful. The nomadic people would try to follow the food, be it US native Indians or… Read more »

Jane
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Jane

My guess is that the people in the traditional societies you mention are much more active than most in our society. I have read that activity helps restore insulin sensitivity.

Jin
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Jin

Hi Sam, No doubt you have heard of the French paradox i.e. they eat more saturated fat than anyone else yet are slimmer and healthier in general but did you know they eat 40% more wheat than UK or USA? Most of Europe is slimmer and healthier than UK or USA. USA and UK have mandatory flour fortification. Could this be the cause? I believe it to be so, as each new wave of fortification has preceded a new wave of obesity and diabetes while non fortifying countries have far less problems.

Walt
Guest
Walt

That is just scary.

Sam
Guest
Sam

yes, the French love their baguette (white bread) and croissants. Difference is, US bread often contains high-fructose corn syrup, i.e. sugar…

seebrina
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seebrina

It dismays me to try and shop due to HFCS added to all foods. While I mostly stick with whole foods, things like yogurt or dressing and such are full of it. They put it in the most unlikely places. I just dont understand the need for that. Its even in savory foods you would never think of needing sugar in any form. Ugh.

Jennifer
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Jennifer

I’ve been on LCHF and intermittent fasting the past couple months and have lost 40 pounds. I dropped my 120 units of insulin and came from an A1C of 9 to 11 (for the past four years) to a projected A1C of 5.8. After 25 days of intermittent fast I dropped my Metformin. It’s been just over 2 weeks now since I quit the metformin, and I think I see my blood sugars rising again. My blood sugar got up to 160 mg/dL today and I injected 20 units of Novalin R to bring it down to 120 mg/dL. This… Read more »

MH
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MH

Thank you, Dr. Fung!

I never could have gotten this well without the groundbreaking information you provide!

I am a 62 year old lady.
I’ve dropped 30 pounds.
My BMI went from 31 to 25.
Fasting blood sugar from 100 to 82.
Blood pressure is 110/70.
Got off the statin medication!
My sleep apnea disappeared. I quit using my CPAP machine.

My daily routine is simple.
Avoid refined carbohydrates, sugar and processed foods.
Eat whole foods.
Eat for 8 hours. Fast for 16.
Walk 5 miles every day.
Rinse. Repeat.

I think I may have avoided metabolic syndrome AND type two diabetes just in the nick of time!

Thank you from the bottom of my heart!

Walt
Guest
Walt

Outstanding post Dr Fung! I did, very much, enjoy the two compartment model, which I encourage all that have not viewed it to do so. However, this post was far more, um, advanced on the subject.

My FBG is now in the 70’s, my A1C is 5.6, my weight is approaching mid normal range of BMI for my height and age. Not too shabby as I was pronounced type 2 diabetic a year ago. Should, anecdotally, anything in my ‘journey’ be helpful in your upcoming books. I’d be happy to share.

Walt
Guest
Walt

lost over 120lbs
A1C 8.5->5.6 in 12 months

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Julia
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Julia

Just binged read your entire blog in order. As of midnight tonight, I have successfully finished my third day of fasting (24-36 hours being my longest and now aiming for 5-10). I have learned so much but I just have a couple minuscule questions that I think will help me on the journey: 1) For holidays or special events, do you recommend fasting before or after? Or both? Fasting before makes sense but then in the anticipation of eating crappy foods (sugar) I would be worried about getting sick or ballooning up after! 2) Lets say I do 5 day… Read more »

Richard S Stone
Guest
Richard S Stone

Julia: Amusing questions, because… If you try to stuff yourself after being on a fasting or IF program you may not be happy. Secondly, you may not even want to stuff yourself, even faced with great quantities of good food. And who says whole grains are healthy? People can eat grains, but people are more adapted to eating root based vegetables and green leafy vegetables compared to grass-based seeds, eaten by mice and birds. Yes I know rice is not very reactive, but it really is just a “sugar” source. My experience and understanding is that one meal of “excess”… Read more »

Julia
Guest
Julia

Thanks for some replies. I however didn’t mean to imply “stuffing myself” on my eating days. More, the best way to eat on those days to keep up with my weightloss goals, and keeping that insulin down before I move on to the next 5 days of fasting.

Warren
Guest
Warren

Hello All, Really appreciate Dr Fung’s blogs and articles on T2D. I was diagnosed with T2D on December of 2013 and have struggled to keep my GL levels in control and I routinely wake up with my GL wround 170-180 even with IDF/ADF fasting. I was on Victoza and had to quit because of how it made me feel, so the only T2D med I am currently taking is 1000mg of Metformin twice daily. After reading this blog I am wondering if I should pursue SGLT-2 type meds in lieu of the metformin with my endocrinologist? I can’t help but… Read more »

Walt
Guest
Walt

Warren, I can not directly address your question but do have one caution. Find a doctor that has a more current view of the problem than “it’s a life-long, chronic progressive disease’. My medical team, HMO, is just too clingy to that notion and, so long as they are, aren’t really trying to cure me, just manage my blood sugars. If you doctors don’t actually believe its curable, they will never find a cure for you. When interviewing any prospective new doctor or endocrinologist, be sure that is your first question.

Amelia
Guest
Amelia

Warren, I recently started taking Invokana (SGLT2 inhibitor). It’s had an immediate positive effect on my blood sugar levels. I went from being at 391 (blood glucose meter reading) down to 146 is three days. Also taking Metformin, 500mg twice a day. I feel really good. I’m also on a LCHF diet. Started a couple of weeks ago. Make sure to drink plenty of water if you do ask your doctor for an SGLT2 inhibitor. Dehydration is one of the main possible side effects. Good luck!

charles grashow
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charles grashow
George Thomas
Guest
George Thomas

Hi Cuckles. I haven’t seen you around lately.

Pablo Sanchez
Guest
Pablo Sanchez

Dr Fung,
Thank you for your interesting work.
One question: if fat not release insulin, and carb release insulin unless protein, then the best diet, to health and weight, would not be a diet whitout protein, but moderate in carbs and fat? Like vegan mediterranean diet? Or only carbs, in case that the fat, a long term, increase the insuline

Nathan Gottschall
Guest
Nathan Gottschall

A caveat I would have regarding lowering the threshold at which the kidneys release glucose in the urine is that this very process, according to my understanding and reading, damages the kidneys when done repeatedly; glucose is crystalline in structure and damaging to the delicate renal mechanism. However, Dr. Fung would have a greater understanding on this than do I.