Inflammation – Not Obesity – Leads to Diabetes

Nice to read that you have received an education.

May reading the following help you shake the delusion:

http://HeartMDPhD.com/StrongMan

I would appreciate an explanation of inflammation.  Are you speaking of swelling, arthritic reactions, innerbody functions or what??  Also, how does that raise your blood sugar?

"I would appreciate an explanation of inflammation. Are you speaking of swelling, arthritic reactions, innerbody functions or what?? " -- renoozie

We are writing about our bodies' inflammatory (immune) cells wreaking havok everywhere internally including "shooting up" our insulin receptors so that we become insulin resistant.

"Also, how does that raise your blood sugar?" -- renoozie

When our bodies no longer respond as readily to insulin because we have become insulin resistant, our blood glucose (aka sugar) will increase.

Would post links but it seems that Krystal has been compelled to delete such posts from me.  Sorry.

Heartdoc

Thanks for your reply.  I think the word immune was the key to my understanding.

Appreciate your input.

"HeartdocThanks for your reply. I think the word immune was the key to my understanding.Appreciate your input." -- renoozie

You are welcome, renoozie :-)

Simply here to help others.

It goes insulin -> obesity AND steatosis AND insulin resistance & inflammation -> more insulin -> more obesity/steatosis/insulin resistance from inflammation...

It starts with insulin.

What makes insulin go up? Carbs, mainly, but also calories (fats, if consumed with carbs, decrease the rate of glucose clearance; carbs, if to the point calories are substantial, obviously increase glucose levels and insulin ).

It stops with insulin, too.

Eating a low carb diet and/or avoiding high calories (the more carbs/proteins one eats the less calories they can eat).

Of course in some people the damage done to their bodies may be such that they require medications for life (e.g. insulin if beta cells are burned out) but for a mild/borderline diabetic arresting the disease and preventing the dearth of complications is as simple as picking up a copy of dr bernsteins book and following the plan.

"It goes insulin -> obesity AND steatosis AND insulin resistance & inflammation -> more insulin -> more obesity/steatosis/insulin resistance from inflammation... It starts with insulin..." --ItsTheWooo

The problem with your premise is that type-1 diabetics can become obese and develop steatosis too and they do not have insulin except that which they inject to match the amount of food they eat.

It logically follows from this latter fact that it starts with the overeating and not the insulin. 

"

The problem with your premise is that type-1 diabetics can become obese and develop steatosis too and they do not have insulin except that which they inject to match the amount of food they eat.

"

Type 1 diabetics only have these symptoms in the presence of insulin. Without insulin they fit the clinical picture of starvation.

The problem is the diet which produces the insulin, as I said... and a type 1 diabetic medicated to diet is susceptable to insulin diseases as the general population. If they are sensitive to develop it, they will, over time, as long as their diet increases their insulin needs.

"It logically follows from this latter fact that it starts with the overeating and not the insulin. "

Availability of energy is a factor in insulin levels, but it is subordinate to carbohydrate. A diet very high in fat, protein to need, and very few carbs, with adequate calories and frequent meals (so as to prevent high sugar from liver) is not going to require lots of insulin.

A diet which is slightly lower in calories but 60% starchy carbs and sugar is going to require much, much more insulin to process.

The different needs for insulin from different macronutrients is why studies repeatedly show that people fail to gain and may even lose excess weight on low carb diets much higher in calories than low fat diets.

Weight is a fail-proof indicator of insulin levels; if a person loses weight (body fat) it is always true their insulin levels decreased. Research consistently proves that people lose more weight on a very low carb diet than a diet with equal calories which is high carb. This, logically, means very low carb diets - calorie per calorie - require a great deal less insulin.

And, if one has a derrangement of metabolism (genetic or aquired), this difference in insulin production for different macronutrients can be extreme. I gain weight rapidly on low calorie intakes of very high carb. On very low carb with high fat, I find it difficult to gain even if I eat a lot of calories, and this can only be accomplished if I start adding a few carbs or extremely high protein intakes.

In summary, I am not necessarily disagreeing with you that calories positively affect insulin levels (they do, otherwise starvation-level calories of low fat diets would produce the same hyperinsulinemia diseases we observe today).
What I am disagreeing with is that it starts with calories. It most certainly does not, because calories are subodrinate to types of calories in their insulinogenic potential. 100 calories of butter requires a lot less insulin than 100 calories of bread... and among different people with different metabolisms, the difference can be quite marked (someone with few insulin receptors on muscle cells, and a great deal on fat cells, will have an even greater difference in how much insulin is produced from that 100 calories of bread). Fat metabolism can produce energy and bring it to cells without nearly as much dependence on insulin levels; the insulin need for energy from fat metabolism is so low it's practically covered by basal insulin. Type 1 diabetics don't medicate to fat, they medicate to carb.

 To deny this fact and to repeatedly state "it starts with over eating and calories" is to simply ignore the vast body of evidence before us on this subject. Calories are a factor, but subordinate to carbohydrate.

Obesity and steatosis are not symptoms but physicial findings. For the type-1 diabetic example, there is no refuting the scientific evidence for the proximate cause being the excessive amount of food eaten and not the insulin.

Here is the relevant thought experiment:

Take any type-1 diabetic and give excessive insulin, there is death, which means no weight gain.

On the other hand, excessive food intake will result in obesity and steatosis. 

"Obesity and steatosis are not symptoms but physicial findings. For the type-1 diabetic example, there is no refuting the scientific evidence for the proximate cause being the excessive amount of food eaten and not the insulin."

Physical findings in a pathological condition are just anotherway of saying signs and symptoms. Obesity and steatosis are signs and symptoms of high insulin (primary or secondary to IR) and insulin resistance.

Food without insulin is for all practical purposes fiber to your body. Without insulin to soften the cell to glucose, it cannot diffuse in (for either metabolism of energy or storage of fat, depending on total glucose load and relative insulin sensitivity/concentration of receptors on different tissues).

Without insulin the sugars builds up in the blood and passes out in urine, because the body can't do anything with it.

Uncontrolled fat burning is also found, because insulin indirectly controls fat burning (though insulin is hardly needed to process fat for energy, it is true insulin controlls the rate of fat burning; the more insulin, the less fat burning, because insulin's job is to send nutrition in cells: mineral, fats, proteins and sugars).

 To say it has to be food and not insulin (in obesity) is like saying atomspheric air will cause oxygenation of body tissues, not hemoglobin in anemia. On one hand it's somewhat true (applying oxygen to an anemic will help their signs/symptoms) but it misses the larger pathology: defective hemoglobin which is causing this sensitivity to low oxygen to begin with.

"Here is the relevant thought experiment:

Take any type-1 diabetic and give excessive insulin, there is death, which means no weight gain.

On the other hand, excessive food intake will result in obesity and steatosis."

This is invalid because insulin production always follows food intake in normal physiology. And, not all foods are equal in insulinogenic potential. That's the key to solving this puzzle.

The only time insulin production does not follow food intake is if there is a malignancy of the pancreas (insulinoma). This BTW really has nothing to do with the topic. The question is what foods make us make too much insulin, or more appropriately, how do we get people to reduce their insulin levels? No one has too much insulin because of overmedication; people have too much insulin because they are sensitive to diets that are insulinogenic.

Your thought experiment is meaningless.

BTW, just a little FYI, the precursor to overt diabetes type 2 is often reactive hypoglycemia (hypoglycemia is the same thing that kills people if they produce insulin without food). The reactive hypoglycemia after eating "normal" carbohydrate meals is an indicator of early hyperinsulinemia and glucose metabolism abnormality (without severe insulin resistance or severe insulin deficiency).

 Hypoglycemia is often what obese people identify as "hunger", and it explains a great deal of over eating behavior found in obesity.

People progress to frank diabetes only when they either lose too many insulin receptors on fat cells OR they burn out their pancreatic beta cells OR a bit of both.

"Physical findings in a pathological condition are just anotherway of saying signs and symptoms."

Not for physicians.

We can describe physical findings for a corpse, which definitely would not have any symptoms. 

"Obesity and steatosis are signs and symptoms of high insulin (primary or secondary to IR) and insulin resistance."

You are forgetting that the primary purpose of insulin is to lower blood glucose.

This is evident by the fact that without insulin, folks die from hyperglycemic shock and not from lack of adipose tissue.  Simply look at the example of our type-1 diabetic friends and their purpose for using insulin.  It certainly is not to become obese or to suffer from steatosis.

" Food without insulin is for all practical purposes fiber to your body."

Incorrect. Would suggest you read up on how our type-1 diabetics survived in the days before exogenous insulin was available.  Hint: they would not have survived without any food even though they did not have any insulin. 

"Without insulin to soften the cell to glucose, it cannot diffuse in (for either metabolism of energy or storage of fat, depending on total glucose load and relative insulin sensitivity/concentration of receptors on different tissues)."

Would suggest you familiarize yourself with the fact that cells that truly need glucose are able to take in glucose even when either insulin or its receptors are either defective or absent. The cells of the brain are notable examples of this. 

"Without insulin the sugars builds up in the blood and passes out in urine, because the body can't do anything with it."

Not when there is no source of glucose either exogenously from the GI tract or endogenously from either gluconeogenesis or glycogenolysis.

"Uncontrolled fat burning is also found, because insulin indirectly controls fat burning (though insulin is hardly needed to process fat for energy, it is true insulin controlls the rate of fat burning; the more insulin, the less fat burning, because insulin's job is to send nutrition in cells: mineral, fats, proteins and sugars)."

It is not clear what you are trying to write here however it seems that you are trying to assign more to insulin than actually is its primary function.

"To say it has to be food and not insulin (in obesity) is like saying atomspheric air will cause oxygenation of body tissues, not hemoglobin in anemia. On one hand it's somewhat true (applying oxygen to an anemic will help their signs/symptoms) but it misses the larger pathology: defective hemoglobin which is causing this sensitivity to low oxygen to begin with."

It seems you would disbelieve the pointed observation that no obesity can be seen where food is scarce either in places of famine or in non-humanitarian prison camps.

"Here is the relevant thought experiment:

Take any type-1 diabetic and give excessive insulin, there is death, which means no weight gain.

On the other hand, excessive food intake will result in obesity and steatosis."

"This is invalid because insulin production always follows food intake in normal physiology."

This remains valid and useful for understanding the purpose and function of insulin.  Whenever, there is controversy about the purpose and function of something, it is useful to do the "knock-out" experiment where we look at instances where the particular something has been "knocked out." For insulin, that would be our type-1 diabetic friends.  Each is illustrative of why insulin is needed.  Each will have no difficulty in clearly expressing to you the purpose and function of insulin and to inform you that insulin does not cause obesity.

This is getting way too long.  Will continue this in a sharepost...

Dear ItsTheWood,

Could you please contact me directly? I would like to write you directly. My email is mendosa@mendosa.com and my phone is (303) 499-5544.

David 

Hi David

My email address is itslikewoowooo@aol.com

You can contact me here if you would like

Thank you,

Nora

Joslin diabetes center is doing a study of the arthritis drug salsalate, which is an anti-inflammatory. If you're close to one of the study centers, you might consider trying that. It not only reduces inflammation but reduces insulin resistance. And being in a study, you get a lot of free lab tests.

I was in the preliminary study, and it reduced my IR and my A1c. 

Hi,

Define "low carb diet". :) The diets most diabetics are low in carbs compared to your macdonalds loving friends but not low enough to really be a metabolic shunt around insulin resistance.

Inflammation <b>results</b> from hyperinsulinemia. Insulin actually encourages the synthesis of pro inflammatory cytokines, which contributes not only to insulin resistance itself but numerous "diabetic complications" like clots/heart disease deaths. And, if you are a poorly controlled diabetic with high insulin levels, you are certainly pro-inflammatory by logical extension.

So the thing we must ask ourselves is, "how do we reduce insulin" because reducing insulin will automatically translate into reducing inflammation and the illnesses associated.

Here is a key: <b>Blood sugar requires insulin to enter the cell; fatty acids require very little insulin to enter the cell </b>.

Here is another key: <b>Insulin resistance occurs in a non-egalitarian fashion; muscle cells and energy-hungry tissues typically have more of an insulin resistance than do fat cells</b>.

If you are eating a diet which yeilds a high glucose load (high protein, or high carb)... this is going to require a lot of insulin for your body to metabolize that glucose created. And, once metabolized, less is sent to supply the needs of vital organs; more is shunted to fat.

The fat created stays put, because the incredible amounts of insulin needed to nourish the more insulin resistant tissues of your body certainly will prevent any fat from leaving your fat cells. This is truly a shame becuase if you were able to burn fat, your energy levels would increase and your tissues would be far better nourished.

The way out of this mess is to eat fat, lots of fat, and almost no carbs with moderate protein. Eating a diet so high in fats will decrease your insulin needs substantially, while simultaneously increasing energy production and availability to all of your body tissues. You'll lose weight and you'll feel no hunger (because your body is shrinking fat cells due to the reduced need for insulin, your need for food is nil and easily supplied by the insulin-hypertrophied fat cell).

The ideal diabetic diet is high in fat and as low in carbohydrate as to just stave off ketosis (not that there is any risk from ketosis, more that ketosis is an important sign of poor control that should not be masked by benign ketosis from carbohydrate restriction.... plus some people report ketosis has side effects ).

I recommend Dr Bernsteins DIabetic Diet as a great book for the diabetic.

Remember the key with diabetes is diet, diet diet. The goal is reduce insulin need / production as much as possible.

<b>Inflammation follows insulin</b>. To say inflammation causes insulin resistance is to miss that important arrow of causation from insulin. And, if you take "tons of insulin" you probably aren't eating a diet sufficiently high enough in fat and low enough in foods that metabolize to substantial glucose (such as carbs and proteins). Over 90% of fat is non-glucogenic and requires no insulin. PRotein requires a great deal of insulin as does carb. For a diabetic with poor control, the key is fat fat fat and little else (protein to needs, but not much more than that, and it goes without saying carb should be a few grams and not more).

Dear Alice,

I would be extremely skeptical that bypass surgery could cure diabetes. 

Our bariatric surgery colleagues are indeed touting a surgical cure for type-2 diabetes.

In our cardiology clinic, we are seeing cures with the non-surgical equivalent 2PD-OMER Approach:

http://HeartMDPhD.com/SermoExposed

If you can't absorb food, you can't spike blood sugar and insulin.

Gastric bypass works like anti-opiate medications works for heroin addiction. After gastric bypass it is almost impossible - by accident or intention - to eat enough to spike blood sugar and cause hyperinsulinemia. Sugar causes massive gastric dumping, and total caloric intake is such that the body is burning tons of body fat simply via calories being so low. Most people on gastric bypass, additionally, are specifically instructed to follow low carb diets (or reduced carb at the very least). The combination of these factors just makes it *impossible* for the sugar to be spiked.

There is nothing this surgery gives that you can't get by doing high fat low carb and reasonable eating. It's a tool, and a dangerous one at that. I'm not against it, I just think it's unnecessary and most people who lose weight with it could have done it on low carb if only they had the proper education and support.

BTW I weigh 120 pounds at 5'5, I lost 160 pounds from a high of 280. Before low carb I had hypoglycemia and PCOS (early signs of high insulin levels). I am living evidence of what I say.

OK--if one is morbidly obese, as I am, how does eating fat, low protein, etc., figure

in trying to reduce fat as a cause of high cholesterol--I thought high protein,low fat,  complex carbs were "the key" for weight/fat loss--am I wrong?

Alice 

Dear Alice,

It's now low protein. All the dispute is whether our diets should be high carb and low fat (the traditional position) or low carb and high fat (what Gary Taubes and Dr. Richard K. Bernstein show makes much more sense). What you thought is what almost all "diabetes experts" think. But it is important for you to read Good Calories, Bad Calories by Gary Taubes to understand how the ground has shifted under us.

Dear Alice,

Please excuse the typo in my previous message -- one little character that changed the entire meaning! I meant to write that it's not low protein. 

Hi momof08,

David Mendosa is correct, very good advice. Dr Bernstein's diet is a great choice for a diabetic, and Taubes book is a must read to appreciate this disease of obesity (and how to prevent, stop, and possibly reverse its course).

To reclaim your health the most important intervention is to eat low carb and high fat. Worrying about protein and stuff like that, isn't very important right now (compared to the damage of carbs, a high protein is actually beneficial...).

I eat less than 60 carbs per day, and as many as 1800 calories. I weigh less than 120 pounds at 5'5.
Before this diet, I was 280 pounds, with reactive hypoglycemia and PCOS (both of these are conditions related to insulin excess). I was most assuredly headed for insulin resistance and possibly diabetes; I was only 20 years old and my health was already that bad! 6 months into the diet I had a cholesterol test done, and my triglycerides were high and my HDL was low (these are hallmark signs of hyperinsulinemia/insulin resistance). Keep in mind I had been low carbing for six months already so you can imagine just how bad my health may have been before the diet.

My A1C was measured at 5.4 after one year on the diet. This is a normal range but considering all of the weight loss and carbohydrate restriction, which should imply a beneficial change in A1C... it is scary to think what it must have been at the start. 

Over the years my cholesterol has slowly improved, with triglycerides getting lower and HDL getting higher. Today my HDL and triglycerides are almost reverse of what they were - my HDL is now like 90 and my triglycerides 36. My last A1c was 5 or 4.9 (I don't remember).

I've been eating low carb for almost 5 years now... it takes the body a long time to heal.

But, the most important thing is to intitiate it and start healing. Please pick up these books, it's the first step to health. 

I am reading the Four Corners Diet recommended by David Mendosa.  I also read Dr. Bernstein's book a couple of years ago and began following his program as I read it with the result I lost about 20#.   After a while, I felt it too restrictive, i.e. no fruit.and guess what? the weight came back on. So, in reading the Four Corners I realize that it too is very similar to Dr.B's. Are you familiar with their program?I  

I

I have llost 35# on Byetta as I can only consume half the amount of food I did before.   Of course, I am concerned about ever gaining it back so am wondering if I should in fact return to the lo carb eating pattern.

Extremes of anything have always raised my guard level and this is certainly extreme.

renoozie

Four Corners is similar to Bernstein, but they allow a little more carb (50 g instead of 30 g) and also allow LC fruits like berries.

I think it's a very healthy diet. If I were you, I'd try low-carbing again because of its effects on BG levels. When you've lost a lot of weight with the help of the diet plus Byetta, then you could see if you could add back more carbs.

I miss fruit, but I find that adding DaVinci fruit-flavored syrups to kefir helps satisfy my yearning for fruit.

Good idea - we never seem to give up that yearning for whatever it is we are not supposed to have!    Thanks

David if you are reading this would you comment on the carbohydrate load in the cereal you use in the am (you order it from the supplier).

Thanks

Dear Renoozie,

Yes, indeed. The serving size, 1/4 cup, has 22 grams of net carbs, according to the Bob's Red Mill website.

Dear Chris,

I thank 9,000 IU/day of Vitamin D myself. Please see my article at:

http://www.healthcentral.com/diabetes/c/17/3112/vitamin/

Best regards,

David