RECOMMENDED ARTICLES ON DIETARY ISSUES

Insulin Reistance and Fatty Liver, at the heart of the storm--Fung

Home
Low Carb management of tyupe-2 diabetes-review
Fructose pathology
Sugar Buzz Lustig & fructose and NAFLD articles
382 day fast
Insulin Reistance and Fatty Liver, at the heart of the storm--Fung
Excess sugar and fatty liver experiment, heart of storm

This and the subsequent (id/2) confirm the outline of how we muck up the metabolic system and thus what to due about it.  See paste at bottom.

https://intensivedietarymanagement.com/insulin-resistance-good-t2d-7/

Insulin Resistance is Good? – T2D 7    Dec 3 2015 

Everybody says that insulin resistance is bad. Very bad. It’s the root cause of type 2 diabetes (T2D), and metabolic syndrome, isn’t it? So, if it is so bad, why do we all develop it in the first place? What’s the root cause? My friend Dr. Gary Fettke from Tasmania wrote an illuminating book called ‘Inversion’ where he describes how you can learn a lot from looking at things from another perspective. Invert (turn upside down) your perspective, and see how your horizons are immensely broadened. So let’s look at why we develop insulin resistance. Why is it good?

Root Cause Analysis

What is the root cause of insulin resistance? Some people say inflammation or oxidative stress or free radicals causes insulin resistance [jk says fatty liver]. Those are total cop-out answers. Inflammation is the body’s non-specific response to injury. But what causes the injury in the first place? That’s the real problem. The inflammation is only the body’s response to whatever is causing the injury.

Think about it this way. Suppose we are battlefield surgeons. After decades on the job, we decide that blood is bad. After all, every time we see blood, bad things are happening. When we don’t see blood, bad things are not happening. It must be the blood that is dangerous. So, deciding that blood is what is killing people, we invent a machine to suction all the blood of people. Genius! The problem, of course, is what’s causing the bleeding, rather than the blood itself. Look for the root cause. Bleeding’s only the response, not the cause. Bleeding is a marker for disease. So is inflammation.

Something causes bleeding, the body’s non-specific response. Something causes inflammation, the body’s non-specific response. Gunshots cause bleeding, knife wounds cause bleeding, and shrapnel causes bleeding. Those are root causes. You got shot. You bleed. But the problem is the gunshot, not the bleeding. The same applies to inflammation [same for hypertension, its atherosclerosis]. 

Whatever is causing the injury (the root cause) is also stimulating inflammation (the nonspecific response to injury). Inflammation is simply the marker for disease. So people say that cardiovascular disease, diabetes, neurodegenerative disorders, obesity and cancers all involve chronic inflammation. But the inflammation is not causing the disease, it is only a marker of it.

If inflammation was actually a root cause of heart disease, for example, then anti-inflammatory medications (prednisone, ibuprofen, NSAIDs) would be effective in reducing heart disease, or obesity, or cancer. But they are not. Whenever people talk about inflammation being the cause of disease, they just bandying around the latest buzzword [put out by pharma’s KOLs].

This is not to say that inflammation (or bleeding) is not useful as a marker of disease. If the bleeding stops, then the treatment (tourniquet) is highly likely to be effective. But it’s not effective because bleeding stopped. It was effective and bleeding stopped (it’s a marker for effectiveness). Similarly in inflammation and T2D, as I previously wrote, insulin therapy does not decrease inflammation, which marks this likely an in-effective treatment overall.

The same goes for oxidative stress (or free radicals). Tell me what is causing the oxidative stress. That’s why antioxidant therapy is so startlingly ineffective. So Vitamin C, or E or N-acetylcysteine or other antioxidant therapies never work whenever they are tested rigorously. Because the oxidative stress is only the response (like inflammation) to whatever the underlying disease process actually is. If somebody goes on and on about oxidative stress (or free radicals or inflammation, or bad gut microbiomes) as the cause of XXX disease, run, don’t walk the other way. “Insulin resistance is caused by inflammation” is like “gunshot wounds are caused by bleeding”.

Insulin Resistance

So, back to insulin resistance. Why does the body develop it so frequently (up to 50% of the American population)? This simply cannot be mal-adaptive. Our bodies are not designed to fail, since we lasted for several millennia before the modern diabesity epidemic. Insulin resistance must serve a protective function, being so common. Maybe this IR is actually protective. Regulation of insulin sensitivity is part of the normal physiologic response – it can go up or down depending on lots of things, including other hormones (eg. pregnancy) or availability of nutrients. So how can IR be protective?Hoarder

Consider this. Excessive glucose in the blood is bad for us (high blood sugars). If this high glucose level is toxic in the blood, why wouldn’t it also be toxic in the body, too?  Shouldn’t we get rid of the toxic levels of glucose instead of merely shoving it from the blood into the tissues of the body? After all, insulin doesn’t actually get rid of the glucose. It shoves the excess glucose out of the blood and forces it into the body. Somewhere. Anywhere. Eyes. Kidneys. Nerves. Heart [that’s bad for those tissues].

Imagine you have too much garbage in your house. But you like to keep your chair nice and neat by moving everything elsewhere. Instead of actually throwing the garbage out of the house, you merely shift it around in the same house. Not a great idea. For glucose, instead of reducing the total amount of whole-body glucose, we merely shove it from the blood into the body.

So, if this high glucose is toxic, then the natural response of the tissue (body) is to protect itself against this excessive glucose load. Suppose you live on a street of houses in Diabetes Ville (each house is a cell of the body). Everybody is friendly and normally leaves their door open (just as a cell is open to glucose in the insulin sensitive state). A truck full of toxic waste (glucose) comes down the street. And the garbage-man (Insulin) really wants to get rid of this slime. So, every time he sees a door open, he shovels in some toxic waste (glucose).

'Toxic Waste Disposal, satisfaction guaranteed or double your waste back.'

After a few days of this, what would you do? You’d bar your f***ing door, is what you’d do! You’d say,”I don’t want this toxic slime!” That’s insulin resistance, baby! You make it really difficult to shove that toxic stuff into your house. It’s not a bad thing, it’s a good thing. The insulin resistance is trying to protect the cell from the toxic levels of glucose that the insulin is trying to shove in the door.

What is Insulin Resistance protecting us from? It’s very name gives the answer away, Insulin Resistance. It’s a reaction against excessive insulin. It’s protecting us from the excessive insulin. In other words, as we’ve written before, Insulin causes Insulin Resistance. But the root cause here is the Insulin, not the Insulin Resistance. The tissues (heart, nerves, kidney, eyes) are all busy increasing their resistance to protect themselves from Insulin which is trying to shove some toxic glucose into their house.

So we call the specialist Dr. Endocrine. Dr. Endo decides that the slime is indeed toxic, and we must get it off the streets immediately. There are some options – like reducing the production of toxic glucose (Low Carb diets) or burning off the toxic glucose (Fasting). But instead, he decides that he will hire more garbage men (insulin) to shove this toxic glucose into the houses. At least then, Dr. Endo won’t be able to see it anymore. Now Dr. Endo can pretend he is doing a great job. Look! The streets are nice and clean. But all the toxic glucose goes into the houses (tissues).

And what happens over time? Well, all the tissues of the body just start to rot. We are inadvertently ‘overcoming’ the tissue-protective insulin resistance developing. Instead of targeting the insulin, and reducing the total amount of glucose that we have to deal with, we are increasing how to get rid of it. So, by prescribing lots of insulin for patients, we are not making things better, we are making them worse.IR is Good

Warning – Technical talk ahead – feel free to skip ahead. Normally, there is an inverse relationship between blood glucose and free fatty acid (FFA). In the fasted state, glucose is low and FFA is high. The body is burning fat for energy. As you eat, insulin goes up, glucose goes up and lipolysis is inhibited and FFA levels fall.

But in T2D, insulin levels are high. Glucose is high. But because of excessive IR, FFA is also high. So, the tissues of the body are now at risk of receiving both excessive glucose and fat, which is now causes the oxidative stress and the inflammatory response. But the inciting factor here, is the excessive glucose and insulin. (See pretty picture above for graphical explanation). Excess glucose to the mitochondrion overloads the electron transport chain and results in excessive ATP production as well as Reactive Oxygen Species – all causing oxidative stress.

Glucose metabolized through the anaplerosis pathways that produce AcCoA and MalCoA which becomes substrate for cholesterol and fatty acid synthesis. MalCoA inhibits FACoA resulting in steatosis, or the production and abnormal deposition of this fat.How to Get Fatty Liver

OK, technical speak over. Welcome back. So, in the liver, excessive insulin produces fatty liver. We can easily demonstrate this in humans. In this study, 16 test subjects were overfed an extra 1000 calories of sugary snacks per day. This consisted of 1 can of Pepsi, 30 ml of fruit juice and a bag of candy. Over 3 weeks, there was only a 2% increase in total body weight. However, there was a disproportionate 27% increase in liver fat due to DeNovo Lipogenesis.  [At http://ajcn.nutrition.org/content/96/4/727.short and http://ajcn.nutrition.org/content/96/4/727.full.  It took them  a subsequent 6 months of energy restricted diet to lose the excess liver fat and another 10%.]

In other words, insulin is driving much of this excess glucose into the liver and it’s being turned into fat. Some of this fat can be exported out of the liver to other tissues such as muscle and pancreas giving you ‘fatty pancreas’.

In the muscle cells, we get fat deposits between the strands of muscle. You could call this ‘fatty muscle’. Technically, this is called intramyocyte lipid accumulation. Many think this causes insulin resistance, but it is more likely the result of   excessive glucose and insulin. The accumulation of fat between muscle fibres (where there should not be any), in cattle, is called delicious.

Cattlemen, of course, know exactly how to develop marbling in cows. The most important determinant is the type of feed. Cows are ruminants, which means that they normally eat grass. However, by feeding a high energy, grain heavy diet, ranchers can increase the growth rate of cows as well as increase marbling.

See if you can spot the difference between well marbled beef and lean beef.CornFedvsGrassFedBeef-steaksonly The grass fed beef develops no marbling, which gives steak much of its flavour. For this reason, many grass fed cows are ‘finished’ with feeding corn in order to develop the fat marbling. Insulin and glucose. No secret. It works in humans as well.

You can see the same sort of fat deposits in the muscle cells of the heart and this may contribute to congestive heart failure. ‘Fatty Heart’.

A New Paradigm

So inversion forces us to see T2D from a new perspective. The toxic agent here is the excessive glucose, and its co-conspirator, insulin. Moving the toxic glucose out of the blood and forcing it into the body has no net benefit, as has been amply demonstrated by multiple long term randomized studies – ACCORD, ADVANCE, VADT, and ORIGIN.

Instead insulin resistance develops precisely because it is a protecting the tissues against the blood trying to shove all its toxic load into the cells. This is why the development of the insulin resistance is universal. It’s a good thing, not a bad one. Giving exogenous insulin to overcome this IR is actually detrimental. So the problem is not the IR at all. Instead, look for the root cause – the excess glucose and excess insulin. Take that away, and the T2D goes away.IR is Good2

So there are good treatments for T2D, and there are bad ones. The bad ones overcome the tissue insulin resistance which is there precisely to protect the tissues. These are insulin and sulfonylureas. The good treatments get rid of the glucose out of the body. You can do this by preventing it from coming into the body in the first place (LCHF diets, Acarbose), or burning it off (Fasting) or urinating it out (SGLT-2 Inhibitors). This explains the power of this new class of medication in terms of cardiac protection.

Insulin resistance is bad?  No, not at all. It is good. Insulin resistance is not the root cause. It’s the natural, protective reaction to the root cause – high insulin levels. It’s the insulin, stupid!

Why We Get Fat,  and what to do about it! --  http://healthfully.org/rc/id23.html 11/23/15

  IR = Insulin Resistance    NAFLD = Non-Alcoholic Fatty Liver Disease     T2D = Type-2 Diabetes--definitions next page

All mammals have a complex regulatory system for appetite, rate of metabolism, and fat storage.  There are over eighty hormones involved in the system.  The Western diet’s high in BOTH the carbs fructose and glucose causes a fatty liver (NAFLD) which can mucks up the regulatory system leading to IR-- with IR to obesity, T2D, etc.  Insulin in response to glucose causes glucose burning & fat storage; high insulin causes excess fat storage.  Causes The carb fructose--a simple sugar--goes to the liver where most is converted to fat, and when insulin is high this fat is stored in the liver.  The high-sugar, high-carb (high insulin and low fat) Western diet will for most result in excess fat storage in the liver.  Gradual over the years, 2 to 3 pounds of fat is stored in the liver (NAFLD); this mucks-up the complex metabolic system to causes IR; and thus for most with IR the yearly gain in weight.  When on an energy-restricted diet the fat tissue through the 4 hormone it produces functions to maintain its current weight by causing an increase in appetite and a reduction in metabolism.  Even after losing weight the system works to restore the fat—the yo-yo diet.  Goals:  A) metabolize the excess fat in the liver and pancreas to reverse IR through a very low carb diet—fasting helps. This forces the body to switch from glucose burning to fat burning.  B) Once fatty liver & IR are cured than carbs can be moderately increased and weight will still be lost.  C) Once ideal weight is obtained; remain on a low carb-sugar diet.  Eventually the weight control system will reset to the ideal weight, this for most takes over 2 years; and avoid the daily Western diet.          

Fix:   2-week very low-carb diet to cause the body to switch from glucose burning to fat burning to cure NAFLD & IR.   

             Fructose is converted to fat only in the liver and insulin causes this fat to be stored in the liver.

Fatty liver >>>> IR in liver >>>> IR in muscle and fat tissues >>>> IR causes abnormal high insulin >>>> excess fat storage

           Carbs raises the insulin level in the body, and insulin causes body to burn glucose and store fat

T2D can be cured with diet.  For example in the first 2-weeks following bariatric surgery over 80% with T2D are cured before weight loss.  With very low carb diet and alternate day-fasting the cure takes from 2-6 months.

Simple fix:  it starts with supermarket.  For B) & C) just buy wholesome, very low net-carb foods (on food label, carbs minus fiber) with low glycemic (table)..  The goal is to stay in the fat burning mode by not eating digestible carbs.         

A)  Good health:    lower carbs, cut sugars, and take JK short fast at least once a weekly and follow JK food table.

B)  Insulin resistant, obesity:   JK short fast daily and the New Atkins Diet (replace carbs with fats for energy). This diet is very low carbs to start, with no other limits, than increase carbs.  JK has added several healthful modifications, at link.  

C)  T2D and morbid obesity:   start with B) and if after 4 months the glucose and HbA-1c are still high then fast every other day for 24 hours or JK short fast.  The goal is to be drug free.  Watch Dr. Jason Fung lectures at “diabetes” on video page.  The more you learn, the more committed you will become to curing T2D and obesity.

I recommend for B) & C) a gradual approach to the low carbs induction phase of the New Atkins diet:  start with quitting sugars and adjusting to that while gradually cutting net carbs to 30 grams daily—it starts in the supermarket. 

JK short fast:  go on a 16 hour fast (7 PM until 11:00 AM) or longer, thus extending the beneficial nighttime fat burning production of ATP (the energy molecule) to midday.  At night because of not eating there is low serum glucose and thus insulin is not secreted by the pancreas.   The body must metabolize fat for energy (ATP).  If hunger becomes an issue than eat a small handful of nuts, green vegetables, cheese, or tea or coffee to kill pangs--the effect of a small portion on insulin production is minimal.  Physical activity prior to and subsequent a meal burns excess glucose thus lowering insulin.

The best source on what to eat for health, for diet, and related topics is at Concise.  In the rh section are articles which lay out the evidence for what is found there.  Important are Part 5 on supplements, Part 6 which covers many of the topics here, and Part 10 on the New Atkins diet.  The Videos library with links confirms the claims here--and other health topic.  The library has brief descriptions.  The ABC, CBC, and BBC national networks expose what U.S. media hides.

Diet-Food Basics

Adipocytes (lipocytes) fat cells compose adipose tissue & secrete hormones resistin, adiponectin, leptin and Apelin.  

ATP, Adenosine TriPhosphate (adenosine with 3 phosphate molecules (PO4) attached), transfers chemical energy within the cell through the loss of one or two of its phosphate groups.  ATP goes from a high state of energy to a low state.  The main way ATP goes back to the high state of energy is through absorbing energy from the metabolism of carbohydrates & fats in the mitochondria, where ATP is restored to three phosphate group.  ATP provides the energy driving over 90% of the biosynthesis processes in the body, such as in the production of hormones, of collagen, and thousands of other compounds.  ATP is used to make muscle fibers contract and in intercellular active transport of large molecules. 

Carbohydrate (carb):  fiber, fructose, glucose-glycogen, galactose, starch, sucrose (net carbs is total carbs minus fiber):

      Fiber, vegetable fiber, roughage, the carbohydrate component not broken down by digestive enzymes--but some is by gut bacteria.  Fiber has more than ten glucose units.  It lowers the insulin spike when consumed with refined carbs. 

     Fructose (fruit sugar) a monosaccharide found in fruits.  Main sources are the disaccharide sucrose, fruits, and high fructose corn syrup.  It is metabolized in the liver into either glucose or fat.  Fructose is converted to fat in the liver, where when insulin is high is stored there, which can cause IR and NAFLD.  Also fructose is 7.5 more reactive then glucose.  Through the process of glycation fructose damages the liver and causes our chronic age-related diseases. 

     Glucose a monosaccharide is the main energy storage molecule for plants; in animals it is stored as long chain called glycogen.  Glucose is one-half of the disaccharide sucrose, and is also obtained from the hydrolysis of starches which are long chains of glucose molecules.  Glucose and fat are the main sources of energy for the production of ATP.

    Starch is long chains of glucose units.  This polysaccharide is produced mostly by green plants for energy storage. 

    Sucrose, table sugar, is the disaccharide consisting of fructose and glucose, and is produced mainly by plants.

Fatty acids and triglycerides are chains of up to 24 carbon molecules with an organic acid on the last carbon.

Glycation:  a process where a monosaccharide (simple sugar) randomly attaches to proteins and thereby adversely affects that protein’s functions.  Fructose’s total glycation is 15 times that of glucose per equal amounts of each.

Insulin regulates other hormones that affect metabolism, appetite, fat, glycogen, proteins storage, blood glucose, etc.  It is produced by the pancreas mainly in response to blood glucose and causes tissues to absorb and burn glucose and also to store fat (not burn). Physicians control elevated glucose with drugs, but it is elevated insulin that produces most of the comorbidities (negative health consequences) associated with IR &T2D, thus dietary carbs should be limited.     

Insulin resistance (IR):   the condition of higher than normal amount of blood insulin to manage blood glucose due to a diminished response to insulin by various tissues.  IR first occurs in the liver cells, and causes fat to accumulate there.  Later the muscle and fat cells develop IR.  The pancreas then releases even more insulin to lower blood glucose.  Since insulin increases fat storage, IR causes excess fat storage, mainly in the muscles and fat tissues to cause obesity. 

Leptin is the satiety hormone; it causes the brain’s hunger center to suppress appetite, while ghrelin has the opposite effect.  Leptin level increases   during the night and thus suppresses hunger. Leptin is produced by fat cells.  Leptin also regulates metabolism.  Leptin is responsible for the 20% reduction in metabolism during an energy-restricted diet.  

Metabolism in reference to diet refers to the metabolic conversion of mainly either fat or carbohydrate into the energy molecule ATP mostly by the mitochondria.  Under conditions of starvation proteins also can be used to make ATP.

NAFLD (Non-Alcoholic Fatty Liver Disease):  the accumulation of fat by liver cells sufficient to significantly downgrade their various functions.  The NHANES survey 2011 found NAFLD in 30% of adult population—similar % for Europe. 

Type-2 diabetes (T2D): occurs when the pancreas fails to produce enough insulin to lower glucose to its normal range. This results from advanced IR and the accumulation of fat in the pancreas, which eventually causes a decline in insulin.

^^^^^^^^^^^^^^^^^^^^^^^^^

Net Carbs while on Atkins ketogenic diet—easy table by JK

Net Carbs = total carbohydrates minus fiber content.

Egg 1 = 0.4 grams

Seafood 6 oz. = 0

Meats 6 oz. = 0

Poultry 6 oz. = 0

Oils 6 oz. = 0

 

Dairy

American processed 1 slice 1.5 grams

Cheeses 1 oz. = 0.7

Cottage cheese c = 5

Cream 1 T  = 0.4

Cream cheese 2 T = 1.2

Milk 1 c = 11.7 to 15

Yogurt plain 1 c = 11.6

Greek Yogurt plain 1 c =  9

 

Raw Vegetables

Avocado = 2 grams

Bell pepper green c= 2.2

Bell pepper red c =3

Broccoli c = 1

Cabbage shredded c = 1.1

Celery stalk = 1

Cauliflower florets c = 1.4

Cucumber c = 1

Green beans c = 2

Nuts

Almonds 24 = 2.5

Brazil 6 = 1.4

Cashews 2 T = 5.1

Mixed nuts 2 T = 2

Peanuts 2 T = 1.4

Pecans 1 oz. = 1.2

Walnuts 1 oz. 1.2

 

Lettice 1 c = 0.36

Olives black 5 = 0.7

Olives green 5 = 0.0

Onion 2 tbs. = 1

Spinach 1 c = 0.2

Squash summer c    2.6

Tomato 1 med = 3.0

Tomato juice 1c = 8

For those off

the induction

(ketogenic) phase

 

Fruits

Apple med = 8

Banana med = 30

Blueberries c = 9

Dates dried 1 oz = 21

Fig dried med = 6

Grapes 1 c = 26

Grapefruit = 9

Melon cantaloupe 1 c  = 12

Orange navel med =15

Peach med = 15

Pear med = 20

Strawberry 5 lg = 5

Legumes

Black bean home cooked 1 c = 8

Canned baked beans 1c = 36

Kidney home cooked 1c = 11

Pinto bean home cooked 1c = 25

Soybean white 1c =10

Vegetables not  leafy

Beets steamed 1c  = 13

Carrots steamed 1c = 8

Corn on cob med steamed 15

Eggplant 1c = 5

Olive cured 7 = 1

Onion 1 c = 12

Peas 1 c = 14

Potato med with skin = 26

 

Snow peas c cooked = 2.7

Squash acorn 1 c = 21

Squash zucchini 1c = 3

Sweet potato med = 20

 

To calculate from the food label simply subtract fiber from total carbohydrates

On the Atkins website (http://files.atkins.com/1501_CarbCounter_Online.pdf) is an extensive table of net carbs.  For simplicity the food label on products can be used, simply subtract fiber from carbohydrates to get an approximate value.  Remember that food manufacturers add sugar to nearly every product plus many of them have various forms of starch as filler and thickening agent (starch is pure glucose). 

 

Enter supporting content here

Looking for a topic, use Google Internal Search Engine

INTERNAL SITE SEARCH ENGINE by Google