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Concise: Diets, health, weight, insulin resistance, and type 2 diabetes


Part 12:  Diets for health, with all the related topics        www./healthfully.org/rh/id8.html  1/13/17 


Sections  #1Western diet health disaster; 2 Definitions, body and food basics; 3 Dietary recommendation and 4 healthful diets; 4 Tables:  net carbs and Insulin Index; 5 Energy, sugar and fats the good and the bad; 6 Fructose alcohol without the buzz; 7 NAFLD and IR are the gateway to MeS and its comorbidities;  8 Why fasting with low-net carbs diet for obesity and T2D; 9 Fasting is easy and essential; 10 Why some don’t get fat; 11 Myth busters; 12 Pathogens causes of CVD; 13 Other cofactors for CVD; 14 How did we get here—Historical; 15 Free will won’t; 16 Outline on metabolic dysfunction; 17 Review and recommendations;  18 Videos and books on diet, bad pharma, and CVD; 19 Conclusion 


AS         Atherosclerosis

 

KD        Ketogenic diet, very low carbs

ATP       Adenosine triphosphate-energy molecule

 

KOL      Key opinion leader

CER       Caloric energy restricted diet    

 

MeS      Metabolic syndrome

CVD      Cardiovascular disease

 

NALFD  Non-alcoholic fatty liver disease

IR          Insulin resistance

 

T2D       Type 2 Diabetes


 


1. Western diet health disaster


The rate of mature adult obesity is over 50%[1], cardiovascular disease (CVD) deaths over 60%, and dementia 47% of those over 84 years, diabetes among seniors over 26%.  Not 1 in 7 by the age of 60 has their slim youthful figure.  Something is much different than a century ago, and much different than those paleo peoples eating a traditional diet.  It started in 1978 when the FDA influenced by commercial interests vilified saturated fats and cholesterol as heart unhealthy.  This resulted in a shift to the cheaper grains, sugars, and polyunsaturated oils from grains.  At the food manufacturers gradually increased the amount of sugars and aggressive advertised sugar drinks.  It starts with fructose (one half of the disaccharide sucrose); we have gone from 15 grams of fructose daily average to over 80 grams in 2010.  Our liver, where it is metabolized, cannot handle the overload.[2]  Fructose’s adverse effects upon the liver causes fatty liver disease (NAFLD) and insulin resistance (IR).  This abnormally high level of insulin send a signal to cells to burn glucose and thus to stop burning fat and store it.  This is why we get fat!  We are getting fat because of the abnormally high insulin is causing weight gain.  This system is why those who are long-term overweight can’t keep it off; because of increased appetite and reduced metabolism they will gradually regain the weight they have lost.  Businesses which profit from illness and manufactured foods promote blaming the victim of the Western diet, thus we get from our corporate media and our physician the message to eat less and exercise more.   That doesn’t fix the weight-regulatory system; thus we have yo-yo dieting.  Like all mammals we have a weight-regulatory system.  What follows is about that system, what science has discovered about it including fructose, the consequences of that damage, and how to fix that system including type-2 diabetes (T2D).  Yes, it can be fixed. 


 


2. Definitions:  body & food basics 9/23/16


Adipocytes (fat cells) for fat storage; they secrete the hormones resistinadiponectinleptin and apelin.  


Amino acids from proteins:  the 20 building different blocks of protein.  Digestion converts proteins to amino acids. 


ATP, Adenosine Triphosphate (adenosine with 3 phosphate molecules (PO4) attached):  the body’s main energy molecule.  ATP transfers chemical energy within the cell through the loss of one or two of its phosphate groups.  ATP returns to the high state of energy 3(PO4) through absorbing energy from the metabolism of carbohydrates & fats in the mitochondria.  ATP provides the energy for over 90% of biosynthesis (hormones, collagen, etc.), for muscle contraction, and for intra & intercellular active transport.  GTP, NADP, NAD and others also function as energy molecules.


Cardiovascular disease (CVD) causes, cigarettes and a high fructose diet.  By causing endothelial dysfunction those cells permit pathogens to colonize in the artery walls to cause inflammation that results in atherosclerosis, and CVD. 


Carbohydrate (carb):  fiber, fructose, glucose, glycogen, starch, sucrose, lactose, net carbs (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 sugar units.  It lowers the insulin spike when consumed with refined carbs. 


Fructose (fruit sugar) a monosaccharide; main sources are fruits, the disaccharide sucrose, and high fructose corn syrup.  Fructose is only metabolized in the liver.   Fructose is a net 15 more reactive then glucose and by glycation damages proteins throughout the body to cause age related chronic diseases.  In the liver it causes IR and NAFLD.  This process is accelerated when insulin is high as the liver’s mitochondria clears first the excess glucose.


Glucose a monosaccharide is the main energy storage molecule for plants; in humans 1-2-lbs is stored as long-chain glycogen a backup energy source stored in muscles, fat, and liver cells.  Glucose is as one half of sucrose, and is also obtained from the hydrolysis of the digestible starches.  Glucose and fat are the main sources for production of ATP.


Glycation:  a process where a monosaccharide (simple sugar mostly fructose) randomly attaches to proteins or lipid; this adversely affects their functions, thus glycation is a major cause of our chronic age-related diseases.


Starch is long chains of glucose units.  This polysaccharide is produced mostly by green plants, seeds, tubers, and other parts of plants.  It is the molecule for energy storage of plants. 


 Sucrose, table sugar, produced by plants; it is the readily hydrolyzed disaccharide consisting of fructose and glucose. 


Diabesity:  the combination of diabetes and obesity; they afflicts those on the Western diet—a recently coined term. 


Fat (Free Fatty acids and triglycerides): up to 24 carbon molecules with an organic acid or glycerol molecule on end.


Glycation:  The non-enzymatic attachment of a monosaccharide (mostly fructose) to a protein which through changing its structure thus often diminishes the protein’s functions It is thus a causal factor for most age related conditions.


Incretins:  a class of hormones secreted by the stomach and intestines into the blood in response to bulky foods to cause satiety and insulin secretion.  They are particular responsive to the presence of proteins and amino acids.


Insulin: a gateway hormone produced by the pancreas.  Its main function is to have cells absorb glucose and store fat, this causes the body to switch from metabolizing fat to that of glucose.  Insulin also regulates other enzymes and hormones including leptin.  Low production of insulin is the cause of type 1 and 2 diabetes.  Insulin also promotes the storage in amino acid, and thus we secret insulin by the incretin system in response to proteins in the stomach. 


Insulin resistance (IR):   Since excess glucose is toxic, cells when full resist the signal by insulin to absorb more glucose. Thus to lower blood sugar, the pancreas releases even more insulin, and thereby cause in a person with IR a higher than normal amount of blood insulin.  IR occurs in the liver cells, and causes fat to accumulate there.  Later the muscle and fat cells develop IR.  As IR progresses, fat storage increases to cause obesity and NAFLD.  Fat also increases in the pancreas to a point which hinders (reduces) the production of insulin to become T2D.  Over 50% of Americans have IR.


Ketogenic diet (KD, very low carbohydrate diet):  the Atkins type diet, a very low carbohydrate diet that causes the body because of lack of glucose to metabolize fatty acids to produce ATP and substances that are collectively known as ketone bodies.  Most KD doesn’t limit calories, only carbohydrates.  Ketogenesis also occurs during fasting. Moderate protein & fasting hasten progress.  The New Atkins diet limits protein so as to avoid the insulin stimulants leptins. 


Ketone bodies:  3 water-soluble molecules (acetoacetate, beta-hydroxybutrate, and their breakdown product acetone) are produced by cells throughout the body that have mitochondria.  Ketone bodies are produced during periods of low food intake (sleeping, fasting, intense exercise, some diets, and starving) and also by those with untreated type-1 (insulin dependent) diabetes.  The beta-hydroxybutrate has been shown to have a number of healthful benefits. 


Key Opinion Leaders (KOLs):  people who rise to top positions in their area of expertise.  In fields relevant to business nearly all of the KOLs violate the standards of science to produce business-favorable spin, and are handsome rewarded for their services.  The term cenotes bad conduct.  Pharma and food industry have used KOLs along with regulatory capture to produce a drug/diet disaster, then sells it to medical students, physicians, politicians, and the public twaddle as cutting- edge science.   


Leptin:  produced by fat cells and functions to maintain a fix level of fat.   Leptin does this by a 25-40% reduction in the rate of metabolism and by creating the feeling that by eating that energy will increase and mood improve, thus the desire to eat more.  Thus leptin functions to maintain fat storage and to restore weight even years later.  


Lipids are a group of naturally occurring fat like molecules including waxes, sterols, fats, phospholipids, and others.


Metabolic syndrome (MeS) “is a is a clustering of at least three of the five following medical conditions: abdominal (central) obesityelevated blood pressureelevated fasting plasma glucosehigh serum triglycerides, and low high-density lipoprotein (HDL) levels”, wiki. It is associated with development of cardiovascular disease and type two-diabetes.  Pharma has framed the discussion of causes of CVD to promote ineffective drug treatments—see cholesterol myth.  A more appropriate list—as its name metabolic denotes--would be insulin resistance, non-alcoholic fatty liver disease, obesity, and type-2 diabetes.  I am using the metabolic list.    


Metabolism in reference to diet refers to the metabolic conversion of mainly either fat or carbohydrate into the energy molecule ATP mostly in 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. 


Tobacco science:  generated by tobacco ethics, industry funded studies which are by design positively distorted to sell products, or for other business objectives such as deflect criticism, attack off patent drugs, to promote diseases, etc.


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


Western diet:  one in which there is over 20% of calories from sugar, under 35% of calories from fat, of which over half of that fat is polyunsaturated.  The most common diet of developed countries and the cause of the diabesity pandemic.


 


3.   Dietary Recommendations and 5 healthful diets


Increase

               Decrease

Avoid/Limit

Saturated and monounsaturated fats (animal fats, lard, & butter are best, followed by palm kernel, coconut, and olive oils), fiber, leafy vegetables, egg, peanuts,, fish, free-ranging beef, nuts, whole milk dairy products including cheese, plain yogurt, and cottage cheese, breakfast protein mix, whole grain products[3], beans.

Meats & poultry unless free ranging[4], large portions of fruits especially melons, bananas, grapes, raisins, and dates[5].  Wanting to lose weight, limit daily to 45 grams of protein male, 35 female--for those of average stature.

Fructose, sugar added foods[6], fruit juices,[7] polyunsaturated and trans-fats, most vegetable oil [8], refined carbohydrates, whole wheat4, large portions of carbs and fruits, potatoes, rice, instant breakfast cereals, alcoholic drinks, artificial sweeteners[9]    

Vinegar,[10] high fiber cereal,[11], tomatoes juice, Karo corn syrup or sorbitol as sweeteners.

Fried foods (unless high in saturated fat), large portions of food with high glycemic index.

Lunch meats unless cooked[12], all GMOs12, corn[13], soy products,[14] most crackers, chain restaurants.  


 


Sugars without fructose:  barley malt, corn syrup (Karol), corn syrup solids, dextran, dextrose, diastatic malt, diatase, ethyl maltol, galactose, glucose, glucose solids, lactose, malt syrup, maltodextrin, maltose, & rice syrup.  For extensive foods recommendations see Fat Chance, pages 199-205 by Prof. Robert Lustig.


FIVE DIETS   9/13/16


1) Healthy diet: For those in good health and normal weight without IR or abdominal; fat.  The goal is to keep fructose low, thus avoid added sugar, juices, & limit fruits.  Increase saturated fats, therefore lower starches.  Increase physical excursion to keep serum glucose lower and thus insulin low.  Low rate of glycation requires very low fructose (see section 6) and taking antioxidant supplements. The short fast at least once a week promotes a healthy liver. 


2)  Fatty liver (abdominal fat) but no major weight issue: follow the above but do the short-term fast every morning.  This must continue until the few extra abdominal pounds are lost, and your middle has that youthful look, then gradually go off the daily fast and see if your weight has stabilized at the lower point; if not than go back to short-term fasting.  Expect to be fasting for 4 months or longer.  Longer fasts speed cleansing of the liver and other organs-- section 8.   


3) Weight loss diet of more than 15%:   Daily the jk short fast and 20% calories from carbs or less.  If progress is slow, then add the New Atkins Diet (ketogenic) with moderate proteins, and/or alternate day fasting. See section 9, below.   


4) T2D diet on 1 or 2 drugs, or obesity:  Daily JK short fast and the new Atkins type diet with moderate protein.  Monitor plasma glucose so as to reduce dependence on drugs.  If after 6 month this hasn’t cured T2D then switch to full alternate-day fasting.  Watch Dr. Jason Fung explain the issues on insulin and diabetes and alternate day fasting diet. 


5) Severe T2D and morbid obesity: Follow a very low carb diet with alternate-day fasting.  T2D is a progressive disease treated with drugs to lower glucose, then more drugs, & then insulin injections.  It is caused by diet and can be cured by diet.  The fast following bariatric surgery cures over 80% of T2D in the first few weeks, before major weight loss.


JK short fast:  go on a 16 hour fast (7 PM until 11:00 AM) or longer, thus extending nighttime fat burning to produce ATP (the energy molecule) to midday.  At night because of not eating there is low glucose and thus low insulin.   If hunger becomes an issue than eat green vegetables, bone broth, black coffee or tea with lemon.  Maximize saturated fat, low protein, very low carbs.  Keep lowering carbs if progress slows and extend the fast. 


Atkins maintenance phase:  Once weight target is reached, the daily intake of carbs is increased by 10 grams per day to find the level where weight is gained, then drop below that level.  Continue to limit refined carbs and foods with high glycemic index to small portions, limit sweets with fructose, & use the JK short fast weekly to maintain a healthy liver.  Vigorous exercise is a general health tonic and mood elevator.  For seniors the addition of natural hormone replacement therapy might be also required, click on estradiol and testosterone; they play a role in fat storage, muscle tone, will to exercise, and general health--things pharma is against. 


 


4.  Tables:  Net Carbs and Insulin Index


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 ½ 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 ½ = 2 grams

Bell pepper green ½ c= 2.2

Bell pepper red ½ c =3

Broccoli ½ c = 1

Cabbage shredded ½ c = 1.1

Celery stalk = 1

Cauliflower florets ½ c = 1.4

Cucumber ½ c = 1

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

 

Green beans ½ c = 2

Lettice 1 c = 0.36Olives black 5 = 0.7

Olives green 5 = 0.0

Onion 2 tbs. = 1

Spinach 1 c = 0.2

Squash summer ½ 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 ½ c = 9

Dates dried 1 oz = 21

Fig dried med = 6

Grapes 1 c = 26

Grapefruit ½ = 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 = 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 pea ½ c cooked = 2.7

Squash acorn 1 c = 21

Squash zucchini 1c = 3

Sweet potato med = 20


 


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). 


Insulin index of common foods


Each portion of food contained 240 Calories—score relative to white bread which was set at 100


Peanuts                   20

 

Fish                            59

 

Grapes                           82

Eggs                          31

 

Oranges                    69

 

Crackers                         87

All bran                    32

 

Potato chips            61

 

Ice cream                       89

Porridge                  40

 

Brown rice               62  

 

Cookies                          92

Brown Pasta          40

 

Special K                   66

 

Whole Bread                96

White Pasta           40

 

Honey smacks         67

 

White Bread               100

Cheese                    45

 

Coco Pops                71 

 

Yogurt sweetened    115

Granola plain         46

 

French Fries             74

 

Baked Beans can       120

Beef                         51

 

Corn Flakes              75

 

Potatoes                      121

Popcorn                  54

 

Croissants                79

 

Mars Bar                      122

Grain bread            56

 

White Rice               79

 

Jelly Beans                  160

Lentils                      58

 

Bananas                   81

 

Fats                                10

Apples                     59

 

Cake                          82

 

 


from http://graemethomasonline.com/wp-content/uploads/2010/06/Insulin-Index.pdf


Detail explanation of testing  http://www.janurky.sk/db/articles/20150703n0(kj_not_kj)/images/insulin_index.pdf


These figures are based on test results for an ideal group:  average age 22 and BMI of 23.  Foods needing preparation such as potatoes and pasta were boiled, stored overnight in the refrigerator then warmed the next day in a microwave.  Test score was based on the average insulin level over 120 minutes divided by that for white bread times 100.   There were 503 tests total test for the 36 listed foods.  Breakfast cereals were served with milk.  “Plasma insulin concentrations were measured in duplicate by using an antibody-coated tube radio-immuonoassy kit (Coat-A-Count; Diagnostic Products Corporation, Los Angeles)”at 1997, p. 1295.  Samples of 1.5 to 2.5 mL. of blood were obtained at 15 minute intervals over the 2 hours test period.  Unfortunately this table lacks important foods of vegetables, milk, soda, diet soda, and fat (which I included from another source--Dr. Fung’s book The Obesity Code p 193).                                                                                                                                                                            


The goal is to maximize the rate of fat burning which requires a low insulin diet.  Insulin causes fat storage.   Since protein is needed to maintain muscle mass, it must be restricted but only somewhat.  The USDA dietary recommendations are high.  Thus I recommend cutting it to 35 grams women, and 45 grams men--for those of average body frame size.  This is sufficient to prevent muscle loss.[15]  The effect of protein upon insulin and thus fat storage explains why short-term and alternate day fasting make a very significant improvement upon the low carb KD.[16]  For most on a KD, after a couple of months the rate of weight loss will decline, the effect of insulin upon leptin.  Fasting prevents this phenomenon of leptin reducing the rate of metabolism.


 


5. Energy:  Carbs, Sugars, and Fats--the bad and good


With the Western diet yearly sugars consumption of added sugar has gone from 35 lbs. in 1909 (43 gm/day) to 152 lbs. in 2000 (751 calories/per day or 189 gm/day) to cause the diabesity (diabetes and obesity) pandemics.  Part of that increase is a result of the vilification of fats and the official government recommendation of lowering carb intakes from a bit over 40% of calories to 30% or less.  With this reduction in calories from fats came it replacement with mostly sugars, but also an increase in grains, mostly wheat and corn.  Starches are a fairly safe source of energy, but the increase of sucrose and HFCS high fructose corn syrup is a bad thing because of the fructose—see next section.   Table sugar (sucrose) is hydrolyzed in the stomach into fructose and glucose, starch in the stomach to glucose.  Glucose and fats are the body’s main sources of ATP (energy molecule)—other monosaccharides such as galactose, fructose, and amino acids contribute to the remaining 20% of the conversion of ADP to ATP.  High blood glucose (a bad thing) is down regulated by increased insulin (also bad) which sends a message for the body to burn glucose and thus store fats.  High insulin levels in response to high glucose will over the decades cause insulin resistance (IR, a reduced response to insulin) in insulin receptor on cell walls.  This is a way of cells to limit its amount of sugar to a safe level.  IR caused high serum glucose results in more insulin secreted by the pancreas.  IR increases fat storage. Gradually many of those on a Western diet accumulate 2-3 extra pounds of stored fat in the liver, nearly doubling the weight of the liver which normally weights 3.2 to 3.7 lb.  This causes mild liver inflammation and what is clinically called Non-Alcoholic Fatty Liver Disease (NAFLD) the starting point the comorbidities from MeS and cirrhosis of the liver (see section 6 on NAFLD).  Excess fat in the pancreas eventually causes a decline in insulin production that result in T2D.  High insulin from IR also causes low leptin a hormone which among many things increases appetite by stimulating the control center in the brain, and leptin also lowers metabolism—2 causes for obesity and the yo-yo diets.  The other problem is the table sugar sucrose, a disaccharide of fructose and glucose.  Fructose in sucrose attaches randomly to proteins in a process called glycation at 7.5 times the rate of glucose, however the slower in vivo clearance doubles that figure.[17]  Glycation damages proteins—the main cause of age related chronic conditions.[18]  Fructose is metabolized only in the liver where it damages the liver by glycation resulting in IR in the liver. With the Western diet’s high carbs, some of the fat in the liver is stored there.  Some of that fat comes from the conversion of fructose to fat and some from conversion of glucose to fat in the liver.  This fat de novo lipolysis (synthesis of fat) plus IR in the liver causes  gradual causes NAFLD.  In other words, if more fat is made than the liver can use, and there is high insulin due to IR and a diet high in carb glucose, this fat accumulates in the liver cells to cause non-alcoholic fatty liver disease (NAFLD).  This fat accumulates in the liver cells and reduces liver functions, as too dose glycation by fructose and glucose; this double assault on the liver adversely affects the many functions of the liver and thereby contributes to IR.[19]  NAFLD with its IR is the main cause of a group of conditions labeled metabolic syndrome (MeS):  NAFLD, IR, and T2D, and its sign obesity (pharma adds the non-metabolic high cholesterol and the resultant hypertension and CVD—for marketing of their drugs).  Sections 6 covers fructose, 7NAFLD.


Fructose:  The very reactive sugar fructose is the starting point for the diabesity pandemic.  As stated above fructose, which accumulates in the liver where it is metabolized, it damages the liver through glycation and fat accumulation.  In the US we have gone from 15 grams per day, mainly from fruits, in 1900 to over 90 grams a day (hh.edu  at) mainly from sucrose and HFCS (high fructose corn syrup).  We have not evolved a system to handle this load since our ancestors only ate moderate amounts of fruit, and in the wild they were smaller and far less sweet.    It isn’t the glucose half of the disaccharide sucrose that is the problem, since grains are pure glucose and mostly paleo peoples ate a high carbohydrate diet.  The traditional oriental diet is high in carbs (up to 75%) but low in fructose (14 grams or less) and as expected their incidents of obesity, CVD, and T2D was and is on that diet quite low, especially among those who don’t smoke.  Fructose among other things damages the liver and this is the starting point for causal chain leading to obesity, MeS, T2D and NAFLD.   See section 6 for an extensive account of harm caused by excess fructose  and watch the documentaries on the health consequences of sugar—link.  Sugar us called “White Poison” because it is one-half fructose.


2) Starches are molecules made up of chains of the monosaccharide glucose; their rate of absorption during digestion varies according to their structure.  Some have a much lower rate than sucrose, and are called resistant starch; thus not all carbohydrates are equal—for tables and more on carbs.  Fiber is a very resistant starch, which lowers insulin by slowing digestion, and which through bacterial action in the intestines approximately a third of it is absorbed as glucose during the next 24 hours.[20]  The portion of and type of starch in meals affects serum glucose, as too the rate of stomach clearance.  Fats, resistant starch, and proteins in the meal slows stomach clearance, thus extending the time in which glucose is absorbed by the duodenum; this lowers the blood insulin spike—a good thing.  There are a number more good things you can do:  see section #12, why some don’t get fat. 


3) Fats, like carbs, are not all equal.  The right fats are the best source of energy.  Two fats are bad:  trans-fats and polyunsaturated fats.  Trans-fats are not natural, but are man made by a process of hydrogenation of polyunsaturated fats.  Their abnormal shapes entail that they don’t function very well in cell walls—a bad thing.  For the same reason polyunsaturated fats are a bad thing.  This is because of their multiple double bonds in the carbon chain (why they are called polyunsaturated).  These double bonds are available to be bonded with reactive chemicals in a process called rancidification, which changes their shapes.  This oxidation can occur on the shelf, it is accelerated when heat is applied as when baking or frying foods, and in the body where reactive chemicals are made during biological processes. The rancid fats, just like trans-fats, don’t function properly in cell walls—a bad thing.  Rancid fats are casual for many, if not most, of the maladies associated with the Western diet.  Rancid fats have been shown, for example as a causal factor for NAFLD, and thus all the comorbidities associated with a fatty liver.  The extent of the health has, like drug side effects, not be a priority of funding.  The evidence is found in scientific studies published in journal:  for rancidification see #25 and for trans-fats (from hydrogenated vegetable oil) see #27.  Another issue arise because polyunsaturated fats are that they are high in omega-6 fatty acids.  The omega-3 fatty acids EPA & DHA are used to limit the immune responses, thus they lower risk for AS & CVD, but too much omega-6 competitively blocks omega-3 usage--a bad thing.  Hunter-gatherer societies averaged about 2 parts omega-6 to one of omega-3; in the U.S. it is 16 to 1 (a bad thing).  Vegetable oils (except from palm & olive trees) are very high in omega-6.    Like trans-fats, the body lack enzymes to metabolism them; thus both types of fat cause AS and thus CVD.  Food manufacturers and restaurants use both of these bad fats.  This leaves us with the safe saturated and monounsaturated fats.  Over the years, data revealed that dietary saturated fatty acids (SFAs) are not associated with CAD [coronary artery disease] and other adverse health effects” in journal.  The same in Wikipedia:There is s no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD” which is based on a meta study of 21 journal articles--and they taste much better.  Saturated fats are best source of energy—see Prof. Miller's for list of their 6 essential functions.


Proteins, though rated at 6 calories per gram, under normal conditions they are not appreciable metabolism for energy (ATP) except on a high protein diet or during starvation.  When fats stores are depleted to 4% during starvation, the cells switch from storing to metabolizing amino acids (the building blocks of proteins)




[1] The worse way to find out what peoples weight and height is to ask them over the phone; and that is how the figures are obtained!  The figure of 35.7% for 2010 does not include the morbidly obese which are 6.3%, giving a total of 42%, at. Adjusting for survey error, a figure of 50% obese (including morbidly obese) is reasonable, with seniors of course have the highest rate by age. 

[2] See Abundance of Fructose, not Good for the Liver and Heart, Harvard Medical School Heart Letter, 2011, hh.edu  at.

[3] Most whole wheat breads are comparable to white bread as to glycemic index (GI) and insulin index (IL) (see  table Part 3), plus they have phytic acid (inositol hexaphosphate (IP6):  Phytic acid has a strong binding affinity to important minerals, such as calcium, iron, and zinc” Wiki that binds to and thus prevents their absorption. Phytic acid is also in beans, peanuts, soybean, brown rice, oat meal, corn, and nuts.  White flour lacks phytic acid.  Sugars are added to mask the rancid taste of phytic acid.  Lustig, Fat Chance 133. 

[4] Cattle are fed a diet of GMO grains.  Certified Organic has been outsourced to companies most of whom do sham inspections. 

[5] High sugar fruits with high glycemic index (raises insulin).   

[6] In 2018 “Sugar added” is to be listed (maybe) under sugar in food labels.  For current labels, how much has been added depends on ingredients, vegetables have natural low levels of sugar, fruits higher. There are 56 different sweeteners used in processed foods.   If in doubt, look at the list of ingredients for sweeteners.  Ingredients are listed in order of percentage by weight.       

[7] Fruit juices having most of the fiber removed, thus produce a serum glucose increase comparable to a like amount of soda. 

[8] Polyunsaturated fats undergo in the body unhealthful rancidification, and they are high in omega-6 fatty acids which block the healthful conversion of omega-3 fatty acids.  Like trans-fats they cause CVD.  US regulations are just a pseudo fix—see fats.

[9] They raise insulin through a hormonal system found in the stomach and intestines.  Studies of the obese show that artificially sweetened drinks do not promote weight loss because their taste stimulates insulin which causes the body to store fat. 

[10] Vinegar reduces insulin resistance and increase satiation. 

[11] These oils are lowest in polyunsaturated fats, including omega 6 fatty acids And because they are from trees they are GMOs free. 

[12] Given the broken food-inspection process, they pose a major risk factor, which has been grossly under reported in our corporate media.  A 2008 study in France showed that their rate of food poisoning was 1/4th the US rate.

[13] Avoid because of high insulin index, and they have a GMO gene that causes corn to produces a pesticide—same for canola, soy.  and others.  Testing and review is a regulatory façade; and the companies do tobacco science to “prove” GMOs are beneficial.  There is very little science on GMOs.  There are several quality documentaries under GMO on the video page.

[14] Soybean has estrogen-testosterone mimic, for which there is evidence that the mimics interfere with their healthful functions.

[15] The science on the effects of elevated insulin due to protein when carbs are low is very incomplete.  For one thing, with a high-protein-low carb diet (once popular in the 1920s and before) proved successful short term.  Obviously, when there is no glucose to burn the body will continue to burn fat.  Insulin also functions to prevent the metabolism the amino acids derived from proteins. 

[16] There is a second hormonal system, incretins, one not affected by blood glucose, that stimulates the release of insulin.

[17] Serum fructose is twice as high from sucrose compared to glucose, thus the 7.5 rate of glycation is multiplied by 2, at 1988.   Fructose unlike glucose exists far more in the linear form rather than the ring form like glucose.  In the ring form of these sugars the reactive aldol or keto groups on not available.  This structural difference entails that fructose is 7.5 times more reactive, Lustig.

[18] Attaching a sugar molecule or its metabolite onto a protein changes its shape and thereby reduces the protein’s biological functions (a bad thing).  Tissues and organs throughout the body gradually experience a decline due to their glucose and fructose caused modifications.  Othe  r reactive chemical such as from metabolism and the carbon monoxide from tobacco smoke are also a bad thing. 

[19] Insulin resistance in the liver entails also elevated glucose because of a reduced production of glycogen by the liver.  Insulin resistance is where the normal level of insulin fails to sufficiently lower serum glucose, and the pancreas thus releases more insulin to obtain the fasting serum level of glucose.  This abnormally high level of insulin slowly causes the body to store more than the normal level of fat.  White adipose (fat) tissue (the most common kind) produces hormones which regulate the level of fat.  With insulin resistance this regulatory system is reset to maintain the weight gain.

[20] This explains in part the benefit to extended fasting, not only does it permit the body to fully adjust to the metabolic changes for fat metabolism which take 3 to 5 day, but also lowers the level of insulin by clearing the intestines of fiber.   The fast following bariatric surgery is why over 80% are cured of T2D 



6.   Fructose alcohol without the Buzz and worse


Fructose is toxic to the liver like alcohol; both are metabolized in the liver, and through various processes compromise liver functions, see Prof. Robert Lustig’s Alcohol without the Buzz.  Like ethanol the quantity consumed determines its toxicity.  Fructose is 15 times net more reactive than equal quantity of glucose to proteins in a process called glycationunregulated bonding to proteins, a bad thing.  Fructose and glucose exist primarily in a ring formation, however because fructose exist to a greater extent in a linear structure for which its carbonyl group on the molecule is exposed, it is more likely to bond with certain amino acids such as lysine on proteins than compared to glucose.   Using fluorescence method of analysis it is estimated to be 7.5 times more reactive than glucose.  The liver is the only significant place for metabolism of fructose, thus fructose is actively transported into the liver from the blood.  Collecting in the liver entails that the liver is subjected to a much greater rate of glycation than other tissues.  That is the first blow to the liver.  Among the process affected in the liver is its major metabolic process of producing glycogen from glucose.  With the slower than normal rate of glycogen production, the glucose accumulates to a higher than normal level in the hepatocytes (liver cells).  Being stuffed with glucose (a bad thing) entails that the hepatocytes are resistant to insulin’s message for to absorb more glucose.  .  This is why the hepatocytes are the first cells to exhibit insulin resistance.  This damage to the hepatocytes also affects the metabolism by the hepatocytes of fructose, thus increasing the rate of damage through glycation.   Second blow comes from IR in the liver:  it causes excess fat storage in the hepatocytes.  In the liver when the insulin level is high, as occurs with a meal high in easily digested carbs, there is an excess of glucose more than the liver can use for metabolism and production of glycogen, this excess glucose is converted through de novo lipogenesis into fats (triglycerides) and stored there.  Glycogen.[1]storage is limited because of builk.   Thus insulin shuts down the metabolism of fats (triglycerides), its transport from the liver as free fatty acids, and also causes the fats to be stored in the liver.   The fructose (glycation) damage liver with a high carb diet accumulates excessive fat storage.  On a steady typical Western diet, very slowly this excess fat accumulates to a toxic level in the liver (2-to-3 pounds).  With that amount it is known as non-alcoholic fatty liver disease (NAFLD).  The three work together, high fructose, glucose and insulin, to cause NAFLD.  (See the next section for the pathologies NAFLD causes.)  This lower rate of utilization of glucose from the blood by the liver raises the level of blood glucose.  The muscle and fat cells being at their maximum level of glucose following a high carb meal, they resist the message from the insulin receptors to absorb more glucose—see Fung on protective mechanism of cells resisting more glucose from the blood.  However, these tissues are resistant to taking up more glucose as signaled by insulin, they nevertheless respond to the message “burn glucose and therefore store fat”. Thus with those developing a fatty liver, NAFLD, they are storing more fat, typically a couple of pounds a year:  the gradual march to obesity.  (See section #10, which list various things that can be done to slow or stop the march to obesity.)  This process of glycation and fat accumulation also occurs in the pancreas, but at a slower rate, since the pancreas’s level of fructose is lower.  After a number of years, however, for about 24% of the seniors it will sufficiently damage the pancreas so that its insulin production will decline about 70% over a period of about a year, and this may become symptomatic or detected by blood work and diagnosed as T2D. 


2)  There is an important point to tease out of the many studies, namely that it isn’t the high carb diet, or refined carbs that is causal for IR and NAFLD, but the inclusion of fructose in that diet.  For example,  those on the traditional diet of Japanese, Chinese, and Okinawans[2] have only a 1% risk for T2D, NAFLD, and obesity, even though they over 70% of their calories come mainly from the quickly absorbed carbs of white rice, noodles, and/or Oriental yams); and among those who don’t smoke their rate of CVD is low.   Sugar, which came from fruits and vegetables, amounted to an average of 15 grams a day—in America the average is over 189 grams a day[3]. And there is experimental evidence that fructose not glucose is the culprit.  Fructose has been linked in an experiment on healthy volunteers without IR in which 25% of calories came from fructose sweetened drinks, compared to a control group with 25% from glucose (corn syrup).  In 2 weeks the volunteers on the fructose group developed IR, while those on the glucose sweetened drink didn’t.   Similar results have been obtain in animal experiments.  Fructose (not glucose) is the sand in the oil that damages the metabolic engine, the liver leading to T2D and obesity, and in addition more comes from glycation in other tissues.   


3)  The diabesity pandemics is not the only reason why Dr. Lustig calls sugar white poison, and state that it should be regulated like alcohol.   He and other scientist call Alzheimer’s disease, whose incidence has increase several fold in the last 4 decades, type-3 diabetes—and there is more.   Allow me here to explain how this reactive sugar when consumed in amounts well above the bodily mechanism for its safe metabolism and repair of glycated proteins. Cellular damage by glycation is not just limited to the liver.  It is a major cause of age related conditions.  ”It degrades the quality of cartilage and affects bone metabolism” at 2013.  Thus we have an explanation for the sharp rise is sport injuries since the 1970s, and also the osteoarthritic joint problems in the general population.  Prior to reading that journal article, I though the increase in osteoporosis and joint problems was driven by the chemical bath we are subject to from drugs, food additives, BPA, and others. Especially those that are sex hormone mimics.[4]. Now it seems that glycation by fructose is the main culprit. Glycated substances are eliminated from the body slowly, since the renal clearance factor is only about 30%.  This occurs in two ways through cell death (apoptosis) and through an enzyme which removes glycated amino acids.  The latter is called proteolysis. The slow clearance by proteolysis entails that for those on the Western diet only about half of the glycation products within the body will be eliminated. “As a consequence, long-lived cells (such as nerves, brain cells) and long-lasting proteins (such as DNA, eye crystalline, and collagen) may accumulate substantial damage over time. Metabolically-active cells such as the glomeruli in the kidneysretina cells in the eyes, [epithelial cells in arteries], and beta cells (insulin-producing) in the pancreas are also at high risk of damage” Wiki.  Some AGEs (advanced glycation end products) are benign, but others are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as cardiovascular diseases (the endothelium, fibrinogen, and collagen are damaged), Alzheimer's disease (amyloid proteins are side-products of the reactions progressing to AGEs),[7][8] cancer (acrylamide and other side-products are released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination).  This range of diseases is the result of the very basic level at which glycations interfere with molecular and cellular functioning throughout the body and the release of highly oxidizing side-products such as hydrogen peroxide.  Long-lived cells (such as nerves and different types of brain cell), long-lasting proteins (such as crystallins of the lens and cornea), and DNA may accumulate substantial damage over time. Cells such as the retina cells in the eyes, and beta cells (insulin-producing) in the pancreas are also at high risk of damage“ Wiki 2015.  Also under-rated is the role of fructose in glycation in retinopathy, nephropathy, and endothelial dysfunction[5] in diabetics, and the over attributing to reactive oxygen species created by metabolism—see Protein Glycation, A firm Link to Endothelial Cell Dysfunction.  Endothelial dysfunction is a starting cause for atherosclerosis and thus CVD--see section 12.  And there are other ways fructose in excess destroys health.


4)  Fructose also chelates minerals in the blood. This effect is especially important with micronutrients such as copper, chromium and zinc. Since these solutes are normally present in small quantities, chelation of small numbers of ions may lead to deficiency diseases, immune system impairment and even insulin resistance, a component of type II diabetes (Higdon).  Compared with consumption of high glucose beverages, drinking high fructose beverages with meals results in lower circulating insulin and leptin levels, and higher ghrelin levels after the meal.[62] Since leptin and insulin decrease appetite and ghrelin increases appetite, some researchers suspect that eating large amounts of fructose increases the likelihood of weight gain[63] Wiki 2014.  Fructose has a glycemic index of 17, while corn syrup compared to pure glucose’s 100 results in a major difference is satiety, thus justifying this type of contribution to obesity.     


5) There are several parallels to ethanol besides there metabolism in the liver and the reactive products damaging the liver proteins (glycation for fructose and the reactive aldehyde from the metabolism of ethanol), at 1991. This can progress to end stage liver disease (cirrhosis of the liver)—see section 7 below . Both ethanol and fructose activate pleasure centers of the brain to produce addictive behavior.  Like ethanol fructose causes a fatty liver, and with the continued over consumption, both can lead to end-stage cirrhosis of the liver.  And both ethanol and fructose have little effect upon the satiety hormones, thus promoting over consumption of food.  Given all these issues, one would assume that the experts would warn the high risk populations of elderly, diabetics, and those with CVD to avoid fructose/sugar.  However, fructose is recommended for diabetics because of its low insulin index, and the other at risk population are not warned; another example of profits before people.   Given the power of advertising to create markets, and our corporatist government, effective regulations are not coming, or an effective program of educating the public concerning the health consequences of sugar.[6] Both the FDA and the American Heart Association now recommend no more than 200 calories from sugar daily, however, few Americans know of this, and given the power of advertisement such a recommendation goes unheeded by most American.   The WHO makes the same recommendation.  Those who limit their sugar are doing so for other reasons than official pronouncements. 


 


7.  NAFLD and IR are the gateway to MeS and its comorbidities


NAFLD “Non-alcoholic fatty liver disease (NAFLD) is one of the causes of fatty liver, occurring when fat is deposited (steatosis) in the liver due to causes other than excessive alcohol use. NAFLD is the most common liver disorder in developed countries….[1][2]  Non-alcoholic steatohepatitis (NASH) is the most extreme form of NAFLD, and is regarded as a major cause of cirrhosis of the liver of unknown cause.[5]  A study using the National Health and Nutrition Examination Survey (NHANES) found a 30% rate of NAFLD in the United States between 2011 and 2012.[7  Most people with NAFLD have few or no symptoms [other than abdominal weight gain, and a propensity to readily put on weight]…. Soft drinks have been linked to NAFLD due to high concentrations of fructose, which may be present either in high-fructose corn syrup or, in similar quantities, as a metabolite of sucrose  Wiki.  Diagnosis of NALD is commonly by ultrasound or biopsy.   No pharmacological treatment has been as of 2015 been approved by the FDA, though pharma has several drug candidates.  However, the condition is responsive to Bariatric surgery, low carbohydrate diet, and diet with fasting.  


 


NAFLD its development:  NAFLD requir7es both high carbs and high fructose.  That it takes both is confirmed by Japanese and other population that eat a traditionally high-carb diet, but with very low sugar—for the Japanese 15 grams per day, and similar amounts for the Okinawans, and Chinese.  These populations have a low rate of CVD and the other age related conditions associated with the Western diet.  Many paleo peoples eat a high carb diet but the Western diseases are very rare among their elders. And there is direct evidence:  a couple of experiments done within a hospital where young healthy volunteers were fed for 2 weeks either high fructose or high glucose, this confirmed the role of fructose, but absolved glucose as to the development of IR.  So how are the two sugars different?  The difference is because of the fructose which is metabolized only in the liver where it is converted mostly to glucose and some fat.  Fructose is also 7.5 times more reactive than glucose through the process of glycation (see definitions section 2), and its slow clearance from the liver compared to glucose doubles that figure to 15.  Glycation damages the liver; it causes inflammation and other signs of liver injury such as high ALT and AST--blood markers for conditions in the liver.  ALT and AST are commonly used as a way to screen for liver problems.   A diet high in fructose is likely high in the sugar glucose both from sucrose.  Starch consists of long chains of pure glucose.  A diet that is high in carbs is necessarily low in fats.  So depending on needs of other tissues (fats and cholesterol are essential for cell membranes) the liver will convert in some of the glucose and fructose through de novo lipogenesis into fats.  Because of the high insulin from IR in the liver and a high carb diet, the high insulin accelerates the accumulation of fat in the liver.  This high carb-sugar diet causes IR in the liver and thus the gradual accumulation of fat in the liver.  The regulation of blood insulin which in part involves the liver, such as through the production of glycogen, will contribute to an excess of blood glucose, which causes other cells, principle the muscle and fat cells to become resistant to insulin.  For those who stay on the high carbohydrate Western diet this is likely to progress to obesity, NAFLD, MeS, and obesity.  Two studies of those with NAFLD found that they consume 2-3 times more fructose than those without NAFLDat, and.   AGEs (advanced glycation end products) in the liver and elsewhere are recognized as foreign substances by the immune system and can in sufficient number produce significant inflammatory response.  The attributing of excess fat in the liver as the primary cause for liver inflammation is questionable given the co-existence of AGEs in the liver and the natural inflammatory response by the immune system to AGEs.  Insulin resistance is like drug resistance where the body responds less to a given dose of a drug, for example alcohol, and a higher dose is thus required for the desired effect.  With insulin resistance the normal level of insulin fails to sufficiently lower serum glucose, and the pancreas thus releases more insulin to obtain the ideal fasting serum level of glucose.  This abnormally high level of insulin slowly causes the body to store more than the normal level of fat.  White adipose (fat) tissue (the most common kind) produces hormones which regulate the level of fat.  With insulin resistance this regulatory system is reset to maintain the weight gained.  High fructose and high glucose from the Western diet is what has lead to the diabesity (obesity & diabetes) epidemic.  


 


Fortunately there is a repair mechanism for NAFLD IR T2D, and obesity, to simply go on a low insulin diet.  This requires fasting made more effective by low fructose and especially the ketogenic diet.  As stated before fasting keeps insulin low and thus keeps the body in the fat burning mode.  Fasting is why about 80% of those who have undergone bariatric surgery cure their diabetes and insulin resistance within the first month. This is because they can’t eat during the first couple of weeks following surgery.  Follow the appropriate fasting programs listed in section 3 duplicates the process that cured those who had bariatric surgery.  And it gets better as weight is lost, the body heals itself, old damaged cells from glycation are replaced with cells whose protein haven’t been damaged.[7]


 


8.   Why a low-net carbs diet for obesity & T2D


There are two common general approaches to dieting, caloric energy restriction (CER) or carbs restriction of which some are the extreme low carbs, the ketogenic (Atkins type) diet without CER—and there are of course many variations of these types of diet.[8]  A third approach, fasting is growing in popularity, mainly in Europe. Unfortunately nearly all of the long-term[9] obese have had their weight regulatory system compromised; it functions to restore weight loss by causing a 25% reduction in metabolism or more, and an increase in hunger through a hormonal system involving insulin and leptin.  Typically around the end of the 2nd month (see chart above), their progress is greatly diminished because of the fat restoring hormone leptin.  Only those with extreme calorie restriction will continue to lose significant weight.  However, once off their diet the weight will be gradually regained (the yo-yo diet).  The main cause is the hormone leptin which is secreted by adipose (fat) tissue; it functions to main the normal level of fat storage.  Leptin intercedes to decrease metabolism--typically 25%-- and through this effect increases appetite.  The dieter feels that if he eats more, he will be mentally sharper, happier and have more energy[10].   Possible there is an approach to solving the affects of leptin which results for the long-term overweight with the restoration of their prior level off.  To address this the government funded a major trial, and they selected a long-term vegetarian to run it, probably want to find evidence against the then very popular Atkins diet, which given its low carbs was unpopular with food manufacturers.   


 The trial was run to compare the CER to the carb restricted diets.  In the funded by government[11] Stanford University international A to Z Weight Loss Study which compared 4 popular diets.  Its lead person was disappointed the Atkins had the best results both in weight loss, blood glucose, and lipid profile.  At 2 moths all 4 cohorts in the trial experience a marked reduction in the rate of weight loss.  At 1 year, the length of the trial, Atkins (ketogenic) cohort loss 9.9, LEARN 5.5, Ornish 5.3, and Zone Diet 3.3 pounds—see JAMA 2007.  Another trial had similar results this time using overweight volunteers:   9.4 kg lost on low carb (20 gm daily) versus the low fat 4.8 kg, at.  In this trial both groups reduced calories between 500 to 1000 calories daily.  In both of the clinical trials the lipid profile and blood pressure were much better for the low carb (thus high fat) cohorts, and more importantly their level of blood sugar improved on the low car diet.  “Insulin levels dropped and insulin sensitivity was restored” (Fung p 101).  A recent journal article interviewed the 2009 group on the television show The Biggest Losers.  A group of 13 morbidly obsess participants were in a boot camp which had an extreme energy restriction, control of foods, and a major exercise program.  They too experienced a major reduction in the energy expended when physically active, a 40% decline.[12] The 5-years later journal review article found that all but one of them regained at least most of their lost weight--see.  A longer period would have produced a bleaker picture.  A large 2015 UK population study of the obese found that 99% of long-term obese adults who lost significant weight that at the end of nine years they were again obese or at best overweight.  The UK data bank lacks information on type of diet, however, it did list those who had bariatric surgery and they were excluded from the study.  But given that the KD is sufficiently popular in the UK, on the face of it, it seems that long-term the Atkins’ maintenance phase was poorly adhered to.  So why did the KDers fare long term?


 


The KD advocates views obesity as a problem with fat storage, and attempts to solve it long term by forcing the body to metabolize fat.  The most popular of these is the New Atkins which calls for moderate protein and uses net carbs (table section 3) instead of total carbs.  It also calls for a lifetime maintenance phase of low carbs.  Its limited success is because of moderate protein consumption.  Eating foods with protein causes the release of insulin through the incretin system of hormones. As stated in the definitions Section 2 above:  Incretin: class of hormones secreted by the stomach and intestines which case insulin secretion and satiety.”  The release of insulin interferes with the process of cleansing the liver and pancreas of fat.  Even with significant weight loss, those with advanced T2D are still dependent upon medications though less.  Unfortunately, KD also has a compliance issue:  like CER, typically have over half the dieters quit before one year.  Moreover both diets for the long-term obese, the diets aren’t sustainable.  As stated above in the CER paragraph above, energy drops and quality of life declines typically about the 8th week and this occurs with the KD.  “Long-term studies of the Atkins diet failed to confirm the much hoped-for benefits” (Fung p. 102). The failure of both diets to have sufficiently long periods of low insulin and thus to cleanse the liver and pancreas of excess fat and permit these organs to heal, this is why the leptin system for maintenance of fat kicks in to restore weight.  In other words they haven’t fixed the lipogenic system where fat tissue releases leptin to restore the level of fat.  So how can the long-term obese and overweight reset their weight regulatory system? 


 


Fortunately, there is a fix:  those who have used fasting in addition to low carbs have had remarkable success. Though not a major player, it has in the 5 years increased and at least in the UK gained the status of a fad diet because of Dr. Michael Mosley of the BBC, his 5-2 fast.  In Europe and Australia where BBC, ABC, and other networks have aired programs extolling fasting, and books there have a greater share their market, more people have tried fasting.  The results from fasting are striking.  Only fasting causes extended periods of low insulin.  During these periods the body cleanses the liver and pancreas of excess fat and thereby cures IR and T2D which drives obesity.  For example, those with bariatric surgery have low insulin because they are fed intravenously, and most of cured of type-2 diabetes within the first 2 weeks. 


There is no drop in metabolism thus weight loss is steady, and the weight-regulatory system is reset.[13]  Once the desired weight is obtain the patient needs merely only to limit sugars and other refined carbs.  There are a number of different approaches from modest food intake to total near restriction of caloric foods.  The most thoroughly research fasting diet is that of alternate day fasting with near zero carbs and proteins, thus no rise in insulin.  Compared to CER and low carbs, its prolonged periods of low insulin make all the difference.[14]  This type of diet will typically within 3 months result in the burning of fat in the liver and pancreas and thus cure IR and T2D and causes the weight regulatory system to eventually adjust to the lower weight.  Proof is found in the success of Intensive Dietary Management—a medical clinic in Toronto Canada-- in curing both obesity and T2D.  The clinic uses low carbs and fasting. Their success, success of others and the journal literature is convincing short-term or alternate day fasting is the best treatment for the obese and the diabetic.[15]  The clinic’s principle scholar is Jason Fung, a nephrologist[16].  He sees end-stage diabetics, and with the clinic’s fasting and diet program he is able to get them off their insulin injections and other drugs to cure their diabetes while losing significant weight. (On October 18 of 2016 The Complete Guide to Fasting is going to press by Jimmy Moor and Dr. Fung.  It probably will contain some figures on the success of his dietary approach.)  The merits of low carb with alternate day fasting is not merely a theory like calories in and calories out but one which has supporting clinical trials and animal experiment—see the 2014 summation article, running 16 pages with 8 more for reference by Metabolism and Diabetes Research Group of the University of Surrey, UK, at.  To make accessible confirmation of the above claims, excerpts from this article are pasted at link and my review article on fasting at.


 


9  Fasting is easy and essential  10/23/16


What has gone wrong:  It all starts with too much of the very reactive sugar fructose (net 15 times more than glucose), which damages the live.  The liver is part of the glucose regulatory system and this damage causes insulin resistance.  Because of insulin functions to cause the cells to take up glucose and burn it; it also causes those cells to stop burning fat and to store it.  With insulin resistance, they require a higher than normal level of insulin to lower the blood sugar, and thus they have a higher than normal rate of fat storage.  Those people are prone to storing more fat than they burn.  Over 90% of people with excess weight have what is called insulin resistance, and its consequence a fatty liver (NAFLD, Non-Alcoholic Fatty Liver Disease).


Why fasting works:  The fix is to burn the excess fat in the liver (and if diabetic in the pancreas), and to continue in the fat burning mode by fasting.  Without a signal from blood insulin, the cells throughout the body switch to burning the stored fat, this is what occurs while sleeping.  Staying in fat burning longer by fasting allows the liver to gradually ship-out and metabolized the excess fat it stored.  Once the liver heals by both lowering the sugar in the diet and by eliminating the excess fat in the liver, the liver’s contributions to the control and metabolism of glucose normalizes and insulin resistance is cured.  A healthy liver is essential in the long-term fix of the weight regulatory system and thus being able to lose weight and keep it off.    


The use of fasting along with a low carb diet reverses obesity and type-2 diabetes.  This fix has been growing in popularity, though food manufacturers and pharma ignores this fix and gives us the wrong message, that of eat less and exercise more.  This doesn’t work for the long-term overweight because their weight-regulatory system has been reset to their current weight, and attempting to lose weight only results in the yo-yo diet.  I have extensively research the topics of diet and fasting.  With the insights of this research I shall use my experiences to illustrate why fasting with reduced carbs is the fix for insulin resistance, NAFLD, and excess fat. 


My Experience:  I never had a protracted weight problem.  By logic I had used the short-term fast when I gained 20 pounds during the winter of 1969-70.  I was in graduate school, philosophy, University of Manitoba.  At the age of 26 during the winter my metabolism slowed down, and so I didn’t burn off rapidly the now excessive calories.  I had developed a fatty liver, and thus was putting on abdominal pounds.  It took 3 months of reduced meals and short-term fasting to lose the weight around my middle.   It stayed off because it was short-term weight gain; my white adipose tissue through leptin had NOT reset my weight to 178 pounds.  After that, whenever I gained 5 pounds, I simply cut back on portions, quit eating by 7 PM, and skipped breakfast several times a week.  The second change was exercise.  I moved from Winnipeg to southern California in 1974 and became in 1975 a sports addict.  I started regularly playing volleyball, cycling, and running, In 1980  I added moderate weight training and singles racquetball.  In 1993 my diet changed for the worse:  following the lead of a very fit friend who both weight trained and ran 7 miles a day, I went on a very low fat (thus high carb) Western diet.  Fortunately I exercised daily and watched my weight; thus I never went more than 5 pounds above my slim weight.  Skipping breakfast, reducing portions, and cutting back on sweets was an easy fix. 


In 2012 I watched Prof. Lustig lecture on YouTube, which had gone viral.  He explained why sugar was poison and I took notes.  A year later, I researched his explanation of the diabesity pandemic (obesity and diabetes);   he presented the evidence on how excess fructose harmed the liver like alcohol and was driving the diabesity pandemic.  In the spring of 2014, I reduced by 75% sugars including fruits.  I also cut back on carbs from grains about to about 30% of calories; thus I increased saturated and monounsaturated fats to replace those calories.  It took about 4 months before candy, fruit juices, ice cream, and melons tasted way too sweet.  Though my weight remained for decades the same, I had 3 pounds more around the lower abdomen than when entered college in 1962.  It was a sign of a fatty liver, so I decided in March of 2016 to experiment with daily short-term fasting. I still ate the rest of the day whatever I desired (my carbs had been reduced a year before and replaced with saturated and monounsaturated fats).  By July of 2016, 4 months later, I lost 4 pounds, waist shrunk 1 inch, and fasting glucose (a measure of IR) was 10% lower.  I noticed that by skipping breakfast, I had reduced my total consumption of food.  I was less hungry especially at dinnertime and there was no decline in metabolism with its negative affect upon physical activity and mood.  The low-insulin diet causes a lower level of hormone leptin, a hormone which reduces metabolism and increases hunger—it is the main cause of the yo-yo diet.  (Leptin produced by fat tissue, functions to restore fat to its normal level.)  A big plus was that I experienced in the morning an increase in mental and physical energy; it is a time when I do most of my studies and writing; and I avoided the decline following breakfast.[17]  I like the short-term fasting. 


One advantage to the lower carbs is that while in the fat burning mode the body increases metabolic rate about 10%.  Secondly neurons releases the catechol amines (adrenalin and noradrenalin, and dopamine) which cause stimulation and mood elevation.  This combination has been inherited because of the survival advantage when food is short—more energy for hunting and gathering.  This is why I now like skipping breakfast.  Morning fasting and not eating at night has convinced me that weight control with short-term fasting is easy and pleasant, much easier than an energy-restricted diet.[18] 


Literature on Fasting:  Dr. Jason Chapter 20, “When to Eat” in his Obesity Code, 2016, p 235-251 covers the history and advantages of fasting; his opening Sentences:  “LONG-TERM DIETING is futile.  After the initial weight loss, the dreaded plateau appears, followed by the even more dreaded weight regain. The body reacts to weight loss by trying to return to its original body set weight…  Even if we eat all the right things, our insulin levels stay elevated…. But we fail to address the other problem insulin resistance.”  The reason for the major drop in metabolism--25 to 40% typically at 2 months on a calorie restricted diet--is leptin[19] (regulated by insulin) Leptin reducing the rate of metabolism has both  physical and emotional consequences:  inactivity and a general decline in psychic energy compounded by an increase in boredom associated with inactivity.  lack of energy with its consequences on moody and activities.  The obese dieter feels that if he eat more he will have more energy to do things and be in a better mood.  Very few of the long-term obese are capable of going on a life-long energy restricted diet—there are numerous long-term studies which show that these obese gain back most or all of their lost weight.[20]  Only fasting addresses insulin resistance.”  His clinical experience (over 1,000 patients) and extensive published research proves that fasting is both easy and works—as too my own experience, and other whom I have consoled. 


From Fung’s Obesity Code:  I shall present what I find of most value in that chapter, sometimes quoted and my additions will be in [brackets].  IR causes excess fat storage and leptin promote reduced metabolism and increased appetite.  [But it is not appetite/hunger exactly, rather the feeling that if I eat a bit more my energy and mental clarity will return to what it ought to be; viz., I will feel better and be in a better mode (this is the effect of leptin on energy)].   All foods promote the release of insulin; only not eating will keep blood insulin level low—see insulin Index table section 3.  As Fung points in other chapters, incretin hormone system responds to digestion in the stomach and small intestine by stimulating the release of insulin from the pancreas [fats and fructose by far produce the least response, insulin index of 10 and 17 respectively.  Incretins explains why meat, fish, and poultry have a higher insulin index than boiled pasta.  Though Fung writes of 24 to 36 hour fasting as curing IR, his clinic also uses the short-term fasting.]  “The term ‘breakfast’ is the meal that breaks the fast—which we do daily”--p 237.  Fasting has been used in most cultures and religions, and our ancestral hunter-gatherer was forced by circumstance.  Hippocrates of Kos (c. 460-370) wrote; “instead of using medicine, better fast today; to eat when you are sick is to feed your illness” p 237.  Humans like most animals do not eat when sick.  Plato and Aristotle were staunch supporters of fasting.  “The body does not burn muscle until all fat store is gone” p 240.  “Blood glucose levels remain normal as the body switches over to burning fat for energy.  This effect occurs with fasting periods as short as twenty-four to thirty six hours.  Longer fasts reduce insulin even more dramatically…. Regular fasting has been shown to significantly improve insulin sensitivity.[21]  This finding is the missing piece in the weight-loss puzzle.  Most diets don’t address insulin resistance,” p240.  One of the most potent stimuli of [human] growth hormone {HGH] secretion during fasting.  Fasting promotes the use of fat as fuel and preserves muscle mass and bone density.  Adrenalin [and noradrenalin] levels go up with fasting,” p 241 they are the natural amphetamines that create alertness and physical energy.  “Breakdown of muscle tissue happens only at extremely low levels of body fat—approximately 4 percent,” p 242.  “The human body has evolved to survive episodic periods of starvation,” p 243.  “Caloric restriction diets do not allow the evolved adaptation that occurs during fasting,” p 244. We have also like all mammals have evolved a system to return to our normal weight when weight has been lost through increased hunger and reduced rate of metabolism.  Its main regulatory hormone is leptin that is produced by the adipose (fat) tissue.  “Studies of eating a single meal per day found significantly more fat loss, compared to eating three meals per day, despite the same caloric intake” 243[22].  “Total energy expenditure is increased during a fast—in a 4-day fast by 12%,” p244.  “In our clinic, experience showed that appetite decreased as duration of fasting increased.  The most astonishing aspect of this study [107 obese subjects unable to lose weight] was the ease with which prolonged starvation was tolerated.  These experiences echoes our own clinical experience at the Intensive Dietary Management Clinic with hundreds of patients,” p245.  The more dangerous visceral fat is preferentially removed with fasting.  There is reference to Dr. Michael Mosley (British on BBC) 5:2 diet, 5 days of full caloric and 2 days of 25% of calories at the end of a short-term fast.  In the trial that compared the 5:2 to the Mediterranean diet with a 25% reduction in calories.  At 6 months both groups lost about the same amount of weight, but the 5:2 group have lower insulin and less IR, at p247. This change (though not measured) indicates that excess liver fat had been metabolism.  The short term fasting made this important difference.  For the long-term overweight fasting reverses insulin and leptin resistance, thus it is essential, and it is used by Dr. Fung to cure type-2 diabetes.     


For those who want to know more of the science behind fasting, I highly recommend that you read my “Evidence of Alternate Day Fasting—Cures Type-2 Diabetes” and Fung’s book The Complete Guide to Fasting.  On P. 204 he states that, “A major advantage of the sixteen-hour fast is that it is fairly simple to incorporate into everyday life.”  The graph on page 202 indicates the amount and duration of the traditional 12 hour fast (7 pm to 7 AM) the 16-hour fast and the 20 hour fast (3, 2, and 1 meals respectively as to the extent of fat metabolism, and fat storage when eating.  My own experience and others whom I have counseled has convinced me that short-term fasting is easy, and the scientific literature confirms that longer periods are also easy; this is because our body has evolved a system to burn the fat reserve and to keep us alert and full of energy so that we more likely to hunt and gather foods.  And as Fung states, “it has a high rate of compliance.”  


10.  Why some don’t get fat --    11/9/16


A variety of factors work to reduce the probability of developing a fatty liver, the starting point for IR and its comorbidities.  It is the combination of fructose and glucose (especially form both sucrose and high glycemic index foods (thus refined carbs and other easily digestible carbs such as potatoes).  The sugar fructose is the starting point thus eating a low sugar diet.  High insulin level driven by high carbs drives liver fat storage.  The traditional Chinese diet though high in white rice (which is comparable to white bread) had little effect.   Experiments have come to the same:  feeding volunteers either a high level of fructose are glucose, only the fructose cohort developed IR. 


A flawed knowledge of the processes and poor recollection makes self-analysis of limited value.  Often the year in which a fatty liver has developed is unknown but surmised based on a gradual gain of weight; however, it is possible that the condition had developed years before, but based on a variety of factors listed below weight gain was minimal. 


Genetics of course make a difference, but not that much.  One authority placed it at 5%.   A major cause is learnt behavior from family, from community, from media.  Another cause for obesity is the prenatal environment.  A fetus is exposed to high level of blood glucose will develop more insulin-secreting cells “and the more insulin the child will secret as it get close to birth.  The baby will now be born with more fat and will become insulin resistant as it ages,” Taubes, supra 132.  The dramatic increase in early childhood obesity, as referred to by Dr. Lustig, is a striking result of unhealthy womb environment and the high sugar diet.  Thus what seems to be an inherited trait is in fact due to the womb environment and the western diet.  For 98% of the obese social factors and the western diet play a much greater role.  A classic review article on Obesity in Scientific American pointed out that while the American Pima Indians of Arizona have the world’s highest rate of diabetes and obesity[23], those on the Mexican side of the boarder have a very low rate.  Since each are from the same genetic pool—104 years of separation, statehood was granted Arizona in 1912—evolution cannot have created that great a difference.  The diversion of the water and the introduction of non-native diet had devastating effects on the health of the people as well”—Wiki.  ‘The genes caused obesity and diabetes’ is simplification that hides the causes, similar to that of the weak will.


Various common ways to avoid the health disaster caused by IR while eating a Western diet (in approximate order of importance): 


Tight weight control and not allowing significant weight of more than 15% above thin body weight to be carried for years (the longer the weight is on the less likely that an energy-restricted diet will keep that weight long-term off)


Mini-fasting when dieting, or alternate day fasting.


Yielding to peer-pressure to be fit and trim


Regular exercise or strenuous lifestyle


Multiple day fasting at least twice a year


Daily average of less than 40 grams for male (30 grams for a woman) of sucrose for an active average size person 


Avoiding regular consumption of high-carb alcoholic beverages such as beer, since glucose competes with ethanol for metabolism in the liver, thereby increasing damage to the liver by slowing the clearance of toxic ethanol.


Major seasonal change in fructose and carb consumption


Having good muscle tone


Avoiding drugs with sedative effects (drowsiness, increasing sleeping, muscle relaxation), thus avoiding nearly all psychotropic drugs, some hypertension drugs, high doses antihistamines, SSRIs, and other drugs that inhibit the functions of neural transmitters.  Even when weight gain is not listed as a side effect, often it is.


For seniors, natural hormone replacement therapy in sufficient dose (see my articles on testosterone and estrogen).


Getting more than 40% of calories from fats


High ratio of saturated fats to unsaturated fats which become rancid in the body (see Part 4 Fats for complex reasons)


Eating a high ratio of natural foods to manufactured foods thus limiting the sugar added foods.  


Major seasonal change in fructose consumption


Limiting the exposure to unnatural chemicals including drugs, food additives, pesticides, hormone mimics, and other sources such as cosmetics.


Aspirin 325 mg or greater per day, it lowers serum glucose—see 1950 Merck Manual, and Aspirin, under “diabetes”.


Genetics, some are more prone, others more resistant. Probably a significant causes in about 15% of those obese. 


The lack of sex hormones has been shown to play a significant role in weight gain.  Estradiol (the best of 4 estrogens) controls fat distribution, which is visually obvious as a girl develops during teen years.  Lack of estrogen cause women to gain abdominal weight following menopause and she loses muscle because her testosterone drops.[24]  The two sex hormones are structurally identical, but for one functional group.  Testosterone makes a different for men past the age of 60 when they do sufficient amount to restore them to a youthful level, which is what I did.  I started in 2004 with natural testosterone[25] from a compounding pharmacy.  It made my weight control easy.  I stopped weighing myself once I realized that my weight-regulatory system kept me between 161 and 166.  Only with fasting did drop to between 155-161 pounds.


     Until 2013 I ate a high carb diet, low fat diet, I avoided the weight gain by doing the most of the above.


 


11.  Myth busters -- (trashing tobacco corporate science)[26]


  1. High serum cholesterol causes CVD.  TRUTH:  High serum cholesterol has not been demonstrated to be a cause of plaque formation.  CVD’s main cause is infective agents within artery walls which damage LDL with toxins and cause an immune response by macrophages that cause atherogenesis.  The cholesterol deposits in the artery walls are a byproduct of the immune response, as too are calcium crystals, foam cells, triglycerides, and lymphocytes.  Cholesterol is a bystander not a cause; thus lowering its production with drugs does not prevent AS or heart attack.  Autopsy studies found no relationship between serum cholesterol and degree of AS in those died violent deaths, see.  The Australian Broadcast Corporation has a documentary which exposes this myth, at and one on the statin scam. 

  2. Avoid saturated fats because they cause CVD by raising the serum level of small-dense LDL which is associated with CVD.  TRUTH:  Saturated fats don’t raise cholesterol levels or small-dense LDL.  And LDL level is not associated with CVD (see #1).  A meta-analysis of 21 studies on saturated fats, “failed to find an association with CVD, Wiki, and also Wiki.  This extends to all types of fats when “increased from 30 to 50% of total energy,” 2004. Moreover, those on an Atkins type KD, their so-called “bad” LDL drops and the “good” HDL rises.

  3. Vegetable oils are preferred to saturated fats (main source animals).  TRUTH:   Vegetable oils are associated with diseases because they are high in polyunsaturated fats that become rancid in the body, when cooking, and on the shelf--link.  Since this process of oxidation changes the shape of the molecule and they are incorporated in cell membranes, they adversely affect the functions of these membranes.  Like trans-fats (also of unnatural shapes) the consequences are disease promoting.  Second, polyunsaturated fats are high in omega-6 fatty acid which blocks conversion of omega 3 oils an anti-inflammatory agent.  Our Paleolithic ancestor averaged 2 parts omega-6 to 1 omega-3; today it’s 16 to 1.  Many people wisely take a fish-oil supplement to improve the ratio of omega-3.  Because of its effect on the immune system and rancidification vegetable oils promote CVD, arthritis, and Alzheimer’s disease.  The more expensive animal fats are the best source of fat followed by the palm kernel, coconut, and olive oils which are high in monounsaturated fats.   There are hundreds of journal articles going back 6 decades on this process, use scholar.google to find them. 

  4. Sugar (the disaccharide sucrose is fructose and glucose), fruit sugar (fructose), and starches (long chains of glucose) are merely empty calories without nutritive value; viz. harmless sources of energy.  A calorie is a calorie.  TRUTH:  sugars and starches (pure glucose) damage tissues.  Fructose and glucose randomly bind to proteins (in a process called “glycation) to damages proteins in your cells.  Thus glycation promotes the degenerative conditions associated with old age:   CVD, atherosclerosis, Alzheimer’s, macular degeneration, et al.  Fructose (fruit sugar and ½ of sucrose) has a glycation rate of 7.5 times that of glucose; actual 15 times because of its slower clearance compared to glucose; moreover, most of the glycation occurs in the liver where it is stored prior to metabolism there.  Since 90% of fructose goes to the liver for metabolism, the damage there through glycation is significant.  Some of the fructose is converted in the liver to fat[27] which can accumulate because of the Western diet with its high carbs.  Damage from glycation and fat accumulation in the liver causes IR and a fatty liver called non-alcoholic fatty liver disease (NAFLD).  NAFLD affect over 30% of the US adult population (NHANES II study).  NAFLD affects the plasma-glucose regulatory function of the liver to cause IR.  Fructose by causing minimal insulin response, it bypasses the appetite regulating system involving leptin and ghrelin which reduces it affect upon the satiation system  of the hippocampus to cause weight gain.  Finally, fructose stimulates the addiction center of the brain (see #6 below) to promote sugar addiction.  Clearly, sugars are not harmless empty calories, nor are starches with high insulin index, and fructose is the worse.

  5. The cause of obesity is a sedentary lifestyle & gluttony.  All one needs to do is eat less and exercise more; viz., burn more calories than one consumes; this is the common advice given by doctors, dieticians, and accepted as the way to lose weight. TRUTH:  For all mammals their weight is controlled by a biological system.  The Western diet with its average of 180 grams of sugars daily causes a fatty liver and IR.  Fatty liver and IR muck up the regulatory system and thus cause obesity.  It is not gluttony and sloth that causes the obesity and diabetes pandemics (blaming the victims) but rather the Western diet which is promoted by food manufacturers and corporatist governments. 

  6. For the obese, a 25% reduction or more in calories will result in significant long-term weight loss.  Truth   The weight regulatory system in an effort to maintain the set weight will reduce the rate of metabolism approximately 25% and increase hunger.  Even those he get past this barrier which occurs typically around the end of the 2nd month, they will once off the diet regain the weigh (yo-yo diet).  The hormone leptin intercedes to decrease metabolism, typically 25% and at the same time increases appetite.  It is secreted by adipose (fat) tissue to main the normal level of fat storage.  Less than 1% of long-term obese adults at the end of nine years will obtain normal body weight through diet.  To prevent this regain of weight, the regulatory system must be reset, and this occurs by fasting and going on a low carb diet.  Fasting will avoid the 2-month drop in metabolism.  This type of diet will eventually result in the burning of fat in the liver and pancreas and thus cure IR and T2D and permit the weight regulatory system to eventually adjust to the lower weight. 

  7. Hormone replacement (HRT) will not promote weight loss.  TRUTH:   Estradiol among other things regulates fat distribution[28] and plays a role in physical well-being.  During and following menopause women experience a precipitous drop in estradiol (the most healthful and active of the 4 human estrogens).  The common post-menopausal reduction in physical activity and associated rate of metabolism contributes to weight gain and abdominal fat.  Natural HRT [estradiol plus progesterone] reduces insulin resistance and fasting glucose in women with diabetes” at.  Since some of estradiol is converted to testosterone NHRT prevents muscle loss with aging, another contributing factor to weight gain.  Men too following andropause experience a reduction in muscle mass and metabolism.  And the heart as a muscle gets weaker.

  8. HRT for men and women poses major health risks which outweigh their benefits.  TRUTH:  natural hormones  lower risk for breast and prostate cancers.  Men in the highest 20% for testosterone have the lowest rate of prostate cancer and heart attacks.  Estradiol moderately lowers the rate of breast cancer.  In sufficient dose NHRT will reset the biological clock to a younger age and thereby significantly reduce the risk of most age-related chronic diseases.  Estradiol with progesterone lowers CVD, Alzheimer’s, cancers, and much more.  Testosterone  decreases the risk of heart attack and cancers.  Current wisdom is based on pharma’s junk science & tobacco ethics:  clinical trials that knowingly used the worst formulate of HRT for women, Prempro.  Read the section on the WHI study which exposes pharma’s and NIH’s tobacco science and ethics.  NHRT is good for people and thus bad for pharma.

  9. Three lies about type-2 diabetes:   a life-long progressive condition; it can’t be cured; and is best managed with drugs that lower blood glucose to normal level.  TRUTH: that once the excess fat stored in the pancreas is cleansed T2D is cured (at the same time the excess fat in the liver is cleansed).  Bariatric surgery reverses often within a month T2D by post operation fasting proves that it can be cured and that fasting is the cure.  Dr. Janson Fung’s dietary treatment of KD (low carb high fat) with alternate-day fasting cures T2D for most within 6 months.  Diet is the cure.   Moreover the cohort who has their glucose tightly controlled has a higher mortality rate in clinical trials.

  10. Pharma is highly regulated by the FD A to protect the public from the tobacco ethics used by corporations to fulfill their fiduciary duties.  Truth:  that there is a revolving door between the FDA and pharma, and that at the highest levels the FDA is ran by executives from pharma and their KOLs.   For a summation of the ways in which the evidence base has been broken—link, or YouTube Dr. Angell.  Our corporatist government enacted the Prescription Drug User Fee Act of 1992 to make the FDA dependent upon pharma for over half of its budget.  Congress wants the FDA to serve the pharmaceutical industry.   Link to Consumer Report on the FDA.  Read Prof. Ben Goldacre’s Bad Pharma.

  11. Doctors know what is best for patients.  Truth:  the education and sources of doctors’ information has been manipulated by pharma so as to turn them into drug pushers.  Pharma runs and owns the results of clinical trials, thus positive bias is the norm--32%.  Pharma determines who becomes a KOLs (Key Opinion Leaders).  They are the lead authors on clinical trials, write the medical textbooks, and give continuing education classes.  The information foundation is thus distorted.  For an insightful explanation of how this has occurred click on linkyou need to know.  Pharma and food manufacturers through junk tobacco science, corporate media, and misinformed doctors cause cognitive dissonance and reliance on their KOLs by both the public and physicians.  Pharma has framed the discussions to promote the sales of patented drugs, and food manufacturers to promote the obesity and diabetes pandemics.  What has been said about pharma applies to the manufactured food and tobacco industries—profits before people.  There is a struggle going by leading men in the medical field who have broken rank over the corruption worked by pharma, but you won’t squarely hear of it in our corporate media.  But you can watch them on YouTube & read their journal articles.  


 


12 Pathogens in artery walls is the main cause of CVD  


The tobacco-science based claim that saturated fats and cholesterol cause CVD; this has been decisively refuted by scientific evidence:   Atherosclerosis (AS) is now recognised as a chronic inflammatory disease occurring within the artery wall and ultimately responsible for myocardial infarction, stroke & peripheral vascular disease.”   There are approximately ten times as many bacterial cells in the human flora as there are human cells in the body”, Wiki,  Not surprisingly some of them are in the interior of the artery walls, the tunica intima.  The inflammatory process starts with white blood cells attempting to eliminate certain bacteria.  They produce an inflammation in response to the virus and bacteria colonies within the artery walls.  A typical study found Chlamydia pneumonia in those with CVD 79% vs 4% without CVD in coronary artery specimens.  LDL functioning as part of the immune system absorb the toxic chemicals produced aby these pathogens.  The “monocytes replenish resident macrophages” (a scavenger white-blood cell) that dispose of the products of the LDL’s immune response--see.   Thus pathogens damage to LDL is part of the process leading to the development of CVD; not high blood cholesterol and high fat diet which are bystanders found within the LDL.  Lesser contributing factors include oxidation & glycation (sugar bonding) which damaging endothelial cells lining the coronary artery walls.  Pharma wants us to believe that the inflammation response is to oxidized LDL in the artery walls.  Wrong again, the contents of LDL is cholesterol and triglycerides which the body needs to grow new cells to promote healing in the artery wall and to replace damage white bloods cells both of which have been damaged by the pathogens.  This explains cogently why atherosclerosis is brought on by an inflammation response.  Pharma says this response is a result of damage to the LDL in the inner layer of the artery; no mention of pathogens. Pharma has ignored a century of artopsy studies of those who died from a heart attack; these studies find pathogens.  But pharma makes billions treating hypercholesterolemia--see.   Then they make billions more hypertension and heart attacks—but not the pathogens that cause AS.  Prevention is not in their business model.  Moreover pharma is very good at marketing--see how.  The scientists who are critics of pharma’s junk science are ignored by corporate media.  Physicians hear pharma’s key opinion leaders (KOLs) at the required continuing education classes funded by pharma.  Having said this, my concern here is with diet’s role of insulin resistance (IR) in obesity, fatty liver disease, diabetes, age-related diseases, and CVD; and also about healthful choices.  Sugars through glycation damage the endothelia cells which line the artery walls, and so damage they increase the risk for pathogens colonizing the inner layer of the arteries—2 links see and more.  


LDL is a lipoprotein-phospholipid wrapped sphere containing about 1500 cholesterol molecules and 3,000 to 6,000 fat molecules including triglycerides, see illustration.  Cholesterol has several essential functions including forming the cell walls, neurons coating, and its conversion into the sex hormones. The liver produces cholesterol--about 70%--and sends it wrapped inside LDL through the blood to cells in need of fats & cholesterol.  Inhibiting the synthesis of cholesterol with a statin drug has many side effects, and it doesn’t prevent CVD.  Numerous books and documentaries expose the cholesterol myth & statin horrors.  But pharma in the production and dissemination of information frames the debate; thus only those who de-nova examine the journal evidence and adjust for their tobacco science can come to the best evidence based answers.


 


13.  Other cofactors for CVD


Pathogens play the key role in the formation of atheroma leading to AS and CVD.  However, excesses in reactive blood-borne chemicals including simple sugars (especially fructose) are contributory.  Their main pathological mechanism is through endothelial dysfunction.   Endothelial cells function as a single layer membrane that lines all the blood vessels and act as the gatekeeper.  These cells have receptors which allow certain chemicals to pass through.  Lymphocytes, for example have a compound which counters adhesiveness that join the endothelial cells together to form a membrane, thus lymphocytes can slip between them.  Various chemicals and foods adversely affect the function of endothelial cells as gatekeepers.[29]


Trans-fats and rancid polyunsaturated fats are statistically associated with CVD.  The abnormal shape of these fats is cause functional issues when they are included in cell membranes. For example, transfats induce platelet aggregation, .…  inhibit activities of Na+ , K+-ATPase and adenylate cyclase and reduce density of B-adrenergic receptors in rat heart membranes [raise blood pressure]…. Recent evidence indicates that trans-fats promote inflammation…. Increased tumor necrosis factor (TNF) system, levels of interleukin-6 and C-reactive protein…. Several studies suggest that trans-fats cause endothelial dysfunction” in the 1984 thorough review by the Department of Agriculture.  Similar affects occur with polyunsaturated fats which are in vivo subject to oxidation.  In addition the high ration of omega-6 to omega-3 fatty acids has been shown to be atherogenic.   Similar association with CVD is associated with a diet high in fructose (but not other carbs).[30]  Hyperinsulinemia, IR, NAFLD, T2D[31] are contributory to endothelial dysfunction.  Like so much that goes on in the body, the causal mechanisms of these condition in the development of endothelia dysfunction is complex and thus process leading to pathology are tentative.  The associations with sugars, smoking, trans and polyunsaturated fats to endothelia dysfunction and CVD are firmly established.  These are the main culprits explaining strong association of CVD to the Western diet, they all promote endothelia dysfunction. 


So what about the standard explanation for atherogenesis?  Pharma’s case for LDL undergoing oxidative damage from metabolites within the tunica intima, and this being the most principle cause of CVD, this is suspect.  Suspect because it ignores pathogens, suspect because it ignores the immune role of LDL, suspect because it fails to explain cogently why LDL is actively transported in large numbers through the epithelial cells into the tunica intima; and downright misleading because it uses the dual meaning of “oxidative” to imply that the products of metabolism is causing the oxidative damage to LDL while in fact it is the toxins that are latching onto the external protein shell of LDL.  Their explanation fails to explain why there is LDL in the intima medial, and to explain cogently why the immune system is involved in the process.  Pharma’s KOLs state that the lymphocytes and macrophages are there to clean up the oxidized LDL—no mention of pathogens. The debris of this process results from the macrophages engulfing large numbers of the oxidized LDL and resultantly undergoing apoptosis that results in the formation of plaque.  Are we to believe in an atypical process involving pathogens, or to think the worse of pharma?  Given pharma’s repeated examples of tobacco science being generated by pharma to promote profits, the plausible conclusion is that this is one more example of bad conduct by pharma.  Pharma has already been proven to have generated the cholesterol and triglyceride myth (see Cholesterol Myth and 2nd article) and to support it pharma has created a factitious modus operandi.  Given the totality of evidence, the healthful choice is to ignore the recommendations of pharma’s KOLs and those, whom they have educated, the majority of physicians.   


 


                          14.  How Did We Get Here--Historical


The prima facie evidence is that the diet adopted by the FDA and Department of Agriculture in the 1977 brought on the health pandemics.  The switch to low fat, low cholesterol, which entails higher carbs, just so happened to favor the products of the food manufactures and the cholesterol lowering drugs of pharma.  In 1977 our government, and later those around the world, ignored over 60 years of dietary science and switched its position as to what is heart healthy.  Based on weak evidence, high serum cholesterol and triglycerides (3-fat molecules joined to 1-glycerol molecule) were accused of being the leading cause of CVD.


 Somehow the Senate panels (McGovern Commission) and their experts on CVD missed cigarettes which at a pack a day doubles the deaths from heart attacks.  The Surgeon General only warned about lung cancer and emphysema in The 1964 Report on Smoking and Health.  Over three times as many deaths are caused by tobacco induced heart attacks and strokes than from lung cancer and emphysema, yet the Surgeon General missed it and a large body of journal literature going back to the turn of the century.   Dr. Kellogg, of cereal fame, published in 1922 a 171 page concise compendium on the published research on tobacco’s known health consequences, including its destructive action on blood vessels, at.  Kellogg’s book has hundreds of scientific citations.  In 1965, 42% of the adult population smoked, yet the McGovern Commissioned missed tobacco.  So why was the evidence on tobacco distorted by the Surgeon in 1964 and ignored by our government in 1977, and why were saturated fats and cholesterol blamed? 


Simply follow the dollars.  Once you realize that serving the public is cloak worn by our corporatist state, than it makes sense, and when we review the details we find that this is standard operating procedure:  serve big dollars while advertising serving the public.  This method explains why our government fingered tobacco for lung cancer, but missed the much bigger killer from CVD:  they were doing damage control for tobacco.  The connection with lung cancer was too obvious, and too well known.  The Surgeon General had done damage control dressed as science in the public’s interest.  So why finger cholesterol and saturated fats?  Animal (saturated) fats cost twice that of vegetable oils; and sugars and refined starches are cheap and addictive.  And most of the products made by food manufacturers are loaded with refined carbs including sugars.   Moreover, pharma doesn’t have drugs to treat the pathogens living inside the artery walls which are the principle cause of AS and CVD, but with drugs they could modestly lower cholesterol and triglycerides in 1977.[32]  Thus pharma was by 1972 (and before) promoting hyperlipidemia and hypertension as causes for CVD and MI.  For example in the 1972, 12th edition of Merck Manual p.374 recommends restrict fats to 30-40 gm/day to lower CVD risk.  And the role of pharma gets more insidious.  If the patient believes X is a risk factor and he tries a cheap fix that must fail, then he is likely to go back to his physician and try patented drugs to fix X.  This is a standard business practice for pharma.  Diet does not significantly lower cholesterol, because the liver makes cholesterol to serve vital needs.  Only about 30% is from diet, lower it and the liver makes more on a need basis.  Moreover, saturated fats don’t raise cholesterol or cause CVD--see Dr. Miller’s lecture.  Thus the low fat and low cholesterol diet fails, so the patient with elevate cholesterol and/or CVD then tries drugs.  This plus the food manufacturers favor their high sugar and starch products over eggs, meats, poultry, and fish, because these foods are a very small part of their product line.  Secondly the vegetable oils are about half the price of animal fats.  The McGovern Committee and the US Department of Agriculture followed the bucks.[33]  The government’s inaction and at times support for tobacco[34] that permits harm from cigarettes is one more example of the power of tobacco (dollar) ethics in a pseudo-democracy, our corporatist state.  The science behind healthy diet was turned upside down by big money and we have a health epidemic.


 


15. Free will won’t, rational control of behavior will


On how to deal with food addiction which seems to trump rational control?  In 1985 applying the standard behavioral analysis for dieting:  I set down various types of behavior that would result in weight loss including food selection. Small portions, peer support, visualization, etc.  I held that thoughts (silent whispers) are merely epiphenomenon that accompanies behavior like a shadow.  Eloquent proof came 2 decades later; one was an experiment that was published in American Scientist (2004, Free Will, Free Won’t).  Electroencephalography was used to measure brain activity and a button was pressed by the participant to indicate when the thought occurred.  The deep brain activity occurred a half-second before the thought of his arm movement.  The thought of the action came after preparatory subconscious neural activity, like the thunder following lightening. Neurological science has since established that thoughts are generated by deep brain processes and accompany an action like a shadow.  To begin with neuroscience has demonstrated that the brain is modular, each of the hundreds of sections has a specific function.  One of these modules functions to create an image of man as being guided by thought.[35]  But rather in the verbal sections of the brain is not aware of what goes on in the motor sections of the cerebellum which acts as a traffic cop coordinating behavior.  In other words the brain has hundreds of specialized modules I call the analytic portions (AP) that function to produce verbal behavior including thoughts.  Thoughts has been by B.F. Skinner labeled as silent whispers.  Consider the behavior process similar to vector algebra (see graphs above on website) where several different forces are acting simultaneously on an object at a point, the result of which will be movement of the object in only one direction.  The deep brain operates according to the diverse force to produce behavior, sometimes contrary to the input from AP.  For diet, based on a complex collection of evidence, the AP has determined that sugars and starches need to be avoided.  At home the AP opposes the eating of refined carbs and sugars, but its contribution to eating choices isn’t sufficient to consistently throughout the day bypass the grapes and candies.  Thus I must influence the arrows of forces in my brain so that at home there aren’t foods high in refined starches and sugars.  The explanation from behavioral psychology:  the closer in time and space to a reinforcer, the greater is the probability that it will affect behavior.  The AP plots that I need to stock the kitchen with items that aren’t high in refined carbs and high sugars.  I also enlisted my wife to use social reinforcers such as praise and she too has changed her diet.  We watch the video Sugar White Poison and other like videos every week.  The AP has set out a program by which I can change my eating behavior life-long.   Moreover, given my extensive education and application of academic skills, my AP is stronger than the norm. 


If it were true that the will (mind, AP) could decide independent of the deep brain process, then there wouldn’t be smokers, drunks, and an obesity epidemic, and certainly there wouldn’t be so many morbidly obese (about 10% with a body mass index, BMI, over 40).  Today I saw a women under the age of 30 whose weight forced her to rely upon a wheel chair.  Does she have a defect in her will (mind)?  Or is it a confluence of genes coupled with dietary causes that have reset her normal weight to a BMI of over 50?  She can think of losing weight, swear that she will, go on a diet, but the deep brain is committed to 400 lbs. and gaining.  The low fat, low calories diet is not her long-term answer.   A bariatric operation is one way, but her stomach will expand sufficiently to accompany many small meals and about half will regain most of their former weight—as two of my friends have done over a period of 6 years.  The wrong expert information spread by doctors and the media has the AP applying a low fat diet with more exercise as the healthful program, and they gained back their weight.       


 


16 Outline on metabolic dysfunction 


This page 6/9/16, is on http://healthfully.org/rc/id23.html


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 is high carbs fructose and glucose that causes a fatty liver (NAFLD) which mucks up the regulatory systems leading to the IR that causes obesity, T2D, CVD, etc.  Glucose raises insulin level, and insulin causes cells to STORE FAT and burn glucose.  IR causes excess fat storage.  Causes:  The carb fructose--a simple sugar--goes to the liver where some is converted to fat, and when insulin is high this fat is stored in the liver.  The low fat, thus high-sugar, high-carb Western diet will for most cause excess fat storage in the liver.  Gradual over the years/decades 2 to 3 pounds of fat is stored in the liver (NAFLD).  This causes IR first in the liver then in other tissues.  IR mucks-up the complex metabolic systems.  With IR comes a gradual gain in weight.  If you have T2D then you have excess fat in the pancreas, and your beta cells no longer produce sufficient insulin to manage your glucose.  When on an energy-restricted diet the fat tissue through the 4 hormone it produces functions to maintain current weight by increasing appetite and reducing metabolism.  Even after losing weight, the system works to restore the fat—the yo-yo diet.  Goals:  to stay in fat burning (low insulin) mode and thus to metabolize the excess fat in the liver and pancreas to reverse IR and T2D.  Once fatty liver & IR are cured than carbs can be moderately increased and weight will still be lost.  Once ideal weight is obtained remain on moderate carb-sugar diet.  Follow the dollars and you will find out why we have the Western diet and the wrong advice—click on link for a list of the misinformation, and much more. 


Fix:   Short-term fasting with low carb diet to stay in fat burning to cleanse the liver and cure NAFLD & IR.   


   Fructose converted to fat in the liver and high glucose via insulin causes fat storage in liver (a 1-2 punch)


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


T2D can be cured with diet.  For example in the first 2-weeks following bariatric surgery over 80% with T2D are cured before major 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 easily digestible carbs.         


17.  Review and recommendations


Glycation cause tissue damage especially in the liver from fructose which leads to IR, fatty liver, & chronic age-related conditions.  High blood glucose causes a 2-hour spike in insulin contributes to IR and NAFLD.  The Western diet with its combination of sugars and refined carbs causes obesity.  Fructose, one-half of sucrose, is the worse sugar (see #4 above).  The traditional Japanese diet is high in carbs but has almost no sugar (15 gm, compared to U.S. 162 gm daily average).  Their carbs from white rice are slowly absorbed because of the large portion of vegetables (fiber) in their meals, and they have a low (healthful) omega-6-to-3 ratio.  The Western diet is also high in polyunsaturated fats, another bad thing.  Their obesity, diabetes, and CVD rates are very low for those following a traditional diet, though many smoke.  The Western high sugar-starches diet is a deadly combo that eventually upset the mechanism that controls appetite, metabolism, and fat storage, and it creates a craving for sweets and other carbs.


Size of portion, rate of absorption, and the amount of exercise prior to and subsequently, these determine the blood sugar and insulin levels.  Avoid large meals and refined carbs to keep insulin low.  Eat frequent-wholesome snacks.  Increase fiber, protein, and the good fats because they delay clearance from the stomach of the carbs; thereby reducing the spike in both glucose and insulin.  Low insulin is for fat burning; low sugar for healthy liver.  Check nutrition labels for the percentage and grams of sugar.  Four grams of sugar equals one teaspoon of sugar.  Avoid manufactured foods with their refined carbs, added sugar, and polyunsaturated fats.  The cure is to go on a very strict low-sugar-low-carb diet (20% of calories from carbs) with small portion (thus low insulin), and also include JK’s 16 hour short fast.  Select the appropriated diet program in Section #2.  You should take better care of your body than your car!


Besides diet, exercise and physical activity contribute to controlling weight and remaining healthy.  In addition there are supplements and drugs that reduce damage from reactive chemical.  Best are Aspirin, CoQ10, vitamin C, & omega-3 fatty acids fish oil—in that order.  Aspirin 325 mg has an assortment of health benefits including reducing the risk of most cancers over 30% by enhancing the action of our body’s system for the destruction of abnormal cells, and aspirin also inhibits the development of AS.  Natural hormone replacement therapy (NHRT) for women and elderly men testosterone in sufficient dose is highly recommended.  These hormones promote weight control and the motivation to be physically active.  Go to their links above for the best usage and their benefits, and you will understand why pharma has with junk science opposed their usage.  For more info, there are links to statins, cholesterol myth, CVD, carbs, fats, and a video library. The video page has links to documentaries and books confirm my claims.  Watch on YouTube CBC on sugar and Australian Broadcast corp.  I Google Chromecast the documentaries to my television which has a stereo connected. The recommended healthfully section has over 1,000 pages involving over 10,000 hours of research and studies of subjects, and counting. To check my research, the articles I wrote have links to medical journals, and a number of their articles are pasted on the website.  The site covers a number of family of drugs, diet, and some very healthful drugs that pharma opposes.  The research exposes a very flawed corporate information system; on point are Marketing Science and Junk treatments.  The global corporate profits-first system produces perverse results including regulatory capture.  Pharma, alcohol, tobacco, manufactured-food, and GMO companies such as Monsanto, cause the greatest harm.  Knowledge is the starting point to better health.  You should take better care of your body than your


 


18.  Videos & books On diet, bad pharma, and CVD  


The page is at http://healthfully.org/rc/id22.html, rg/4, and rh/id7 for the complete, current collection


Videos are the best method for teaching and reinforcing the lessons within this article.  I have collected with summations a list of over 130 videos on health related topics, the largest section is on diet.  Please view them.   For a list of books on diet, bad pharma, and related topics click on link.  You should take better care of your health than your car.




[1] “f the human body relied on carbohydrates to store energy, then a person would need to carry 31 kg (67.5 lb) of hydrated glycogen to have the energy equivalent to 4.5 kg (10 lb) of fatWiki.

[2]  It is not just the race of Mongoloids, for a number of tribal societies consume a high-carb diet without Western consequences. 

[3] In 2000 the USDA placed added sugar at 152 lbs/year, that doesn’t count sugar from fruits and vegetables, thus about 200 lbs. yearly.  Being an average half the people are above average.  Nearly half that figure is fructose. 

[4] Estradiol and testosterone both promote bone remodeling, and thus are the most effective way to prevent osteoporosis and stop its progression.   The older medical literature confirms see estradiol and Testosterone.

[5] A high glycemic index diet with its sugars: ”Consuming higher GI diets was associated with > 3 fold higher accumulation of advanced glycation end products (AGEs) in retina, lens, liver, and brain in the age-matched mice, suggesting that higher GI diets induce systemic glycative stress that is etiologic for lesions” at 2011.

[6] Canada, Australia, and the UK have through documentaries warned the people about sugar. 

[7] The DNA is housed within a membrane in the nucleus to protect it from reactive chemicals such as fructose.  Another layer of protection is the mitochondria, a vessula for metabolism and the reactive chemical produced in the process.   

[8] NutraSweet for example uses low carb (not extreme) with energy restriction and weekly counseling—a bit like Weight Watchers.

[9] Long-term makes a different for after several years it is likely that their weight control system has reset to the obese level of fat.  Unfortunately, this conclusion is observational; viz., I have been unable to find significant research on this issue, as of now. 

[10] This is an important difference from the normal hunger, which with our Western diet is the up down blood glucose cycle caused by insulin clearing the high carb meal.  This type of hunger occurs even when at full energy.  It causes the Western graving phenomena:  3 meals a day with snacking in between meals.  Fasting with merely low carbs eliminates that phenomenon.

[11] The government clearly on the side of food manufactures and grain grower, expected that the Atkins low card diet would fare worse than the others (at least on cardiac measurements of lipids and blood pressure, it came out best); therefore the lead person selected for the study, Christopher Gardner, a long-term vegetarian, was clearly on the low fat energy restricted camp.  The results disappointed both.  In measurements of LDL, HDL where higher is better, blood pressure triglycerides and weight Atkins was best.  See Gary Taubes, Why We Get Fat and What to Do About It, 2009, p  190-192.

[12] “Energy expenditure attributed to physical activity increased by 10.2 ± 5.1 kcal/kg.d at wk 6 and 6.0 ± 4.1 kcal/kg.d at wk 30 [10.2 – 6.0 = 4.2 less energy expenditure when physically active (i.e., awake)] …. CONCLUSIONS: Despite relative preservation of FFM, exercise did not prevent dramatic slowing of resting metabolism out of proportion to weight loss. This metabolic adaptation may persist during weight maintenance and predispose to weight regain unless high levels of physical activity or caloric restriction are maintained.  Journal of Clinical Endocrinology Metabolism 2012

[13] There is an evolutionary reason why fasting doesn’t kick in the drop in metabolism.  Our ancestors when out of food need the energy to search and hunt for food.  Thus there is an increase in HGH and catechol amines to increase energy, improve mood, and mental activity.   People feel good when fasting because of these biological mechanisms.. 

[14] See my development of the topic at link, Dr. Jason Fung’s blogs, his book The Obesity Code 2016, and  in October 2016 The complete Guide to Fasting

[15] In a testimonial (Richard’s Story) of Richard’s, his wife who is only obese states that she uses the short term fasting.  I then wrote Dr. Fung, and he replied that the clinic also uses the short-term fasting and the results are similar.  

[16] Kidney failure is one of the 4 major comorbidities caused by late stage T2D, the others being cardiovascular disease, and two related to leaking capillaries, namely blindness and leg amputation. 

[17] Seniors, much more than people under the age of 60, experience postprandial a major decline in energy because of the major reduction in metabolism by the mitochondria as it switches to glucose metabolism to produce the energy molecule ATP.  The lower store and reduced rate of production of ATP has profound effects upon seniors.

[18] As I age (73 years in 2016), the diversion of energy and blood to promote digestion entails a low point after eating a full meal.  

[19] Leptin is produces by the fat (adipose) cells and among its functions is the restoration of fat to the set level.   

[20] This topic is masterfully covered in the two books of Dr. Jason Fung, The Obesity Code, part 2, p 29-66, and The Complete Guide to Fasting, 97 to 109.  Repeated failures accounts for the reluctance of seniors to try one more time.  

[21] This could well make a daily skipping of breakfast equal or better than alternate day fasting.  There is journal evidence to decide this possibility.  

[22] I two friends have lost significant weight on one meal a day.  One a Dr. Evans lost over 150 pounds, and both kept the w eight off.   

[23] See Gary Taubes, Why We Get Fat and What to Do About It, 2009 pgs.  19-24.

[24] Part of the estradiol produced is converted to testosterone, and testosterone maintains muscle.  Reduced muscles are replaced by increased fat.  Less muscles increase the sedentary lifestyle of women who aren’t exercise addicts. A similar issue for elderly men and testosterone.  Both hormones significantly reduce the risk atherosclerosis and its comorbidities, osteoporosis, arthritis, dementia, some cancers.  This explains why pharma is against hormone replacement therapy. .  

[25] Pharma is against hormone replacement, and thus too are most doctors.  You must tell your doctor that a friend (me) has great success by raising his testosterone to a youthful level (above 700 ng/dl) and you want to do the same.  From a compounding pharmacy ¼ tsp. of 15% lotion (60 gm/mo.).  Tell him that you are willing to be at greater risk of prostate cancer and heart attacks which is what your doctor believes.  Both are false, and the opposite is the case, but pharma is against health and has generated junk science with the support of our government.  Androgel, the strongest of pharma’s testosterone products is less than half the dose required for significant benefits.  See Gary Taubes Why We Get Fat, his account of Wades rat, p 89-94, and elsewhere, where he discusses sex hormones’ roles in fat distribution.  Testosterone improves muscle tone, mass, and mood, for active lifestyle.  

[26]   "’Science’ done on behalf of an interest defending its cash cow from overwhelming credible science that shows it is harmful or detrimental to public benefit in some way at”.  Through the use of KOLs and supported by government and corporate media the industry or corporation can frame the discussion of the subject and discredited or worse critics.       

[27] “Like ethanol, fructose increases de novo lipogenesis (DNL), inhibits fatty acid oxidation, and has been implicated in NAFLD” at

[28] Girls during menarche put fat on their buttock; and women abdominal fat following menopause—like men.  Steatopygia (huge butt) is a sexually selected trait among African pygmy women, which occurs following menarche.  It is an extreme example of the effect of estradiol—see Gary Taubes Why We Get Fat, and What to Do About It, p 63, also read Wades experiments on rats.   

[29] Why veins are immune to formation of plaque and endothelial dysfunction is due to the much lower blood pressure in the veins.  Just how the higher arterial blood pressure effect endothelial cell functions remains a mystery.  Evidence for the role of increased blood pressure resides in the fact that when a section of vein is transplanted to a artery in a bypass operation approximately half of them will be subject to atherogenesis.   

[30] The traditional diet of the Japanese which is very low in sugar, though high in carbs, has a far lower incidence of CVD.  Some primitive tribes have a high fruit diet, yet they too have very low rates of CVD.  The likely reason is the seasonal nature of fruits, which thereby entail that those peoples do not develop IR and NAFLD which requires years to develop.  The body thus has time to burn the excess liver fat before it accumulates to a pathological level. 

[31] T2D affects the adhesion between adjacent endothelial cells thus causing them to leak.  This phenomena results from the high the leaking of blood, especially in the lower legs & feet, the eyes, and kidneys.  T2D is the leading cause of amputation of legs, and major cause of kidney failure, and blindness.  

[32] Moreover cholesterol and triglycerides are not causal associated with CVD, and pharma doesn’t profits from preventing disease, thus they with their KOLs created the lipid hypothesis for CVD.  Worth reading is chapter 3 of Good Calories, Bad Calories by Gary Taubes, 2008, which goes describes 2 major clinical trials and McGovern Commission’s agenda. 

[33] The Soft Science of Dietary Fat, Science Vol. 291, 3/30/01, Gary Taubes; and also in his 2 books Why we get fat & Good Calories. 

[34] One example was that during WWII there was a program for the distribution of free cigarettes to the fighting soldiers.

[35]  Chapter 3 and 4 of Who’s In charge?:  Free Will and the Science of the Brain, by Michael Gazzaniga, is on how “the interpreter” part of the brain gives us the story of thoughts leading actions.  


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5. On sources of energy, sugars and fats the bad and good


With the Western diet yearly sugars consumption all sources has gone from 35 lbs. in 1909 (43 gm/day) to 151 lbs. in 2010 (751 calories/per day or 188 gm/day) to cause the diabesity (diabetes and obesity) pandemics.  Table sugar (sucrose) is hydrolyzed in the stomach into fructose and glucose, starch in the stomach to glucose.  Glucose and fats are the body’s main sources of ATP (energy)—other monosaccharides such as galactose and amino acids the remaining 10%.  High blood glucose (a bad thing) is down regulated by increased insulin (also bad) which sends a message for the body to burn glucose and thus store fats.  High insulin levels in response to high glucose will over the decades cause insulin resistance (IR, a reduced response to insulin) in insulin receptor on cell walls.  This is a way of cells to limit its amount of sugar to a safe level.  IR caused high serum glucose results in more insulin secreted by the pancreas.  IR increases fat storage. Gradually many of those on a Western diet accumulate 2-3 extra pounds of stored fat in the liver, nearly doubling the weight of the liver which normally weights 3.2 to 3.7 lb.  This causes mild liver inflammation and what is clinically called Non-Alcoholic Fatty Liver Disease (NAFLD) the starting point the comorbidities from MeS and cirrhosis of the liver (see section 6 on NAFLD).  excess fat in the pancreas eventually causes a decline in insulin production that result in T2D.  High insulin from IR also causes low leptin a hormone which among many things increases appetite by stimulating the control center in the brain, and leptin also lowers metabolism—2 causes for obesity and the yo-yo diets.  The other problem is the table sugar sucrose, a disaccharide of fructose and glucose.  Fructose in sucrose attaches randomly to proteins in a process called glycation at 7.5 times the rate of glucose.[1]  Glycation damages proteins—the main cause of age related chronic conditions.[2]  Fructose is metabolized only in the liver where it damages the liver by glycation resulting in IR in the liver. With the Western diet’s high carbs, some of the fat in the liver is stored there.  Some of that fat comes from the conversion of fructose to fat and some from conversion of glucose to fat in the liver.  This fat de novo synthesized fat driven by high insulin causes a gradual accumulation to cause NAFLD.   In other words, if more fat is made than the liver can use, and there is high insulin due to glucose, this fat accumulates in the liver cells to cause non-alcoholic fatty liver disease (NAFLD).  This fat in cells reduces liver functions, as too dose glycation by fructose and glucose; this double assault on the liver adversely affects the many functions of the liver and thereby contributes to IR.[3]  NAFLD with its IR is the main cause of a group of conditions labeled metabolic syndrome (MeS):  NAFLD, IR, and T2D, and its sign obesity (pharma adds the non-metabolic high cholesterol and the resultant hypertension and CVD—for marketing of their drugs).  


Fructose:  The very reactive sugar fructose is the starting point for the diabesity pandemic.  As stated above fructose, which accumulates in the liver where it is metabolized, it damages the liver through glycation and fat accumulation.  In the US we have gone from 15 grams per day, mainly from fruits, in 1900 to over 90 grams a day (hh.edu  at) mainly from sucrose and HFCS (high fructose corn syrup).  We have not evolved a system to handle this load since our ancestors only ate moderate amounts of fruit, and in the wild they were smaller and far less sweet.    It isn’t the glucose half of the disaccharide sucrose that is the problem, since grains are pure glucose and mostly paleo peoples eat a high carbohydrate diet.  Paleo peoples on a traditional diet have a fasting glucose level that is much lower than our norm; for example, the Tokelau off of New Zealand their average is lower than the bottom 10% of the Swedes.  It isn’t the carbs but the fructose.  The Western diet overwhelms the repair system for damage proteins by glycation.  The traditional oriental diet is high in carbs (up to 75%) but low in fructose (14 grams or less) and as expected their incidents of obesity, CVD, and T2D is quite low, especially among those who don’t smoke.  Fructose among other things damages the liver (see next section) and this is the starting---watch the documentaries on the health consequences of sugars—link.


2) Starches are molecules made up of chains of the sugar glucose; their rate of absorption during digestion varies according to their structure.  Some have a much lower rate than sucrose, and are called resistant starch; thus not all carbohydrates are equal—for tables and more on carbs.  Fiber is a very resistant starch, which lowers insulin by slowing digestion.  The portion of and type of starch in meals affects serum glucose, as too the rate of stomach clearance.  Fats, resistant starch, and proteins in the meal, they slow stomach clearance, thus extending the time in which glucose is absorbed by the duodenum; this lowers the blood insulin spike—a good thing.  There are a number more good things you can do:  see section #12, why some don’t get fat. 


3) Fats, like carbs, are not all equal.  The right fats are the best source of energy.  Two fats are bad:  trans-fats and polyunsaturated fats.  Trans-fats are not natural, but are man made by a process of hydrogenation of polyunsaturated fats.  Their abnormal shapes entail that they don’t function very well in cell walls—a bad thing.  For the same reason polyunsaturated fats are a bad thing.  This is because of their multiple double bonds in the carbon chain (why they are called polyunsaturated).  These double bonds are available to be bonded with reactive chemicals in a process called rancidification, which changes their shapes.  This oxidation can occur on the shelf, it is accelerated when heat is applied as when baking or frying foods, and in the body where reactive chemicals are made during biological processes. The rancid fats, just like trans-fats, don’t function properly in cell walls—a bad thing.  Rancid fats are casual for many, if not most, of the maladies associated with the Western diet.  Rancid fats has been shown, for example as a causal factor for NAFLD, and thus all the comorbidities associated with a fatty liver.  The extent of the health has, like drug side effects, not be a priority of funding.  The evidence is found in scientific studies published in journal:  for rancidification see #25 and for trans-fats (from hydrogenated vegetable oil) see #27.  Another issue arise because polyunsaturated fats are that they are high in omega-6 fatty acids.  The omega-3 fatty acids EPA & DHA are used to limit the immune responses, thus they lower risk for AS & CVD, but too much omega-6 competitively blocks omega-3 usage--a bad thing.  Hunter-gatherer societies averaged about 2 parts omega-6 to one of omega-3; in the U.S. it is 16 to 1 (a bad thing).  Vegetable oils (except from palm & olive trees) are very high in omega-6.    Like trans-fats, the body lack enzymes to metabolism them; thus both types of fat cause AS and thus CVD.  Food manufacturers and restaurants use both of these bad fats.  This leaves us with the safe saturated and monounsaturated fats.  Over the years, data revealed that dietary saturated fatty acids (SFAs) are not associated with CAD [coronary artery disease] and other adverse health effects” in journal.  The same in Wikipedia: ”There is s no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD” which is based on a meta study of 21 journal articles--and they taste much better.  Saturated fats are best source of energy—see Prof. Miller's for list of their 6 essential functions.


Proteins, though rated at 6 calories per gram, under normal conditions they are not appreciable metabolism for energy (ATP).  However during starvation they are used in the production of ATP.  The cells switch from storing to metabolism amino acids (the building blocks of proteins) when fats stores are depleted to 4%. 


 


6.   Fructose alcohol without the Buzz


Fructose is toxic to the liver like alcohol:  Prof. Lustig a leading research on childhood obesity in his The Complete Skinny on Obesity states:  “fructose is a poison like alcohol.”   He then explains why it is addicting and how it damages the liver.  The same is repeated in a series of lectures and documentaries of his on YouTube, and UCTV—link to list.  Both are metabolized in the liver, and through various processes compromise liver functions.  And like ethanol the quantity consumed determines the toxicity.  (For detailed review of the scientific evidence on how fructose causes insulin resistance)  Fructose is 15 times more reactive than glucose, and through the unregulated attachment to proteins it damages protein.  Over a 2 hour period of bolus of fructose compared to a bolus of glucose will result in 15 times more bonding to proteins.[4]  Science it accumulates in the liver where it is metabolized the liver more than other organs are damaged. This process is called glycation (see section 2, definitions).  That is the first blow to the liver.  In the liver when the insulin level is high, and there is an excess fructose from sweets, some of the excess is converted through de novo lipogenesis to fat along with lipogenesis of the excess glucose and this excess fat because of insulin is stored in the liver.  Very slowly this fat on a typical Western diet accumulates to a toxic level (2-to-3 pounds), and becomes a clinical condition known as non-alcoholic fatty liver disease (NAFLD).  The two work together, fructose and insulin (in response to blood glucose) to cause NAFLD.  See the next section for the pathologies NAFLD causes.  An important point to tease out of the many studies is that it is not the high carb diet itself that is causal for IR and NAFLD, but the inclusion of fructose in that diet.  A proof is that those on traditional diet of Japanese, Chinese, and Okinawans diet all of which are above 70% calories from quickly absorbed carbs from white rice, noodles, and/or Oriental yams, they have about a 1% risk for type-2 diabetes, NAFLD, and obesity, and a low rate among those who don’t smoke of CVD.  Sugar, which came from fruits and vegetables, amounted to an average of just 14 grams a day.  It was the addition of fructose from sucrose to their diet that has changed all that, their rates of obesity and T2D has soared.  Numerous lab experiments have shown that fructose causes liver changes leading to IR. High fructose sugar diet is the cause for the diabetes pandemic.   


Number can be misleading:  USDA chart:  The per-capita yearly consumption of ADDED sweeteners was 109 lbs. in 1950 and 152 lbs. in 2000.[5]  With the major reduction in corn syrup (pure glucose), which has been replaced with HFCS (high fructose corn syrup) our fructose consumption has doubles.  Thus the harm done is far greater than the increase in 43 pounds of added sweeteners would indicate.[6]


But this is only the picture of why Dr. Lustig calls sugar white poison, and should be regulated like alcohol.  Glycation is not just limited to the liver.  It is a major cause of age related conditions. I just found an article describing how it degrades the quality of cartilage and affects bone metabolism, at 2013.  Prior to that I though the increase in osteoporosis and joint problems was driven by the chemical bath we are subject to in drugs and food additives. Now it seems that glycation by fructose is the main culprit.  Glycated substances are eliminated from the body slowly.  On a high sugar diet, the renal clearance is only about 30%. This implies that the half-life of a glycation within the body is about double the average cell life. Red blood cells are the shortest-lived cells in the body (120 days), so, the half-life is about 120 days. (This fact is used in monitoring blood sugar control in diabetes by monitoring the glycated hemoglobin level.)  As a consequence, long-lived cells (such as nerves, brain cells) and long-lasting proteins (such as DNA, eye crystalline, and collagen) may accumulate substantial damage over time. Metabolically-active cells such as the glomeruli in the kidney, retina cells in the eyes, and beta cells (insulin-producing) in the pancreas are also at high risk of damage” Wiki. “It appears that fructose and galactose have approximately ten times the glycation activity of glucose, the primary body fuel.[7] Glycation is the first step in the evolution of these molecules through a complex series of very slow reactions in the body known as Amadori reactions, Schiff base reactions, and Maillard reactions; which lead to advanced glycation end products (AGEs) Some AGEs (advanced glycation end products) are benign, but others are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as cardiovascular diseases (the endothelium, fibrinogen, and collagen are damaged), Alzheimer's disease (amyloid proteins are side-products of the reactions progressing to AGEs),[7][8] cancer (acrylamide and other side-products are released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination).  This range of diseases is the result of the very basic level at which glycations interfere with molecular and cellular functioning throughout the body and the release of highly oxidizing side-products such as hydrogen peroxide.  Long-lived cells (such as nerves and different types of brain cell), long-lasting proteins (such as crystallins of the lens and cornea), and DNA may accumulate substantial damage over time. Cells such as the retina cells in the eyes, and beta cells (insulin-producing) in the pancreas are also at high risk of damage“ Wiki 2015.  Also under-rated is the role of glycation in retinopathy, nephropathy, and endothelial dysfunction[7] in diabetics, and the over attributing to reactive oxygen species created by metabolism—see  Protein Glycation, A firm Link to Endothelial Cell Dysfunction.  Endothelial dysfunction is the immediate cause of CVD, see section 12.  Fructose also chelates minerals in the blood. This effect is especially important with micronutrients such as copper, chromium and zinc.  Since these solutes are normally present in small quantities, chelation of small numbers of ions may lead to deficiency diseases, immune system impairment and even insulin resistance,  a component of type II diabetes (Higdon)” Wiki 2012.[8]  Yes, the lipid (cholesterol and fats) hypothesis another  example of pharma and the food manufacturers framing the discussion to promote their  profits.    


 


7.  NAFLD and IR are the gateway to MeS and its comorbidities


NAFLD its development:  NAFLD requires both high carbs and high fructose.  That it takes both is confirmed by Japanese and other population that eat a traditionally high-carb diet, but with very low sugar—for the Japanese 15 grams per day, and similar amounts for the Okinawans, and Chinese .  These populations have a low rate of CVD and the other age related conditions associated with the Western diet.  And there is direct evidence:  a couple of experiments done within a hospital where young healthy volunteers were fed for 2 weeks either high fructose or high glucose, this confirmed the role of fructose, but absolved glucose as to the development of IR.  So how are the two sugars different?  The difference is because of the fructose which is metabolized only in the liver where it is converted mostly to glucose and some fat.  Fructose is also 7.5 times more reactive than glucose through the process of glycation (see definitions section 2), and its slow clearance from the liver compared to glucose doubles that figure to 15.  Glycation damages the liver, and too much fructose causes inflammation and other signs of liver injury such as high ALT, a blood marker for conditions of the liver.  ALT is commonly used as a way to screen for liver problems.  AST another liver marker is commonly also tested for in blood work, and it too test high from a diet with excessive fructose.  A diet high in fructose is likely high in the sugar glucose both from sucrose.  Starch consists of long chains of pure glucose.  A diet that is high in carbs is necessarily low in fats.  So depending on needs of other tissues (fats and cholesterol are essential for cell membranes) the liver will convert in some of the glucose and fructose through de novo lipogenesis into fats.  Because of the high insulin from IR in the liver and a high carb diet, the high insulin accelerates the accumulation of fat in the liver.  This high carb-sugar diet causes IR in the liver and thus the gradual accumulation of fat in the liver.  The regulation of blood insulin which in part involves the liver, such as through the production of glycogen, will contribute to an excess of blood glucose, which causes other cells, principle the muscle and fat cells to become resistant to insulin.  For those who stay on the high carbohydrate Western diet this is likely to progress to obesity, NAFLD, MeS, and obesity.  Two studies of those with NAFLD found that they consume 2-3 times more fructose than those without NAFLD—at, and.   AGEs (advanced glycation end products) in the liver and elsewhere are recognized as foreign substances by the immune system and can in sufficient number produce significant inflammatory response.  The attributing of excess fat in the liver as the primary cause for liver inflammation is questionable given the co-existence of AGEs in the liver and the natural inflammatory response by the immune system to AGEs.  Insulin resistance is like drug resistance where the body responds less to a given dose of a drug, for example alcohol, and a higher dose is thus required for the desired effect.  With insulin resistance the normal level of insulin fails to sufficiently lower serum glucose, and the pancreas thus releases more insulin to obtain the ideal fasting serum level of glucose.  This abnormally high level of insulin slowly causes the body to store more than the normal level of fat.  White adipose (fat) tissue (the most common kind) produces hormones which regulate the level of fat.  With insulin resistance this regulatory system is reset to maintain the weight gained.  High fructose and high glucose from the Western diet is what has led to the diabesity (obesity & diabetes) epidemic. 


 


Fortunately there is a repair mechanism for NAFLD IR T2D, and obesity, to simply go on a low insulin diet.  This requires fasting made more effective by low fructose and other carbs.  As stated before fasting keeps insulin low and thus keeps the body in the fat burning mode.  Fasting is why about 80% of those who have undergone bariatric surgery cure their diabetes and insulin resistance within the first month. This is because they can’t eat during the first couple of weeks following surgery.  Follow the appropriate fasting programs listed in section 3 duplicates the process that cured those who had bariatric surgery.  And it gets better as the weight goes away the body heals itself, old damaged cells from glycation are replaced with cells whose protein haven’t been damaged.[9]


 


8.   Why fasting with low-net carbs diet for obesity & T2D


There are two common general approaches to dieting, caloric energy restriction (CER) or carbs restriction of which some are the extreme low carbs, the ketogenic (Atkins type) diet without CER—and there are of course many variations of these types of diet.[10]  A third approach, fasting is growing in popularity, mainly in Europe. Unfortunately nearly all of the long-term[11] obese have had their weight regulatory system compromised; it functions to restore weight loss by causing a 25% reduction in metabolism or more, and an increase in hunger through a hormonal system involving insulin and leptin.  Typically around the end of the 2nd month (see chart above), their progress is greatly diminished because of the fat restoring hormone leptin.  Only those with extreme calorie restriction will continue to lose significant weight.  However, once off their diet the weight will be gradually regained (the yo-yo diet).  The main cause is the hormone leptin which is secreted by adipose (fat) tissue; it functions to main the normal level of fat storage.  Leptin intercedes to decrease metabolism--typically 25%-- and through this effect increases appetite.  The dieter feels that if he eats more, he will be mentally sharper, happier and have more energy[12].  A trial was run to compare the CER to the carb restricted diets.  In the funded by government[13] Stanford University international A to Z Weight Loss Study which compared 4 popular diets, Atkins had the best results both in weight loss, blood glucose, and lipid profile.  At 2 moths all 4 cohorts in the trial experience a marked reduction in the rate of weight loss.  At 1 year, the length of the trial, Atkins (ketogenic) cohort loss 9.9, LEARN 5.5, Ornish 5.3, and Zone Diet 3.3 pounds—see JAMA 2007.  Another trial had similar results this time using overweight volunteers:   9.4 kg lost on low carb (20 gm daily) versus the low fat 4.8 kg, at.  In this trial both groups reduced calories between 500 to 1000 calories daily.  In both of the clinical trials the lipid profile and blood pressure were much better for the low carb (thus high fat) cohorts, and more importantly their level of blood sugar improved on the low car diet.  “Insulin levels dropped and insulin sensitivity was restored” (Fung p 101).  A recent journal article interviewed the 2009 group on the television show The Biggest Losers.  A group of 13 morbidly obsess participants were in a boot camp which had an extreme energy restriction, control of foods, and a major exercise program.  They too experienced a major reduction in the energy expended when physically active, a 40% decline.[14] The 5-years later journal review article found that all but one of them regained at least most of their lost weight--see.  A longer period would have produced a bleaker picture.  A large 2015 UK population study of the obese found that 99% of long-term obese adults who lost significant weight that at the end of nine years they were again obese or at best overweight.  The UK data bank lacks information on type of diet, however, it did list those who had bariatric surgery and they were excluded from the study.  But given that the KD is sufficiently popular in the UK, on the face of it, it seems that long-term the Atkins’ maintenance phase was poorly adhered to.  So why did the KDers fare long term?


 


The KD views obesity as a problem with fat storage, and attempts to solve it long term by forcing the body to metabolize fat.  The most popular of these is the New Atkins which calls for moderate protein and uses net carbs (table section 3) instead of total carbs.  It also calls for a lifetime maintenance phase of low carbs.  Its limited success is because of moderate protein consumption.  Eating foods with protein causes the release of insulin through the incretin system of hormones. As stated in the definitions Section 2 above:  Incretin: class of hormones secreted by the stomach and intestines which case insulin secretion and satiety.”  The release of insulin interferes with the process cleansing the excess fat in the pancreas and liver.  Even with significant weight loss, those with advanced T2D are still dependent upon medications though less.  Unfortunately, KD also has a compliance issue:  like CER, typically have over half the dieters quit before one year.  Moreover both diets for the long-term obese, the diets aren’t sustainable.  As stated above in the CER paragraph above, energy drops and quality of life declines typically about the 8th week and this occurs with the KD.  “Long-term studies of the Atkins diet failed to confirm the much hoped-for benefits” (Fung p. 102). The failure of both diets to have sufficiently long periods of low insulin and thus to cleanse the liver and pancreas of excess fat and permit these organs to heal, this is why the leptin system for maintenance of fat kicks in to restore weight.  In other words they haven’t fixed the lipogenic system where fat tissue releases leptin to restore the level of fat.  So how can the long-term obese and overweight reset their weight regulatory system? 


 


Fortunately, there is a fix:  those who have used fasting in addition to low carbs have had remarkable success. Though not a major player, it has in the 5 years increased and at least in the UK gained the status of a fad diet because of Dr. Michael Mosley of the BBC, his 5-2 fast.  In Europe and Australia where BBC, ABC, and other networks have aired programs extolling fasting, and books there have a greater share their market, more people have tried fasting.  The results from fasting are striking.  Only fasting causes extended periods of low insulin.  During these periods the body cleanses the liver and the pancreas of excess and thereby cures IR and T2D which drives obesity.  For example, those with bariatric surgery have low insulin because they are fed intravenously, and most of cured of type-2 diabetes within the first 2 weeks. 


There is no drop in metabolism thus weight loss is steady, and the weight-regulatory system is reset.[15]  Once the desired weight is obtain the patient needs merely only to limit sugars and other refined carbs.  There are a number of different approaches from modest food intake to total near restriction of caloric foods.  The most thoroughly research fasting diet is that of alternate day fasting with near zero carbs and proteins, thus no rise in insulin.  Compared to CER and low carbs, its prolonged periods of low insulin make all the difference.[16]  This type of diet will typically within 3 months result in the burning of fat in the liver and pancreas and thus cure IR and T2D and causes the weight regulatory system to eventually adjust to the lower weight.  Proof is found in the success of Intensive Dietary Management—a medical clinic in Toronto Canada-- in curing both obesity and T2D.  The clinic uses low carbs and fasting. Their success, success of others and the journal literature is convincing short-term or alternate day fasting is the best treatment for the obese and the diabetic.[17]  The clinic’s principle scholar is Jason Fung, a nephrologist[18].  He sees end-stage diabetics, and with the clinic’s fasting and diet program he is able to get them off their insulin injections and other drugs to cure their diabetes.  The merits of low carb with alternate day fasting is not merely a theory like calories in and calories out but one which has supporting clinical trials and animal experiment—see the 2014 summation article, running 16 pages with 8 more for reference by Metabolism and Diabetes Research Group of the University of Surrey, UK, at.  To make accessible confirmation of the above claims, excerpts from this article are pasted at link and my review article on fasting at.


 


9.   Fasting is easy and essential


I never had a protracted weight problem.  By chance I had used the short-term fast when I gained 20 pounds during the winter of 1969-70.  At the age of 26 my metabolism slowed down, and so I didn’t burn off rapidly the excess glucose and fructose.  I had developed a fatty liver, and thus was putting the pounds on.  It took 3 months of reduced meals and fasting to lose it.  It stayed off because it was short-term weight gain:  my white adipose tissue through leptin had not rest my weight to 170.  After that, whenever I gained 5 pounds, I simply cut back on portions, quit eating by 7 PM, and skipped breakfast several times a week.  The second change was exercise.  I moved from Winnipeg to Southern California and became in 1975 a sports addict.  I started playing volley ball and cycling, then over the next 7 years I added moderate weight training and singles racquet ball.  In 1993 my diet changed for the worse:  following the lead of a very fit friend Robert Fischer, I went on a very low fat (thus high carb) Western diet.  Fortunately I watched my weight, thus I never went more than 5 pounds above my youthful weight.  Skipping breakfast is easy.  In 2012 I watched Prof. Lustig lecture on YouTube, which had gone viral.  He explained why sugar was poison and I took notes.  In 2013 I researched his explanation of the diabesity epidemic.  In the spring of 2014, I reduced sugars including fruits, and carbs from grains, thus I increased fats.  It took 4 months before candies, fruit juices, ice creams, and sweet melons tasted way too sweet.  Though my weight remained for decades the same, I had 3 pounds more around the lower abdomen than when I was 25.  It probably was a sign of a fatty liver, so I decided in the spring of 2016 to experiment with daily short fasting.  By July of 2016, 4 months later, I lost 4   pounds, waist shrunk 1 inch, and fasting glucose (a measure of IR) was lower.  I noticed that by skipping breakfast, I had reduced my total consumption of food.  I was less hungry especially at dinner time.  A big plus was that I experienced no decline in mental or physical energy in the morning, and avoided the decline following breakfast.[19]   After a couple of months of adjusting, I now like skipping breakfast.  I stopped eating a handful of nuts or some celery mind morning, and now I have just 16 ounces of tea with a teaspoon of lime juice. Morning fasting and not eating at night has convinced me that weight control with short-term fasting is easy and pleasant, easier than an energy-restricted diet.[20] 


The lack of sex hormones has been shown to play a significant role in weight gain.  Estradiol (the best of 4 estrogens) controls fat distribution, which is visually obvious as a girl develops during teen years.  The low estradiol causes women to gain abdominal weight following menopause.  The natural estradiol with progesterone from a compounding pharmacy has many benefits including helping avoid abdominal weight.  The two sex hormones are nearly structurally identical, but for on functional group.  Testosterone makes a different for men past the age of 60 when they do sufficient amount to restore them to a youthful level, which is what I did.  Starting in 2004 was the use of natural testosterone[21] from a compounding pharmacy.  It made my weight control easy.  I stopped weighing myself once I realized that my weight regulatory system kept me between 161 and 165.  Again we have an example of why corporations should not be allowed to dominate medical science; and those who know of the benefits of hormone replacement therapy are marginalized.[22] 


Dr. Jason Chapter 20 “When to Eat” in his Obesity Code, 2016, p 235-251 covers the history and advantages of fasting; his opening words “LONG-TERM DIETING is futile”.  The reason is the major drop in metabolism due to leptin and it physical and emotional consequences; thus few are capable of going on a life-long energy restricted diet—there are numerous long-term studies which show that the obese gain back most or all of their lost weight.   “The body reacts to weight loss by trying to return to its original body set weight…  [because] our insulin level stays elevated” which is due to insulin resistance; thus leptin also is elevated.   Only fasting addresses IR.  His clinical experience and extensive research proves that fasting is both easy and works.   Here I stand upon his shoulders:  I shall present what I find of most value in that chapter, sometimes quoted and my additions will be in [brackets].  IR causes excess fat storage and leptin promote reduced metabolism and increased appetite.  [But it is not appetite/hunger exactly, rather the feeling that if I eat a bit more my energy and mental clarity will return to what it ought to be; this is the effect of leptin on energy.]   All foods promote the release of insulin; only not eating will keep blood insulin level low.   As Fung points in other chapters, incretin hormone system responds to digestion in the stomach and small intestine by stimulating the release of insulin from the pancreas [fats and fructose by far produce the least leptin response].  It explains why meat, fish, and poultry have a higher insulin index than boiled pasta.  Though Fung writes of 24 to 36 hour fast as curing IR, his clinic also uses the short-term fast.  “The term ‘breakfast’ is the meal that breaks the fast—which we do daily”--p 237.  Fasting has been involved used in most cultures and religions, and among the hunter-gatherer was forced by circumstance.  Hippocrates of Kos (c. 460-370) wrote; “instead of using medicine, better fast today; to eat when you are sick is to feed your illness” p 237.  Humans like most animals do not eat when sick.  Plato and Aristotle were staunch supporters of fasting.  “The body does not burn muscle until all fat store is gone” p 240.  “Blood glucose levels remain normal as the body switches over to burning fat for energy.  This effect occurs with fasting periods as short as twenty-four to thirty six hours.  Longer fasts reduce insulin even more dramatically…. Regular fasting has been shown to significantly improve insulin sensitivity.  This finding is the missing piece in the weight-loss puzzle.  Most diets don’t address insulin resistance,” p240.  One of the most potent stimuli of growth hormone {HGH] secretion is fasting.  Fasting promotes the use of fat as fuel and preserves muscle mass and bone density.  Adrenalin [and noradrenalin] levels go up with fasting,” p 241 they are the natural amphetamines- that create alertness and physical energy.  “Breakdown of muscle tissue happens only at extremely low levels of body fat—approximately 4 percent,” p242.  “The human body has evolved to survive episodic periods of starvation,” p 243.  “Caloric restriction diets do not allow the evolved adaptation that occurs during fasting,” p 244.  “Studies of eating a single meal per day found significantly more fat loss, compared to eating three meals per day, despite the same caloric intake” 243[23].  “Total energy expenditure is increased during a fast—in a 4-day fast by 12%,” p244.  “In our clinic experience showed that appetite decreased as duration of fasting increased.  The most astonishing aspect of this study [107 obese subjects unable to lose weight] was the ease with which prolonged starvation was tolerated.  These experiences echo our own clinical experience at the Intensive Dietary Management Clinic with hundreds of patients,” p245.  The more dangerous visceral fat is preferentially removed with fasting. There is reference to Dr. Michael Mosley (British on BBC) 5:2 diet, 5 days of full caloric and 2 days of 25% of calories at the end of a short-term fast.  In the trial that compared the 5:2 to the Mediterranean diet with a 25% reduction in calories.  At 6 months both groups lost about the same amount of weight, but the 5:2 group have lower insulin and less IR, at p247.  The short term fasting made this important difference.  Fasting because it corrects insulin resistance is essential for long-term dieting success. 


For those who want to know more of the science behind fasting, I highly recommend that you read my “Evidence of Alternate Day Fasting—Cures Type-2 Diabetes”  and Fung’s book on Fasting that is scheduled for release October 2016.  For a concise refresher as to the details of what has caused the weight control system to crash click on link.  My own experience, an others whom I have talked to and counseled, this has convinced me that short-term fasting is easy, and the scientific literature confirms that longer periods are also easy; this is because our body has evolved a system to burn the fat reserve and to keep us alert and full of energy so that we more likely to hunt and gather foods.   


 


10.  Why some don’t get fat


A variety of factors work to reduce the probability of developing a fatty liver, the starting point for IR and its comorbidities.  It is the combination of fructose and glucose (especially form both sucrose and high glycemic index foods (thus refined carbs and other easily digestible carbs such as potatoes).  The sugar fructose is the starting point thus eating a low sugar diet.  High insulin level driven by high carbs drives liver fat storage.  The traditional Chinese diet though high in white rice (which is comparable to white bread) had little effect.   Experiments have come to the same:  feeding volunteers either a high level of fructose are glucose, only the fructose cohort developed IR. 


Recollection of events prior and imperfect knowledge of causes makes self-analysis of limited value.  Often the year in which a fatty liver has developed is unknown but surmised based on a gradual gain of weight; however, it is possible that the condition had developed years before, but based on a variety of factors listed below weight gain was minimal.  Moreover, given the typical imperfect method of diagnosis (ultra sound or biopsy) there might be a false negative, or the test was ran during a period were the amount of fat stored in the liver had decreased to a temporary subclinical level. 


Genetics of course make a difference, but not that much.  One authority placed it at 5%.   A major cause is learnt behavior from family, from community, from media.  Another cause for obesity is the prenatal environment.  A fetus is exposed to high level of blood glucose will develop more insulin-secreting cells “and the more insulin the child will secret as it get close to birth.  The baby will now be born with more fat and will become insulin resistant as it ages,” Taubes, supra 132.  The dramatic increase in early childhood obesity, as referred to by Dr. Lustig, is a striking result of unhealthy womb environment and its effect upon the weight regulatory system. Thus what seems to be an inherited trait is in fact due to the womb environment.  This is not to deny the relevance of genes, only clear examples of a specific gene cause a group or sizeable subgroup to have the debilitating biological disadvantages genes is contra evolution, except when promoted by sexual selection.  A classic review article on Obesity in Scientific American pointed out that while the American Pima Indians of Arizona have the world’s highest rate of diabetes and obesity[24], those on the Mexican side of the boarder have a very low rate.  Since each come from the same genetic pool—104 years of separation, statehood was granted Arizona in 1912—evolution cannot have created that great a difference.  The diversion of the water and the introduction of non-native diet had devastating effects on the health of the people as well”—Wiki.  ‘The genes caused obesity and diabetes’ is simplification that hides the causes:  it is like saying, “god made the earth”:  explains everything and nothing. 


Childhood malnourishment results in adjustments made that promote fat storage.  Such children have a greater response to the refined carbs including sugars.  Thus countries with high childhood soda consumption coupled by poor nutrition (lack of protein), there is a high rate of childhood and young adult obesity and diabetes.  Three noted examples are the poor in Mexico, India, and China. 


Steady high fructose childhood diet of sodas, fruits, table sugar along with plenty of carbs will—all things being average—cause obesity.  Note native peoples on a traditional diet don’t become obese.  And the Japanese, and Chinese on the traditional diet high in high carbs (over 70% of calories) yet less than 20 grams of fructose don’t have an issue with either obesity or diabetes—see Dr. Fung 160-65 for more evidence.      


Various common ways to avoid the health disaster caused by IR while eating a Western diet (in approximate order of importance): 


Daily average of less than 40 grams for male (30 grams for a woman) of fructose for an active average size person 


Regular exercise or strenuous lifestyle


Tight weight control and not allowing significant weight of more than 5% above lean body weight.  The longer the excess fat is carried the less likely is it that an energy-restricted diet will keep that weight long-term off.


Mini-fasting when dieting


Yielding to peer-pressure to be fit and trim


Major seasonal change in fructose and carb consumption


Limiting high sugar beverages


Natural hormone replacement therapy (testosterone or estradiol with progesterone from a compounding phamacy.


Having good muscle tone


Getting more than 40% of calories from fats of which over half is saturated fats


High ratio of saturated fats to unsaturated fats (see Part 4 Fats for complex reasons)


Eating a high ratio of natural foods to manufactured foods thus limiting the sugar added foods and polyunsaturated fats.  


Choosing fruits and pure dark chocolates as a desert or snack over items high in sucrose such as fruit juices, candies, cookies, sodas, and like. 


 


11.  Myth busters -- (trashing tobacco corporate science)[25]


  1. High serum cholesterol causes CVD.  TRUTH:  High serum cholesterol has not been demonstrated to be a cause of plaque formation.  CVD’s main cause is infective agents within artery walls which damage LDL with toxins and cause an immune response by macrophages that cause atherogenesis.  The cholesterol deposits in the artery walls are a byproduct of the immune response, as too are calcium crystals, foam cells, triglycerides, and lymphocytes.  Cholesterol is a bystander not a cause; thus lowering its production with drugs does not prevent AS or heart attack.  Autopsy studies found no relationship between serum cholesterol and degree of AS in those died violent deaths, see.  The Australian Broadcast Corporation has a documentary which exposes this myth, at and one on the statin scam. 

  2. Avoid saturated fats because they cause CVD by raising the serum level of small-dense LDL which is associated with CVD.  TRUTH:  Saturated fats don’t raise cholesterol levels or small-dense LDL.  And LDL level is not associated with CVD (see #1).  A meta-analysis of 21 studies on saturated fats, “failed to find an association with CVD, Wiki, and also Wiki.  This extends to all types of fats when “increased from 30 to 50% of total energy,” 2004. Moreover, those on an Atkins type KD, their so-called “bad” LDL drops and the “good” HDL rises.

  3. Vegetable oils are preferred to saturated fats (main source animals).  TRUTH:   Vegetable oils are associated with diseases because they are high in polyunsaturated fats that become rancid in the body, when cooking, and on the shelf--link.  Since this process of oxidation changes the shape of the molecule and they are incorporated in cell membranes, they adversely affect the functions of these membranes.  Like trans-fats (also of unnatural shapes) the consequences are disease promoting.  Second, polyunsaturated fats are high in omega-6 fatty acid which blocks conversion of omega 3 oils an anti-inflammatory agent.  Our Paleolithic ancestor averaged 2 parts omega-6 to 1 omega-3; today it’s 16 to 1.  Many people wisely take a fish-oil supplement to improve the ratio of omega-3.  Because of its effect on the immune system and rancidification vegetable oils promote CVD, arthritis, and Alzheimer’s disease.  The more expensive animal fats are the best source of fat followed by the palm kernel, coconut, and olive oils which are high in monounsaturated fats.   There are hundreds of journal articles going back 6 decades on this process, use scholar.google to find them. 

  4. Sugar (the disaccharide sucrose is fructose and glucose), fruit sugar (fructose), and starches (long chains of glucose) are merely empty calories without nutritive value; viz. harmless sources of energy.  A calorie is a calorie.  TRUTH:  sugars and starches (pure glucose) damage tissues.  Fructose and glucose randomly bind to proteins (in a process called “glycation) to damages proteins in your cells.  Thus glycation promotes the degenerative conditions associated with old age:   CVD, atherosclerosis, Alzheimer’s, macular degeneration, et al.  Fructose (fruit sugar and ½ of sucrose) has a glycation rate of 7.5 times that of glucose; actual 15 times because of its slower clearance compared to glucose; moreover, most of the glycation occurs in the liver where it is stored prior to metabolism there.  Since 90% of fructose goes to the liver for metabolism, the damage there through glycation is significant.  Some of the fructose is converted in the liver to fat[26] which can accumulate because of the Western diet with its high carbs.  Damage from glycation and fat accumulation in the liver causes IR and a fatty liver called non-alcoholic fatty liver disease (NAFLD).  NAFLD affect over 30% of the US adult population (NHANES II study).  NAFLD affects the plasma-glucose regulatory function of the liver to cause IR.  Fructose by causing minimal insulin response, it bypasses the appetite regulating system involving leptin and ghrelin which reduces it affect upon the satiation system  of the hippocampus to cause weight gain.  Finally, fructose stimulates the addiction center of the brain (see #6 below) to promote sugar addiction.  Clearly, sugars are not harmless empty calories, nor are starches with high insulin index, and fructose is the worse.

  5. The cause of obesity is a sedentary lifestyle & gluttony.  All one needs to do is eat less and exercise more; viz., burn more calories than one consumes; this is the common advice given by doctors, dieticians, and accepted as the way to lose weight. TRUTH:  For all mammals their weight is controlled by a biological system.  The Western diet with its average of 180 grams of sugars daily causes a fatty liver and IR.  Fatty liver and IR muck up the regulatory system and thus cause obesity.  It is not gluttony and sloth that causes the obesity and diabetes pandemics (blaming the victims) but rather the Western diet which is promoted by food manufacturers and corporatist governments. 

  6. For the obese, a 25% reduction or more in calories will result in significant long-term weight loss.  Truth   The weight regulatory system in an effort to maintain the set weight will reduce the rate of metabolism approximately 25% and increase hunger.  Even those he get past this barrier which occurs typically around the end of the 2nd month, they will once off the diet regain the weigh (yo-yo diet).  The hormone leptin intercedes to decrease metabolism, typically 25% and at the same time increases appetite.  It is secreted by adipose (fat) tissue to main the normal level of fat storage.  Less than 1% of long-term obese adults at the end of nine years will obtain normal body weight through diet.  To prevent this regain of weight, the regulatory system must be reset, and this occurs by fasting and going on a low carb diet.  Fasting will avoid the 2-month drop in metabolism.  This type of diet will eventually result in the burning of fat in the liver and pancreas and thus cure IR and T2D and permit the weight regulatory system to eventually adjust to the lower weight. 

  7. Hormone replacement (HRT) will not promote weight loss.  TRUTH:   Estradiol among other things regulates fat distribution[27] and plays a role in physical well-being.  During and following menopause women experience a precipitous drop in estradiol (the most healthful and active of the 4 human estrogens).  The common post-menopausal reduction in physical activity and associated rate of metabolism contributes to weight gain and abdominal fat.  Natural HRT [estradiol plus progesterone] reduces insulin resistance and fasting glucose in women with diabetes” at.  Since some of estradiol is converted to testosterone NHRT prevents muscle loss with aging, another contributing factor to weight gain.  Men too following andropause experience a reduction in muscle mass and metabolism.  And the heart as a muscle gets weaker.

  8. HRT for men and women poses major health risks which outweigh their benefits.  TRUTH:  natural hormones  lower risk for breast and prostate cancers.  Men in the highest 20% for testosterone have the lowest rate of prostate cancer and heart attacks.  Estradiol moderately lowers the rate of breast cancer.  In sufficient dose NHRT will reset the biological clock to a younger age and thereby significantly reduce the risk of most age-related chronic diseases.  Estradiol with progesterone lowers CVD, Alzheimer’s, cancers, and much more.  Testosterone  decreases the risk of heart attack and cancers.  Current wisdom is based on pharma’s junk science & tobacco ethics:  clinical trials that knowingly used the worst formulate of HRT for women, Prempro.  Read the section on the WHI study which exposes pharma’s and NIH’s tobacco science and ethics.  NHRT is good for people and thus bad for pharma.

  9. Three lies about type-2 diabetes:   a life-long progressive condition; it can’t be cured; and is best managed with drugs that lower blood glucose to normal level.  TRUTH: that once the excess fat stored in the pancreas is cleansed T2D is cured (at the same time the excess fat in the liver is cleansed).  Bariatric surgery reverses often within a month T2D by post operation fasting proves that it can be cured and that fasting is the cure.  Dr. Janson Fung’s dietary treatment of KD (low carb high fat) with alternate-day fasting cures T2D for most within 6 months.  Diet is the cure.   Moreover the cohort who has their glucose tightly controlled has a higher mortality rate in clinical trials.

  10. Pharma is highly regulated by the FD A to protect the public from the tobacco ethics used by corporations to fulfill their fiduciary duties.  Truth:  that there is a revolving door between the FDA and pharma, and that at the highest levels the FDA is ran by executives from pharma and their KOLs.   For a summation of the ways in which the evidence base has been broken—link, or YouTube Dr. Angell.  Our corporatist government enacted the Prescription Drug User Fee Act of 1992 to make the FDA dependent upon pharma for over half of its budget.  Congress wants the FDA to serve the pharmaceutical industry.   Link to Consumer Report on the FDA.  Read Prof. Ben Goldacre’s Bad Pharma.

  11. Doctors know what is best for patients.  Truth:  the education and sources of doctors’ information has been manipulated by pharma so as to turn them into drug pushers.  Pharma runs and owns the results of clinical trials, thus positive bias is the norm--32%.  Pharma determines who becomes a KOLs (Key Opinion Leaders).  They are the lead authors on clinical trials, write the medical textbooks, and give continuing education classes.  The information foundation is thus distorted.  For an insightful explanation of how this has occurred click on linkyou need to know.  Pharma and food manufacturers through junk tobacco science, corporate media, and misinformed doctors cause cognitive dissonance and reliance on their KOLs by both the public and physicians.  Pharma has framed the discussions to promote the sales of patented drugs, and food manufacturers to promote the obesity and diabetes pandemics.  What has been said about pharma applies to the manufactured food and tobacco industries—profits before people.  There is a struggle going by leading men in the medical field who have broken rank over the corruption worked by pharma, but you won’t squarely hear of it in our corporate media.  But you can watch them on YouTube & read their journal articles.  


 


12 Pathogens in artery walls is the main cause of CVD  


The tobacco-science based claim that saturated fats and cholesterol cause CVD; this has been decisively refuted by scientific evidence:   Atherosclerosis (AS) is now recognised as a chronic inflammatory disease occurring within the artery wall and ultimately responsible for myocardial infarction, stroke & peripheral vascular disease.”   There are approximately ten times as many bacterial cells in the human flora as there are human cells in the body”, Wiki,  Not surprisingly some of them are in the interior of the artery walls, the tunica intima.  The inflammatory process starts with white blood cells attempting to eliminate certain bacteria.  They produce an inflammation in response to the virus and bacteria colonies within the artery walls.  A typical study found Chlamydia pneumonia in those with CVD 79% vs 4% without CVD in coronary artery specimens.  LDL functioning as part of the immune system absorb the toxic chemicals produced aby these pathogens.  The “monocytes replenish resident macrophages” (a scavenger white-blood cell) that dispose of the products of the LDL’s immune response--see.   Thus pathogens damage to LDL is part of the process leading to the development of CVD; not high blood cholesterol and high fat diet which are bystanders found within the LDL.  Lesser contributing factors include oxidation & glycation (sugar bonding) which damaging endothelial cells lining the coronary artery walls.  Pharma wants us to believe that the inflammation response is to oxidized LDL in the artery walls.  Wrong again, the contents of LDL is cholesterol and triglycerides which the body needs to grow new cells to promote healing in the artery wall and to replace damage white bloods cells both of which have been damaged by the pathogens.  This explains cogently why atherosclerosis is brought on by an inflammation response.  Pharma says this response is a result of damage to the LDL in the inner layer of the artery; no mention of pathogens. Pharma has ignored a century of autopsy studies of those who died from a heart attack; these studies find pathogens.  But pharma makes billions treating hypercholesterolemia--see.   Then they make billions more hypertension and heart attacks—but not the pathogens that cause AS.  Prevention is not in their business model.  Moreover pharma is very good at marketing--see how.  The scientists who are critics of pharma’s junk science are ignored by corporate media.  Physicians hear pharma’s key opinion leaders (KOLs) at the required continuing education classes funded by pharma.  Having said this, my concern here is with diet’s role of insulin resistance (IR) in obesity, fatty liver disease, diabetes, age-related diseases, and CVD; and also about healthful choices.  Sugars through glycation damage the endothelia cells which line the artery walls, and so damage they increase the risk for pathogens colonizing the inner layer of the arteries—2 links see and more.  


LDL is a lipoprotein-phospholipid wrapped sphere containing about 1500 cholesterol molecules and 3,000 to 6,000 fat molecules including triglycerides, see illustration.  Cholesterol has several essential functions including forming the cell walls, neurons coating, and its conversion into the sex hormones. The liver produces cholesterol--about 70%--and sends it wrapped inside LDL through the blood to cells in need of fats & cholesterol.  Inhibiting the synthesis of cholesterol with a statin drug has many side effects, and it doesn’t prevent CVD.  Numerous books and documentaries expose the cholesterol myth & statin horrors.  But pharma in the production and dissemination of information frames the debate; thus only those who de-nova examine the journal evidence and adjust for their tobacco science can come to the best evidence based answers.


 


13.  Other cofactors for CVD


Pathogens play the key role in the formation of atheroma leading to AS and CVD.  However, excesses in reactive blood-borne chemicals including simple sugars (especially fructose) are contributory.  Their main pathological mechanism is through endothelial dysfunction.   Endothelial cells function as a single layer membrane that lines all the blood vessels and act as the gatekeeper.  These cells have receptors which allow certain chemicals to pass through, others such as lymphocytes posses a compound which effects the adhesiveness that join the endothelial cells to form a membrane and thereby permit the lymphocytes to slip between them.  harm the gateway cells that line blood vessels.[28]


Trans-fats and rancid polyunsaturated fats are statistically associated with CVD.  The abnormal shape of these fats is thought to contribute to various disposal issues that are pathological.  For example, transfats induce platelet aggregation, .…  inhibit activities of Na+ , K+-ATPase and adenylate cyclase and reduce density of B-adrenergic receptors in rat heart membranes [raise blood pressure]…. Recent evidence indicates that trans-fats promote inflammation…. Increased tumor necrosis factor (TNF) system, levels of interleukin-6 and C-reactive protein…. Several studies suggest that trans-fats cause endothelial dysfunction” in the 1984 thorough review by the Department of Agriculture.  Similar affects occur with polyunsaturated fats which are in vivo subject to oxidation.  In addition the high ration of omega-6 to omega-3 fatty acids has been shown to be atherogenic.   Similar association with CVD is associated with a diet high in sugars (but not carbs).[29]  Hyperinsulinemia, IR, NAFLD, T2D[30] are contributory to endothelial dysfunction.  Like so much that goes on in the body, the causal mechanisms of these condition in the development of endothelia dysfunction is complex and thus tentative.  The associations with sugars, smoking, trans and polyunsaturated fats to endothelia dysfunction and CVD are firmly established.  The strong association of CVD with Western diet is based on carbs with sugar causing IR and IR’s role in endothelia dysfunction. 


So what about the standard explanation for atherogenesis?  Pharma’s case for LDL undergoing oxidative damage from metabolites within the tunica intima, and this being the most principle cause of CVD, this is suspect.  Suspect because it ignores pathogens, suspect because it ignores the immune role of LDL, suspect because it fails to explain cogently why LDL is actively transported in large numbers through the epithelial cells into the tunica intima; and downright misleading because it uses the dual meaning of “oxidative” to imply that the products of metabolism is causing the oxidative damage to LDL while in fact it is the toxins that are latching onto the external protein shell of LDL.  Their explanation fails to explain why there is LDL in the intima medial, and to explain cogently why the immune system is involved in the process.  Pharma’s KOLs state that the lymphocytes and macrophages are there to clean up the oxidized LDL—no mention of pathogens. The debris of this process results from the macrophages engulfing large numbers of the oxidized LDL and resultantly undergoing apoptosis that results in the formation of plaque.  Are we to believe in an atypical process involving pathogens, or to think the worse of pharma?  Given pharma’s repeated examples of tobacco science being generated by pharma to promote profits, the plausible conclusion is that this is one more example of bad conduct by pharma.  Pharma has already been proven to have generated the cholesterol and triglyceride myth (see Cholesterol Myth and 2nd article) and to support it pharma has created a factitious modus operandi.  Given the totality of evidence, the healthful choice is to ignore the recommendations of pharma’s KOLs and those, whom they have educated, the majority of physicians.   


 


                          14.  How Did We Get Here--Historical


The prima facie evidence is that the diet adopted by the FDA and Department of Agriculture in the 1977 brought on the health pandemics.  The switch to low fat, low cholesterol, which entails higher carbs, just so happened to favor the products of the food manufactures and the cholesterol lowering drugs of pharma.  In 1977 our government, and later those around the world, ignored over 60 years of dietary science and switched its position as to what is heart healthy.  Based on weak evidence, high serum cholesterol and triglycerides (3-fat molecules joined to 1-glycerol molecule) were accused of being the leading cause of CVD.


 Somehow the Senate panels (McGovern Commission) and their experts on CVD missed cigarettes which at a pack a day doubles the deaths from heart attacks.  The Surgeon General only warned about lung cancer and emphysema in The 1964 Report on Smoking and Health.  Over three times as many deaths are caused by tobacco induced heart attacks and strokes than from lung cancer and emphysema, yet the Surgeon General missed it and a large body of journal literature going back to the turn of the century.   Dr. Kellogg, of cereal fame, published in 1922 a 171 page concise compendium on the published research on tobacco’s known health consequences, including its destructive action on blood vessels, at.  Kellogg’s book has hundreds of scientific citations.  In 1965, 42% of the adult population smoked, yet the McGovern Commissioned missed tobacco.  So why was the evidence on tobacco distorted by the Surgeon in 1964 and ignored by our government in 1977, and why were saturated fats and cholesterol blamed? 


Simply follow the dollars.  Once you realize that serving the public is cloak worn by our corporatist state, than it makes sense, and when we review the details we find that this is standard operating procedure:  serve big dollars while advertising serving the public.  This method explains why our government fingered tobacco for lung cancer, but missed the much bigger killer from CVD:  they were doing damage control for tobacco.  The connection with lung cancer was too obvious, and too well known.  The Surgeon General had done damage control dressed as science in the public’s interest.  So why finger cholesterol and saturated fats?  Animal (saturated) fats cost twice that of vegetable oils; and sugars and refined starches are cheap and addictive.  And most of the products made by food manufacturers are loaded with refined carbs including sugars.   Moreover, pharma doesn’t have drugs to treat the pathogens living inside the artery walls which are the principle cause of AS and CVD, but with drugs they could modestly lower cholesterol and triglycerides in 1977.[31]  Thus pharma was by 1972 (and before) promoting hyperlipidemia and hypertension as causes for CVD and MI.  For example in the 1972, 12th edition of Merck Manual p.374 recommends restrict fats to 30-40 gm/day to lower CVD risk.  And the role of pharma gets more insidious.  If the patient believes X is a risk factor and he tries a cheap fix that must fail, then he is likely to go back to his physician and try patented drugs to fix X.  This is a standard business practice for pharma.  Diet does not significantly lower cholesterol, because the liver makes cholesterol to serve vital needs.  Only about 30% is from diet, lower it and the liver makes more on a need basis.  Moreover, saturated fats don’t raise cholesterol or cause CVD--see Dr. Miller’s lecture.  Thus the low fat and low cholesterol diet fails, so the patient with elevate cholesterol and/or CVD then tries drugs.  This plus the food manufacturers favor their high sugar and starch products over eggs, meats, poultry, and fish, because these foods are a very small part of their product line.  Secondly the vegetable oils are about half the price of animal fats.  The McGovern Committee and the US Department of Agriculture followed the bucks.[32]  The government’s inaction and at times support for tobacco[33] that permits harm from cigarettes is one more example of the power of tobacco (dollar) ethics in a pseudo-democracy, our corporatist state.  The science behind healthy diet was turned upside down by big money and we have a health epidemic.


 


15. Free will won’t, rational control of behavior will


On how to deal with food addiction which seems to trump rational control?  In 1985 applying the standard behavioral analysis for dieting:  I set down various types of behavior that would result in weight loss including food selection. Small portions, peer support, visualization, etc.  I held that thoughts (silent whispers) are merely epiphenomenon that accompanies behavior like a shadow.  Eloquent proof came 2 decades later; one was an experiment that was published in American Scientist (2004, Free Will, Free Won’t).  Electroencephalography was used to measure brain activity and a button was pressed by the participant to indicate when the thought occurred.  The deep brain activity occurred a half-second before the thought of his arm movement.  The thought of the action came after preparatory subconscious neural activity, like the thunder following lightening. Neurological science has since established that thoughts are generated by deep brain processes and accompany an action like a shadow.  To begin with neuroscience has demonstrated that the brain is modular, each of the hundreds of sections has a specific function.  One of these modules functions to create an image of man as being guided by thought.[34]  But rather in the verbal sections of the brain is not aware of what goes on in the motor sections of the cerebellum which acts as a traffic cop coordinating behavior.  In other words the brain has hundreds of specialized modules I call the analytic portions (AP) that function to produce verbal behavior including thoughts.  Thoughts has been by B.F. Skinner labeled as silent whispers.  Consider the behavior process similar to vector algebra (see graphs above on website) where several different forces are acting simultaneously on an object at a point, the result of which will be movement of the object in only one direction.  The deep brain operates according to the diverse force to produce behavior, sometimes contrary to the input from AP.  For diet, based on a complex collection of evidence, the AP has determined that sugars and starches need to be avoided.  At home the AP opposes the eating of refined carbs and sugars, but its contribution to eating choices isn’t sufficient to consistently throughout the day bypass the grapes and candies.  Thus I must influence the arrows of forces in my brain so that at home there aren’t foods high in refined starches and sugars.  The explanation from behavioral psychology:  the closer in time and space to a reinforcer, the greater is the probability that it will affect behavior.  The AP plots that I need to stock the kitchen with items that aren’t high in refined carbs and high sugars.  I also enlisted my wife to use social reinforcers such as praise and she too has changed her diet.  We watch the video Sugar White Poison and other like videos every week.  The AP has set out a program by which I can change my eating behavior life-long.   Moreover, given my extensive education and application of academic skills, my AP is stronger than the norm. 


If it were true that the will (mind, AP) could decide independent of the deep brain process, then there wouldn’t be smokers, drunks, and an obesity epidemic, and certainly there wouldn’t be so many morbidly obese (about 10% with a body mass index, BMI, over 40).  Today I saw a women under the age of 30 whose weight forced her to rely upon a wheel chair.  Does she have a defect in her will (mind)?  Or is it a confluence of genes coupled with dietary causes that have reset her normal weight to a BMI of over 50?  She can think of losing weight, swear that she will, go on a diet, but the deep brain is committed to 400 lbs. and gaining.  The low fat, low calories diet is not her long-term answer.   A bariatric operation is one way, but her stomach will expand sufficiently to accompany many small meals and about half will regain most of their former weight—as two of my friends have done over a period of 6 years.  The wrong expert information spread by doctors and the media has the AP applying a low fat diet with more exercise as the healthful program, and they gained back their weight.       


 


16 Outline on metabolic dysfunction 


This page 6/9/16, is on http://healthfully.org/rc/id23.html


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 is high carbs fructose and glucose that causes a fatty liver (NAFLD) which mucks up the regulatory systems leading to the IR that causes obesity, T2D, CVD, etc.  Glucose raises insulin level, and insulin causes cells to STORE FAT and burn glucose.  IR causes excess fat storage.  Causes:  The carb fructose--a simple sugar--goes to the liver where some is converted to fat, and when insulin is high this fat is stored in the liver.  The low fat, thus high-sugar, high-carb Western diet will for most cause excess fat storage in the liver.  Gradual over the years/decades 2 to 3 pounds of fat is stored in the liver (NAFLD).  This causes IR first in the liver then in other tissues.  IR mucks-up the complex metabolic systems.  With IR comes a gradual gain in weight.  If you have T2D then you have excess fat in the pancreas, and your beta cells no longer produce sufficient insulin to manage your glucose.  When on an energy-restricted diet the fat tissue through the 4 hormone it produces functions to maintain current weight by increasing appetite and reducing metabolism.  Even after losing weight, the system works to restore the fat—the yo-yo diet.  Goals:  to stay in fat burning (low insulin) mode and thus to metabolize the excess fat in the liver and pancreas to reverse IR and T2D.  Once fatty liver & IR are cured than carbs can be moderately increased and weight will still be lost.  Once ideal weight is obtained remain on moderate carb-sugar diet.  Follow the dollars and you will find out why we have the Western diet and the wrong advice—click on link for a list of the misinformation, and much more. 


Fix:   Short-term fasting with low carb diet to stay in fat burning to cleanse the liver and cure NAFLD & IR.   


   Fructose converted to fat in the liver and high glucose via insulin causes fat storage in liver (a 1-2 punch)


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


T2D can be cured with diet.  For example in the first 2-weeks following bariatric surgery over 80% with T2D are cured before major 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 easily digestible carbs.