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Part 6: Ill-health pandemic: conditons, causes, and dietary fixes

MYSTERY SOVLED AS TO THE OBESITY AND DIABETES PANEDMICS.  The process leading to metabolic dysfunction is complex.  It starts with a one-two punch of too much carbs (glucose) with fructose over a prolonged period of time Fructose is converted to fat in the liver, and the glucose regulatory hormone insulin causes fat storage (and glucose burning).  Fat accumulation in the liver is the starting mucks up the metabolic-weight regulatory system.  This excess in 80% of the cases causes IR first in the liver and then in the muscle and fat cells (myocytes and adipocytes).  This excess liver fat often progresses to NAFLD.  Other factors affect this process:  especially frequency eating the Western diet, rate of absorption of refined carbs, physical activity, tight regulatory control of weight to prevent obesity, alcohol consumption, and fasting, to name the principle factors determining the risk for metabolic dysfunction.  Once fatty liver is established and allowed to progress, the conditions upon which healing occurs are not likely to happen without bariatric surgery or long-term Atkins-paleo type dietary changes. 

  Part 6:  Ill-health Pandemic:  Conditions, Causes & Fixes  --  http://healthfully.org/rh/id12.html  10/23/15

AS        Atherosclerosis


N3         Omega 3 fatty acids   

CVD     Cardiovascular disease


N6         Omega 6 fatty acids   

HT        Hypertension


MeS      Metabolic syndrome[1][1]

IR         Insulin resistance


NALFD  Non-alcoholic fatty liver disease

KOL     Key opinion leader


T2D       Type 2 Diabetes

MI        Myocardial infarction


TC          Total Cholesterol


Important fact:  Corporations, especially pharma in pursuit of profits pollutes the scientific process with tobacco science and their dollar influence frames the discussion.  A perverse system produces perverse results. 

1)  Table sugar (sucrose) is a disaccharide which is hydrolyzed in the stomach to fructose and glucose.   A diet high in sucrose is essential for the development of insulin resistance (IR).  It also requires high insulin  which develops into metabolic syndrome (MES). 

2)  Metabolic syndrome (MeS) is the result of damage to the metabolic system that involves insulin and leptin resistance and non-alcoholic fatty liver disease (NAFLD) which can develop into type-2 diabetes (T2D)—bad pharma adds others.

3)  IR, MeS T2D and obesity are associated with the Western diet, and not associated with the Paleolithic diet. 

4)  The starting cause for insulin resistance is a high fructose diet combined with high level of insulin.  It is a one-two punch.  Fructose is converted to fat in the liver, and insulin cases the storage of fat in the liver.  Overloads with fat the liver is damaged, and this mucks up its metabolic functions (see #s14-16) which cause first insulin resistance in the liver and then in the adipocytes and myocytes.  When the latter occurs it is considered IR.

5)   Insulin is released by the pancreas in response to high serum level of glucose. Insulin causes cells--mainly muscle and fat--to absorb and store lipids (fats) and to metabolize glucose.  High insulin level up-regulates (increases) leptin.  Low levels of leptin or leptin resistance causes obesity. 

6)  High level of leptin reduces hunger through actin upon the hypothalamus in the brain.  A low level of leptin functions to increase appetite and lowers the rate of metabolism.  Leptin resistance increases appetite and lowers metabolism.

7)  Leptin is produce in adipose (fat) tissue. Among its functions is the maintenance of current level of fat, thus making long-term loss though energy restricted diet a failure.  Fasting and extremely low car diets have highest success rates.

8)  Prolonged high serum levels of insulin over the years will result in a diminished response by insulin receptor in cells—especially by the muscle & adipose (fat) cells.  This reduced response (tolerance to insulin) is termed insulin resistance (IR).   With IR, the pancreas releases even more insulin to lower the level of glucose.  Damage to the liver by fructose starts the process (#4, 14-16).

9)  Starches are pure glucose.   Primary sources are grains, potatoes, sucrose (table sugar), starchy vegetables, and legumes.  Their effect upon serum glucose and thus insulin varies with quantity, exercise, and rate of absorption--see and.  Also important is the type of starch, some are readily digested other are resistant starches of varying degree. 

10)  T2D results from the accumulation of fat in the pancreatic beta cells.  This is brought about by the high level of serum insulin form IR, which causes the storage of fat.  Though IR often exist for years, the decline in insulin production resulting in T2D occurs in a few months due to fat accumulation in beta cells in the pancreas. 

11) Following guidelines for T2D results in a progressive condition which starts with one drug that lowers serum insulin (usually metformin), then when resistance to medication occurs, additional drugs, and finally injections of insulin.

12) Genetics and lack of physical exertion play important roles in exacerbating the unhealthy high fructose Western diet.  However genes are only 10% of the cause.  Amount of physical activity is under the control of hormones that strive to preserve the store of fat.   E.g., obese children are less active than their normal weight brothers. 

13) Of those with T2D, 40% are not obese, and of those obese, 80% will develop T2D.  The principle cause of obesity is insulin and leptin resistance which promotes fat storage, increased appetite, and reduces metabolism when dieting.

14) Fructose is metabolized in the liver in the same way that alcohol is, and like ethanol damages the liver. Both are converted to fats which through accumulation damages the liver.  Liver cells accumulate fat that compromise functions, and enlarges the liver.  Alcohol causes fatty liver disease (FLD) and fructose causes NAFALD.  Both also effect the location of storage of fat resulting in in visceral (abdominal) fat accumulation.

15) Fructose undergoes a non-enzymatic Maillard reaction which damage proteins and thereby is a main cause in most age related chronic conditions and insulin resistance in the liver.  The process of random attachment of sugar to a protein or lipid is called glycation.  Fructose glycation rate is 7.5 times that of glucose multiplied by 2 because of higher serum level & slower clearance than glucose.  With fatty liver, because of slower clearance, glycation is accelerated, especially in the liver, where the damage contributes to metabolic dysfunctions that can develop into IR.

16) Only about 20% of glucose is metabolized in the liver into glycogen a storage form.  However 100% of fructose is metabolized in the liver, of which about 80% is converted to fat. 

17) Starches and corn syrup are pure glucose are relatively safe source of energy for people without IR on a low sugar diet.  But those who are eating regular a large amount of sugar, the high insulin as a result of the refined carbs causes the liver to store fat a product of the conversion of fructose.  See diet for more details on how to reduce the rate of harm caused by carbohydrates, nutrients, and some chemicals.  

18) A number of other conditions are associated with IR and T2D, including cardiovascular disease, and most other age-related chronic conditions including Alzheimer’s disease, cancers, and macular degeneration.  

19) The main controllable dietary cause of atherosclerosis including cardiovascular disease  (CVD) is a diet high in sugar, refined carbohydrates, and polyunsaturated fats (in that order of importance)—all part of the Western diet. Other very significant causes are carbon monoxide from cigarettes and pathogens living inside the artery walls—cholesterol isn't.

20) Cholesterol and triglycerides are bystanders, not causal factors for atherosclerosis (AS) and CVD (see cholesterol myth, and).  The elderly with high serum cholesterol live longer and have lower rate of CVD--Framingham Heart Study. 

21) A diet low in fats & cholesterol results in increased in carbohydrates, thus rather than preventing CVD, promotes it.

22) Man’s weight--like all mammals’--is controlled by a complex biological hormonal control system.  The Western diet which is high in sugars and carbohydrates negatively affects this weight control system. 

23) When calories are reduced this hormonal system reduces metabolism and increases appetite so as to maintain the set level of weight.  Going off a diet, with few exceptions, results in a gradual return to the previous weight. 

24) The sex hormones of estradiol and testosterone are part of this weight control system; thus as they decline with age most people will gradually increase abdominal fat.  Taking sufficient dose of Testosterone or estradiol is effective.  They also affect muscle tone, thus through exercise reduces serum glucose.

25) Tobacco ethic refers to the principle which all large corporations operate under.  Corporate performance is measured by short-term profits.  In the present mature state of capitalism, corporate ethics has produced the Western diet, framed the discussion of diet, influenced corporate media, and block government intervention. 

26) Tobaccos (junk) science refers to the distortion worked by corporations upon the scientific process in violation of the principles of sciences--done to promote financial gain.  Corporations fund tobacco science and use their influence to distort the evidence base and spread beliefs that are not supported by science. 

27) The http://healthfully.org/rg/ website focuses upon exposing the tobacco science.  There you will find a table of contents and library of internet documentaries and lectures with evaluation and links.

OUTLINE OF aetiology of insulin & leptin resistance--Main Causal Factors:

Insulin and leptin resistance are necessary conditions for development of T2D, NAFLD, & MeS

  1. Womb environment.  A pregnant woman that has high levels of insulin and serum glucose (associated with obesity during pregnancy) is more likely to have a child who will becomes insulin resistant (IR).  Her fetus is likely to respond less to insulin (IR) since her high level of insulin & glucose has crossed the placental barrier. 

  2. Over 20 genes are statistically associated with the development T2D.  Their causal input to T2D is about 10%, the remainder is environmental, and thus everyone is at risk.  What follows is a result of a high carb-sugar diet. 

  3. Fructose which is only metabolized in the liver accumulates into fat and glycogen (storage form of glucose).  Some of the fat is stored in the liver.  Stored liver fat along with fructose’s in vivo 15-fold rate of glycation compared to glucose creates NAFLD & liver IR.  This compromises the liver’s dozens of functions.    

  4. The liver normally consumes 20% of serum glucose, much less with NAFLD.  This raises serum glucose which results in more insulin to lower glucose.  Gradually muscle and fat cells become tolerant to (resistant to) the higher level insulin thus resulting even more insulin to lower serum glucose to a safe level. Prolonged high serum insulin over the years causes IR.

  5. High serum insulin causes weight gain in 2-main ways:  signals cells to store fat and burn glucose[2] and by increasing the amount of leptin, which over time causes leptin resistance.

  6. With leptin resistance there is increased appetite and reduced metabolism through the reduction in thyroid hormones thus promoting weight gain[3].     

  7. With weight gain (increase in adipose cells size) there is an increase in the hormones which adipose tissue secrets. “ In recent years, been recognized as a major endocrine organ,[1] as it produces hormones such as leptin, estrogen, resistin, and the cytokineTNFαWiki.  These hormones control among other things metabolism, appetite, weight, and fat distribution. 

  8. The high fructose diet with carbs causes fat accumulation ins certain glandular tissues including the pancreas.  As fat accumulates (like with a fatty liver), the function of the beta cells in the pancreas declines.  In response to serum that is a rather sharp drop in insulin production.  If sufficient T2D results.     



1)  There is a major health epidemic because of unhealthful Western diet which is grouped as a collection of conditions named metabolic syndrome (MeS); this includes obesity conservatively estimated at 36% of adults, non-alcoholic fatty liver disease (NAFLD) at 30% in the NHANES Survey.  Insulin resistance (IR) is 51% of seniors over age of 65, type-2diabetes (T2D) at over 26% of seniors, 2012.  Type-2diabetes is typically a chronic disease associated with a ten-year-shorter life expectancy. This is partly due to a number of complications with which it is associated, including: two to four times th e risk of cardiovascular disease, including ischemic heart disease and stroke,” (Wiki) and an assortment of other age-related chronic conditions including blindness, kidney failure, cognitive dysfunction, dementia, sexual dysfunction, lower limb amputation, atherosclerosis and thus hypertension.  Their main causes are our government’s recommendation in the late 70’s for a low fat and low cholesterol diet.  American following this recommendation, and the manufactured (processed) food industry lowered of fat content and replaced it with sugars.  This has caused a health disaster which consumes over 70% of all medical expenses.  There is compelling evidence that the increase in sugar (fructose being the worse) damages the liver and the regulatory system for insulin and leptin to cause MeS.  However, in our corporatist state this information on cause and its dietary fix are not effectively disseminated.  What follows below is an explanation of how a high sugar-starch diet that makes us sick and why it is so difficult to correct the problem.  What I am about to describe is supported by journal articles and the subject of several quality documentaries—links provided.   

2)  Like so much of what I have done elsewhere & published at healthfully.org, I questioned everything, especially in areas that could be spun for the promotion of the sales of patented drugs, and for food I examined the dietary recommendations.  I have examined the biology behind a medical issue concerning the bodily production and utilization of insulin and I uncovered major differences between sound science and pharma-generated spin.  The spin is in dietary recommendations and metabolic syndrome, and NAFLD.  To MeS pharma added high serum triglycerides and LDL, low HDL and hypertension (see Wiki) which are neither from IR or a significant cause for ischemic events.  The core issue is that of a metabolic disturbance brought on by fructose which is the main causes MeS, obesity, and T2D.  Having created these causal myths, pharma sells patented medication to lower cholesterol and blood pressure.  This is another example of their junk-science chasing the wrong causes—read cholesterol myth also and, or watch the documentary on the Australian Broadcast Corporation, and read on hypertension.  These myths are woven into metabolic syndrome, diet, hypertension, diabetes, cardiovascular disease, and high serum cholesterol (labeled hypercholesterolemia and dyslipidemia) which pharma treats with drugs.  The role of fructose with carbs is downplayed and the critics ignored by pharma, corporate media, medical text books, and by key opinion leaders (KOLs) who educate doctors.  Pharma does junk science to minimalize the role of the dietary cause:  long-term high fructose diet with refined carbs damages the liver through fat accumulation ; this is the starting point for MeS.  It is essential to understand the corporate role of the food industry in promoting our Western diet.     

3) There are more distortions engineered by pharma and the manufactured foods industry[4] concerning the role of diet.  Among them are the calories-in, calories-out and the personal responsibility hypothesis of weak willed-gluttony.  Prof. Robert Lustig MD, on University of California Television has rebutted these standard obesity myths on calories, and on personal responsibility.  I have come to the same answers as Dr. Lustig after researching fulltime for the year 2014 the issues he and others has raised.  Prof. Lustig explains why a high carb-sugar diet causes health problems, and comes to the conclusion that fructose is toxic, like ethanol. 

4) Western diet: Two dietary shifts since the 1946 brought on the obesity-diabetes epidemic. One is the increase of fructose consumption from 20 gm/day in 1946 to 95 in 2008[5], most of which comes through the increase use of the disaccharide sucrose (table sugar), which consists of the molecules of glucose and fructose.  Sugar consumption now averages 152 lbs. per year in the U.S.  Fructose is metabolized just like alcohol in the liver, where like alcohol it slowly damages that organ (see Non-alcohol fatty liver disease, NAFLD below).  This damage and through glycation (see below) also promotes insulin resistance in the liver.  Insulin functions in the liver to regulate the liver’s production of glucose, glycogen, and free fatty acids, and affects other process of the liver.  The second related cause is the increase in carbohydrates. Increased consumption resulted from our governments holding in 1977 that fats and cholesterol were unhealthy and should be reduced.  We went from 44% of total calories in 1970 to 30% now; thus resulting in an increase in carbs.  The cause of this shift to a low fat diet based not upon science but the manufactured food industry influence upon the Senate’s committee investigating the rise is CVD—follow the bucks to food manufacturers and pharma—see cholesterol myth.  Carbs (mostly starches and one-half the disaccharide sucrose) both are converted to glucose in the stomach.  Insulin is secreted in by the pancreas to lowering the glucose level through metabolism,; at the same time insulin causes cells to store fat.  The fat produced in the liver from the high fructose diet is store in the liver.  This excess fat mucks-up various liver functions which over the decades for a variety of reasons causes insulin resistant, which requires more insulin to lower serum  glucose.  IR often progresses to type-2 diabetes, and obesity because the excess insulin increases fat storage.  Too much fat in the pancreas causes T2D.    This shift in diet to lower fat has made the U.S. the fattest nation.  The comorbidities associated with elevated insulin[6] and not the glucose.  Since it is a dietary problem, the fix is dietary—for documentary video, or my brief diet summary.  


[2] Note:  high serum glucose plays a minor role in pathology compared to insulin.  Pharma generated spin stresses glucose not insulin. 

[3] “The PI-3K pathway also is activated by Insulin receptor and is therefore an important area where leptin and insulin act together as part of energy homeostasis… can cause POMC neurons to become insensitive to leptin through hyperpoloarization” Wiki.

[4] For manufactured (processed) foods their goal is to promote sales through added sugar and salt.  Sugar not only tastes good but stimulates the same brain centers that cause drug addiction, for which there is strong evidence, watch, and, also

[5] In 1 century, Americans have increased fructose consumption from 15 g/d (4% of total energy) to 95 g/d (12% of total energy)… fructose exerts 3 different negative impacts on human metabolism…. 2013 A. Nutrition.  The 95 grams is derived from 154 of added sugar, The New Atkins, p. 31, and that doesn’t include natural occurring as in fruits and juices. 

[6] As mentioned in above section it is not the elevated serum glucose, but the elevated insulin that is the most significant causal factory for the various conditions.  For example those with T2D who are tightly managed their serum glucose have more MI and other causes of deaths that those who don’t if such manage is through increase in insulin.  Thus treatments of T2D with insulin or drugs that raises the insulin is good for pharma but not the patient—see Fung for over a dozen studies on point.  Both obesity and T2D have dietary fix.

5)  Obesity and diet:  “Obesity is a chronic health problem. It is the major factor for type II diabetes, cardiovascular disease. It is also associated with cancer, osteoarthritis, liver disease, sleep apnea, depression and other medical conditions that affect mortality and morbidity” Wiki.  The official rate of 36% is based on the CDC phone survey, a method that grossly underestimates. "Asking someone how much they weigh is probably the second worst question behind how much money they make… From past research, we know that women tend to under-report their weight, and men tend to over-report their height, Wiki.  And it is worse: the 6.3 % of the population who are morbidly obese (BMI above 40) are not included in with the 36% in the category of obesity--see.  “The consumption of sweet soda and fruit drinks has more than doubled since the 1970s… drinking sugary drinks was affecting genes that regulate weight and increased the genetic predisposition of a person to gain weight…. giving to children and adolescents calorie-free drinks like mineral water or soft drinks sweetened with artificial sweeteners resulted in weight loss” Wiki.   Other studies have shown that in just 2 weeks a diet consisting of 25% of calories from sugar resulted in insulin resistance--watch the CBC program on sugar.  The full impact of the increase in sugar takes years to develop, since obesity is a defect in the fat storage mechanism from hyperinsulinemia (high insulin), and this take years to decades to manifest (see #s 8, 9, 18, 19).  What follow mainly centers upon the regulatory system that control metabolism and appetite, and thus weight, physical energy, and the results of these homeostatic systems malfunctioning as a consequence of the Western diet. 

6)  Biological controls for weight gain:  Gary Taubes- (book list, at p. 112-125) convincing argues that the sedentary lifestyle is not a cause of obesity but a result of the biological process that causes the increase in adiposity. He argues that just like the biological mechanisms which set height and hair distribution, there is one for weight.  Gary uses animal examples of hippo, elephant, blue whale, and squirrels prior to hibernation as illustration of this mechanism.  Insulin has the greatest regulatory function, though over a dozen hormones and enzymes are involved.  When hormones set weight to obese, they control not just the rate of conversion of carbohydrates to fat and the storage of fat, but also the rate of metabolism and appetite. Thus not only does obesity through the load of extra weight diminish capacity for an active lifestyle, but obesity affects the hormonal mechanisms driving weight gain also zaps the energy needed to be active.  Those who are very active are so because of hormones and heredity. Obesity is not a result of over eating, but of excessive fat storage. “Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller.  Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger” Tabues-1 454.  Taubes also argues that to control weight long term requires resetting the hormonal mechanism so that a lower percentage of fat is stored and appetite diminished.  This explains why over 90% of people who after a diet fail to long-term maintain their weight loss, their weight control mechanism has not been reset.  To reset the mechanism requires a low sugar, low carb diet with the source of energy replaced by fats.  The sex hormones are also extensive involved.  Taubes 1 (page 373-4) writes of the experiments by George Wade on rats which the controlling effects of estradiol.  Taubes2 ends the discussion by pointing out the all the other mechanisms such as growth are tightly controlled by hormones, why should we expect fat storage to be different?  A similar view is expressed by Prof. Lustig. 

7) Leptin A high level of leptin decreases appetite through signaling the brain; leptin resistance entails a defect in the signaling and thus causes weight gain.  “Administration of leptin to rodents decreases food intake and increases energy expenditure.  In contrast to starvation, weight loss after peripheral or central leptin administration is restricted to adipose tissue “Physiology.  The same results have been obtained with patients with leptin deficiency.  “Leptin (Greek meaning "thin") is a 16-kD adipokine that plays a key role in regulating energy intake and expenditure, including appetite and hunger, metabolism, and behavior. It is one of the most important adipose-derived hormones.  This hormone circulates in and acts on the hypothalamus to regulate food intake and energy expenditure. When fat mass falls, serum leptin levels fall stimulating appetite and suppressing energy expenditure until fat mass is restored.  This hormone circulates in and acts on the hypothalamus to regulate food intake and energy expenditure. Leptin acts on receptors in the hypothalamus of the brain, where it inhibits appetite.  This appetite inhibition is long-term, in contrast to the rapid inhibition of eating by cholecystokinin (CCK) and the slower suppression of hunger between meals mediated by PYY3-36.   Leptin signals the brain that the body has had enough to eat, producing a feeling of satiety.  In humans, low circulating serum leptin has been associated with cognitive changes associated with anorexia, depression, HIV, and the development of Alzheimer's disease.  Yet another proposed mechanism involves the phenomenon known as leptin resistanceLeptin is a hormone that regulates long-term energy balance in many mammals. An important role of leptin is long-term inhibition of appetite in response to formation of body fat. This mechanism is known to be disrupted in many obese individuals: even though their leptin levels are commonly elevated, this does not result in reduction of appetite and caloric intake. Leptin resistance can be triggered in rats by ad libitum consumption of energy-dense, highly palatable foods over a period of several days.[36] Chronic consumption of fructose in rats ultimately results in leptin resistance (however, this has only been demonstrated in a diet where fructose provided 60% of calories; the actual consumption by humans in a typical Western diet is several times lower. Once leptin signaling has been disrupted, the individual becomes prone to further overeating, weight gain, and insulin resistance” Wiki.  Dieters who lose weight, particularly those with an overabundance of fat cells, experience a drop in levels of circulating leptin. This drop causes reversible decreases in thyroid activity, sympathetic tone, and energy expenditure in skeletal muscle, and increases in muscle efficiency and parasympathetic tone. The result is that a person who has lost weight below their natural body fat set-point has a lower basal metabolic rate than an individual at the same weight who is of that natural weight; these changes are leptin-mediated, homeostatic responses meant to reduce energy expenditure and promote weight regain as a result of fat cells being shrunken below normal size. Many of these changes are reversed by peripheral administration of recombinant leptin to restore pre-diet levels…. Studies on leptin cerebrospinal fluid (CSF) levels provide evidence for the reduction in leptin crossing the BBB [-brain barrier] and reaching obesity-relevant targets, such as the hypothalamus, in obese people.  It is likely that the leptin resistance in these individuals is due to a post leptin-receptor deficit, similar to the post-insulin receptor defect seen in type-2diabetesWiki.  Adipose tissues produce a hormone, adiponectin, which provides the mechanism for regulating the amount of adipose tissue including effecting glucose flux, lipid catabolism, protection from endothelial dysfunction (factor in atherogenesis), insulin sensitivity weight loss, control of energy metabolism, reduction of TNF-alpha.  Obesity is associated with decreased adiponectin.  Another major regulatory hormone is Ghrelin which is similar to leptin in extent of regulatory functions.  Ghrelin is produced in the gastrointestinal track and has sites of action in the pancreas, nervous system, reproductive system and immune systems. It, like leptin, helps regulate metabolism and hunger. Having covered briefly ghrelin and adiponectin, for simplicity their roles are dropped out of the analysis along with others.  The purpose is to see the forest and understand the processes, not to present a description of each important species of tree.  Leptin regulation in part is influence by insulin, and both are the main cause for obesity, and like insulin, leptin has many other roles.[1]  Dr. Lustig, in his Fat Chance, p. 47 states:  No matter the mechanism, insulin blocks leptin signaling both in rodents and in humans… In the brain insulin causes leptin resistance and “brain starvation.”  In summary, IR entails high level of insulin and that among functions of insulin is the down regulation of leptin, which thereby results in an increase in the drive to eat (what is called hunger) and reduction in satiation upon eating. 

8)  Insulin and glucagon in glucose regulation:  The Isle of Langerhans in the pancreas produces the hormones glucagon, insulin and amylin, somatostatin, and pancreatic polypeptides, all of which play a role in the regulation of glucose-glycogen levels.  Glucagon and insulin play major roles in the regulation of cellular glucose-glycogen levels.  Glucagon raises glucose levels by promoting gluceogensis & glycogenolysis.  Its effect is opposite that of insulin, which lowers glucose levels. The pancreas releases glucagon when glucose levels fall too low. Glucagon causes the liver to convert stored glycogen  polymers into glucose, which is released into the stream. As these stores become depleted, glucagon then encourages the liver and kidney to synthesize additional glucose by gluconeogenesis.  Glucagon turns off glycolysis in the liver [the production of ATP], causing glycolytic intermediates to be shuttled to gluconeogenesis.  High glucose levels stimulate the release of insulin” Wiki.  Insulin causes cells in the skeletal muscles, and fat tissue to absorb glucose from the  [for metabolism].  Insulin stops the use of fat as an energy source by inhibiting the release of glucagon.  Insulin is provided within the body in a constant proportion to remove excess glucose from the, which otherwise would be toxic. When glucose levels fall below a certain level, the body begins to use stored sugar as an energy source through glycogenolysis, which breaks down the glycogen stored in the liver and muscles into glucose, which can then be utilized as an energy source.[2]  When control of insulin levels fails, diabetes mellitus can result.  Patients with type-2 diabetes are insulin resistant [or fail to produce sufficient insulin, see discussion below on variations in T2D].  Over 40% of those with Type-2diabetes require insulin as part of their diabetes management plan” Wiki.   “Insulin causes esterification of fatty acids–-forces adipose tissue to make fats (i.e., triglycerides) from fatty acid esters and thereby forces its storage and its lack the reverse” Wiki.

9)  Insulin resistance (IR):   Insulin is promoted by a number of mechanisms describe throughout this paper.  These include glycation by fructose in the liver, non-alcoholic fatty liver disease, insulin resistance in the liver, reduce secretion in the adipose tissue of adiponectin (a process associated with obesity), and by prolonged elevated serum insulin level.  High level of insulin from a high carb diet reduces the responsiveness of insulin receptors on cell walls.  With lower response there is high serum glucose.  The pancreas thus secrets even more insulin to lower the serum glucose to a safe target level.  This high insulin promotes fat storage and thus obesity.  It also reduces the production of leptin which affect the process that controls the body’s set “normal weight” through increased appetite and if necessary reducing metabolism to maintain that higher weight.  Most of the adverse health consequences of high serum glucose results from its affect upon adhesion factors joining cells and damage through glycation.  Insulin resistance promotes glycation through the higher level of serum sugars for a longer period of time.[3] When the glucose and fructose levels are high, glycation damages the proteins on the cell wall (endothelial cells) lining the arteries.  Overtime the reactive sugars, carbon monoxide, and various drugs can significantly compromise the endothelial cells’ functions.  This can cause endothelial dysfunction.  IR is a risk factor for ischemic events, because it increases by higher level of circulating sugars glycation which damages the endothelial cells.  So damaged there is an increased probability of leakage of plaque from the tunica intima into the blood stream.[4]  Since insulin upregulates leptin, IR increases serum leptin, which can develop into leptin resistance.  Leptin resistance can be triggered in rats by ad libitum [at ones pleasure] consumption of energy-dense, highly palatable foods [sugar and starches] over a period of several days…. IR stimulates the formation of new fatty tissue and accelerates weight gain.  Obesity should therefore not be regarded as a pathology or disease, but rather as the normal, physiologic response to sustained caloric surplus…  Sedentary lifestyle increases the likelihood of development of insulin resistance.  It's been estimated that each 500 kcal/week increment in physical activity related energy expenditure reduces the lifetime risk of type-2 diabetes by 6%.  A different study found that vigorous exercise at least once a week reduced the risk of type-2 diabetes in women by 33%” Wiki. Exercise lowers serum glucose.   In Science 2003 a study confirmed an age  association with IR in that there is among the elderly approximately a  40% reduction in oxidative and phosphorylation activity in the mitochondria; viz., the person with IR, his mitochondria clears glucose at a  slower rate.  A further complication is that adipose tissue through reduced production of adiponectin causes insulin resistance.  With obesity the production of adiponectin decreases.  This effect results from increased expression of molecules involved in both fatty-acid combustion and energy dissipation in muscle. Moreover, insulin resistance in lipoatrophic mice was completely reversed by the combination of physiological doses of adiponectin[5] and leptin, but only partially by either adiponectin or leptin alone” at 2001 and 2002, also 1989.  

10) High-fructose diet role in causing Insulin resistance (IR) and other consequences:  On Pages 123-24 of Fat Chance by Dr. Robert Lustig is listed “the unique metabolism of fructose can induce each of the phenomena associated with metabolic syndrome.”  Fructose which is only metabolized in the liver in several ways starts the process leading to IR and MeS.  Dr. Lustig lists them.  1) Fructose when metabolized in the liver depletes the liver’s store of ATP[6].   Among its affects is the accumulation of uric acid which increases blood pressure and causes gout.  2)  Fructose is metabolized in the mitochondria of the liver where it produces an excess of acetyl-CoA which leaves the mitochondria.  3)  This acetyl-CoA is converted to fat within the liver, which causes non-alcoholic fatty liver disease (NAFLD, see #15 below).  4) Fructose activates an enzyme in the liver that leads liver insulin resistance.  To this I would add that glucose is stored as glycogen, and that this process is impaired through damage cause by fructose.  Reduced production of glycogen entail elevated serum glucose and thus increased insulin, one way liver dysfunction promotes IR.  5) This insulin resistance in the liver causes a rise in the level of serum glucose.  6) This higher level of glucose in the causes the pancreas to release more insulin.  6) This higher level of insulin increases fat storage (width gain). 7) Leptin level is lowered in response to higher insulin, and this sends a message to the hypothalamus in the brain to increase hunger.  8) Fructose as a reactive chemical damages proteins at 7.5 times the rate of glucose through the Maillard reaction, moreover since there is much more in the liver as site of metabolism then the measured serum level, the rate of liver damage is highest.  The serum level over 2 hours from a 75 gm bolus of sucrose is twice that of glucose.  9) Two experiments on young healthy subjects comparing the effects of 1000 kcal of extra fructose to that of 1000 gm of glucose.  At 9 weeks out there was a 25% greater insulin insensitivity in the fructose group, at 1980, and 2005 and, in rats[7], also.  10)  This effect of fructose damaging the liver contributes to the association of a high fructose diet with cancer, Alzheimer’s disease, and other age related conditions.  As prof. Lustig puts it:  “Fructose isn’t the only cause of obesity, but it is the primary cause of chronic metabolic diseases which kills . . . slowly.  Fructose can fry your liver and cause all the same diseases as alcohol [on point 2013].  We know we must limit our ethanol consumption or face the consequences.  But sugar flies under the radar” Lustig supra 125.  Population studies also shed light.  The Chinese and Japanese traditional diet is high in the refined carbohydrate white rice, yet T2D is just 1 percent.  With the introduction of the Western diet with its sugar laden beverages, the rate of obesity has shot up in Japan to over 20 percent, at.  Since the traditional Japanese diet is high in carbs, yet obesity, CVD, and diabetes is very low, this demonstrates the role of fructose, not glucose in pathology. 

11) High sugar diet:  The disaccharide sucrose is the principle sugar which is readily converted during digestion into glucose and fructose.  High fructose corn syrup (HFCS) found only in process foods is cheaper and sweeter than sucrose.  It is made from corn starch which is pure glucose by an enzymatic process developed in Japan and became a commercial success in the 1980s.  It usually consists of 55% fructose and 43% glucose, thus HFCS’s effect is similar to sucrose.  Being water soluble and readily hydrolyzed, HFCS and sucrose are rapidly cleared from the stomach as monosaccharides. Both sucrose and HFCS are readily absorbed by the duodenum.  Glucose stimulates the production of insulin which causes cells to absorb the glucose for metabolism and to store fat, while fructose is transported directly to the liver for metabolism.  The duration and amount of insulin follow consumption of sugar, starches, and other sources of glucose has major health consequences.  A chain of interconnected conditions arise from decades-long elevation in glucose in the serum and of fructose in the liver.  Metabolic syndrome, insulin resistance, obesity, and fatty live are results of fructose-initiated damage to the liver, and other causes.  The liver can synthesize glucose from certain amino acids, lactate, and glycerol.  The liver can break down glycogen into glucose, and convert glucose to glycogen which it can store.   Sugars cause oxidative and glycation damage to the liver which diminish its functions.  Fructose has a reaction constant 7.5 times as high as that of glucose in its non-enzymatic reaction with protein in vitro” at 1988; moreover their graphs shows over a 3 hour period following ingestion of 75 grams of sucrose twice the serum level of fructose, thereby resulting in 15 times the amount of fructose.  Both sugars attach to proteins and lipid in a process called glycation by the Millard reaction.  Thus fructose in theory causes damage at 15 times the rate of glucose—no in vivo studies have been performed for confirmation.   In Hippocampus 2008:  Here, we used functional and structural assays to characterize the effects of excessive caloric intake on the hippocampus, a brain region important for learning and memory.  We conclude that a high-caloric diet reduces hippocampal synaptic plasticity and impairs cognitive function, possibly through BDNF-mediated effects on dendritic spines.”  High sugar diet causes fatty liver and metabolic syndrome; this is supported both by population studies and laboratory research (# 17 below).  High sugar diet is linked to tooth decay insulin intolerance, gout, obesity, diabetes, CVD, Alzheimer’s disease, cognitive decline, and many other age-related chronic conditions.  Since fructose is only metabolized in the liver, the liver is particularly prone to damage through glycation.  This liver damage among other things causes IR in the liver.  A high level of serum glucose raises the insulin level, to which over decades the muscles and other cells become resistant to the insulin, thus causing even more insulin resistance.  A high carb diet in itself is not sufficient.  As pointed out at the end of #10, the traditional high carb Japanese diet had both a low rate of obesity and T2D.  Add the Sugars from sodas and manufactured foods of the Western diet, and it has all changed.  The high sugar/fructose diet is a health disaster.

12) Fructose, the differences from glucose:  Unlike glucose, which is metabolized widely in the body, fructose is metabolized almost completely in the liver in humans, where it is directed toward replenishment of liver glycogen and triglyceride synthesis.[8]  Fructose is also not metabolized in insulin-sensitive peripheral tissues. Fructose is selectively taken up and almost completely metabolized by liver hepatocytes, while much of dietary glucose passes through the liver where it is metabolized in skeletal muscle to CO2, H2O and ATPWiki. Fructose is often recommended for diabetics because it does not trigger the production of insulin by pancreatic β cells, probably because β cells have low levels of GLUT5 [transport system into pancreas] although its net effect is debated.  Fructose has a very low glycemic index of 19 ± 2, compared with 100 for glucose and 68 ± 5 for sucrose [for glycemic index table at article on carbohydrates].  Fructose is also seventy-three percent sweeter than sucrose.  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.  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” Wiki.  “Since fructose consumption has been hypothesized to be a cause of insulin resistance, obesity, … and, leading to metabolic syndrome. In preliminary research, fructose consumption was correlated with obesity.  A study in mice showed that a high fructose intakes increases adiposity.  While a few other tissues (e.g., sperm  cells and some intestinal cells) do use fructose directly, fructose is metabolized primarily in the liver.  A preliminary human study indicated that fructose may influence metabolic activity or  flow in brain regions regulating satiety ("fullness"), and so may promote overeating.  Excessive fructose consumption may contribute to the development of non-alcoholic fatty liver disease [#15 below]Wiki.  Typical findings: “For effects of high fructose diet include:  Fructose is more lipogenic than glucose or starches, and usually causes greater elevations in triglycerides and sometimes cholesterol than other carbohydrates.   Dietary fructose has resulted in increases in serum pressure, uric acid, and lactic acid.  People who are hypertensive, hyperinsulinemia, hypertriglyceridinemia[9], non-insulin-dependent diabetes, or postmenopausal women are more susceptible to these adverse effects of dietary fructose than healthy young subjects.”  “[Evidence] suggest that fructose stimulates triglyceride production but impairs triglyceride removal, whereas glucose stimulates both of them" Wiki, relying on 1996.  In Fructose, weight gain and insulin resistance syndrome, 2002 journal article states:  Because leptin production is regulated by insulin responses to meals [and fructose doesn’t stimulate insulin production], fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae [injury].”  The rise in CVD and obesity results from its dietary increase.  USDA chart:  The per-capita yearly consumption of sweeteners was 109 lbs. in 1950 and 152 lbs. in 2000.  The USDA states: “The food consumption in 1970 was 2275 calories and in 2000 was 2,750 calories per person per day, 475 calories above the 1970 level.”  Though both glucose and fructose are about equally efficient at producing ATP (the body’s energy source), fructose rate of glycation is “7.5 times higher than glucose” (at).  Adjusting for its higher serum level and longer duration, the in vivo rate is 15 times that of glucose.  In addition fructose has a greater role than glucose in causing obesity, IR, MeS, and NAFLD.  The role in fructose leading to insulin resistance entails collateral damage to the immune system, and as a consequence an association with atherosclerosis.  Pathogens within the tunica intima of the arteries is the leading cause of AS and thus CVD.  Fructose’s negative effect upon the immune system explains in part why those with T2D have twice the risk of heart attack (AMI).[10]Increasing experimental evidence indicates that several factors that influence metabolism also play a role in the regulation of immune responses” at.  Though I have relied upon Wikipedia as a source, those with a financial interest spin Wikipedia articles to downplay the role of fructose and promote the cholesterol–fat myths.  Thus I have turned to other sources on diet and journal articles to counter the pharma and food manufacturers’ tobacco-science distortions.  The statement repeatedly made by Prof. Robert Lustig (see Video Library) that fructose is poison and should be regulated like alcohol is supported by the evidence. A 2013 nutritional journal article is titled Fructose is alcohol without the Buzz; both are metabolized the same way in the liver and are equally toxic to the liver—thus proving Dr. Lustig’s fructose is poison claim.     


13)  Sugar addiction:  “The hedonic pathway comprises a neural conduit between two brain areas:  the ventral tegmental area (VTA) and the nucleus accumbens (NA also known as the reward center)… Pleasure occurs when the VTA signals the NA to release dopamine, a neurotransmitter…. When the released dopamine binds to its specific dopamine D­3 receptor in the NA, the sense of pleasure is experienced.  Sugars are also key players in the hedonic pathway, modulating reward to response to meals.  In normal circumstances, after you’ve eaten a sufficient amount, leptin sends a signal to the VTA to suppress the release of dopamine, thereby reducing the reward of food…. If you feed a rodent a palatable food (e.g., a high-fat, high-sugar food such as cookie dough), the animal experiences reward because dopamine is released from VTA and binds to D­­3 receptor in the NA…. Dopamine stimulation in the NA reinforces the intake of drugs or alcohol and also of food…. After you’ve eaten a sufficient amount, leptin sends a signal to the VTA to suppress the release of dopamine, thereby reducing the reward of food.  That’s what obesity is:  leptin resistance.   What about insulin, leptin’s accomplice?  Normally, people are sufficiently sensitive to insulin.  Insulin’s job is to clear dopamine from the synapses…. Thus the rise in insulin that occurs during a meal blunts the reward of further food intake.  This acts as a servo-mechanism built into the hedonic pathway to prevent overfeeding.  Insulin resistance leads to leptin resistance in the VTA, contributing to increased caloric intake by preventing dopamine clearance from the NA.  Increase pleasure is then derived from food when energy stores are full…. Thus, the combination of high fat along with high sugar is likely to be more addictive than high fat alone.  All the criteria for sugar addiction have been demonstrated in rodent models.   Evolutionary, sweetness was the signal to our ancestors that something was safe to eat“, Prof. Robert Lustig, Fat Chance 2013, p 50-56.  If you doubt the sugar addiction theory, try cutting your sugar intake to 24 grams a day (6 teaspoons).  Use the food labels to determine sugar content and USDA Handbook for the bulk foods (mainly fruits, vegetables).  I tried it, and though fairly good at eliminating sugar added products, I keep nibbling on apples, bananas, raisins, and grapefruit juice. I have eliminated the sugar added at the source, the grocery store, but not those on the shelf at home; they simply aren’t getting replaced, and the worse of them have been trashed.  Secondly observe the behavior of children between the ages of 3 and 6, most crave sugar added products, and let their parents in the super market know it.  “When the nucleus accumbens is excessively activated by sweet food or powerful drugs, says Bartley Hoeble of Princeton, ‘it can lead to abuse and even addiction.  When this system is underactive, signs of depression ensure.  Rats can be easily addicted to sugar,’ according to Hoebel, ‘and will demonstrate the physical symptoms of opiate withdrawal when forced to abstain.’  [This] implies that the addiction can be overcome with sufficient time, effort, and motivation, which is not the case with hunger itself…. Avoiding carbohydrates will lower insulin levels even in the obese, and so ameliorate the hyperinsulinemia that causes the carbohydrate craving itself.  ‘After a year to eighteen months the appetite is normalized and the craving for sweets is lost’, said James Sidbury, Jr. about the effects on children of his carbohydrate-restricted diet.”   Taubes 446.   


14) The breakdown of the regulatory system for serum glucose and weight control:  it is a 4 step process that begins with a high sugar and refined carbohydrate diet.  This results in fructose damaging the liver in ways that result in insulin resistance in the liver and also to produce non-alcoholic fatty liver disease (NAFLD).  This causes both insulin and leptin resistance. Damage to the pancreas beta cells will cause T2D.  At the same time weight is gained.  And with drug treatment resistance develops which result in injections of insulin. The weight gained through insulin results in an increase in adipose tissue, which produces hormones that are resistant to calorie restricted diets that include carbs.  The weight regulatory much of which is in the adipose tissue is resistant to reduction in adipose tissue. 

15) Fetal environment IR, T2D, and obesity:  “Insulin is a gateway hormone affecting others whereby the overproduction of insulin plays a key role in the process.  Beside the question of predisposition to obesity based on genes, there is also the fetal insulin-glucose load from the mother.  In the near-term fetus, high glucose level result in increased production of insulin by the fetus and increase in the isle of Langhorne cells which produce insulin.  These changes predispose the person to an increased sensitivity to sucrose.  Fortunately predisposed does not mean beyond cure.  Additional evidence comes from that the fact that over the last twenty-five years, birth weight has increased worldwide, by as much as 200 grams (half a pound)… it is likely that maternal weight gain is translated into fetal body fat; the more weight the mother gains during pregnancy the great the birth of the newborn, and the more fat cells early on, the greater the risk later on” Lustig 76.  “The number of fat cells is determined before you are born” Lustig 77.  Over-nourished infants are predisposed to obesity if their mother developed gestational diabetes.  The picture is complicated by the fact that undernourished fetuses are also predisposed to obesity.  “Newborns in Pune, India versus those born in London demonstrated that, despite the fact those new born in India weighed 700 grams less at birth, their insulin levels were markedly elevated… the India-born babies demonstrated increased adiposity four times higher insulin, and two times higher leptin levels than their London-born counterpart… they were predestined to develop obesity and metabolic syndrome” Lustig 79.  “Worse yet premature babies also manifest insulin resistance… enormously high risk for metabolic syndrome in childhood or in adulthood” Lustig 79-80.  Clearly fetal environment affects risk factors.  Most significant is the drift towards overweight and obese mothers:  given its causal relationship to the next generation of overweight mothers, we are evolving to a fat species.   

16) Role of genetics: “A large number of genes increase the sensitivity to a high carbohydrate study.  We identified four loci containing variants that confer type-2diabetes risk, in addition to confirming the known association with the TCF7L2 gene. These loci include a non-synonymous polymorphism in the zinc transporter SKC30A8, which is expressed exclusively in insulin-producing beta-cells, and two linkage disequilibrium blocks that contain genes potentially involved in beta-cell development or function (IDE–KIF11–HHEX and EXT2–ALX4). These associations explain a substantial portion of disease risk and constitute proof of principle for the genome-wide approach to the elucidation of complex genetic traits" at Nature 2007.  For over 99% the populace these genes are merely a risk factor dependent upon environment (high fructose diet), thus obesity is rare among hunter-gatherers.  

17) Non-alcoholic fatty liver disease (NAFLD) and its extreme form NASH:  A recent study using the National Health and Nutrition Examination Survey (NHANES) found a 30% prevalence of NAFLD in the United States between 2011 and 2012.  NAFLD is related to insulin resistance and the metabolic syndrome.  Most patients with NAFLD have few or no symptoms. Patients may complain of fatigue, malaise, and dull right-upper-quadrant abdominal discomfort. Mild jaundice may be noticed although this is rare. More commonly NAFLD is diagnosed following abnormal liver function tests during routine tests.  Soft drinks have been linked to NAFLD due to high concentrations of fructose[11], which may be present either in high-fructose corn syrup or, in similar quantities, as a metabolite of sucrose. The quantity of fructose delivered by soft drinks may cause increased deposition of fat in the abdomenWiki. Non-alcoholic fatty liver disease (NAFLD) is the term for a wide range of conditions caused by a build-up of fat within the liver cells. It is usually seen in people who are overweight or obese.  NAFLD is related to insulin resistance and the metabolic syndrome and may respond to exercise, diet change, and weight loss.   It is a spectrum disease, and at the low end of NAFLD, few have symptoms.  Some patients complain of fatigue and malaise.  A healthy liver should contain little or no fat. Most people with NAFLD only carry small amounts of fat in their liver, which doesn't usually cause any symptoms. This early form of the disease is known as simple fatty liver, or steatosis.  (“Steatosis” is also used to refered to the disease condition NASH, see below.) Simple fatty liver is very common in the UK, reflecting the number of people who are obese or overweight.  It is one of the most common forms of liver disease, with an estimated 25-30% people in the UK having early forms of NAFLDNHS.   It is difficult to distinguish alcoholic FLD from NFLD, and both show micro-vesicular and macro-vesicular fatty changes at different stages.  Fatty change represents the intra-cytoserumtic accumulation of triglycerides (neutral fats).  At the beginning, the hepatocytes present small fat vacuoles (liposomes) around the nucleus (micro-vesicular fatty change). In this stage, liver cells are filled with multiple fat droplets that do not displace the centrally located nucleus. In the late stages, the size of the vacuoles increases, pushing the nucleus to the periphery of the cell, thus giving characteristic signet ring  appearance (macro-vesicular fatty change).  Large vacuoles may coalesce and produce fatty cysts, which are irreversible lesions.  Defects in fatty acid metabolism are responsible for pathogenesis of FLD, which may be due to imbalance in energy consumption and its combustion, resulting in lipid storage, or can be a consequence of peripheral resistance to insulin, whereby the transport of fatty acids from adipose tissue to the liver is increased.  Impairment or inhibition of receptor molecules (PPAR-α, PPAR-γ and SREBP1) that control the enzymes responsible for the oxidation and synthesis of fatty acids appears to contribute to fat accumulation. On the other hand, nonalcoholic FLD may begin as excess of unmetabolised energy in liver cells.  Hepatic steatosis [fat build up in liver] is considered reversible and to some extent non-progressive if the underlying cause is reduced or removed.  FLD is observed in up to 75% of obese people, 35% of whom progressing to NAFLD   Wiki.   A liver can remain fatty without disturbing liver function, but by varying mechanisms and possible insults to the liver may also progress to become non-alcoholic steatohepatitis (NASH), a state in which steatosis is combined with inflammation and fibrosis (steatohepatitis).  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.  NASH is a progressive disease: over a 10-year period, up to 20% of patients with NASH will develop cirrhosis of the liver, and 10% will suffer death related to liver disease.[8]  Cigarette smoking is not associated with an increased risk of developing NASH. The exact cause of NAFLD is still unknown [business-spin leaving out the role of fructose].  However, both obesity and insulin resistance probably play a strong role in the disease process. The exact reasons and mechanisms by which the disease progresses from one stage to the next are not known.  One debated mechanism proposes a "second hit", or further injury, enough to cause change that leads from hepatic steatosis to hepatic inflammation.  Oxidative stress, hormonal imbalances, and mitochondrial abnormalities are potential causes for this "second hit" phenomenon.  Common findings are elevated liver enzymes and a liver ultrasound showing steatosis[12]Wiki.  “Steatosis suggests that the accumulation of fat due to fructose metabolism causes a disruption of those functions of the liver affecting serum insulin level.  High serum insulin is defined as insulin resistance.  The association of NAFLD with obesity (70-90% of the obese have NAFLD at) is strong evidence for the role of insulin and fructose[13]  So too is NAFLD associated with glycation, at 2008.  For example, “bariatric surgery patients show an improvement in NASH symptoms [the extreme form of NAFLD] in around 80% of patients” journal and Wiki.  The fructose conversion to fat in the liver accumulates not only in visible clumps in the liver (which when extensive develops into clinical cirrhosis of the liver) but also with droplets of fat within hepatic cells.  The liver goes from about 3 pound to about 5 pounds with NAFLD.

17B) NASH, Non-alcoholic steatohepatitis:  “is the most extreme form of NAFLD and is regarded as a major cause of cirrhosis of the liver of unknown causes” Wiki.  Weight gain is accelerated as fat content of the liver progress and the effects of IR worsen.  Thus 60 to 70% of the obese have NAFLD and have progressed to 18.5% NASH, while of the morbidly obese (BMI > 40) 91% have NAFLD of which 29% have NASHsee.  NASH is a progressive disease: over a 10-year period, up to 20% of patients with NASH will develop cirrhosis of the liver, and 10% will suffer death related to liver disease.”  [For cause] one debated mechanism proposes a "second hit", or further injury, enough to cause change that leads from hepatic steatosis to hepatic inflammation.  Oxidative stress, hormonal imbalances, and mitochondrial abnormalities are potential causes for this ‘second hit’ phenomenonWiki.   For reasons still being investigated, inflammation in the liver is associated with the conversion of NAFLD to NASH and cirrhosis.  Definitive diagnosis of NASH requires a liver biopsy with over 60% of a hepatocytes weight consisting of fat.  On one biopsy 24% of those with NAFLD are missed.  [This is because] “histologic lesions of NASH are unevenly distributed throughout the liver parenchyma; therefore, sampling error of liver biopsy can result in substantial misdiagnosis and staging inaccuracies”see.  Though both caloric restriction (<1500 calories/d, and carb restriction ( < 20gm/d) produced lower hepatic triglycerides and weight loss, the low carb diet produced significantly superior results at 2011.  Given the 95% long-term failure rate of energy restriction, the benefits are but short-term and thus carb restriction is the preferred therapeutic approach.      

18) Fructose and non-alcoholic fatty liver disease (NAFLD):  Fructose brings about this condition in much the same way as alcohol:  ethanol is metabolized in the liver and used in the production of fatty acids, the same for fructose.[14]  Insulin in the liver causes the hepatocytes to burn glucose and store the fat that they are producing from fructose.  This accumulation of fat will modify metabolic processes outside the liver, which will result in IR.  Over many years the high fructose diet will cause sufficient fat for a diagnosis of NAFLD, which afflicts 30% of the adult population.  Moreover, glycation by fructose in the liver occurs at rate 15 times that of glucose when consumed in equal portions (see #12), and.   This random latching on to proteins in the liver cause more havoc with liver functions, and can progress to a point where it shows up on liver function tests.    “The degradation of the metabolic processes in the liver entails a decrease in energy and subsequent related emotional problems such as depression.  The close parallel in fructose metabolism results in metabolic consequences which resemble those from alcoholism.  Given the many functions of the liver, a healthy liver has numerous varied benefits” Wiki.  In Gastroenterologysoft drink consumption is the most common risk factor for fatty infiltration of the liver in patients without classic risk factors” like finding, and.   The role of sugar is found in hundreds of journal article on NAFLD.  Fructose It’s Alcohol Without the Buzz” (the title of a 2013 journal article) describes the similarity to alcohol caused liver damage.  This parallel to alcohol has been used by Dr. Lustig and others.   


19) Role of insulin in developing insulin resistance:  Liver damage through fructose metabolism in the liver is associated with NAFLD though the conversion of fructose to fat.  Though the exact cause of the gradual process of developing insulin resistance in the liver is not known, in the aetiology of bodily insulin resistance, liver insulin resistance comes first.  This order of events is supported by the observation concerning hepatitis C, an infection of the liver:  The extra insulin resistance caused by Hepatitis C apparently brings on diabetes at 35 or 40, instead of 65 or 70….  Eventually, type-2diabetes or latent autoimmune diabetes occurs when glucose levels become higher throughout the day as the resistance increases and compensatory insulin secretion fails.  The elevated insulin levels also have additional effects (see insulin) that cause further abnormal biological effects throughout the body” Wiki.   The body has developed a system for preventing IR; it secretes insulin in cycles of 3 to 6 minutes.  However, the body has not evolved a way to handle the high sugar-carbohydrate Western diet.  Elevated insulin from the Western diet is a direct cause of IR by decreasing the response of the insulin receptors on the surface of muscle and adipose cells.   Strong evidence for this comes from bariatric surgery, which results in fasting following the operation as the stomach heals.  Within 1 week 90% of patients are cured of T2D and IR, thus showing that insulin is the main direct cause and not the quantity of adipose tissue is the cause of IR—at 2006, also see #23 for discussion of bariatric surgery. 

19b) The role of refined carbohydrates in develop IR and MeS. The spike in glucose and thus insulin from refined carbohydrates elevates insulin and will with a steady diet cause IR as stated above.  However, the influence of corporate bucks has kept out the role of refined carbs.  Pharma makes too much treating diabetes and the comorbidities from IR to implicate carbohydrates and thus insulin.  “There was no mention that carbohydrates might be responsible for the causing or exacerbating either metabolic syndrome or the combination of low HDL, high triglycerides, and small, dense LDL,… In the now established version of the alternative hypothesis—that metabolic syndrome leads to heart disease—the carbohydrates that had always been considered the causative agent had been officially rendered harmless.  They had been removed from the equation of nutrition and chronic disease, despite the decades of research and observations suggesting the critical causal role they played.” Gary Taubes, Good Calories, Bad Calories, 2005, p183.  And it gets worse the fix gets blamed as the cause:  the doubling of the risk of MI for those with T2D is blamed on low-carb diet with its increased saturated fats.  “Traditional restriction of carbohydrate intake in persons with diabetes and thus an increased intake of fat, usually saturated” quoting the 1988 Surgeon General’s Report, supra 186. This is the logic that led the American Diabetes Association, from the early 1970s to recommend that diabetics eat more carbohydrates rather than less, despite a complete absence of clinical trials that might demonstrate the benefits of so…” supra 186-7.    

 20) Role of adipose tissue in developing insulin resistance and obesity:  The accumulation of fat within the hepatocytes (liver cells) in addition to clump of fat in the liver adversely affects liver functions and intra cellular fat in the pancreas causes T2D.  Having once been thought of as merely containers for fat storage, in the last 3 decades adipose (fat) tissue has been shown to produce a number of hormones.   “In recent years, been recognized as a major endocrine organ,[1] as it produces hormones such as leptinestrogenresistin, and the cytokineTNFαWiki.  These hormones control among other things metabolism, appetite, weight, and fat distribution.  The reduced secretion of adiponectin by adipose tissue has been shown in conjunction with reduced leptin as causes of IR—see #7-9 above.  “In the fat cells of obese individuals, there is increased production of metabolism modulators, such as glycerol, hormones, and pro-inflammatory cytokines, leading to the development of insulin resistance.” Wiki.   With obesity through decreased leptin there is an increase in appetite and a lower rate of metabolism and this lower rate entail a higher blood glucose level and thus damage through glycation.  Obesity is a marker for a malfunctioning glucose-leptin-insulin regulatory system--80% of those with T2D are obese.  High carb diet contributes to obesity by stimulating insulin production.  “Fat production in adipocytes is strongly stimulated by insulin. By controlling the activity of the pyruvate dehydrogenase and the acetyl-CoA carboxylase enzymes, insulin promotes unsaturated fatty acid synthesis. It also promotes glucose uptake and induces SREBF1, which activates the transcription of genes that stimulate lipogenesis” Wiki.   Adipose tissue produces estriol, which is an antagonist (suppresses) of estradiol.  Estradiol causes fat to be stored in the buttocks, thighs, and hips in women.  Following menopause when estradiol declines the fat migrates to the abdomen, which is strongly associated with MIs (heart attacks).  In these ways through estriol synthesis is women obesity is associated with health issues seen with a decline in estradiol following menopause.  See HRT for the benefits and tobacco science pharma uses. 


2 hour glucose

Fasting glucose








<7.8 (<140)

<6.1 (<110)



Impaired fasting glycaemia

<7.8 (<140)

≥6.1(≥110) & <7.0(<126)



Impaired glucose tolerance

≥7.8 (≥140)

<7.0 (<126)



Diabetes mellitus

≥11.1 (≥200)

≥7.0 (≥126)



HbA1c (glycated hemoglobin) is a measure of the amount of glycation that occurs during the life of a red-blood cell over the previous 90 days which is indicative of the management of serum glucose, and thus a test for diabetes.  Note: all these values for diabetes have been lowered in the last decade so as to increase the number treated.    

21) Treating pre-diabetics e 2 common forms of type-2-diabetes:  Most cases of T2D have low serum insulin.  For all types of T2D, as stated when describing NAFLD (# 16 & 17) and the associated IR,  It all starts with insulin resistance in the liver through the action of fructose.  About 20% of glucose metabolism occurs in the liver and all of fructose metabolism.  Eventually due to the action of insulin excess cellular fat accumulates in the beta cells of the pancreas and the insulin production sharply declines resulting in symptomatic hyperglycemia.  However, in pharma’s push to sell drugs, some who are predi

Unlike type 1 diabetes that is a result of autoimmune destruction of the beta cells, T2D can be reversed through diet.  T2D can also be managed with drugs other than insulin.  A second more acute form of T2D develops when tolerance develops to those drugs, and insulin must be administered.  Because of the action of insulin on fat storage, glucose conversion to fat, and its action upon leptin which increases appetite about 80% of those who are obese have T2D.  With the addition of insulin, for most the rate of weight gain increases as does the comorbidity rates. 

22) Latent Autoimmune Diabetes of Adults (LADA):  Of those diagnosed with T2D about 5%, are not obese and appear to have adult onset type-1 diabetes, which is commonly mistakenly treated as T2D.[15]  The concept of LADA was first introduced in 1993….  It is estimated that more than 50% of persons diagnosed as having non-obesity-related type-2 diabetes may actually have LADA… Not all people having LADA are thin or skinny, however—there are overweight individuals with LADA who are misdiagnosed because of their weight” Wiki. “It is clear that type-2 diabetes is not a single disorder but is rather a syndrome of great heterogeneity… When diabetes is associated with obesity, the disease usually seems to be caused by insulin resistance plus an impaired ability of the pancreas to compensate for the resistance. The present data suggest that non-obese diabetic [LADA] elderly male subjects form another subgroup of the disease where peripheral insulin action is normal and the insulin secretory defect is the major cause of the disease….  In non-obese hyperglycaemic subjects, however, there was no evidence of peripheral insulin resistance… only a marked secretory defect involving both the first-and second-phase response” Diabetologia, 1991 at 486.  Though it has since ancient times been known that dietary management is an effective treatment at reducing morbidity and mortality, because of damage to the pancreas, with LADA  for most neither alternate day fasting diet or bariatric surgery (see #31) will be curative.  LADA occurs in 5-10% of those diagnosed with T2D.  Possible some subset will be cured as the islets of Langerhans beta cells in the pancreas regenerate.  Unfortunately the literature is sparse. 

[1]In the periphery leptin is a modulator of energy expenditure, modulator between fetal and maternal metabolism, permissive factor in puberty, activator of immune cells, activator of beta islet cells, and a growth factor. Further, it interacts with other hormones and energy regulators: insulin, glucagon, insulin-like growth factor, growth hormone, glucocorticoids, cytokines, and metabolites...  Leptin affect bone metabolism….  Factors that acutely affect leptin levels are also factors that influence other markers of inflammation, e.g., testosterone, sleep, emotional stress, caloric restriction, and body fat levels. While it is well-established that leptin is involved in the regulation of the inflammatory response, it has been further theorized that leptin's role as an inflammatory marker is to respond specifically to adipose-derived inflammatory cytokinesWiki.  Cytokines are a broad class of compounds including the interleukins which play important immune system roles.  Elevated levels of cytokines are associated with an assortment of pathological conditions.   

[2]  Although other cells can use other fuels (most prominently fatty acids), neurons depend on glucose as a source of energy in the non-starving human. They do not require insulin to absorb glucose, unlike muscle and adipose tissue, and they have very small internal stores of glycogen. Glycogen stored in liver cells (unlike glycogen stored in muscle cells) can be converted to glucose, and released into the blood when glucose from digestion is low or absent, and the glycerol backbone in triglycerides can also be used to produce  glucose” Wiki.

[3]  Resistance is common when a hormone is at a stead peak state.  The body adjust to this high level to reduce its affect.  To prevent this the pancreas release insulin every 3 to 6 minutes, for graph.  This tolerance is similar to tolerance to alcohol, where with repeated usage a greater dose is required for inebriation.

[4] This is quite different than the way pharma frames the discussion of CVD—see endothelial dysfunction.  A series of articles expose the tobacco science taught by KOLs—see  http://healthfully.org/rh/id1.html, id2, rl/id5, rl/id8, rl/id9, rl/id5, rl/id10.

[5] Adiponectin is a hormone secreted by adipose tissue which modulates a number of metabolic processes including glucose regulation and fatty acid oxidation.  Its level increases during energy restriction. 

[6] ATP, Adenosine triphosphate the body’s energy molecule:   is a nucleoside triphosphate used in cells as a coenzyme. It is often called the "molecular unit of currency" of intracellular energy transfer.  ATP transports chemical energy within cells for metabolism. It is one of the end products of photophosphorylation, cellular respiration, and fermentation and used by enzymes and structural proteins in many cellular processes, including biosynthetic reactions, motility, and cell division.  It’s depletion plays a major role in death during heart attack and from congestive heart failure, since ATP is the molecule which is the energy source used by the heart.  Statins, for example, deplete the ATP supply by 40%, thus pharma doesn’t test their statins on those with congestive heart failure—though it is often given to them.  

[7]In summary, fructose but not glucose feeding led to impaired insulin action in both the liver and peripheral tissues” at 1989.

[8] As evidence clearly shows (see Aetiology of insulin and leptin resistance on page 2, which goes over the steps starting with high fructose consumption --listed at above 50 grams a day) that causes the liver damage which can ultimately lead to all cases of T2D.  

[9] High levels of triglycerides are good because they are a safer source of energy than carbs which cause glycation and thus CVD.

[10] The other casual factor is that diabetes promotes a reduction in cellular adhesion, which facilitates the leaking of plaque from within artery walls.  This reduction in adhesion which promotes the leaking of erythrocytes (red blood cells) from capillaries which causes  blindness, kidney failure, and gangrene in legs. 

[11]  Those who claim the high-fat diet is the cause of NAFD are doing tobacco science.  It is based on a rat model—for example-see.  However, though not vegetarians--like rabbits used for cholesterol myth--their diet is relative to man low in fats.  Eskimos who ate a high fat low carb diet, yet  have a very low rate of NAFLD & CVD.  NAFLD is associated with the high carb-fructose Western diet.  

[12]  In cellular pathology, steatosis (also called fatty change, fatty degeneration or adipose degeneration) is the process describing the abnormal retention of lipids within a cell. It reflects an impairment of the normal processes of synthesis and elimination of triglyceride fat. Excess lipid accumulates in vesicles that displace the cytoplasm. When the vesicles are large enough to distort the nucleus, the condition is known as macrovesicular steatosis; otherwise, the condition is known as microvesicular steatosis. While not particularly detrimental to the cell in mild cases, large accumulations can disrupt cell constituents, and in severe cases the cell may even burst. Mo direct is that “Short-term high fat feeding in rats results specifically in hepatic fat accumulation…caused a ~3-fold increase in liver triglycerides and total fatty acyl-CoA content without any significant increase in visceral or skeletal muscle fat content [parallels human development of NAFD for those who are not obese]… suppression of endogenous glucose production by insulin was diminished and insulin-stimulated peripheral glucose disposal [IR]… In conclusion, these data supported the hypothesis hepatic steatosis leads to hepatic insulin resistance…” at 2004.

[13] The role of fructose as the starting point for the progress to IR, NAFLD, MeS, and,T2D is based upon strong evidence, yet Wikipedia on NAFLD, merely sates that it is “due to other causes than excessive alcohol use” and one sentence on fructose in the context of soft drinks:  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. The quantity of fructose delivered by soft drinks may cause increased deposition of fat in the abdomen.[6][7]  But is not merely soft drinks as a source of fructose, but the excessive amount of sugar and refined carbs in the Western diet, all sources. The foot print of corporations is found throughout Wikipedia. 

[14] American Association for the study of Liver Disease, 2013:“Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in adults and children. A number of genetic and environmental factors are known to predispose individuals to NAFLD. Certain dietary sugars, particularly fructose, are suspected to contribute to the development of NAFLD and its progression. The increasing quantity of fructose in the diet comes from sugar additives (most commonly sucrose and high fructose corn syrup) in beverages and processed foods. Substantial links have been demonstrated between increased fructose consumption and obesity, dyslipidemia, and insulin resistance. Growing evidence suggests that fructose contributes to the development and severity of NAFLD. In human studies, fructose is associated with increasing hepatic fat, inflammation, and possibly fibrosis. Whether fructose alone can cause NAFLD or if it serves only as a contributor when consumed excessively in the setting of insulin resistance, positive energy balance, and sedentary lifestyle is unknown. Sufficient evidence exists to support clinical recommendations that fructose intake be limited through decreasing foods and drinks high in added (fructose-containing) sugars.”  Pharma has drugs for NAFLD. 

[15] Type 1 diabetes is caused by the immune-mediated destruction of islet insulin-secreting β-cells. This chronic destructive process is associated with both cellular and humoral immune changes in the peripheral blood that can be detected months or even years before the onset of clinical diabetes. Throughout this prediabetic period, metabolic changes, including altered glucose tolerance and reduced insulin secretion, deteriorate at variable rates and eventually result in clinical diabetes. A fraction of individuals with humoral immunological changes have clinical diabetes that initially is not insulin-requiring. The onset of diabetes in these patients is usually in adult life, and because their diabetes is at least initially not insulin-requiring, they appear clinically to be affected by type 2 diabetes. Such patients probably have the same disease process as patients with type 1 diabetes in that they have similar HLA genetic susceptibility as well as autoantibodies to islet antigens, low insulin secretion, and a higher rate of progression to insulin dependency. These patients are defined as being affected by an autoimmune type of diabetes not requiring insulin at diagnosis, which is also named latent autoimmune diabetes of the adult (LADA)” ADA 2001, full.

23) Bad pharma and type-2 diabetes:  Like so much that occurs in today’s medicine, what is sold as beneficial isn’t best for the patient.  It is corporate tobacco ethic producing tobacco science which is used to promote junk treatments.  The common pattern used by pharma is to identify a surrogate endpoint; in this case high serum glucose, claim that this surrogate endpoint is strongly associated with pathologies (serum glucose at a very high level), treat the surrogate endpoint with drugs.  Clinical trials are designed to sell the product.  Once give FDA approval, pharma next expands the market by doing more tobacco science to provide “evidence” for benefits to a much larger population including an asymptomatic population with modestly elevated serum glucose.  At the same time treatment choices counter to pharma’s financial interest are both attacked by tobacco science and downplayed.  Thus over example through education in diet can often reverse the need for medications.  “Only 13% of diabetics are instructed by their physician and 25 percent of those instructed by dietitians showed a sound knowledge of their dietary requirements” at.  Failure to follow a strict diet hastens the rate of decline resulting in more drugs.  Finally insulin is added.  All of these drugs have under-reported side effects.  Moreover, there is the additive effect, where by multiple drugs, often in unexpected ways overload various bodily organs such as the kidney or affect catalytic process such as cytochrome P450 and thereby produce unexpected side effects.   These consequences polypharmacy are often treated with more drugs.  Organizations that set out treatment guidelines such as the NIH and American Heart Association knowingly use this tobacco science to expand the drug market.  Our corporatist government promotes the regulatory façade.  And it gets worse.  :  Pharma following the standard pattern of expanding the market for its drugs has through their KOLs (key opinion leaders) expanded late 2014 the disease population by lower its surrogate markers high serum glucose and glycation of hemoglobin (HAC1) and thereby include a population without symptoms.  The sales pitch is that its drugs lower the risk of morbidity and mortality associated with elevated glucose.[1]  The 2014 article by John S. Yudkin Jr. in the British Medical Journal goes over the new standards and their consequences.  Over half of those placed on drugs for elevated glucose, shouldn’t.  Moreover this elevation of glucose is a natural part of aging.  The cure for T2D is a very low carbohydrate diet with alternate day fasting (see #30).  Instead doctors educated by pharma fail to warn their patient about refined carbs.  Instead of a cure, billions are spent on drugs that only slow the progression of T2D.  For a person who develops T2D at the age of 50, their life is shortened an average of 7-10 years—their mortality rate has doubled.   And it gets worse the dietary recommendation is a low-fat diet, thus high carbs, the Western diet.  And they hold that fructose, because of its low glycemic index, is a safe sweetener.  The dietary switch to carbohydrates has been convincing shown not to prevent cardiovascular disease (as claimed) but to promote it.  This dietary switch is made worse by recommending the replacement of saturated fats with polyunsaturated fats which like carbohydrates promote atherosclerosis.  (Note at the end of this paper are a list of quality documentaries and University of California Television programs and some lectures by Dr. Jason Fung which confirm the key points here made on diet and its effects upon T2D, NAFLD, insulin resistance, leptin resistance, obesity, etc.).   What can be said about bad pharma failing to act in the public interest equally applies to food manufacturers.  What follows is a discussion of the good and bad fats; to lump them together is good marketing science, and more tobacco science.   

http://upload.wikimedia.org/wikipedia/commons/thumb/a/a9/Isomers_of_oleic_acid.png/300px-Isomers_of_oleic_acid.png Cis-2-butene.svgcis-2-butene—both-CH3 are on same side; with trans-fat they are on different sides of the carbon chain, and thus form a straight carbon chain—above left. 

24) Polyunsaturated too much omega 6 fatty acids:  one of the 2-major health issues is that most plant source of fats is high in polyunsaturated fats, one is rancidification (section below) the other is that they have about 20 times as much omega 6 (N-6) fatty acids to omega-3 (N-3).  Tree nuts are not high in polyunsaturated fats.  They include avocado, olive, coconut, almond, and thus are not rich in the bad polyunsaturated N-6.  The paleo-diet main source of fat came from animals—very few societies consumed significant quantities of grains and nuts.  Many experimental studies have provided evidence that incorporation of alternative fatty acids into tissues may modify inflammatory and immune reactions and that omega-3 fatty acids in particular are potent therapeutic agents for inflammatory diseases… When humans ingest fish or fish oil, the EPA and DHA from the diet partially replace the omega-6 fatty acids, especially AA, in the membranes of probably all cells, but especially in the membranes of platelets, erythrocytes, neutrophils, monocytes, and liver cells.  Inflammation plays an important role in both the initiation of atherosclerosis and the development of atherothrombotic events” 2002 Biomed. In other words, the high amount of N-6 blocks most of the conversion of N-3 to anti-inflammatory agents.  Excess omega−6 fatty acids from vegetable oils interfere with the health benefits of omega−3 fats, in part because they compete for the same rate-limiting enzymes.   A high proportion of omega−6 to omega−3 fat in the diet shifts the physiological state in the tissues toward the pathogenesis of many diseases: prothrombotic, pro-inflammatory and pro-constrictive.  A ratio of 2–3/1 omega 6 to omega 3 helped reduce inflammation in patients with rheumatoid arthritis   A ratio of 5/1 had a beneficial effect on patients with asthma but a 10/1 ratio had a negative effect.  A ratio of 2.5/1 reduced rectal cell proliferation in patients with colorectal cancer, whereas a ratio of 4/1 had no effect” Wiki.   Paleo diet has a ratio of N-3 to N-6 is less than 1 to 4; the Western diet ratio is 1 to 15 or greater.  Thus it is wise to avoid corn, canola, sunflowers, and soya oils.  Olive and palm oils are low in polyunsaturated fats, even lower are animal fats.   

25) Polyunsaturated fats are subject to rancidification:  is the hydrolysis and/or autoxidation of fats into short-chain aldehydes and ketones which are objectionable in taste and odor.  Hydrolytic rancidity refers to the odor that develops when triglycerides are hydrolyzed and free fatty acids are released to form free tatty acids and salts of free fatty acids.  Oxidation primarily occurs with unsaturated fats. Microbial rancidity refers to a process in which microorganisms, such as bacteria or molds, use their enzymes such as lipases to break down fat.[2]  Rancidification can produce potentially toxic compounds associated with long-term harmful health effects concerning advanced aging, neurological disorders, heart disease, and cancer. A combination of water-soluble and fat-soluble antioxidants is ideal” Wiki.  Lipid peroxidation refers to the oxidative degradation of lipids. It is the process in which free radicals "steal" electrons from the lipids in cell membranes, resulting in cell damage.  It most often affects polyunsaturated fatty acids, because they contain multiple double bonds in between which lie methylene bridges (-CH2-) that possess especially reactive hydrogens.  If not terminated fast enough, there will be damage to the cell membrane, which consists mainly


of lipids. In addition, end-products of lipid peroxidation may be mutagenic and carcinogenic.  For instance, the end-product malondialdehyde  reacts with deoxyadenosine and deoxyguanosine in DNA, forming DNA adducts to them, primarily M1GWiki.  The detailed 2010 article Pathological Aspects of Lipid Peroxidation list aging,  Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), atherosclerosis (and thus CVD and other related conditions), pre-eclampsia (pregnancy disorder affecting about 4%), diabetes, renal diseases, chronic lymphedema (also known as lymphatic obstruction, causing swelling by compromised lymphatic system), hepatic diseases including liver IR, NAFLD, NASH (#16), exacerbating hepatitis C and cirrhosis of the liver, and a causal factor for cancers.  The various authors of each section of this in-depth article describe the process by which the lipid peroxidation causes pathology.  The role of oxidation of fats and cholesterol within the artery walls as being atherogenic is clearly made in that article.  The effects of rancidification in the body are beyond dispute.  Also contributing are dietary sources of rancid oils.  The possibility that the body fats might undergo a similar kind of degradation is still largely ignoredperhaps because the irregular irreversible pattern of this type of process seems at odds with the enzyme-controlled reversible pathways of traditional biochemistry. Yet work with mitochondria and other biological preparations has shown that the processes commonly grouped together as " degeneration ", " fatigue ", and " ageing " (none of which have a basis in classical enzymology) develop in close parallel with evidence of Rancidification” at 1969.  The source can either be dietary rancid fats or in vivo oxidation—in vivo causing the greatest issues.  Now let us follow the chain of events concerning IR and CVD.  Rancid fats contribute to liver dysfunction NAFLD and IR by accumulating in the liver in a form that the liver can’t dispose of.  Similarly they contribute to atherosclerosis and CVD by being in a form with the muscle cells in the tunica intima (muscular layer) of the artery walls cannot uptake and metabolized these rancid fats.  The macrophages in the tunica intima similarly can’t dispose of the rancid fats.  Thus like trans-fats (see section below) rancid fats contribute to CVD and atherosclerosis.  Accumulating evidence suggests that oxidized fats and lipid oxidation products in the diet can contribute to the pathogenesis of atherosclerosis” at 2002, and 1998. Non-enzymatic oxidation causes the failure of the body to dispose of them; they accumulate like those of the unnatural, man-made trans-fats. 

26) Trans-fats:  Beside polyunsaturated fats being subjected to in vivo oxidation, they are commercially catalytically hydrogenated to prevent oxidation and improve properties: they retain flavors of the products baked and deep fried than unsaturated fats, and being a solid like lard produced products with a superior texture to the polyunsaturated fats.  And follow the dollar:  hydrogenated polyunsaturated fats are much cheaper than natural saturated fats.   During hydrogenation of the double bonds in polyunsaturated fats, an assortment of cis-and-trans bonding occurs.  In this way trans-fats are preferentially created over cis-fats because of their lower energy of reaction.  Not found in nature but in trace amounts, we lack an enzyme to metabolize trans-fats.  The daily intake of about 5 g of trans-fat (1.5 teaspoons) is associated with a 25 percent increase in the risk of ischemic heart diseaseNEJM, at.  “Trans-fats are found only in trace amounts in meat and dairy products.  Their major source is in food production: liquid cis-unsaturated fats such as vegetable oils are hydrogenated to produce saturated fats, which have more desirable physical properties[3] [namely,  flavorful baked and fried foods, longer shelf life, and at half the price of animal fats and cheaper than palm and olive oils].  Trans-fats are a contaminant introduced by a side reaction on the catalyst in partial hydrogenation of vegetable oils.  However, partial hydrogenation reconfigures most of the double bonds that do not become chemically saturated, twisting them so that the hydrogen atoms end up on different sides of the chain. This type of configuration is called trans, from the Latin, meaning "across".[39] The trans configuration is the lower energy form, and is favored when catalytically equilibrated as a side reaction in hydrogenation” Wiki.   In 1975, 5.6 billion Ib. of hydrogenated vegetable oil were produced in the United States, which is an average of 28 Ib/year/person (113)” ARN 1984. This amounts to 35 grams per day.  Based on population studies and clinical trials, trans-fats are blamed for high levels of cholesterol, lower the good HDL, and as a major cause of CVD, but it is their effect upon prostaglandins that is the way they cause CVD and MI.  This is more pharma spin.  An experiment on rats using feed high in trans-fats and HFCS was able in 16 weeks to produce in the rats NASH, IR, MeS, and T2D trans fed rats, 2008 Thus trans-fats and as discussed in #s 24-25 the polyunsaturated fats are driving along with fructose the association of CVD with diet--not the cholesterol and saturated fats.  The abnormal and thus lacking a bio-pathway for disposal trans and rancid fats and excess fructose are the main villains.  But as pointed out in the section on the Mediterranean diet, complex population studies are like data mining, where you dig determines what you find.  Far better are laboratory animal and in vitro experiments.

27) Laboratory evidence that trans-fats cause CVD:   Pharma’s KOLs (key opinion leaders) push the cholesterol myth:  trans-fats increases the risk of coronary heart disease by raising levels of the lipoprotein LDL (so-called "bad cholesterol") and lowering levels of the lipoprotein HDL ("good cholesterol") “ Wiki.  “It is now well known that the hydrogenation process and particularly the formation of trans-fatty acids has led to increases in serum cholesterol concentrations whereas LA [linoleic acid] in its regular state in oil is associated with a reduced serum cholesterol concentration” Biomed.  This has been confirmed with high trans-fat in clinical experiment on volunteers.  But it has been shown (see part 2) that pharma pushes the high LDL, high total cholesterol, and high-fat diet as causes of CVD for to promote drug sales of their statins.  What follows are from articles which explain the damaging cellular effects of transfats.  In a 2006 review article on trans-fats:  “Because of their effects on the metabolism of gamma-linoleic and arachidonic acid, ingestion of trans-fatty acids can affect the metabolism of prostaglandin and other eicosanoids and may alter platelet aggregation and vascular function.  In addition incorporation of trans-isomers into membrane phospholipids may influence the physical properties of the membrane as well as the activities of the membrane-associated enzymes…. Effect collagen 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 [affects wall of arteries and other tissues]… soluble vascular-cell adhesion factor…reflected by reduction in brachial artery flow-mediated vasodilation by 29 percent [raises blood pressure], as compared with intake of saturated fats.  Other effects include consumption of trans-fats reduced the activity of serum paroxonase, an enzyme that is closely associated with HDL cholesterol, and impaired the postprandial activity of tissue plasminogen activator.  Trans-fats appear to affect lipid metabolism through several pathways….”  The same finding with much greater detail is in the 1984 thorough review by the Department of Agriculture.  Several epidemiological studies found a significant association of trans-fats with CDV and MI, including those studies which controlled for contravening variables.[4]  As previously stated LDL and high total cholesterol are bystanders.  Pro-inflammatory effects of pathogen colonies within the artery walls has been incontrovertible demonstrated to be major cause of CVD.   Given the clear association in dozens of population studies and clinical trials of trans-fats to CVD, governments have responded to this health hazard created by the food industry.  With the body of experimentation upon rats revealing the mechanism, the deleterious effects of trans-fats has been established, the principle one being it effect upon blocking the conversion of the essential omega-3 fatty acid, at.  For more on trans-fats see Part 4.  The smoking gun lines with the fact that trans-fats exert a pro-inflammatory effect, and the inflammatory processes in artery walls in response to damaged LDL causes atherogenesis.  “Because the presence of inflammation is an independent risk factor for atherosclerosis… the production of interleukin-6 and TNF-a by cultured mononuclear cells was greater after one month…” NEJMsee also, a 2006 summary article.  Through fat accumulation, trans-fats cause a fatty liver and thus promote NAFLD--at 2008 “It seems that a strong relationship exists between the consumption of TFA in the oxidized oils and lipid peroxidation and non-alcoholic fatty liver disease (NAFLD)” at 2011.  Based on lab and population studies, assiduously avoid artificially produced trans-fats[5].  

28) What are the regulations:  Official response has been prohibiting trans-fats in a number of countries, but not the U.S.  According to the FDA, the average American consumes 5.8 grams of trans-fat per day (2.6% of energy intake).  This is government figure is low because trans fatty acids that are part of mono- and diglyceride [bound with glycerol] are not required to be listed on the ingredients label as making contributions to calorie count or trans fatty acid content.  Trans-fats in the form of monoglycerides and diglycerides are not considered fats by the FDA, though upon absorption from digestive track they yield trans-fats.  Another gap in calculation is that trans-fat levels of less than 0.5 grams per serving are listed as 0 grams trans-fat on the food label.  There is no requirement to list trans-fats on institutional food packaging; thus bulk purchasers such as schools, hospitals, [restaurants], and cafeterias are unable to evaluate the trans-fat content of commercial food items [nor is there an incentive to spend more for trans-free foods]” Wiki.  The major source of trans-fats in the U.S. is in fried foods from restaurants, and this source is not included in US dietary figures for trans-fats.   A number of countries have simplified the process of controlling trans-fatty acids by banning them, starting with Denmark in 2003 and now also Iceland, Sweden, Switzerland .  “Spain … no significant levels of trans-fats were found in any of the anaylsed products, regardless of brand of origin” at Bakery.  The regulations might make a difference, because death rate per 100,000 2011 from coronary heart disease is 80.5 US, 55.9 for Denmark, for Spain 43, Switzerland 52, Japan 31, Israel 46, Italy 51, Greece 60, U.K. 69, and France 29, source LeDuc Media.  And France consumes the highest rate of saturated fats.  The highest rate of obesity and diabetes is in the US, which corresponds to the highest consumption of fructose.  Let us not become distracted by what could by the minor causes such as fats when the elephant in the kitchen are refined carbs and sugars.  The weakness of lab work on fats make the case,[6] we need to look at the Western high carb diet.   However the manufactured food industry and fast-food restaurants prefer unsaturated fats because they are about half the price, and they prefer hydrogenated fats because they taste better and have a longer shelf life; thus another example of what Prof. Ben Goldacre calls “pretend regulatory fixes”.  The zero trans-fats on food label is deceptive for 2 reasons, at up to 0.5 grams per portion the entry is 0, and since no one is checking food content; there is an incentive to manufacture the dietary numbers on product labels.  It is like having a speed limit for Freeways but no traffic cops enforcing the limit.   

29) Saturated fats are good for you:  We have all heard repeatedly that saturated fats are bad: they cause CVD by clogging blood vessels.  This claim is accepted as proven, yet a meta-analysis of 21 studies considered the  effects of saturated fat intake and found that Intake of saturated fat was not associated with an increased risk of coronary heart disease, stroke, and cardiovascular disease" Wiki.  Though this fat myth was stated in #12, I need to repeat this along with the myth that dietary cholesterol also promotes CVD.  This too is false; the chorus of professors and doctors who expose these myths are not given space in the corporate press or time on corporate television—the exception is Australia Broadcast Corporation.  Compelling evidence shows that the high refined carb-fructose diet has resulted in the current health disaster, and that carbs should be replaced with saturated fats and monounsaturated fats, because polyunsaturated fats promote through omega 6-fatty acids (N6) their affect negative effect upon the immune system that increases age related diseases, and also through rancidification.  The Paleolithic diet had a ration of N6 to N3 of under 4 to 1, with the Western diet the ratio is 16 to 1.   Excess omega−6 fatty acids from vegetable oils interfere with the health benefits of omega−3 fats, in part because they compete for the same rate-limiting enzymes.  Through this negative affect upon omega-3 fatty acids which omega-6 fatty action competitively blocks its action; also when rancid, polyunsaturated fat through oxidation, has an affect comparable to that of transfats in promoting cardiovascular disease.   Prof. Donald Miller, MD presents the compilation to an audience of physicians the evidence which shows that saturated fats are good for you--on YouTube; watch it if in doubt.  France of the developed countries has the highest consumption of fats and saturated fats has the lows death rate of developed nations from CVD—and it ain’t because of red wine. France also has of the developed western countries the lowest consumption of sugars; 27 kg per person per year as reported for 2000 by the CEDUS—at p122, from the book, The Rise of Obesity in Europe.  The control group in the rat experiment (#26 above)  has a human equivalent in the French who eat no trans-fats and low fructose diet. 

30) Managing T2D, obesity, NAFLD, IR and MeS with diet:  Diet has been used to manage the intractable type-1 and type-2 diabetes since the ancient Greeks (see Hippocrates).  The rise in frequency with the Western diet and that there are now 5 categories of drugs used to manage serum glucose entail that pharma has expanded the guidelines to include a much larger population. This section just deals with those who are managed by just oral medications; section #32 for those who are also on insulin.  Extreme low-carb Atkins type diets are successful.  Several small dietary trials have been done in hospitals which produced results within 2 weeks.  One on 10 obese patients with T2D establishes the benefits of diet.  All 10 patients were obese, 7 with hypertension, 5 dyslipidemia, and 2 with coronary artery disease.  To set baseline, the first week consisted of normal diet and thus included foods from fast-food establishment, the next two weeks they followed an Atkins diet with 21 g of carbohydrates per day and all the protein and fat they wanted.  Patients on Atkins diet spontaneously reduced their mean energy intake from 3,111 to 2164/day. Diabetes medications were adjusted according to their improvements. In just two weeks their body weight decreased by 2.02 kg to an average of 112.41 kg, but after adjusting for water loss the mean change was 1.65 kg.  Hemoglobin A1c (HA1c) decreased from 7.3% to 6.8%, insulin sensitive improved by 75%, and mean serum triglyceride and cholesterol levels decreased 35% and 10% respectively (more proof that saturated fats don’t promote hypercholesterolemia) at p. 19.  Another trial of 6 months using a ketogenic diet cured NAFLD in 4 of the 5 participants, and the mean weight loss was an average of 28 lbs.[7]   Other similar experiments have confirmed reduced rate of metabolism when on a diet and the effects of high sucrose diet upon IR.  The extremely low-carb diet work and should be followed by those whose T2D hasn’t progressed to the stage of requiring insulin.

31)  Why drugs fail:   T2D is caused by diet, and it is reversible through diet.  There are three strong indications of this is the cure for T2D. One, for over 90% of those undergoing bariatric surgery they are cured before significant weight loss.  Second, that prior to insulin both type1 and type 2 diabetes were managed with diet.  The low-carb diet was used to manage serum glucose; see for example, Sir William Osler, The Principles and Practice of Medicine, 7th Ed. 1909, p420. Third, is that Dr. Fung has cured many of his T2D patients with ADF.  As Dr. Jason Fung clearly explains the problem is not glucose but insulin.  As stated repeated insulin causes fat storage, which leads to obesity and fat in the insulin producing cells in the pancreas which eventually causes a decline in insulin product that results on high serum glucose resulting in T2D.  Insulin through leptin regulation increases hunger.  What is needed is not more insulin or increased insulin sensitivity, but less insulin.  The two mainstays of diabetes medication don’t lower insulin.  Metformin type drugs decreases hyperglycemia primarily by suppressing glucose production by the liver (hepatic gluconeogenesis), though action in the mitochondria, and metformin increase peripheral insulin sensitivity, and decreases the absorption of glucose from the intestinal track.  The "average" person with type 2 diabetes has three times the normal rate of gluconeogenesis; metformin treatment reduces this by over one-third” Wiki.  “The other leading type of diabetic drugs is the sulfonylureas.  They bind ATP in a process which increases the secretion of insulin, and they limit glucose production in the liver” Wiki. Binding glucose is not a fix, nor more than binding fats which some weight loss medications do.  This is because the glucose (and fat) go the intestines where the bacterial flora their digest these carbs; and this result in gas, intestinal pain, diarrhea, and other side effects.  The best solution is to go on a very low-carb diet—something pharma and food manufactures oppose.   Moreover when serum sugar is managed by drugs, there is no reduction in cardiovascular events are death but instead for most types of drugs is increased, and the tighter the management the greater the morbidity.  Doctors should be recommending as first line the extreme low-carb diet.     

32)  Bariatric surgery cures T2D and MeS:   There are major health benefits for the morbidly obese (BMI over 40). Study of 232 patients who had either bariatric surgery or none, the mortality rate in the surgery group was 1%, in those without treatment 4.5% per year.  Mean glucose level in the surgery group fell for 187 to 140 mg/dl.  The surgery group needing medical management of glucose fell from 31.8% to 8.6 and the non-treatment group increased  from 56.4% to 87.5%, 1997.   Dr. Jason Fung states that 90% of those who undergo bariatric surgery are cured of T2D.  Series with long-term follow-up show that gastric bypass and biliopancreatic diversion achieve durable normal levels of serum glucose, serum insulin, and glycosylated hemoglobin in 80% to 100% of severely obese diabetic patients, usually within days after surgery” 2002. On point is a study that used blood tests designed to measure improved function of beta cells in pancreas and insulin sensitivity.  All ten subjects tested at end of 1 week following bariatric surgery and all 10 were cured of T2D.  The study showed that the cure was a result of fasting rather than weight loss--2006.[8]  Among the panoply of obesity-related co-morbidities that are ameliorated by bariatric surgery, perhaps the most impressive and scientifically interesting is the rapid, dependable resolution of type 2 diabetes. Numerous studies, including a meta-analysis of 22,094 patients, confirm that 83% to 86% of patients with diabetes experience complete remission of their disease after Roux-en-Y gastric bypass (RYGB)…. After biliopancreatic diversion (BPD), the remission rate is greater than 95%,”at.  “Most reported series show that return to euglycemia and normal insulin levels occur within days after surgery, long before there is any significant weight loss. 15,24,25  In 1995, Pories et al 24 reported the results of GBP in a series of 608 morbidly obese patients. Preoperatively, 146 patients were diabetic (type 2) and 152 had impaired glucose tolerance. GBP achieved normal levels of serum glucose, insulin, and glycosylated hemoglobin in 83% of diabetic patients and in 98.7% of patients with impaired glucose tolerance within 4 months after surgery, without the need for any diabetic medication or special diet, and before any weight reduction occurred” at.  “Immediately after bariatric surgery, the patient is restricted to a clear liquid diet, which includes foods such as clear broth, diluted fruit juices or sugar-free drinks and gelatin desserts. This diet is continued until the gastrointestinal tract has recovered somewhat from the surgery. The next stage provides a blended or pureed sugar-free diet for at least two weeks. This may consist of high protein, liquid or soft foods such as protein shakes, soft meats, and dairy products. Foods high in carbohydrates are usually avoided when possible during the initial weight loss period.  Post-surgery overeating is curbed because exceeding the capacity of the stomach causes nausea and vomitingWiki.  The evidence clearly shows that fasting--not weight loss--cures T2D. Fasting entails very low serum insulin, and this permits the body to burn the fat with hepatic liver and beta pancreatic cells.  The latter restores insulin production.  As stated earlier those with T2D,[9] have a decline in insulin production. 

33) The diabetes cure fasting diet for insulin dependent T2D:  Similar in effect to bariatric surgery is fasting.  The alternate-day fasting regime as proposed by Dr. Jason Fung  has proven success.  Fung’s diet incorporates on the off-fasting day the low-carb diet (actually low insulin diet).  Dr. Fung refers to a 6-month study which compared intermittent fasting (IER) to conventional reduced energy diet (CER)—both groups consumed the same number of calories.  The IER group significantly outperformed the CER group as to weight loss by 15% and insulin sensitive—at 2011.  Unfortunately this diet was not low carb, which is part of Dr. Fung’s low insulin diet.  Dr. Fung explains the dynamic of intermittent fasting with his low insulin diet.  Fasting for obese patients is easy since their body merely switches to burning fat and hunger is only moderate.  Restoration of insulin sensitivity, thus lower serum, entails increased metabolism of fat and lower leptin thus less hunger.  Also on his diet there isn’t the reduction in metabolism that develops with the low-calorie diet, thus increased weight loss, and avoids the yo-yo effect of ordinary diets.  My own proposal would be to go on a program like the one recommended by Dr. Richard Bernstein; a very low carbohydrate diet[10], which “was the standard treatment for diabetes throughout the 19th century Wiki.  The low-carb diet should also be low insulin, thus small meals and frequent small snacks.  Since insulin is part of a complex regulatory system and all foods produce an insulin response (see table on Insulin Index at end of this paper), those on 3 or more diabetic drugs and or insulin should take an aggressive dietary approach of alternate-day fasting.  If compliance with the very-low carb diet proves difficult, then start out with three changes. One, small meals to keep the insulin level low (most foods will cause some rise in insulin).  Two, substitute resistant starches and increase vegetables.  Three, gradually reduce sugars.    The Use of two metabolic pathways results in the mitochondria over producing acetyl-CoA; so warns Prof. Lustig MD in Fat Chance, p. 108[11].  Click on link for the details on healthful diet divided into 6 parts; for choices of foods the section at length, for 6 pages summation with the 2nd and 3rd sections devoted to food selection.  I recommend the YouTube lectures by Dr. Jason Fung which explains T2D and how to reverse T2D with diet.  He explains how pharma treats glucose instead of the cause excessive insulin. The drugs pharma offers do not stop its progression. T2D shortens life an average of 7 years.

[1]  For a number of these medications there is no net long-term patient benefit for the population of those with moderate symptoms when compared to a low carb diet.  This is strong reason to conclude that there are no positive major health benefits for those without symptoms.  The net benefit claims  are based upon pharma’s clinical trial, well below the standard of sound science.  What is true of psychotropic drugs is true of other classes (click on Positive Bias) for these results are consistent with pharma’s business model.

[2] This affect by bacteria is one of the causes for atherosclerosis.  Bacteria are found in the tunica media (muscle of artery walls) and are a major cause for CVD. Another example of pharma distorting the beliefs about CVD—for confirmation of infectious agent role.  Thus the toxins from bacteria damage both the LDL and its fatty acid content. 

[3] Desirable properties of not being subject to oxidation (they lack a double bond unsaturated fats), which improves flavor, and they “melt at a desirable temperature (30-40° C)” Wiki.  Removing trans-fats following hydrogenation of vegetable oil adds to its cost.  Thus for flavor, shelf-life, and price hydrogenated vegetable oils are commercially valued.  

[4] A well designed study in Boston looked at the dietary intake of 239 hospital patients with their first MI were matched to 282 control subjects.  A questionnaire was used to estimate dietary intake of trans-fats, and adjustments were made for contravening variable.  “Relative risk for the highest quintile, 2.44.”  Trans-fats constituted 1.6% of daily energy intake.  The highest quintiles consumed twice the daily intake of the lowest.   “The association could not be explained by other established risk factors.”

[5] Trans-isomers of fatty acids constitute about 5% to 6% of dietary fat in the average US diet, mostly derived from partial hydrogenation of vegetable oils…. Typical margarines  in the US market range from 10% to 30% of total fat… more than 10% of total fat are also frequent in cookies, crackers, breads, pastries, and French-fried potatoes” at AHA.

[6] There are just two studies using a Google Scholar search of the literature.  One population wing of the Nurses’ Health Study found a clear association after controlling for confounding variables of transfats with CHD (coronary heart disease).  The other was trial using rats of 4 cohorts (6 in each):  trans-fat + HFCS, lard + HFCS, trans-fat, and control (without  t forced sedentary lifestyle).  The combo of HFCS and trans-fat had had the greatest weight gain, and liver weight gain, but there was no indication as the CHD (possible by deliberate omission).  Liver damage is not a proven surrogate for CHD.  The lack of an animal study is telling.      

[7] That one participant showed 0 lbs. loss, this makes me believe that this person didn’t comply with the diet, and was the one who’s  NAFLD wasn’t cured.  The diet was on the honor system.  Possible the person only complied a couple days prior to monthly testing.

[8] Those who undergo bariatric surgery undergo fasting.  “The oral glucose load, together with the circulating levels of intestinal incretins and adipocytokines has been studied in 10 diabetic morbidly obese subjects before and shortly after biliopancreatic diversion (BPD) [bariatric surgery]to avoid the weight loss interference. Diabetes disappeared 1 week after BPD, while insulin sensitivity (32.96 ± 4.3 to 65.73 ± 3.22 μmol · kg fat-free mass−1 · min−1at 1 week and to 64.73 ± 3.42 μmol · kg fat-free mass−1 · min−1 at 4 weeks; P < 0.0001) was fully normalized.  Fasting insulin secretion rate (148.16 ± 20.07 to 70.0.2 ± 8.14 and 83.24 ± 8.28 pmol/min per m2; P < 0.01) and total insulin output (43.76 ± 4.07 to 25.48 ± 1.69 and 30.50 ± 4.71 nmol/m2; P < 0.05) dramatically decreased, while a significant improvement in β-cell glucose sensitivity was observed,” 2006. 

[9] Pharma, of course, wants to treat those who are merely IR, who show up on the HAc1 test with or fasting glucose tolerance test as IR. The guideline has recently been changed from just manage through exercise and diet to also including the use of drugs. 

·        [10] The Bernstein diet:  The allowed carbohydrate amounts are a maximum of 6 grams for breakfast, 12 grams for lunch, & 12 grams for dinner.

·        Avoiding all foods with added sugar or honey such as desserts, candies, and pastries; all foods made from grains and grain flours such as breads, cereals, pasta, and rice; all starchy vegetables such as potatoes, corn, carrots, peas, tomatoes, and beans; all fresh or preserved fruits and fruit juices; all dairy products except for butter, cream, and fermented cheeses.

·        The patient takes responsibility for blood sugar control including blood glucose testing up to 8 times per day.

·        Target blood glucose levels that are nearly constant for the entire day.

·        Weight loss for obese people with type 2 diabetes.

·        Exercise for all those with type 2 diabetes.

·        Basal and bolus dosing for insulin users.


[11]   The evidence support this aspect of the Western diet contributing to its unhealthy consequences is supported by population studies.  As for the role of Acetyl-CoA, a search of Googlescholar failed to find confirmation of its role, and his book lacks a reference.  


34) 4 Diets for health, moderate weight loss, obesity, severe T2D and morbid obesity:  DIETS -- 10/23/15

1) Healthy diet: For those in good health and normal weight.  The goal is to keep serum fructose & insulin low, thus avoid added sugar & easily digestible starches.  Small meals, with fiber, fats, and proteins along with increased physical excursion keeps serum glucose and thus insulin low.  Low rate of glycation requires very low fructose (see section 5, #4).  At least 2 days a week keep carbs to under 25% of total calories; for an average male and women that would be 600 and 500 calories which is 170 and 143 grams respectively.  The jk short fast at least once weekly promotes a healthy liver.     

2) Weight loss diet of less than 20%:   Daily the jk short fast and 20% calories from carbs or less.  If progress is slow, then add the New Atkins Diet.  Very low carbs with fasting cleanses the liver to cure NAFLD[1], IR, MeS, and T2D. 

3) T2D diet on one drug, &/or obesity:  Daily JK short fast and the new Atkins type diet.  Monitor plasma glucose so as to reduce dependence on drugs.  If after 6 month this hasn’t cured T2D then replace the JK short fast with full alternate-day fasting.  Watch Dr. Janson Fung explain the issues on insulin and diabetes and alternate day fasting diet.[2]  

4) 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 the beneficial nighttime fat burning production of ATP (the energy molecule) to midday.  At night because of not eating there is low glucose and thus insulin is not secreted by the pancreas.   The body then metabolizes fat for energy (ATP).  If hunger becomes an issue than eat a small handful of nuts, green vegetables, or low-carb power bar to kill pangs; the effect of a small portion on insulin production is minimal.  (Another version of the fast is to consume just 20% of calories, all low carbs; thus if on a non-fasting day you eat 2,500 calories, then on the fasting day just 500 calories.  Choose whichever fast has the best compliance.)  Always select low net-carb snacks.

Atkins maintenance phase:  Once weight target is reached, the daily intake of carbs is increased by 10 grams per week 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, limits sweets with fructose, and use the JK short fast to maintain a healthy liver.  Set up a routine of vigorous exercise since it is a general health tonic and mood elevator. 

Healthful food choices  10/23/15




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]. 60 grams of protein male, 45 female daily ideal.

Fructose, sugar added foods[6], fruit juices,[7],polyunsaturated and transfats, vegetable oil [8], refined carbohydrates, whole wheat4, large portions of carbs and fruit, potatoes, rice, instant breakfast cereals.  

Vinegar,[9] high fiber cereal,[10], 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[11], all GMOs12, corn[12], soy products,[13] most crackers, chain restaurants.  

Sugars without fructose:  barley malt, corn syrup, 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 use Fat Chance, pages 199-205 by Prof. Robert Lustig.

35) Healthful choices:  What is beneficial for senior as listed at Diets, supplements & drugs is all the more so for diabetics because of their higher risks. Of special merit is high dose aspirin (325 mgs with meals).  From the paper on aspirin:  Diabetes treatment of type 2 (T2D) with high dose aspirin or other salicylates has a positive effect upon obesity and diet induced insulin resistance; thus by improving the function of insulin it lowers serum glucose level through improved in glucose metabolism.  Increased inflammation of diabetics is associated with morbidities for which aspirin is a treatment.”  Given the positive effect upon insulin resistance and glucose management, a reasonable inference would be that aspirin reduces the risk of developing T2D and the related NAFLD and IR.  This benefit has been long known:  Administration of salicylates was shown over a century ago to lower glucose levels in patients with diabetes.”  A review of the research on aspirin provides compelling evidence for its daily usage and is proof of the power of pharma to direct medical practice to maximize their profits.  Aspirin benefits are detailed in hundreds of journal articles summation, history and uses, cancer prevention, prevention of atherosclerosis and thus CVD and hypertension.  There are two concise papers on what to eat.  The longer one has related topics, at id8.  I highly recommend a careful reading and adopting the recommendations.  There is a list of supplements including CoQ10, Vitamin C (both are effective antioxidants, one fat soluble and the other water soluble), omega-3 fish oil, and the sex hormones (estradiol with progesterone, and testosterone) for the elderly in sufficient dose.  Read the papers on these hormones carefully so as to avoid pharma’s less than ideal products.  Pharm is against all of these because they prevent diseases; thus pharma does tobacco science to education the physicians and warn the public. 




Diet-Food Basics

Adipocytes (lipocytes) fat cells compose adipose tissue & secrete hormones resistinadiponectinleptin and Apelin.  

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

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

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

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

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

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

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

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

Glycation:  a process where a monosaccharide (simple sugar) randomly attaches to proteins or lipid; this  adversely affects the proteins’ functions.  Fructose binding reaction to proteins over 2 hours is 14 times that of glucose. 

Insulin regulates other hormones that affect metabolism, appetite, fat and amino acid storage, blood glucose, etc.  It is produced by the pancreas mainly in response to blood glucose and causes tissues to absorb and burn glucose and also to store fat (not burn). Though Pharma has doctors control elevated glucose with drugs, it is insulin elevated that  produces the comorbidities (negative health consequences) associated with T2D, thus dietary carbs should be limited.     

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

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

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

Mitochondria an organelle function is to produce ATP through metabolism of fatty acids and glucose.

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

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


5.  Setting the Record Straight on points relevant to diet-- (exposing tobacco science)

  1. High plasma cholesterol causes CVD.  TRUTH:  High plasma 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 plasma cholesterol and degree of AS in those died violent deaths, see.

  2. Avoid saturated fats because they cause CVD by raising the plasma level of small-dense LDL which is associated with CVD.  TRUTH:  Saturated fats don’t raise cholesterol levels or small-dense LDL.  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.

  3. Vegetable oils are preferred to animal fats.  TRUTH:   Vegetable oils are associated with diseases because they are high in polyunsaturated fats and become rancid in the body and on the shelf--1945 and. Some of their oxidation products are harmful.  Second, they are high in omega-6 fatty acid which blocks conversion of omega 3 oils to 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 the diseases involving inflammation, including CVD, arthritis, and Alzheimer’s disease and other conditions.  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.  

  4. Sugar (the disaccharide sucrose, 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) has a glycation rate of 7-10 times that of glucose.  Actual 15 times as great a rate of glycation because of its slower clearance compared to glucose.  Fructose is converted in the liver to fat which can causes liver dysfunction that progresses to non-alcoholic fatty liver disease (NAFLD), and that affects the plasma-glucose  regulatory function of the liver to cause IR.  Fructose by minimal insulin response, it bypasses the appetite regulating system involving leptin & ghrelin, which causes weight gain.  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.

  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 low-calorie diet of 75% or less than normal 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 20% and increase hunger.  Eating less simply results in yo-yo diets.  Less than 1% of obese adults at the end of nine years will obtain normal body weight.  To prevent this regain of weight, the regulatory system must be reset, and this occurs by going from carb burning metabolism to fat burning metabolism. by going on an extremely low carb (ketogenic, Atkins type) diet.   Fasting also promotes fat burning.  This type of diet will eventually result in the burning of fat in the liver and pancreas which will allow cure IR and thus permit the weight regulatory system to eventually adjust to a lower weight. 

  7. Hormone replacement (HRT) will not promote weight loss.  TRUTH:  during and following menopause women experience a precipitous drop in estradiol (the most healthful and active of the 4 nat  ural estrogens).  This drop in estradiol increases LPL  which regulates weight, distribution of fat, and physical activity.  Natural HRT [NHRT, estradiol plus progesterone] reduces insulin resistance and fasting glucose in women with diabetes” at.  Numerous studies have found similar benefit for men on testosterone due to its androgen effect which increases metabolism.

  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 group for testosterone, have the lowest rate of prostate cancer.  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 risk.   Testosterone  decreases the risk of heart attack.  Current wisdom is based on pharma’s junk science & tobacco ethics.  Read the section on the WHI study which exposes NIH’s use of Prempro, the worse HRT.

  9. Two lies about type-2 diabetes:  that it is caused by high plasma sugar therefore drugs are given to lower sugar, and that it is a life-long condition; viz. it can’t be cured.  Truth: IR is the problem which is cured by either bariatric surgery or by Dr. Janson Fung’s dietary treatment of ketogenic diet (low carb high fat) with alternate day fasting. 

  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 for 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 leads on clinical trials, write the medical text books, 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 causes cognitive dissonance  and reliance on their KOLs.  Pharma has framed the discussions to produce promote the sales of patented drugs.    What has been said about pharma applies to the manufactured food and tobacco industries—profits before people.


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

Net Carbs = total carbohydrates minus fiber content.

Egg 1 = 0.4 grams

Seafood 6 oz. = 0

Meats 6 oz. = 0

Poultry 6 oz. = 0

Oils 6 oz. = 0



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


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



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


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


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

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

[1]  Dr. Fung’s clinic has documented many cures, and the fasting that occurs with bariatric surgery cures T2D in the first 2 weeks prior to significant weight loss.  T2D, NAFLD and “resolution of NASH in around 80% of patients”[20]  Wiki and.

[2] Watch Dr. Fung explain how the body switches from glucose to fat burning.  Burning excess fat in the liver to promotes overall metabolic health.  The fructose in the Western diet causes fatty liver. This is caused by fructose, which causes insulin resistance.

[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 compared to most other fruits. 

[6] In 2015 “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 produce a serum glucose increase comparable to 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] Vinegar reduces insulin resistance and increase satiation. 

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

[11] 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

[12] Avoid because of high insulin index, and they have a GMO gene that causes corn to produces a pesticide—same for other crops such as canola, soya bean and others.  Testing and review is a regulatory façade:  and the companies do tobacco science to “prove” the changes in the crops are beneficial, and the FDA is business friendly. There is very little true science on GMOs.

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

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