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Pharma's tobacco science, diet, Inuslin Resistance, diabetes

A lesson on how pharma tweaks the basic science behind Insulin Resistance to treat signs instead of causes, and the dietary fix   7/27/15

Pharma profits from the Western-diet health disaster.  Instead of sending the right message about diet, pharma educates doctors on the cluster of conditions and signs caused by the effects of the Western diet.  It is not in pharma’s financial interest to inform doctors about the dietary fix to those conditions.    The article below is about how pharma has manipulated the information about the satellite of conditions made common by the Western diet.

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


Part 1:  Wiki’s tweaks by pharma’s KOLs on diet related conditions

For those who want to know of the actual process leading to the obesity and diabetes pandemics and how this has been spun by pharma.  For those who when told they are Insulin Resistant (IR), or have Metabolic Syndrome (MeS)[2], Non Alcoholic Fatty Liver Disease (NAFLD), Type-2 Diabetes (T2D, NIDDM, Non-Insulin Dependent Diabetes Mellitus), this article is for you.  There are pharma’s drugs; they aren’t a fix because they don’t treat the cause,[3] and there is a dietary fix that is not mentioned.  Nine out of ten of physicians repeat pharma’s spin rather than the correct dietary fix--why.   If you wish to know of bad pharma then attend Prof Marcia Angell’s President’s Lecture—link.  If you wish to read about diet and/or the science behind it, then click on link.  And for a library of quality- documentaries on diet, bad pharma, and their tobacco science, then click on this link.  What follows is about the spin, what I call “tobacco science” which is generated to promote profits.  Once exposed, the best fix to the Western-diet health disaster is revealed.     

Wikipedia has become a source for pharma to spread their spin; not at all surprising given that pharma frames the discussion of the topic that promote their profits.  Again and again pharma’s Key Opinion Leaders (KOLs)[4] simply ignore the fix, and proceed indirectly to promote pharma’s drugs by elevating bystanders to causes.  This pharmaceutical approach fails to reduce morbidity or mortality.  Pharma has through their KOLs spun medical textbooks, medical-university classes, mandated continuing-education classes for doctors, and medical journal contents. This article is about pharma’s spin in Wikipedia on the above conditions listed in the first paragraph.  For example Wikipedia’s article on NAFLD has 2 sentences about soft drinks and fructose, but missed/ignores the role of fat deposits in the liver in the liver as a result of the liver’s metabolism of fructose[5] (“may cause increased deposit of fat in the abdomen”.  Not may, there is only 1 cause, fructose).   On MeS more of the same:  The metabolic syndrome can be induced by overfeeding with sugar or fructose, particularly concomitantly with high-fat diet.”  Sugar is 50% fructose.  More spin:  fats are not causal, and the experiment evidence shows that high fructose diet at 9 weeks has a much greater effect on insulin resistance then glucose.  On Insulin resistance the science improves, but “Fructose is metabolized by the liver into triglycerides, and, as mentioned above, tends to raise their levels in the blood stream”.  However, feeding rats a high fat diet produces, results not applicable to humans[6] and high blood fatty acids does has not been shown to cause CAD.  “Therefore, it may contribute to insulin resistance through the same mechanisms as the dietary fat.”   But fat doesn’t contribute to IR.  More spin the article on type-2  diabetes:  primary causes are obesity and overweight, lack of physical activity, stress, and urbanization.  In the subsequent paragraph comes sugar-sweetened drinks, and fructose isn’t mentioned.  The article on obesity doesn’t mention fructose or refined carbohydrates, and there are but 2 sentences on sugar.  “Diet quality can be improved by reducing the consumption of energy-dense foods, such as those high in fat and sugars, and by increasing the intake of dietary fiber.”  This is the wrong message, since fat is not the problem as Eskimos prove.  The article on the obesity epidemic makes no mention of fructose, sugar, or refined carbs.   Pharma and food manufacturers are very good at influencing the production of information.  Reading Wikipedia leads to the wrong conclusions. 

Wikipedia doesn’t mention government’s role in the diabetes and obesity pandemics.  It started with a government commission making a political rather than scientific choice.  Industry then used those who believed in unhealthy fats and dietary cholesterol to get that message out through government and corporate media.  The low-fat dietary recommendation issued by the FDA in 1977 was to replace fat with carbs.  Saturated fats make foods taste better, thus industry responded by enhancing flavor with sugar and transfats.  The government’s change in the food pyramid and the farm subsidies for grain made manufactured foods cheap, and thus permitted the growth of the Western diet in and abroad; thus obesity MeS pandemics.

Wikipedia and in general the food literature needs to place to address the problems.  Government created the problem, government needs to step up with the fix.   Public health emergencies like with cigarettes worked.  We had legislative action to get out the message that cigarettes kill, banned advertising on television, and through increased taxes dissuaded people from smoking.  Government needs to do the same with sugar added, low-fat, refined-carbohydrate, rich foods.  And our government needs to provide the food manufactures with incentives to increase saturated fat[7] and lower refined carbohydrates.  

Part 2, The process leading to insulin resistance (not spun by KOLs): 

Fructose is metabolized only in the liver.  About 80% of fructose is used to synthesize through acetyl CoA into fat in the liver where some of it is stored. About 20% is converted in the liver to glycogen.  Selection as to which is mediated by insulin.  A meal high in carbs and fructose will result in some of that fat being stored by hepatic (liver) cells.  (Fructose is slowly cleared from the blood at a significantly slower rate than glucose).    Depending on diet (high carbs and sugar), exercise, and sex hormones IR develops in the liver and progresses into non-alcoholic fatty liver disease (NAFLD) which is clinically similar to alcoholic fatty liver disease (AFLD).  With NAFLD, IR develops in the fat and muscle cells.  Another contributing factor is that fructose is 15 times in vivo more reactive that glucose (7.5 x 2)--the “2” because of its slower clearance than glucose.  Blood sugars can latch on to certain amino acids in proteins (glycation) and thereby impede their functions.  When fructose in sufficient numbers latch on to endothelia cells that line the walls of arteries, through glycation it causes endothelia dysfunction (like carbon monoxide from cigarettes).   Endothelia dysfunction is a risk factor for ischemic events including heart attacks and strokes (see atheroma, pathogens, and cholesterol myth and Australian government’s documentaries on the dietary villains and the cholesterol myth).   Based on incontrovertible scientific studies the actual process leading to CAD starts with IR in the liver.  This is quite different that the spin the paragraphs above and the article below. 

Part 2.  Journal article by KOL:   

So how does pharma and their KOLs deal with this dietary evidence?  Simple, they ignore it.  Since pharma controls the teaching process, the generation of treatment guidelines, and has captured the regulatory system, we have a healthcare nightmare.  If you doubt the ugly picture I have painted, watch the documentaries and lectures by professors which I have collected with links at (http://healthfully.org/rh/id7.html).  As Harvard Professor Marcia Angell puts, “what can the 800 pound gorilla do? Pretty much anything it wants.”   The 800 alludes to the global sales of $800 billion per year industry.  The critics are buried under the avalanche of misinformation, and marginalized by the corporate media.  Pharma’s power to ruin careers sends a chilling message to the medical community.  It limits the content of criticism.[8] 

The article below is a well-argued piece dressed in tobacco science.   Strong evidence of industry authorship is found in that there are 4,783 citations of this article, and it has 9 different journal versions—revealed by scholar.google.com.   Pharma relies upon ghost writers to get their message out.  KOLs attach their names to the ghost written articles—see Prof. Ben Goldacre’s Bad pharma 2013 pages 287-299 for the evidence.  The article below is part of pharma’s effort to expand the market for their diabetic drugs to include those with insulin resistance--see, and, and. [9]  Pharma sell the condition insulin resistance, then the drugs which are supposed to prevent its progression to MeS and T2D.  Prof. Marcia Angell--and others—call this “disease mongering”. Long-term clinical trials have failed to find a statistically significant benefit at this stage for treating IR to prevent T2D and CAD’s acute consequences.  For a cohesive analysis of the evidence and the issues Dr. Jason Fung’s YouTube lectures are excellent—for links.  However physicians are encouraged through guidelines to lower the bar for T2D based upon the surrogate endpoints of fasting serum glucose and HBA­­1c.  Under some circumstance this includes treating aggressively IR.  This again is the wrong message, because the drug course leads to a chronic deteriorating condition.  The right message is a low refined-carb diet with strenuous physical activity.   


[2]   Metabolic syndrome is a cluster of signs which are associated with the conditions of coronary artery disease, atherosclerosis, which include Insulin resistance, obesity, and type-2 diabetes.  Pharma has added to MeS the bystanders:  high cholesterol (hyperlipidemia also called dyslipidemia), high triglycerides (fats) and hypertension.  However, these three are not causal, but rather signs of underlying conditions.  They are like the fever associated with influenza.  Cholesterol and fat found in plaque are signs of an immune response to pathogens, and hypertension is a sign of atherosclerosis.  Treating fever does not cure the underlying influenza, nor does treating hypertension, high blood cholesterol, and triglycerides reduce morbidity or mortality—though KOLs teach otherwise.  As taught doctors treat the bystanders, and the results aren’t worth their side effects.     

[3]  High blood glucose is not the problem, but rather a sign of the problem which is a fatty liver that has mucked up the metabolic control system.  Fatty liver is caused by excessive fructose in the diet.  The fix is to metabolize liver fat by an extremely low carb diet. 

[4] In medicine a doctor becomes a KOL only through providing services for pharma.  The selection process determine prominence.

[5] Fructose is metabolized only in the liver where it becomes fatty acids (fat) and glycogen. However, fructose at most contributes to only 20-30 for glycogen—at—the rest comes from glucose.  Glycogen is the storage form of glucose--under 3 kg are stored.  This fat from fructose accumulates in the liver cells (hepatocytes).  When in excess, it adversely affects various processes in the liver.  This results in insulin resistance in the liver.  Insulin promotes fat storage; thus high liver insulin entails increased fat storage in hepatocytes.   The fatty liver with a high carb diet causes insulin resistance in the rest of the body. 

[6] Rat (and rabbits) is primarily a vegetarian.  Rats have not evolved for a high fat or high cholesterol diet; man has.  The Eskimo and certain African tribes eat a very high fat-cholesterol diet, yet their lipid profiles are normal and they don’t suffer from CAD.

[7] Cheap plant fats that are high in polyunsaturated fats are unhealthy because of rancidification in the body, and the high amount of omega 6 fatty acids—see fats.  Monounsaturated and saturated fats are far better.  

[8] For example I find it hard to believe that such diligent researches as Prof. Robert Lustig, Ben Goldacre, and Marcia Angell, science writer Gary Taubes and Dr. Jason Fung--all with a public presence--don’t know of the cholesterol myth,  They are all on YouTube, links.  Finding a publisher is difficult, Prof. Uffe Ravnskov MD, Dr. Duane Graveline, and Anthony Colpo had to self-publish their important summary books on the cholesterol myth; however, Dr. Stephen Sinatra, who has a large public following, found a publisher.  Other accesses to the mass media are barred, and very little is found in the medical journals on the cholesterol myth.  

[9] The issue of bias in pharma-funded studies is complex and damning—see Bad Pharma Supra reference to studies which show that industry funded studies favor the sponsor. A study of 74 journal articles that used the raw data found Positive bias averaged 32%.    


Typical of pharma is this sample abstract which is tweaked.  Missing in this case is a diet high in fructose and other carbs which is the starting point for IR through its causing NFALD.  The article weaves a tale of how IR progresses to MeS.  For every condition there are two biological pathways, one tweaked by pharma, the other usually is found in fragments in the journal literature, and is based upon laboratory studies, mostly on rats.  After this article (below) is three appendixes, all of which piece together the complex aetiology of metabolic dysfunction and the expose the various food manufacturers and pharma-generated myths.   

http://care.diabetesjournals.org/content/14/3/173.short  diacare.14.3.173Diabetes Care March 1991 vol. 14 no. 3 173-194

Insulin Resistance: A Multifaceted Syndrome Responsible for NIDDM [T2D], Obesity, Hypertension, Dyslipidemia, and Atherosclerotic Cardiovascular Disease


Diabetes mellitus is commonly associated with systolic/diastolic hyperten sion, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive control subjects, a heightened plasma insulin response to a glucose challenge is consistently found. A state of cellular resistance to insulin action subtends the observed hyperinsulinemia. With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to non-oxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: Na+ retention, sympathetic nervous system over-activity, disturbed membrane ion transport, and proliferation of vascular smooth muscle cells. Physiological maneuvers, such as calorie restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; evidence indicates that these maneuvers can also lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia are also associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate-density and low-density lipoproteins, both of which are atherogenic. Last, insulin, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of various growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including non-insulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.

  • Copyright 1991 by the American Diabetes Association

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