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VI.   Blaming elevated glucose for the comorbidities of t2d, obesity, and MeSassociation doesn’t prove significant causality but profits industries   6/6/18

            a.  Evolutionary question:  evolution does a very good job of protecting mammals from common environmental hazards.  Why don’t LSP on a high starch diet have high fasting glucose and HbA1c?  And why don’t they have conditions associated with the western diet in proportion to their serum glucose level? Their level is below 95% of Swedes in 1999, see Section 1c, yet the conditions are virtually unknown?  These questions suggest that dietary glucose is not the problem, nor elevated serum glucose, but rather recent dietary changes, in particular fructose. 

The pattern repeats:  Pharma profits from treating a sign and searching for new drugs to treat signs while burying the major causes under a stack of KOLs’ journal articles.  Managing glucose and the chronic conditions that develop is very profitable.                                             

a.  Glycation by glucose is not a major cause for CVD and other CAWDs:  This bromide of medical wisdom was born out of t1d study, however, it is much different condition than t2d:  one condition has near zero production of insulin, the t2d patients have IR, insensitivity to insulin.  When their pancreas production of insulin declines (because of fat accumulation), their IR becomes mildly symptomatic.  The response to drugs that raise insulin or promote its activity are much different for these patients. 

 Dr. Jason Fung points this out in the Obesity Code, p. 80 that pharma used a trial for t1d the lower side effects, to “educate” doctors with this trial (and other subsequent trials); however, the logic is flawed because most t1d patients were never insulin resistant.  And it gets worse in that pharma ignored the weight gain of 9.8 pounds more for the tight control group—insulin promotes fat storage.  By not following the long-term consequence, pharma avoids the side effects associated with MeS including obesity including cancer.  This and in other ways they produced results which supported the role of glucose as the major pathogenic factor, and thus that diabetics both type 1 and 2 needed to tightly control the level of glucose.  

Several types of evidence presented here show that glucose alone is not pathogenic.  For example those life-long low-sugar diet high starch diet:  traditional Japanese diet which is high in the refined carbohydrate white rice; they have a low rate of CAWD—and it would have been lower if they didn’t smoke and drink.  So too does other societies such as Kitavans and Okinawans who eat starchy root crops as a staple.  All of them average less than 30 grams of sugar daily from all sources.  A high glucose/starch diet doesn’t cause IR, t2d, MeS, or CAWD.  Thus the association of the western diet doesn’t prove causality for refined carbs--merely removing the nutritional parts from grains is not causal.[1]  As shown above it is the fructose mainly obtained from sucrose that is causal. 

Another consideration is the lack of linear association of CADW with the increase in serum glucose:  the normal level of serum glucose for those on a western diet and the elevated level of prediabetics.  The diabetic is not considered because their level is now similar to the prediebetic.  START

c.   A historical prospective:   Gary Taubes in The Case Against Sugar reviews the biological effects of fructose and how industry has deflected criticism.   Sugar came into the 20th century with a bad rap, that of causing the health problems of the upper class, since until about the 1850s only the affluent could afford those luxury foods.  Then with the extraction of sugar from cane and beats the price dropped, but usage was for most of the working class limited.  The market for sugar laden product grew but was still one third of our present consumption.  Gout and obesity were the most visible conditions of the affluent, and it was popularly held to be caused by sugar.   


 The difference is about 30%, but for most conditions the risk is doubled or greater.   When that person drifts toward t2d, the period of elevation is typically under a year, which is two short a period for the pathologies that normally develop after 10 years and longer.  The biological evidence for cause of those conditions as being linked to glucose is weak, made all the weaker when compared to the same type of evidence for fructose.  Thus elevation of the less reactive glucose is insufficient to account for the increase in CAWD. 

[1] Importance detail is that glucose in cells is metabolized first, thus in a chart I saw the area under the graph indicates that fructose has twice the area for glucose under the graph for equal amounts of both, thus doubling fructose potential for damage.

VII  Prevention and signs of insulin resistance

a.     Prevention: Prevention is easy simply limit sugar.  How much depends on metabolism.  An elite athlete can consume about 4 times the average 70-year old without developing insulin resistance.  For a person who isn’t IR the average male, active 30-year old can consume can consume about 60 grams a day, and a woman about 40 grams.   Teens can consume more.  Activity level and rate of metabolism make a big difference.  But why endure the fate of Prometheus?[1] damage the liver with fructose and then have it repaired Of course the best diet is to stay low fructose.[2]

b.    How to tell if you are insulin resistant:  A person who is insulin resistant can have normal HbA1c and normal fasting glucose because they are secreting excessive insulin to lower blood glucose.  Only in more advanced state of IR dose that person have a rise in both of the glucose measurements.  The gold standard is to perform a glucose tolerance test in which insulin is measured, not the serum glucose.  See below the Joseph R. Kraft section; he performed this test on over 14,000 patients.  Other signs strongly associated with IR are 1) a fatty liver (NAFLD) for which a sonogram is the preferred test; 2) elevated HbA1c and/or fasting glucose; 3) to gain weight and need to diet to lose it; 4) yo-yo diets; 5) a non-smoker who has atherosclerosis thus CVD; 6) hypertension, which is a sign of atherosclerosis and kidney damage; 7); elevated uric acid which is causal for kidney damage and ED; 8) and CAWD—see  Section I.  Given that when compared to the Kitavans who eat a high starch diet which is low in sugar, by their standards about 90% of adults by the age of 30 are insulin resistant—see Staffan Lindeberg, are the work of Joseph Kraft in appendix. 


VIII The error of blaming palmitic acid or other saturated fats for CVD

“Since the 1990s, these researchers have established certain findings unambiguously.  First, feed animals enough pure fructose or enough sugar (glucose and fructose) and their liver converts some of the fructose into fat—the saturated fat palmitic acid, to be precise, which is the one that supposedly gives us heart disease when we eat it, by raising LDL cholesterol [see cholesterol myth].  The biochemical pathways involved are clear and not particularly controversial.  Feed animals enough fructose for long enough and this fat accumulates in the liver, cause the kind of fatty liver seen in obese children and adults.  The fat accumulation accompanies insulin resistance, first in the liver and then other cells as well, resulting in metabolic syndrome, at least in laboratory animals.  . . . The effects may take several months to appear if the animal are fed something closer to what humans in America actually consumer—around 20 percent of calories in their diet.  Stop feeding them the sugar and the fatty liver goes away and with it insulin resistance .  In a 2011 study in which twenty-nine rhesus monkeys were given the opportunity to drink a fructose-sweetened beverage along with their unusual monkey chow, every last one of them developed “insulin resistance and many features of the metabolic syndrome” within a year, and four had progressed to type 2 diabetes”--Taubes, p204-5.  De novo lipogenesis produces palmitic acid[3].  The association with CVD is through the fructose which is converted to palmitic acid, thus it is the fructose that is causing CVD.  This is one way that palmitic acid and in general saturated fats get blame form CVD and ischemic events.  The fire caused by the high starch plus fructose in the liver is ignored while the blamed is placed upon their conversion product palmitic acid. 


XI  Dietary fix   insulin resistance, type-2 diabetes,  obesity, fatty liver,  TOFI, and CAWD

a. What doesn’t work:  eat less and move more   Pharma’s and food manufacturer’s fix is to eat less, exercise more, frequent small portions, and replace energy dense fats with carbs; thus a high insulin diet.  It work for those who don’t have long-term (over 2 years) weight issue, because by the end of 2 years most with the exception of some children, have had their weight regulatory system rest through the hormones secreted by the adipose tissue to the increased weight.  The standard advice  doesn’t fix the mammalian weight-regulatory system because it doesn’t cure IR; thus, we have the yo-yo diets.  Yo-yo because—as mentioned above—leptin secreted by the adipose tissue functions to restore the amount of fat to a set point, and in this case because of insulin resistance, that point has been set in their recent past.  Leptin then will cause an increase in appetite and a reduction in metabolism of 20—40%; and with that reduction the dieter will fell that he needs to eat more to feel better.  This is why for most gradually over the next 6 years their weight increases to the set point and frequently higher if that person is sufficient insulin resistant; this is the fate of nearly all those who attempt to restore their health by the caloric-restricted diet recommended by physicians. 

b.  Obesity and t2d are dietary problems with a dietary fix.  The path to health is illuminated by the results of bariatric surgery.  Bariatric surgery is able to cure 80% of the diabetics, and 51% at 12 year follow up.  Most diabetics following the surgery are off their medication in the first two months, before major weight loss.  Following surgery the intravenous feeding limits calories to around 500 per day; this indicates that the forced fasting is curative vector—not weight loss.  Other studies have shown that fasting and for some the ketogenic diet cures through metabolism of excess stored fat in the liver, and for diabetics in the pancreas.  Following surgery they are on an extremely low calorie, low insulin diet; their body metabolizes the excess fat in the liver and pancreas which cures their diabetes and insulin resistance—excess insulin increases fat storage.[4]  The long-term cure rate would be higher if those surgery patients had been warned of the roll of fructose and had a low carb diet in the hospital and afterwards.  A small but growing group of physicians (Dr. Jason Fung and Dr. Michael Mosley[5] are the best known) are now advocating fasting (both intermittent and alternate day) and lowing carbs or a ketogenic diet.  They have been able to cure type-2 diabetes and obesity by curing insulin resistance and fat storage in the liver and pancreas.  With low insulin, the body continues the process of autophagy—started while sleeping—that metabolizes the excess fat in the pancreas which causes the reduction in the production of insulin for those with t2d.  The metabolism of the excess fat in the liver cures NAFLD and IR.  Since insulin causes fat storage, the low insulin diet accelerates weight loss.      

Mediterranean diet is healthy because of the high consumption of olive oil; wrong, it is the low consumption of sugar.  This is part of the mountains of proposed causes and fixes currently circulating.  That which explains what has gone wrong and the fixes are buried within the mountain of media stimulated social twaddle.  Switching to a Mediterranean diet won’t fix the fatty liver, insulin resistance, and diabetes, thus what is offered as a fix, isn’t: nor will it cure IR, because of the failure to warn about sugar.      

Good and bad fats:   The type of fats in the diet are important, with saturated fats and trans fatty acids increasing the risk, and polyunsaturated and monounsaturated fat decreasing the risk[26]Wikipedia (contrary to the mass of evidence, see rancid fats and saturated fats). The only way to sort out the tobacco science is to question everything, and rely upon the modus operandi.  The modus operandi:  Polyunsaturated and to a lesser extent monounsaturated fats because of their double bond(s) have free electrons which is available for attachment to by reactive chemicals, which when in sufficient amounts and occurring within cell walls, it becomes a healthy issue.   Because of oxidation, milk is high in saturated fats.   

The Dietary Fix and in concise, some links:  The question isn’t how can I lower my risk factor for CAWD to that of those who live on Crete (Mediterranean diet),[6] but to lower it to the level of the Kitavans (footnote 11).  This requires undoing the damage done to our complex weight regulatory system, and then not damaging it again by excessive fructose.[7]  The simple answer is fasting made more effective with a low carb diet.   To learn more I highly recommend reading the two books by Dr. Jason Fung and watching his lectures on YouTube.  In a more concise form then his books, you will find my dietary advice and a longer version (my advice was arrived at prior to reading and watching his lectures).  It is easier not to eat than to significantly reduce calories long term.  With fasting the body burns fats, not conserve it, and increases metabolism to promote searching for foods.   It is as Dr. Fung wrote in Obesity Code, “It is more important not to eat than what you eat.”  In one clinical trial, skipping breakfast resulted in a reduction of 539 calories per day.  An easy start is intermittent fasting (skipping a meal or 2) and progress into alternat e day fasting and thereby avoid the metabolic consequences of being in the starvation mode.   Going on a low carb (insulin) extends autophagy and accelerates the rate of weight loss.   

In summary:  The role of uric acid is complex in that it can at subclinical levels be pathogenic through the blood borne micro-sharp crystal that damage endothelial cells and kidney cells. However, it doesn't seem in itself to amount to a pathogenic level unless the person is insulin resistant, especial in the extreme form of type-2 diabetes.  Insulin resistance is caused by the excessive dietary fructose, which overwhelms cellular repair systems. These cells being compromised are less able to function properly and repair damage due to uric acid crystals, underproduction of collagen, compromised proteins due to fructosylation, reduced production of ATP by the mitochondria and an assortment of other cellular changes.  The fix is a cleansing diet as described in the next section. 

[1] Prometheus is a Titan that had the ability to see the future.  As punishment for not revealing how Zeus would be overthrown, Zeus had the Titan chained to a rock and every day an eagal would eat out the Titan’s liver.  It would grow back during the night.  For a  dramatic account watch Aeschylus’s Prometheus Bound and closer to the original performance.

[2] Galactose is the other reactive sugar, and it too is metabolized mainly in the liver.  However, unlike fructose whose metabolism is delayed by glucose metabolism, galactose is metabolized to glucose rapidly in the Leloir pathway.  Thus a young infant has about 40% of it calories from lactose, yet doesn’t develop fatty liver or insulin resistance.  See Disorders of Carbohydrate Metabolism, 13,    

[3]Hepatic de novo lipogenesis and TG secretion. The DNL process begins with the conversion of acetyl-CoA into malonyl-CoA by ACC. Malonyl-CoA is condensed with several acetyl-CoA moieties by FASN to produce a 16-carbon palmitic acyl-CoA…. De novo fatty acids. The saturated fatty acid palmitic acid is the main product of fatty acid synthase. Long-chain elongase (LCE) can extend palmitic acid by 2-carbons to generate stearic acid. Palmitic and stearic acids serve as precursors for palmitoleic and oleic fatty acids respectively, where a double bond is incorporated into the fatty acid chain by sterol-CoA desaturase (SCD)”  Lipid health Dis 2016.  Without the sugar, there wouldn’t be production of palmitic acid in the liver—as proven by LSP consuming mostly fats. 

[4] Prior to bariatric surgery the effective treatment for the morbidly obese was prolonged water fasting with some electrolytes and vitamins (no protein)—apoptosis of adipocytes provides amino acids.  Fasts typical ran about 100 days, the record is 382 days. 

[5] Dr. Mosley, a BBC documentary producer, wrote in 2015, The 8-Week Blood Sugar Diet:  How to beat diabetes fast (and Stay off medications--#1 international bestseller.  Links for their documentaries and books are provided in this web section. 

[6] If the Mediterranean diet was very low in sugar like the traditional Oriental the risks would be much lower.    

[7] This happens to about half of those who have bariatric surgery, which cures about 80% of those with type-2 diabetes so that they are off their medications.  The food restriction allows the body to metabolize the excess pancreatic fat that causes their diabetes.  However, the distains and physicians not knowing the cause, give bad advice with its unfortunate consequences. 

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What can the 1,300 pound gorilla do, pretty much anything it want--prof. Marcia Angell, Harvard

DISCLAIMER:  As Ben Franklin said, we all keep our own time; thus what I write is what I believe & thus would do; however, I am not recommending others to violate clinical guidelines or their doctors’ recommendations