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Evidence for Alternate Day Fasting--Cures diabetes

INTRODUCTION  12/23/16

Obesity (25% above thin body weight) is over 40% of adult population.  There are 10 million people with T2D and 26% of those over the age of 65, and there are 81 million pre-diabetics, of which 51% of those over the age of 65.  Over 30% of the population has non-alcoholic fatty liver disease.  These conditions are a result of a defect in fat storage driven by abnormally high level of insulin that causes excessive fat storage starting in the liver.  The fix is long periods of not eating (fasting) which can be complimented by  a low insulin diet (low carb-sugar and moderate protein).  

Part 11, Fasting, fixing the weight regulatory system

rh/id13.html  12/23/16 (latest update)

It’s much easier to do a short-term fast daily than to cut back calories 30% on a diet!

Cleanse your liver to reset your weight regulatory controls & thus lose fat naturally

Abbreviations:

ADF Alternate Day fasting     

ATP Adenosine Triphosphate    

CER Caloric Energy Restriction      

CVD CardioVascular Disease    

IR Insulin Resistance    

KD Ketogenic Diet    

KOL Key Opinion Leader    

NAFLD Non-Alcoholic Fatty Liver Disease   

T2D Type 2 Diabetes      

 

Sections

1.   Definitions, dietary & metabolic  -- 19 terms used here

2.   The science behind weight gain & dieting

3.   Five diets depending on situation/goals

4.   Different types of fasts,  their evidence

5.   Fasting is easy

6.    Tables:  Net Carbs, Insulin Index

 

1.  Definitions:  food & body basics

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

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

Cardiovascular disease (CVD) main cause (besides cigarettes) is a high carb diet which causes endothelial dysfunction of the cells lining the artery walls, which in turn causes the inflammatory response that leads to  atherosclerosis thus CVD

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

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

Fructose (fruit sugar) a monosaccharide found in fruits.  Main sources are the disaccharide sucrose, fruits, and high   fructose corn syrup.  It is metabolized only in the liver into either glucose, or fat which when insulin is stored there to cause fatty liver.  Also fructose is 7.5 more reactive then glucose & by glycation damages the liver, blood vessels etc.

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

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

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

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

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

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

Insulin: a gateway hormone is produced by the pancreas.  Its main function is to have cells absorb glucose and store fat.  Insulin also regulates other enzymes and hormones including leptin.  Chronic low insulin is the immediate cause of type 1 and 2 diabetes.  Insulin also, modifies action of many enzymes, increases DNA production, decreases production of glucose replication, increases production of triglycerides, contributes to the co-ordination of a wide variety of homeostatic and regulatory functions  by enhancing brain signaling, etc.  Half-life 4-6 minutes. 

Insulin resistance (IR):   Since excess glucose is toxic, cells resist the signal by insulin to absorb more glucose. Thus to promote absorption, the pancreas releases even more insulin, and thereby cause in a person with IR a higher than normal amount of blood insulin.  IR occurs first in the liver cells, and causes fat to accumulate there.  Later the muscle and fat cells develop IR.  As IR progresses, fat storage increases to cause obesity and NAFLD.  Fat in the pancreas also  increases to a point which hinders (reduces) the production of insulin to cause T2D. Over 40% of Americans are IR.

Ketogenic diet (very low carbohydrate diet) with high fat and adequate-protein, named from the ketones produced by the liver to supply energy to the brain, which doesn’t store or burn fat.  With low insulin the mitochondria burns fats. 

Leptin:  produced by fat cells is in part regulated by insulin.  Leptin in the brain suppresses appetite and it also regulates metabolism.  Leptin is responsible for the 25% reduction in metabolism plus increased appetite that eventually occurs during an energy-restricted diet.  Leptin functions to maintain fat storage and to restore weight even years later.  

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

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

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

2.  The science behind weight gain & loss

1)   Fasting is one of the two best tools for resetting the weight/fat-regulatory system to a youthful weight, the other is bariatric surgery; at the same time they frequently cure T2D, IR, & NAFLD.[1]  To understand the need for fasting we must understand way the weight-regulatory system works and what is causing it to malfunction.  The short answer to cause:  a diet high in reactive fructose (table sugar sucrose is 2 saccharides, fructose and glucose).  Fructose damages the liver in ways that has caused a malfunction in the hormonal fat storage-appetite regulatory system through the development of insulin resistance (IR).  This damage results from a combination of two process:  1) the reactive sugar fructose, which accumulates in the liver for metabolism; it has reacted with proteins in the hepatic (liver) cells through the process of glycation to affect its cellular functions; 2) one effect of this damage is to develop IR (excess insulin) in the liver; 3) Insulin signals cells to accept and metabolize glucose and thus to store rather than metabolize fat; thus IR causes excess fat to  accumulated in the liver sufficient to further comprise various liver functions; 4) one consequence of fatty liver (NAFLD) is to cause IR in muscles and adipose (fat) tissues; 5) this, like causes obesity.

High dietary fructose sugar Western diet has caused our diabesity (obesity & diabetes) pandemic.  This is what we all should know, yet our corporate media & KOLs have led us to look in the wrong places, namely gluttony and sloth, thus not finding the causes fructose and IR, or fix low sugar & fasting.  I am posting this explanation a second time (from link): 

2) A Summary:  All mammals have a complex regulatory system for appetite, metabolism, and fat storage.  There are over eighty hormones involved in the system.  The Western diet is high the carbs fructose and glucose.  Fructose causes a fatty liver (NAFLD) which mucks up the regulatory systems leading to the IR, & that to obesity, T2D, CVD, etc.  Glucose and proteins raise insulin levels, and insulin causes cells to burn glucose and thus to STORE FAT!  IR causes excess fat storage.  Causes:  The reactive sugar fructose (1/2 of sucrose) goes to the liver to be metabolized, and there through glycation it damages the liver cells.  This causes IR in the liver and thus excess fat storage (NAFLD) there.  The liver now fails to properly help regulate blood glucose to cause in IR in muscles, fat cells, etc. which causes their excess fat storage there and other tissues.  Excess fat in the pancreas causes T2D.  Fat tissue produces the hormone leptin which control the amount of fat.  On an energy-restricted diet leptin functions to maintain current weight by reducing metabolism which makes the dieter feel like he needs to eat more to feel mentally and physically better.  Even after losing weight, this system functions to restore the fat—the yo-yo diet.[2]  Goals:  to metabolize the excess fat in the liver and pancreas which resets the regulatory system by curing T2D, IR & also leptin resistance.  To do this requires both fasting & sugar-carb restriction.  Follow the dollars and you will find out why we have the high sugar (151 lbs. US average 2000) western diet and the wrong advice (diet & exercise)--for long version.

Fix:   Short-term or alternate day fasting with very low carb & high fat  diet to metabolize fat metabolizing mode.     

   Fructose by glycation damages the liver and high glucose via insulin causes fat storage in liver (the 1-2 punch)

Fructose glycation damages liver >>>IR in liver >>> NAFLD >>> IR in muscle and fat tissues >>>>  excess fat storage

T2D and obesity are cured with fasting.  For example in the first 2-weeks following bariatric surgery over 80% with T2D are cured before major weight loss.  With low carb diet and alternate day-fasting the cure takes 2-12 months.

3)  Arriving at the above analysis has consumed 4 years, 50 hours per week, studies.  Having extensive academic training in science and philosophy (12-years in 3 universities and 1 college over a span 2 decades), I was able to meander my way through the tobacco fields of misinformation on diet, metabolism, and the causes of the resulting pathologies from the western diet.  I had exposed tobacco science on a dozen select topics starting in 2004 when I posted my first articles on healthfully.org.  In time I discovered how far we had gone down the corporate path since the Regan era changes.  Exposing tobacco myths became the central theme of the healthfully.org/recommended sections started in 2010.  For issues on diet, this required an extensive study of the basic in the biological processes involved in the production of ATP from fats and carbohydrates and how the Western diet went beyond what our biological systems could safely handle.  By the end of the 2nd year, January  2015, I had an overall theory of processes and causes for the health disaster brought on by a diet high in refined carbs with its average of over 90 grams for fructose daily.  From that point on I was just modifying details, such as on how fructose damages the liver[3] and how glycation damages endothelial cells to promote CVD.  This knowledge allowed me to spot the tobacco science on diet, fats, sugars, fasting and so on.   

4)  My personal experience with fasting along with exercise is why, though I eat a Western diet, I didn’t gain weight long-term.  In 1970 I did my first short-term fast.  I had gained 20 pounds during the summer and fall, so that winter I decided to lose it.  My diet plan was to not eat at night and in the morning along with smaller meals (see jk short fast section #3 for details).  I was going to graduate school in the morning without having breakfast.  It was easy; my wife Barbara, also a student, was always counting calories; we had been on school mornings skimping on breakfast.  I simply skipped evening snacks and the toast or cereal and milk.  I was going without for 17 hour (7 PM until 12:00 AM).  I quickly lost the weight.  After that I bought a scale, and whenever I gained about 5 pounds I used the short-term fast and small meals to lose that weight.  Upon moving to San Diego area from Winnipeg, I started vigorous exercise[4] cycling and 2-man volley ball.  Another reason why as I grew older and my testosterone and metabolism declined, that I didn’t gain weight though I ate a typical Western diet (ice cream instead of sodas) was because at the age of 60 I started to take from a prescription topical testosterone at twice the dose of Androgel.[5]   Unfortunately in 1990 I bought into FDA dietary recommendations and at a very low fat diet which was high in carbs including sugars.  Yet still I kept the weight within the 5 pound limit.  Only in 2013 when I was researching the diabetes (obesity-diabetes) pandemic I become aware that I was doing 3 bad things: high sugar and carbs (thus very low fat) and polyunsaturated fats.[6]  I started by cutting sugars, and in 4 months I lost my taste for sweets; at the same time I increased by fats, mostly butter.  In 2014 I further cut my carbs by limiting cereals for breakfast and averaging 2 slice of bread a day, cut back on milk from a quart a day to an average of 2 ounces, etc.  I didn’t suffer from my diet all those years is because I used short-term fasting, tightly controlled my weight, exercised vigorously, and took testosterone.  I am in my seventh decade and at the top 2 percent of my age group for strength and endurance, and I don’t take unnatural drugs.   

5)  For those with a long-term weight issue the ketogenic diet with fasting is proven fixes for IR, NAFLD, obesity & T2D.  The two are complementary:  with fasting  there is a much higher success rate than just a ketogenic diet.  Based on animal studies of KD or fasting, their benefits:  extends maximum life, better insulin control, reduces injury to nerve cell, reduces risks of diabetes, heart disease, certain types of cancer, and improves immune system.  In human studies of fasting there reduced inflammatory markers (CRP, interleukin 6, and homocysteine), heart rate, blood pressure, and risks for diabetes, neurological disorders including Alzheimer’s and Parkinson’s disease, and an increase in human growth hormone (HgH).  KD has been used successfully to manage intractable epilepsy and to stop the growth of cancer.[7]    

6)   Having hopefully wet-your appetite and convinced you that fasting is good for you; I now am moving on to answer the questions about fasting.  This paper is a review of the research and literature on fasting with the goal of arriving at the best evidence based conclusion for each of the various goals depending on situations.   Consequently after laying the research foundation, follows the best dietary approach to restoring health and what is a healthful diet.  Being a moderately technical article, I will assume that the reader is aware of dietary basics (section1 above has 20 definitions) and also that businesses frame the discussion and thus beliefs of physicians, scientists, and the public;--for an on point essay. 

7)   There are many variations on fasting; I will review some of them, then in section 2 present 4 choices depending upon your goals and personal preference.  Most of the ADF clinical trials permit unrestricted food consumption (carbs) on the non-fasting day, and some on fasting days aren’t true fast since they allow caloric foods (Moseley 5:2 being the most popular of those which permits 500 calories).  The failure to restrict carbs and sugar causes me to suspect that corporations are lurking in the background.[8]  Fasting works by extending the time of fat-burning metabolism from night sleep for a total of 16 or more hours.  Fasting has become popular in both diet books and YouTube videos, but not still lagging behind the CER and the KD diets.  Those that steer dieters to include carbs or 6 small meals are influenced by KOLs.  Those diets are also flawed by the cholesterol and saturated fats myths, and they miss the role of insulin and leptin in the weight regulatory system.  The business generated “saturated fats are bad“ has been laid to rest in the science literature, but the myth still lives on.  It is safe (actually best to eat saturated fats), watch prof. Miller’s lecture on fats.  The cholesterol myth has generated dozens of critical books and several foreign documentaries.  Because the press repeats the lies frequently and doctors are fed tobacco science, the myth lives on.  For example webmd, which always presents pharma’s position, repeats the aforementioned myths.  The dailyburn errs in the same way as Wedmd; it lists 5 popular ADF diet plans, than makes a few suggestions.  Dr Mercola is the second best that I reviewed on the web: he recommends very low carbs, exercise, and considers as better monounsaturated (nut fats), but by omission repeats the cholesterol and saturated fat myths. 

8)   By the end of the 2nd year of my study of nutrition, I came upon the work of Dr. Jason Fung, a Canadian nephrologist.  He digs through the journals to organize the experimental data into a cohesive explanation of the processes (another worthy is Gary Taubes).[9]  They confirmed my conclusion, and Dr. Fung had the practical experience of curing end-stage obese type-2 diabetics in his clinic.  Dr. Fung is excellent; he combines ADF with the low carb diet, and presents the research evidence in college freshman-level lectures carried on YouTube some of which are given to an audience of doctors; the same is also covered in his blog.  His 2016  book The Obesity Code and The Complete Guide to Fasting are the best available.  In Fung’s lectures on obesity and T2D (on YouTube) he states insulin is the culprit and the fix is an extremely low-insulin—thus carbs--with ADF.  Insulin tells the body to store fat and burn carbs, thus insulin resistance (excessively high) promotes obesity.  IR causes leptin resistance, which on a CER diet typically at about 2 months lowers metabolism and increase the sensation of hunger.  High insulin from IR is the immediate cause for obesity and T2D.  Fung states that it is insanity to try the same thing over and over again referring to eat less and exercise more and though physicians know it doesn’t work it is their advice.  The problem is with the fat storage system, not the calories.  Insulin the most important of the fat-regulatory hormones, thus the problem is with insulin.[10]  CER (continuous energy restriction) does not keep insulin low, while the KD (ketogenic diet) with fasting does.  With this low insulin diet and ADF his clinic has successfully treated advanced T2D and/or obesity—for his lectures on YouTube. 

9)  As with nearly every bodily process, the details are complex:  there are over 80 hormones which directly or indirectly affect fat storage, weight, glucose level, metabolism, and appetite.  Insulin is the most important of those hormones; it regulates many of those hormones.  Our system is essentially the same complex system found in other mammals. Insulin is secreted by the pancreas to lower serum glucose, insulin is also secreted in response to incretins, hormones secreted into the blood by cells in the stomach and duodenum in response to certain amino acids (the building blocks of proteins)—see insulin index table below[11].  Meats, poultry, and fish have an insulin index around 55, which is above most pasta.  This is because the incretin system in the stomach and intestines is stimulated by the presence of food, and another system in the mouth responds to the taste of food, and still another based on the presence of amino acids (the soluble form from proteins) in the blood, all these systems cause the pancreas to release insulin.[12]

“Insulin can increase independently of blood sugar.  With carbohydrates, there is a very tight correlation between blood glucose and insulin levels.  But overall, blood glucose was responsible for only 23 of the variability of the insulin response.  The vast majority of the insulin response (77 percent) has nothing to do with blood sugars.  Insulin not glucose drives weight gain, and this changes everything…. In the end, the insulin response is what matters.”  Dr. Jason Fung, Obesity Code, 2016, p 190

Insulin is low only when we haven’t eaten for several hours, as when sleeping on an empty stomach.  The body shifts into beta oxidation which metabolizes the stored fat to produce ATP, the energy molecule.  When insulin is low, so too is the hormone leptin and thus reduces hunger.[13]  This is why we are not hungry upon waking up in the morning.  It is easy from that starting point to remain on a fast.  It is even easier to fast for those on a ketogenic diet (KD); their body has adjusted to the shift in metabolism on a long-term basis, and they have lost their craving for sweets and carbs.  Moreover the meals on a KD have on an average a significantly higher satiation quotient, meaning that they are more filling then one high in easily digested carbs.  Proteins and fats have a slower clearance from the stomach.  And the low-carb dieter doesn’t have the yo-yo effect of blood glucoses going up from the carbs then being cleared and low because of the insulin, and thus hungry again in a couple of hours.  This high-low blood glucose cycle is the main reason for the phenomena called grazing:  we have gone from 3 meals a day the norm until the 80s to frequent snacking.   These phenomena explain why the average calories on a KD is lower that pre-diet even though KD does not restrict calories—just carbs restricted.  Because the level of the catecholamines epinephrine and norepinephrine increases when fasting, the metabolism goes up about 10% and this creates a feeling of well-being.  These neurotransmitters increase metabolism and alertness.[14]  When fasting insulin is low and fat metabolism accelerates, and this will result gradually in the burning off the excess fat stored in the liver and pancreas, the fat which had caused IR, leptin resistance, and T2D.[15]  Once healed the weight regulatory system will gradually rest to maintain the lower weight; thereby avoiding the yoyo-diet effect that plagues CER diets and makes KD less effective than when fasting is added.    

10)     A low insulin, ketogenic diet more details: requires very low carbs, small meals, moderate protein, and when hungry low net-carb[16] snacks.  Physical exertion by burning glucose lowers insulin level, thereby promoting fat burning.  This change in diet entails an increase in green vegetables, cheese, and fats.   Further complexity is add in that that there are classes of carbohydrates—see sections on resistant carbohydrates and fibers.  For example, there is a much lower insulin response from 100 grams of carbs from home cooked black beans compared to 100 grams of carbs from baked potatoes.  However for those on a ketogenic diet, these complexities are of no concern; simply count grams of net carbs (see section 5 for table).   The healing process is accelerated by adding fasting to KD. 

 

3.  Five Diet choices

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

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

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

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

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

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

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

4. Different fasts, the evidence

1)   A review of the journal evidence shows that ADF can, like bariatric surgery[17], cure T2D before significant weight loss due to a change in metabolism from glucose burning to fat burning (this also cures insulin resistance by metabolizing the excess fat in the liver).[18]  Ninety percent of bariatric patients are cured in the first 2 weeks--at NEJM 2012.  A similar though slower improvement occurs with the combo of ADF & KD as demonstrated by Dr. Fung’s patients, most are off insulin within 2 months.  So is Dr. Fung’s results supported by animal experiments and clinical trials?

2)  What follow below relies heavily upon a published research article The Effects of Intermittent Energy Restriction on Indices of Cardiometabolic Health, Research in Endocrinololgy, 2014, Nutrition, Metabolism and Diabetes Research Group, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK, Rona Antoni et al, all 26 pages at http://ibima.net/articles/ENDO/2014/459119/459119.pdf.  After weight loss, if low refined carbs is maintained, the weight stays off, see2014.   “Accumulating data suggests that ADF may also activate hormesis[19], and there has been some suggestion that it is the stress associated with fasting, or the alternating periods of anabolism and catabolism, rather than an overall ER is responsible” at p 15.  Halberg et al had significant improvement in whole-body glucose uptake after as little as two weeks of ADF” p14.  “Leptin secretion with ADF consisting of 75% energy restriction had a 24% reduction in the hunger hormone leptin compared to baseline” (Bhutani et al study at 2014).  Moreover, the longer the fasting period (2-days is superior to 1 day) the greater metabolic improvement—p 13.  The clinical trials and animal experiments do not compare ADF to low insulin diet.  Only Harvie et al (48) in 2014 have used the low carb protocol with 2 days of 75% energy restriction compared to CER and obtain a 43% drop in leptin compared to 23% for CER.  “A large portion of the evidence comes from rodent studies’, at p 16.  Several studies have shown that favorable results with short-term fasting or 50% energy restriction on fasting days; however “the evidence is relatively sparse for those with established T2D” at 16.   There is need for much more research on humans.

3)  Given Jason Fung’s positive results the combination of low carb with ADF, it is the best choice for the long-term obese and those with T2D who have progressed to a reliance upon insulin—answering Antoni et al question supra about established T2D.  For those whose issues are less, start with the short term fasting because of its higher compliance, while at the same time reducing carbohydrates.  Fung’s clinic uses short-term fasting when compliance is an issue with positive results.  Fung’s clinic has yet to publish a summary of the results.  Hopefully his book Complete Guide to Fasting, scheduled for October 2016, will provide a summary of their clinical experience, and also answer questions such about leptin and rate of metabolism, need for a Atkins type maintenance phase, etc.  I highly recommend watching Dr. Fung’s lectures on diabetes and its cure--for a list of them, and reading his The Obesity Code, 2016, chapter 19 is on fasting.   Dr. Fung’s clinic in Toronto has a program set up to works long distance as a guide with the patient’s physicians—see https://intensivedietarymanagement.com/join/.  If appropriate, make use of the this service, it runs under $300/year.  Highly recommended is a short paper healthful diet, which covers what to eat and exposes the major disinformation generated by food manufacturers and bad pharma.  There is a large collection of diet related papers at http://healthfully.org/rh/. For motivation, watch frequently the documentaries and lectures on diet; the best are listed at http://healthfully.org/rg/id4.html--each with a short description and evaluation. 

 

5.   Fasting is easy and essential

By chance I have used the short-term fast the first time.  I gained 20 pounds, the winter of 1969-70.  I the age of 27 my metabolism slowed down, but not my appetite.  It took 3 months of reduced meals and fasting to lose it.  After that, whenever I gained 5 pounds, I simply cut back on portions, quit eat by 7 PM, and skipped breakfast several times a week.  The second change was exercise.  I moved from Winnipeg to southern California and became in 1975 a sports addict.  I started playing volley ball and cycling, then over the next 7 years I added moderate weight training and singles racquet ball.  In 1993 my diet changed for the worse:  following the lead of a very fit friend, I went on a very low fat (thus high carb) Western diet.  Fortunately I watched my weight, thus I never went more than 5 pounds above my youthful weight.  Skipping breakfast is easy.  In 2013 I watched Prof. Lustig lecture on YouTube which had gone viral.  He explain why sugar was poison and I took notes.  In 2014 I researched his explanation of the diabesity epidemic.  In the spring of 2014, I reduced sugars including fruits, and carbs from grains, thus I increased fats. It took about 4 months before candy, soda and sweet melons tasted way too sweet.  Though my weight remained for decades the same, I had a bit more around the lower abdomen than when I was young.  It could be a sign of a fatty liver, so I decided in the spring of 2016 to experiment with daily short fasting.  By July of 2016, 4 months later, I lost 4   pounds, waist shrunk 1 inch, and fasting glucose (a measure of IR) was lower.  I noticed that by skipping breakfast, I had reduced my total consumption of food.  I was less hungry especially at dinner time.  A big plus was that I experienced no decline in mental or physical energy in the morning, and avoided the decline following breakfast.  After a couple of months of adjusting, I now like skipping breakfast.  Morning fasting and not eating at night has convinced me that weight control with short-term fasting is easy and pleasant.[20] 

The lack of sex hormones has been shown to play a significant role in weight gain.  Estrogen controls fat distribution, which is visually obvious as a girl develops during teen years, and the weight gained for most following menopause.  The two sex hormones are nearly structurally identical, but for on functional group.  Testosterone makes a different for men past the age of 60, if they do sufficient amount to restore them to a youthful level.  I started in 2003 using natural testosterone[21] from a compounding pharmacy.  It made my weight control easy.  I stopped regular weighing myself once I realized that my weight regulatory system now keeps me from gaining weight, but I still continued the, low-fat thus high-carbohydrate diet until to2013. 

Dr. Jason Chapter 20 “When to Eat” in his Obesity Code, 2016, p 235-251 covers the history and advantages of fasting; his opening words “LONG-TERM DIETING is futile”;

“Two major factors maintain our insulin at a high level.  The first is the foods that we eat—which are what we usually change when we go on a diet.  But we fail to address the other factor:  The long-term problem  of insulin resistance. This problem is one of meal timing.  Insulin resistance keeps our insulin levels high.  High insulin maintains our high body set weight.  Inexorably our high body set weight erodes our weight-loss efforts.  We start feeling hungrier.[22]  Our metabolism (that is our total energy expenditure) relentlessly decreases until it falls below the level of our energy intake.  Our weight plateaus and ruthlessly climbs back up to our original body set weight, even as we keep dieting.  Clearly changing what we eat is not always enough [for those who are long-term overweight]… To break the insulin resistance cycle [of gradual ever increasing insulin resistance] we must have recurrent periods of very low insulin…. If all foods raise insulin [see Insulin Index, section 6], then the only way for us to lower it is to completely abstain from food…. Fasting…fasting to break insulin resistance and to loose weight…. A tried and true healing tradition.,,, has been part of the practice of virtually every culture and religion on earth ” p 235-236. Hippocrates of Kos (c. 460-370 BC) wrote, “instead of using medicine, better fast today; to eat when you are sick is to feed your illness…. “The term ‘breakfast’ is the meal that breaks the fast—which we do daily”--p 237. 

Fung goes one to describe the role of insulin through in part regulation of leptin which in increasing appetite and lower metabolism.  Though Fung writes of 24 to 36 hour fasting as curing IR, his clinic also uses short-term fasting.  “The body does not burn muscle until all fat store is gone… Blood glucose levels remain normal as the body switches over to burning fat for energy.  This effect occurs with fasting periods as short as twenty-four to thirty six hours.  Longer fasts reduce insulin even more dramatically…. Regular fasting has been shown to significantly improve insulin sensitivity.  This finding is the missing piece in the weight-loss puzzle.  Most diets don’t address insulin resistance” p240.  One of the most potent stimuli of growth hormone {HGH] secretion is fasting.  “Fasting promotes the use of fat as fuel and preserves muscle mass and bone density.  Adrenalin [and noradrenalin] levels go up with fasting.... Breakdown of muscle tissue happens only at extremely low levels of body fat—approximately 4 percent” p242.  “The human body has evolved to survive episodic periods of starvation,” p 243.  “Caloric restriction diets do not allow the evolved adaptation that occurs during fasting,” p 244.  “Studies of eating a single meal per day found significantly more fat loss, compared to eating three meals per day, despite the same caloric intake” 243[23].  “Total energy expenditure is increased during a fast—in a 4-day fast by 12%,” p244.  “In our clinic experience showed that appetite decreased as duration of fasting increased.  “The most astonishing aspect of this study [107 obese subjects unable to lose weight] was the ease with which prolonged starvation was tolerated.  These experiences echo our own clinical experience at the Intensive Dietary Management Clinic with hundreds of patients,” p245.  The more dangerous visceral fat is preferentially removed with fasting. There is reference to Dr. Michael Mosley (British on BBC) 5:2 diet, 5 days of full caloric and 2 days of 25% of calories at the end of a short-term fast.  In the trail this was compared to a Mediterranean diet with a 25% reduction in calories.  At 6 months both groups lost about the same amount of weight, but the 5:2 group have lower insulin and less IR, at p247.  The short term fasting made this important difference.  Fasting because it corrects insulin resistance is essential for long-term dieting success. 

For those who want to know more of the science behind fasting, I highly recommend that you also read Fung’s The Complete Guide to Fasting, October 2016.  My own experience and other whom I have talked and counseled has convinced me that short-term fasting is easy, and the scientific literature confirms that longer periods are also easy; this is because our body has evolved a system to burn the fat reserve and to keep us alert and full of energy so that we more likely to hunt and gather foods.   



[1] The likely cause of failure is Latent Autoimmune Diabetes of Adults  Adults with LADA may initially be diagnosed incorrectly as having type 2 diabetes based on their age, particularly if they have risk factors for type 2 diabetes such as a strong family history or obesity.   a low C-peptide and raised antibodies against the islets of Langerhans support the diagnosis. It can only be treated with the usual oral treatments for type 2 diabetes for a certain period of time,[2][3] after which insulin treatment is usually necessary, as monitoring for complications. 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.  Glutamic acid decarboxylase autoantibody (GADA), islet cell autoantibody (ICA), insulinoma-associated (IA-2) autoantibody, and zinc transporter autoantibody (ZnT8) testing should be performed on all adults who are not obese who are diagnosed with diabetes.[4]

[2] See Dr. Jason Fung’s “The Complete Guide to Fasting (2016) p101-of the 13 participants, at 6 years 3 weighed more, 6 regained most of their weight, 2 were at their pre-show weight, and the one who had bariatric surgery at year 4 reversed his weight gain, though was still 80 pounds above his weight at the end of the show.

[3] Journal articles showed that under 10% of fructose was in the liver converted to fat, moreover, fat was normally stored in a limited amount for blood transport as need through the liver’s production of LDL.  Excess glucose was also converted to both glycogen and fat in the liver.  Eventually I reversed my positon and decided that the damage to the liver through glycation which causes IR in the liver and only then would insulin cause excess of fat storage in the liver--over 30% of adults results in the condition of NAFLD, many of whom have only moderate abdominal fat.  Thus I am editing my papers to place glycation first among causes.      

[4]  Dr. Fung develops the topic of elite athletes on low carbs and performance.  A number of elite athletes are on a low carb diet.   

[5] The decline in hormones for men and for women is a causal factor for weight gain and thus T2D.  The current beliefs about hormone replacement therapy are another example of how pharma frames the discussion because they profit from illness. 

[6] Polyunsaturated fats are as bad as trans-fats because their multiple double bonds are subject to oxidation (the process is also called “rancidification”).   See link for details and links to research articles.   Soy, canola, corn oils are cheap).

[7]The vast majority of cancer disable fat metabolism, thus relying on glucose--for more on cancer click on link. 

[8]  Having uncovered over the last decades numerous cases of bad pharma deliberately though their KOLs (key opinion leaders) doing bad (tobacco) science to “prove” that an alternative to their drugs is inferior.  I suspect that most of the clinical trials of ADF trials are deliberately flawed to get fasters out of fat burning mode.  The muck of tobacco science is buried within the hidden details.

[9] The other authority to put the pieces together is Gary Taubes a science writer who in his 2011, Why We Get Fat, and What to Do About It, eloquently explains the historical science behind dieting, the process leading to obesity, the current bad advice, and the fix for obesity, but he defers in 2011 from taking a position on fasting and misses incretin  and the need to keep insulin low through fasting (not just a KD diet) to fix the weight-regulatory system.  It is 2nd on the best book on obesity. 

[10] Pharma sells patented modifications of insulin to lower glucose.  One of its side effects for those with T-2D is increased fat storage. 

[11] Because Glycemic Load and Glycemic Index tables don’t measure the effects of protein and fructose on insulin, they are only an imperfect gauge  of the insulin response to various foods.

[12]    "Many factors stimulate insulin secretion, but the main one is blood glucose. Incretins, especially GIP and GLP-1 secreted, respectively, by K and L cells in the gut are also important", (Rang and Dale's Pharmacology (2015)). Wiki  We have reported previously that the oral or intravenous administration of the amino acid l-leucine to healthy subjects results in increases in plasma insulin and decreases in blood glucose and plasma free fatty acids” p 1479. “We speculate that the purpose of the insulogenic response to protein ingestion is to aid both in the utilization of absorbed amino acids and in their synthesis to protein” 1486 Journal 1966.   

[13]  Leptin functions to maintain adiposity; thus there is a reduction in metabolism of 25% or more by about 2nd month, thus reduced physical excursion and mental energy.  Leptin is the main reason for both the low compliance with and subsequent weight gain. 

[14] This is a survival advantage we inherited that promotes the drive to search for food and to hunt. 

[15] This phenomenon cures T2D bariatric patients, they undergo  post-operative fasting,  Cure rates (other than band) is between75%, and 100% and it occurs before a major reduction in weight at, and 100% (“All patients in the surgical groups discontinued pharmacologic treatment (oral hypoglycemic agents and insulin) within 15 days after the operation on the basis of daily seven-point glucose profiles (pre-meal, post-meal, and bedtime… and 19 of 20 (95%) undergoing biliopancreatic diversion) at NEJM 2012.   

[16] Net carbs are the total carbs listed minus the fiber.  It is an approximation of total carbs, because some of the resistant carbs, which includes fiber, are fiber are slowly digested by bacteria in the digestive track and some of the resultant glucose is absorbed.  Some of these resistant carbs are also converted to ethanol and absorbed.    

[17] Bariatric surgery cures between 70 and 95% of T2D, most within the first 2 weeks, depending on type of surgery- at NEJM 2012 

[18] Insulin resistance:  the condition in which cells have reduced response to hormone insulin, and this causes high-blood sugar.  Insulin resistance first occurs in the liver, then depending upon diet it can also develop in the muscles and adipose (fat) cells.  The pancreas produces more insulin in response to the elevated glucose.  Due to the accumulation of fat in the pancreas, for some the beta cells drastically reduce their production of insulin which results in type-2 diabetes.

[19] Hormesis is a generally favorable biological response to a low exposure s to toxins or other stressors—the stress of going between two different systems of metabolism.  Anabolism is the construction of larger from smaller molecules while catabolism is the reverse process of breaking down into smaller units.  However, I don’t understand how metabolism fat and that of glucose, that one of these could be anabolism, is both starting molecules are converted to simpler ones, unless the author is referring the conversion of pyruvates to larger molecules in the metabolism of triglycerides.  

[20] As I age (73 years in 2016), the diversion of energy and blood to promote digestion entails a low point after eating a full meal.   Not eating breakfast, I find the best time for studies and writing in the morning, I also have plenty of energy for gardening. 

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

[22] It id s type of hunger which persists, not the short-term hunger caused by the need to replenish blood glucose, such as when not eating for several hours or following strenuous work or exercise.  CER hunger comes from the decline in metabolism that makes one feel consistently tired, mentally less sharp, and more moody, and the feeling the cure is to eat more.

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

6.  Two tables, Net Carbs & Insulin Index

Net Carbs = total carbohydrates minus fiber content.

Egg 1 = 0.4 grams

Seafood 6 oz. = 0

Meats 6 oz. = 0

Poultry 6 oz. = 0

Oils 6 oz. = 0

 

Dairy

American processed 1 slice 1.5 grams

Cheeses 1 oz. = 0.7

Cottage cheese c = 5

Cream 1 T  = 0.4

Cream cheese 2 T = 1.2

Milk 1 c = 11.7 to 15

Yogurt plain 1 c = 11.6

Greek Yogurt plain 1 c =  9

 

Raw Vegetables

Avocado = 2 grams

Bell pepper green c= 2.2

Bell pepper red c =3

Broccoli c = 1

Cabbage shredded c = 1.1

Celery stalk = 1

Cauliflower florets c = 1.4

Cucumber c = 1

Nuts

Almonds 24 = 2.5

Brazil 6 = 1.4

Cashews 2 T = 5.1

Mixed nuts 2 T = 2

Peanuts 2 T = 1.4

Pecans 1 oz. = 1.2

Walnuts 1 oz. 1.2

 

Green beans c = 2

Lettice 1 c = 0.36

Olives black 5 = 0.7

Olives green 5 = 0.0

Onion 2 tbs. = 1

Spinach 1 c = 0.2

Squash summer c    2.6

Tomato 1 med = 3.0

Tomato juice 1c = 8

For those off

the induction

Phase

 

Fruits

Apple med = 8

Banana med = 30

Blueberries c = 9

Dates dried 1 oz = 21

Fig dried med = 6

Grapes 1 c = 26

Grapefruit = 9

Melon cantaloupe 1 c  = 12

Orange navel med =15

Peach med = 15

Pear med = 20

Strawberry 5 lg = 5

Legumes

Black bean home cooked 1 c = 8

Canned baked beans 1c = 36

Kidney home cooked 1c = 11

Pinto bean home cooked = 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 c cooked = 2.7

Squash acorn 1 c = 21

Squash zucchini 1c = 3

Sweet potato med = 20

 

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

Insulin index of common foods

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

 

Peanuts                   20

 

Fish                            59

 

Grapes                           82

 

Eggs                          31

 

Oranges                    69

 

Crackers                         87

 

All bran                    32

 

Potato chips            61

 

Ice cream                       89

 

Porridge                  40

 

Brown rice               62  

 

Milk whole or skim     90

 

Brown Pasta          40

 

Special K                   66

 

Cookies                          92

 

White Pasta           40

 

Honey smacks         67

 

Whole Bread                96

 

Cheese                    45

 

Coco Pops                71 

 

White Bread               100

 

Granola plain         46

 

French Fries             74

 

Yogurt sweetened    115

 

Beef                         51

 

Corn Flakes              75

 

Baked Beans can       120

 

Popcorn                  54

 

Croissants                79

 

Potatoes                      121

 

Grain bread            56

 

White Rice               79

 

Mars Bar                      122

 

Lentils                      58

 

Bananas                   81

 

Jelly Beans                  160

Apples                     59

 

Cake                          82

 

Fat                                  10

 

from http://graemethomasonline.com/wp-content/uploads/2010/06/Insulin-Index.pdf and also http://www.janurky.sk/db/articles/20150703n0(kj_not_kj)/images/insulin_index.pdf

For measure of digestible carbs see glycemic index and glycemic load tables at id3.html

Detail explanation of testing: 

These figures are based on test results for an ideal group:  average age 22 and BMI of 23.  Foods needing preparation such as potatoes and pasta were boiled, stored overnight in the refrigerator then warmed the next day in a microwave.  Test score was based on the average insulin level over 120 minutes divided by that for white bread times 100.  There were 539 tests total test for the 39 listed foods.  Breakfast cereals were served with milk.  “Plasma insulin concentrations were measured in duplicate by using an antibody-coated tube radioinmmuonoassy kit (Coat-A-Count; Diagnostic Products Corporation, Los Angeles)”at 1997, p. 1295.  Samples of 1.5 to 2.5 mL of blood were obtained at 15-minute intervals over the 2 hours test period.  Unfortunately this table lacks important foods of vegetables, soda, diet soda, and fat (which I included from another source--Dr. Fung’s book The Obesity Code p 193).                                                                                                                                                                            

The goal is to maximize the rate of fat burning which requires a low insulin diet.  Insulin causes fat storage.  Since protein is needed to maintain muscle mass, it must be restricted, but only somewhat.  The USDA dietary recommendations are high.  Thus I recommend cutting protein to 35 grams women, and 45 grams men--for those of average body frame size.  This is sufficient to prevent muscle loss.[1]  The effect of protein upon insulin and thus fat storage explains why short-term and alternate day fasting make a very significant improvement upon the low carb ketogenic diet.[2]  For most on a ketogenic diet after 2-months the rate of weight loss will decline, the effect of insulin upon leptin, this lowers metabolism.  Fasting prevents this phenomenon.



[1] The science on the effects of elevated insulin due to protein when carbs are low is very incomplete.  For one thing, with a high-protein-low carb diet (once popular in the 1920s and before) proved successful.  Obviously the when there is no glucose to burn the body will continue to burn fat; however there could be for those who don’t fast a point where metabolism declines. 

[2] There is a second hormonal system, one not affected by glucose, stimulating the release of insulin from the pancreas.

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