Home | Book outline by chapters and subheadings | Letter on project to physicians | 1B-low fructose-avoids conditions associeted with western diet | 6:2 HORMONAL HEALTH | 2:1 The basic on sugar, and related topics | 3-1 Mitochondrdial structures and maintenance | 4:4 Polyunsaturated fatty acids in cell membranes | 6:1 AUTOPHAGY, repair, replace, recycle, and defense systems | 6:3 Diet basics: Energy restriction, keto, and fasting diets | 6:4 type-2 diabetes diet versus drugs


Book outline by chapters and subheadings

Why We Get Sick, the High Sugar Diet and Mitochondrial Dysfunction:  Textbook on conditions associated with the western diet, and what to do about it    3/3/20.



1) Intro CAWD

1) Uric acid—sensitivity to and consequences

2) Burkitt and Trowel’s CAWD book, historical accounts


3) LSP markers differ HSP

2) Under production of collagen  & cholesterol 

4) Nature of biological systems--touchstones

3) Endothelial dysfunction uric acid, collagen & PUFAs


4) Rancid PUFAs in cell membranes and good fats

1) Basic-background knowledge

5) Chemical causes for MTDD and CC for CAWD

2) Fructose receptors jejunum

6) A review of sections 3 through 4

3)  Fructose consumption, numbers, KOLs


4) Fructose through fructation causes MTDD

1) CAWD1) B-4 and risk measurements

5)  Polyol pathway—glucose to fructose in every cell

2) List of conditions associated with the western diet

SECTION 3:  MITOCHONDRIAL DYSFUNCTION (MTDD)and the consequences of the underproduction of ATP

SECTION 6:  THE FIXEs, what’s good

1) MTD structure and metabolism

1) Autophagy the repair replace, and recycle systems

2) MTD functions other than metabolism

2) Sex hormones fine tune autophagy, other supplements

3) Inherited mtDNA & nDNA mutations

3) Diet basics, energy restriction, keto, and fasting diets

4) MTD lipid droplets, and NAFLD

4) Type 2 diabetes and diet, low carbs vs. drugs

5) MTDD CC IR, LR,  lipophilia, NAFLD, type 2 diabetes

5) Fixing social environment

B-4 fructose, MTDD, RATP, RRA, CAWD conditions associated with the western diet, CC contributing cause, HSP high sugar population, IR insulin resistance, KOL key opinion leader, LR Leptin resistance, LSP low sugar population MTD mitochondria (/al), MTDD mitochondrial dysfunction, NAFLD non-alcoholic liver disease, PUFA polyunsaturated fatty acids, RATP reduce ATP, RRA reduced rate of autophagy

STYLE: address (2:6,3) section, chapter, item.    Calibri:  inserts under illustrations; in Sections are bold and brick red      Book Antiqua: Chapters 2-4-blue 16 pica.   Lucida sans Items in chapters; Sections in blue   time Roman:  footnote       Green for lack of evidence or I missed it  NEED TO lower # of abbreviations used throughout to less than half the size and then have special ones that are used in a few chapters, & eliminate ADA, WHO, TE etc. as too infrequent.     


Section 1, Low Sugar Populations (LSP), Next project-changes

Chapters:  1.  Introduction   2. Burkitt and Trowell’s CAWD book    3.     4. How industries frame the topics; some consequences.

Chapter 1. Introduction   2. Exposing tobacco science   3. Framing and un-framing topics  4. CAWD  

Chapter 2 Burkitt & Trowell’s CAWD Book 1. review of their book and related works

Chapter 3: Biomarkers   1. LSPs compared to HSPs biomarkers    2. Wearing the right glasses, a glimpse of what to come, the difference 

Chapter 4 Seeing the forest, on mother nature  

Section 2, Fructose,

Chapters:    1. Basic background knowledge   2. Fructose receptors jejunum    3. Fructose consumption, numbers, KOLs    4. Fructose through fructation causes MTDD    5. Polyol pathway makes fructose from glucose in every cell

Chapter 1:  1. Basic background knowledge, 1.  ????  2. Metabolism in the cytosol:  glycolysis, fructolysis, pyruvic acid, lactic acid fermentation, amino acid catabolism, pentose phosphate pathway, glutathione, cAMP, (cyclic adenosine monophosphate), acetyl CoA, phospholipid.  3. Metabolism in the mitochondria: Krebs cycle, lipolysis, fasting state, beta-oxidation (fat metabolism), ketone bodies, oxidative phosphorylation (ADP converted to ATP), electron chain transport in the MTD, superoxide   4. Major sugar facts   5. The Sugars: sucrose, glucose, galactose, ribose, sorbitol, glycogen, glycogenolysis, gluconeogenesis   6. Fructose as a poison--basic flow chart   7. On fructose, fructation by fructose is different than glucose   8. Industries being industries   

Chapter 2:  Fructose receptors jejunum   1. Reactive sugars cause MTDD    2. Location of fructose metabolism (2018 macAMP or update)  

Chapter 3. Fructose consumption, numbers, Gov.  1. The road to a health disaster   2. All sugars with fructose count   3. A brief history of sugar consumption    4.  Hedonic pathway causes sugar addiction   5. On the obesity numbers    6. The pathogenic consequences   7. Fructose causes MTDD, an introduction   8. The information system is marketing  


Chapter 4 Fructose through fructation causes MTDD   1. Introduction fructation causing MTDD   2. An Overview   3. mtDNA and IR   4. Fructation causing MTDD, the evidence   5. Reactive oxygen species (ROS) a CC for MTDD   6. Milliard reaction, Strecker degradation   7. Advanced glycation end-products (AGEs).    8. Lysine deficiency   9. NADPH depletion    10. Some other effects of fructation of the MTD    11. Fructose and the kidney   12. Fructation a brief summary   13.  KOLs’ exoneration of fructose    14. A couple of lessons from the above    15. JK’s answer to MTDD, fructation of imports

Chapter 5 polyol pathway, conversion of glucose to fructose in every cell:  1. Introduction    2. Osmotic pressure from excess sorbitol and glucose, pharma’s position    3. Another statement of Pharma’s theory    4. Hypertonicity challenged    5.  The polyol pathway and NADH depletion—possibly   7.  A drug to block the polyol pathway thus lower sorbitol    8. Fructose through PP damages kidney   9. Why blame pharma    10. The rat lab, the smell of methylamine--8 issues   11. Blaming glucose instead of insulin and drugs   12. Blaming glucose instead of insulin resistance   13.  Why LSP on high carb diet don’t through PP have CAWD   14. Evidence for fructose’s pathogenic role through PP   15. Fructose is cleared last from cells and from blood

Section 3, Mitochondrial Dysfunction, the consequences,

Chapters:  1. MTD structures & metabolism   2. MTD functions other than metabolism   3. MTDD CC for DNL, lipid droplets, and NAFLD   4. MTDD CC IR lipophilia, t2d   

Chapter 1, Mitochondria structures and processes   1. MTD basics   2. Mitochondria structures and functions    3. External connections, microtubules    4.  mtDNA repair systems   5. Fission and fusion   6. Mitophagy   7. Sex hormones are protective    8. ATP, adenosine triphosphate production   9. MTDD and under production of ATP. 

Chapter 2, MTD functions other than metabolism:  1. Regulating processes   2. Synthesizing molecules   3. Urea cycle   4. Pregnenolone   5. Heme      6. iron sulfur cluster   7. Calcium storage and signaling    8. Senescence and apoptosis     

Chapter 3, Defective metabolism of cancer, mtDNA nDNA, and mutations 1. Historical background   2. Warburg and the Warburg effect   3. On starving cancer         4. Golden era of medicine   5 Consequences of mutations   6 Inherited mtDNA mutations   7. Reactive chemical assault   8. Inherited nDNA mutations  INCOMPLETE 

§Chapter 4, MTDD, the assault DNL, lipid droplets and NFLD 1. Historical, my standing on the shoulders   2. Briefly on IR and t2d   3. Lipid droplets and NAFLD   4. NAFLD non-alcoholic fatty liver disease   5. The assault upon mtDNA     6. The vulnerable mtDNA criticized by KOLs   7. The repair systems fails & tables   8. What is causing MTDD     9. How fructose causes MTDD   10. Lipid droplets (ectopic fat) 

Chapter 5, MTDD CC for IR, LR, lipophilia:   1. Introduction   2. Insulin resistance and cellular glucose stuffing   3. MTDD and other CCS for IR    4.  The road to IR through the liver   5. Insulin functions   6. Excess insulin, a marker and a problem   7. Leptin functions    8. Some comments on leptin functions     9. Weight regulatory system causes obesity   10. more on weight-regulatory system   11. Conflating the 2 very different types of diabetes in murine research   12. Murines produce vitamin C   13. T2d, extreme IR & beta cells burnout 2/20-HEADINGS CHECKED

Chapter 6 MTDD review:  MAYBE   --   or for physician’s


Section 4, More major contributing causes for CAWD

Chapters:  1. Uric Acid & urate sensitivity   2.  Collagen issues     3. Endothelial dysfunction, uric acid, collagen and PUFAs   4 Rancid PUFAs in cell membranes and good fats   5. Chemical CC for MTDD and CAWD   7. Combined theory of aging

Chapter 1:  Uric Acid & urate sensitivity:  1. Introduction   2. Purine family of compounds   3. Urates and uric acid    4. KOL’s version of hyperuricemia    5. Hyperuricemia and fructose    6. Loss of uricase gene in big-brain primates    7. Gout, hyperuricemia, and micro monosodium urate crystals     7.  Hyperuricemia and it consequences   8. Causes fatty liver   9.  MSO and endothelia dysfunction   10. MSO and nephropathy   11. MSO and oxidative stress [possible just a sign of 8, 9, and 10    11.  MSO and MTDD

Chapter 2:  Collagen issues: 1. Collagen basics   2. B-4 and the reduced collagen replacement (RCR).   3. Low ascorbate and collagen cross links (and Pauling-cancer footnote—develop in 3:3).  4. Low ascorbate in the polyol pathway   5. Ignoring the obvious, ascorbate   6. Insulin and insulin like growth affect upon collagen   7.  Stem cells and autophagy in collagen production   8. Collagen in endothelial dysfunction and CVD  9. Contributing causes for ED.  10. Endogenous antioxidants    11. The path to CAWD 

Chapter 3:  Endothelial dysfunction, CCs uric acid crystals, collagen and PUFAs:   1. Endothelium and cells    2. Endothelium dysfunction   3. Uric acid and urate crystals damage endothelial cells   4. Endothelial dysfunction, a CC for CVD   5. Nephropathy   6. Collagen, IR, ascorbate, and ED   7. Rancid fats and ED

Chapter 4:  Rancid PUFAs in cell membranes and good fats:  1. Diet and their message   2. Nature’s choice   3. Extraction vegetables oils and rancidification   4. Why rancid in cells?  5. Health consequences   6. Palmitic acid, glycogen, and omega 3 & 6 fatty acids   7. Oxidized cholesterol and lipoproteins as cause for atheromas   8. Trans-fats, are they bad?  9. What are the regulations of trans-fatty acids?  10. What is good?   11. Evidence that coconut oil stimulates neurotrophins   12. Other ways to stimulate neurotrophins

Chapter 5:  Chemical CC for MTDD and CAWD:  1. Introduction   2. Sensitivity to chemicals   3. Mitochondrial link   4. How chemicals damage the MTD   5. MTDD conditions    6. Markers associated with MTDD   7. Measurements of MTD functions in vivo   8. List of drugs which cause MTD damage   9. Hall of shame:  a) Vioxx, b) antiarrhythmic, c) statins, d) neuroleptics e) diabetes mellitus   10. So how bad is it?   11. What have we learnt?  12. Scientists for hire, mass delusion, and bias  

Chapter 6:  A Review of sections 3 & 4:  Chapter 5, Mitochondria consequences—survey:   1.  Measuring MTDD using serum glucose    2. Fructation, MTDD & IR   3. Insulin resistance is on a continuum     4.  Type-2 Diabetes is the extreme form of IR    5. Low ascorbate   6. Fructation affects all proteins   6. The polyol pathway relieves osmotic pressure   7.  Low ascorbate in diabetics   8. The polyol pathway and NADH depletion    9. Fructation and MTDD     10. MTDD and the underproduction of ATP and thus hypoxia    11. Quality of and under production of collagen    12. Uric acid   13. Endothelium, endothelia and dysfunctions    14. De novo lipogenesis   15.  Fatty liver--NAFLD and NASH    16. Cellular repair systems   17. Markers for MTDD  18. Cytotoxicity   19.  Fetal environment   20. MTD theory of aging and the role of the western diet




Section 5, Conditions Associated with the Western diet

Chapters 1. B-4 and risk measurements   2. B-4 and CAWD   3  Brief review of CAWD

Section 6, The Fixes

Chapters 1. Autophagy and the repair systems; 2. Sex hormone;  3. Diet basics;  4. Diet for diabetes versus medication 5. Social environment and organize

Chapter 1, Autophagy the repair, replace and recycle system:  1. introduction to autophagy   2. Autophagy: organelle, lysosome, phagosome, Golgi apparatus, autophagosome, macroautophagy, microautophagy, Barbieri’s 382 day fast, chaperone-mediated autophagy (CMA), mitophagy, lipophagy, xenophagy, peroxisome, endosome, 3. Apoptosis   4. Necroptosis in response to pathogens   5. Autophagy’s role in cancer suppression   6. Aspirin and cancer    7. AMPK   8. Switches, AMPK, mTOR, & insulin   9. Drug fixes    10.  Autophagy immune and clearing functions [examples needed]

Chapter 2, Sex hormones and others hormones fine tune autophagy:  1. Sex hormone connection     2. InCHIANTI longevity study   3.  Sex hormones benefits   4. Estradiol and testosterone protect MTD   5. Testosterone, and neurosteroid    6. Estradiol HRT is healthful    7. HERS, WHI, horse estrogen and MPA    8. Osteoporosis and estrogen    9. Epidemic of osteoporosis and osteoarthritis    10. My historical note on hormones    11. Why menopause and andropause?   12. DHEA and DHEAS introduction   13. DHEA turns on autophagy   14. DHEA neurosteroid   15. IGF-1 and InCHIANTI Study   16. IGF-1 autophagy, and CC for MTDD   17. Pregnenolone a major neurosteroid   18. Progesterone and progesterin   19. Neurosteroid summary   20. Testosterone, estradiol 

Chapter 3:  Diet Basics:  energy restriction, keto and fasting diets:  1. Mediterranean diet   2. Why the Mediterranean diet works    3. Weight regulatory system and Tbe Biggest Loser   4. Blaming the victims    5 Three types of diets: caloric energy restriction, low carbs, and Atkins-keto diet   6. How bariatric surgery causes permanent weight loss    7. Going without food, fasting    8. Extended water fasting—Angus Barbieri record   9. Amino acids and insulin   10. Wasting t1d prior insulin days   11. Ketogenic diet    13. Short list of what is best for dieting   14.  Personal note, how I ate the western diet and avoided CAWD   15. Fixing the cause.   

Chapter 4:  Diabetes, diet versus meds:  1. Introduction   2. The tidal wave of t2d   3.  Early western history of diabetes   4. Modern health care before the drugs for t2d    5. Dietary low-carb management of t2d, Merck 1950-61    6. Low carb diet for diabetes mellitus   7.  Fructose damaging MTD is the starting point.  8. NAFLD to IR and fatty pancreas leads to t2d    9. Bariatric surgery and t2d    10. Curing t2d with ketogenic diet or fasting   11. Supplements and exercise   12.  Confusion from the past, on ketoacidosis and hypoglycemia   13. Homeostasis and don’t upset the apple cart   14. Treating the sign, glucotoxicity, instead of the cause IR    15. Drugs for treating t2d    16. The wonder drug, metformin?     17. The ADA 2019 guidelines     18. Prediabetic treatment   19. Short list of what is weight loss, managing t2d and lowering risk for CAWD    19. What causes t1d  

20. What causes wasting in untreated t1d      




Chapter 5:  Social environment

~~~~~~~~~~~~~~~~~~~~~From 4:6 on psychiatric drugs

Psychiatric section chapter 6 section 4  1 Intro   2 Psychiatric drugs as sedatives, consequences reduced boredom, CAWD, dementia    3 recreational sedatives, sedatives for non-psychiatric uses    4 non-psychiatric drugs that cause sedation   5 fog promoted conditions   6 Theory of chemical imbalance   7 Breaking blind 87%  8 Inert placebo bias   Citalopram KOLs trial bias   10 about citalopram   12 Hamilton Scale, many ways to assure improvement   13 FDA accepts 2 trials and ignored the negative 5   14 Citalopram 4-6 week trials, no mention of 5 others   15 85% benefited claim   16 Gotzsche on STAR*D  description & results   17 Gotzsche attacks   18 Doctors resistant to helping patients quit   19 withdrawal syndrome    20  Wiki’s KOLs missed symptoms   21 Tardive dyskinesia split 20 ways   22 Terminal acts (TA) suicide/murders sedatives as CC  23 Why are TA much more common than in the 50s? sedatives  24  5 categories of causes:  neurotransmitter imbalance, chemical lobotomy, cognitive decline, withdrawal syndrome  & dopamine reduction   23 sedatives cause TA   25 neurotransmitters   26 chemical lobotomy   27 Alzheimer’s disease, diminished housekeeping  28 reduced brain size and poor functioning   29 dopamine   30 Dopamine reduction promotes TA  31 cognitive decline & other 4 categories promote TA   32  Greater the dose and longer the increased chance for TA, also extreme withdrawal agitation   33 Dopamine’s role stated again  34 genes CYP450   the complexity of the brain, 200 chemical messengers 

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On how daily excessive fructose damages the mitochondria and thus is the main cause for the conditions associated with the Western diet--much, much, more than insulin resistance, type-2 diabetes, and weight gain