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![“Lipids, risk factors and Ischaemic heart disease” Atherosclerosis 124 Suppl. (1996) S1-S9
“The [Total/HDL] RATIO was found to be a better predictor of CHD
than TC, LDL, HDL and triglyceride -- not only in the Framingham Study,
but also in the Physician's Health Study and many other studies.”
“Unless LDL levels are very high - 7.8 mmol/L (300mg/dL) or higher - they
have no value, in isolation, in predicting those individuals at risk of CHD”
- William P. Castelli (Framingham Director)](https://image.slidesharecdn.com/4-221016195846-6eb42942/75/4-The-Power-of-Real-Nutrition-Science-Unvbelievable-Benefits-Accrued-pptx-23-2048.jpg)
Uploaded byIvor Cummins
4. The Power of Real Nutrition Science - Unvbelievable Benefits Accrued.pptx
The document discusses the relationship between diet, particularly carbohydrate and fat intake, and chronic diseases, emphasizing the impact of processed foods and metabolic syndrome. It highlights the importance of measuring insulin and cholesterol levels in understanding health risks, as well as noting rising rates of pre-diabetes among adults. The text critiques traditional dietary guidelines and advocates for a low carbohydrate, high healthy fat diet to address chronic health issues.
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4. The Power of Real Nutrition Science - Unvbelievable Benefits Accrued.pptx
- 1. 2017 Ivor CumminsBE(Chem) CEng Chronic Disease Realities - Nutritional Details Ivor Cummins BE(Chem) CEng MIEI PMP®
- 2. Serum GGT Serum Ferritin Ivor’s Story (2013) Cholesterol <200 approx < 5 112 530 6.8 <35 approx
- 3. When the expertsdon’t know…
- 4. July 2013 -Singapore It’s Root Causing Time
- 6. EXCESSIVE CARBOHYDRATE MEDIUM FAT/PROTEIN HIGHISH FRUCTOSELOW FRUCTOSE LOTS OF NON-STARCHY VEG! BUT LOW STARCHY CARBOHYDRATES HIGH HEALTHY FAT / MODERATE PROTEIN Root Cause Solution
- 7. GGT U/L 25 50 75 100 112 Start 6 Weeks 125 8Weeks 42 35 The Power of a Proper Pyramid Ferritin 530 230 BP 145/90 130/80 Cholesterol Weight 95kg 83kg Waist 35” 32”
- 8. How did theworld abandon… Good Science?
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- 15. Men Only (12k) 7Countries Manual Analysis Cherry Picked Men/Women (180k) 18 Countries Modern Technology Unbiased Team Krazy Keys Proper PURE
- 16. “In the WHIrandomized clinical trial (n=48 835), reduction of total fat consumption from 37.8% energy (baseline) to 24.3% energy … had no effect on incidence of Coronary Heart Disease, Stroke or total CVD” “This was consistent with null results of 4 prior randomized clinical trials and multiple large prospective cohort studies…” In a pooled analysis of individual-level data from 11 prospective cohort studies in the United States, Europe, and Israel that included 344 696 participants, “each 5% higher energy consumption of carbohydrate in place of saturated fat was associated with a 7% higher risk of CHD”
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- 20. The Lipoprotein Particles– Boats for Cargo The Chylomicron is the big one, created to ferry dietary fat and cholesterol, for energy and healing Chylomicron VLDL is made in the liver to ferry Trigs and Chol… VLDL 2013 Ivor Cummins BE(Chem) MIEI HDL HDL is the so-called “GOOD Cholesterol” LDL LDL (from VLDL) is the so-called “BAD Cholesterol” sdLDL Oxidized LDL is the real “BAD Cholesterol” The LIPOPROTEIN PARTICLES are transport vessels (“boats”) created in the body to deliver Triglyceride and Cholesterol (“cargo”), for energy transfer, critical synthesis, and healing purposes…. Triglyceride/ Cholesterol An Apo- Lipoprotein Phospholipids
- 21. 2013 Ivor CumminsBE(Chem) MIEI The LDL Species Created by your Liver, for Triglyceride (and Cholesterol) Delivery…
- 22. VLDL, IDL,LDL…..and SmallDense LDL C II C II LPL LDLR SR-B1 Ch Ch Ch 2013 Ivor Cummins BE(Chem) MIEI Ch To tissues and cells Ch Moderate Uptake Res Time >2 days Poor Uptake Res Time = ?? Tg HL Tg Ch Ch Ch LDL B100 IDL E B100 Tg Tg Ch Ch Ch Ch Tg LDL SD LDL OX HL Gluc B100 B100 Tg Ch Ch Ch Tg Ch Ch Ch VLDL Tg Tg Tg Tg Tg Tg Tg Tg Ch Ch Ch Ch E C II B100 Ch Ch Ch IMMUNE SYSTEM MACROPHAGE / FOAM CELL
- 23. “Lipids, risk factorsand Ischaemic heart disease” Atherosclerosis 124 Suppl. (1996) S1-S9 “The [Total/HDL] RATIO was found to be a better predictor of CHD than TC, LDL, HDL and triglyceride -- not only in the Framingham Study, but also in the Physician's Health Study and many other studies.” “Unless LDL levels are very high - 7.8 mmol/L (300mg/dL) or higher - they have no value, in isolation, in predicting those individuals at risk of CHD” - William P. Castelli (Framingham Director)
- 24. “If You Don’tMeasure It …it Don’t Get Fixed” “If You Don’t Measure It …you Can’t Understand It”
- 25. Hyperinsulinemic syndrome: themetabolic syndrome is broader than you think. Surgery. 2014 Aug;156(2):405-11.
- 26. Hyperinsulinemic syndrome: themetabolic syndrome is broader than you think. Surgery. 2014 Aug;156(2):405-11. 423 Metabolic Syndrome Disease Papers Researched Selected the 70 Papers which had actually measured Insulin So how did Insulin relate to the myriad MS Diseases ???
- 27. Array of ChronicDiseases Hyperinsulin Signal Present Cardiovascular Disease / Atherosclerosis 12 / 12 studies Diabetes / Polycystic Ovary Syndrome 12 / 13 studies Central Obesity / Sleep Apnea / Met Syn 15 / 15 studies Hypertension 9 / 10 studies Non-Alcoholic Liver Disease / Renal Failure 9 / 9 studies Dyslipidaemia / Met Syn 6 / 6 studies Certain Cancers 4 / 5 studies Hyperinsulinemic syndrome: the metabolic syndrome is broader than you think. Surgery. 2014 Aug;156(2):405-11.
- 28. Array of ChronicDiseases Hyperinsulin Signal Present Cardiovascular Disease / Atherosclerosis 12 / 12 studies Diabetes / Polycystic Ovary Syndrome 12 / 13 studies Central Obesity / Sleep Apnea / Met Syn 15 / 15 studies Hypertension 9 / 10 studies Non-Alcoholic Liver Disease / Renal Failure 9 / 9 studies Dyslipidaemia / Met Syn 6 / 6 studies Certain Cancers 4 / 5 studies Data source: 2011–2014 National Health and Nutrition Examination Survey and 2015 U.S. Census Bureau ~65% of US adults over 45 …are pre-Diabetic or Diabetic. Pre-Diabetic ≈ Diabetic ≈ Insulin Resistant ≈ Hyperinsulinemic
- 29. KNOWN Diabetics ! MORE Diabetics ! YET MORE Diabetics ! If INSULIN Tested ??? Surveyed all Coronary Disease The 2015 EuroAspire Study Patients aged 18 to 80 Across 24 European countries “If You Don’t Measure It …you Can’t Understand It”
- 30. 40% ofNon-Obese are TOFI The TOFI Epidemic? TOFI Heart Attack Risk is right up there with the Obese “Thin Outside, Fat Inside” “If You Don’t Measure It …you Can’t Understand It”
- 32. Modern Processed Foodsand Lifestyles are the Drivers “Coronary atherosclerosis in indigenous South American Tsimane: a cross-sectional cohort study” Lancet. 2017 Apr 29;389(10080):1730-1739. Homework: Google “Insulin Resistance” and the Disease of your Choice
- 33. Welcome to theElephant in the Room:
- 34. Welcome to theElephant in the Room:
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- 37. “Soybean Oil IsMore Obesogenic and Diabetogenic Than Coconut Oil and Fructose in Mouse: Potential Role for the Liver.” 2015 PLoS ONE 10(7): e0132672. “Dietary Linoleic Acid Elevates Endogenous 2- AG and Anandamide and Induces Obesity,” Obesity 20, no. 10 (October 2012): 1984–94. “Adipose Tissue Immune Response: Novel Triggers and Consequences for Chronic Inflammatory Conditions.” Inflammation 37, no. 4 (2014): 1337–53. “Dietary Linoleic Acid Is Required for Development of Experimentally Induced Alcoholic Liver Injury,” Life Science 44, no. 3 (1989): 223–7. “Alcoholic Liver Disease: Update on the Role of Dietary Fat,” Biomolecules 6, no. 1 (March 2016): 1. “Linoleic Acid Recommendations—A House of Cards,” Prostaglandins, Leukotrienes and Essential Fatty Acids 85, no. 6 (2011): 399–402. “The Importance of the Ratio of Omega-6/ Omega-3 Essential Fatty Acids.” Biomedicine & Pharmacotherapy Volume 56, Issue 8, October 2002, Pages 365-379
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- 39. ”The Gut isGround Zero”
- 40. The Gut isGround Zero The incretin effect in healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH
- 41. The Gut isGround Zero The incretin effect in healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH
- 42. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 INSULIN Adipose Storage STOMACH The Gut is Ground Zero
- 43. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH INSULIN Adipose Storage The Gut is Ground Zero
- 44. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 Pancreatic Function Satiety STOMACH INSULIN Adipose Storage The Gut is Ground Zero
- 45. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 Pancreatic Function Satiety STOMACH INSULIN Adipose Storage The Gut is Ground Zero
- 46. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 Pancreatic Function Satiety STOMACH INSULIN Adipose Storage The Gut is Ground Zero
- 47. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH INSULIN Adipose Storage The Gut is Ground Zero Pancreatic Function Satiety ?? ? ? ?
- 48. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 Pancreatic Function Satiety STOMACH INSULIN Adipose Storage The Gut is Ground Zero
- 49. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH Pancreatic Function Satiety INSULIN Adipose Storage The Gut is Ground Zero 1 2
- 50. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH The Gut is Ground Zero Pancreatic Function Satiety INSULIN Adipose Storage
- 51. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH The Gut is Ground Zero Pancreatic Function Satiety INSULIN Adipose Storage
- 52. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH The Gut is Ground Zero Pancreatic Function Satiety INSULIN Adipose Storage
- 53. The incretin effectin healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions www.thelancet.com/diabetes-endocrinology Published online February 11, 2016 STOMACH The Gut is Ground Zero Pancreatic Function Satiety INSULIN Adipose Storage 1 2
- 54. A Teeny Sampleof the correct science…
- 55. “Effectiveness and Safetyof a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non- Randomized, Controlled Study” Diabetes Therapy April 2018, Volume 9, Issue 2, pp 583–612 Professor Jeff S. Volek, Ph.D., R.D. “Dietary Carbohydrate Restriction Uniquely Targets the Features of Metabolic Syndrome” ? KETO / LOW CARB
- 56. “Effectiveness and Safetyof a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non- Randomized, Controlled Study” Diabetes Therapy April 2018, Volume 9, Issue 2, pp 583–612 Professor Jeff S. Volek, Ph.D., R.D. “Dietary Carbohydrate Restriction Uniquely Targets the Features of Metabolic Syndrome” KETO / LOW CARB
- 57. “Effectiveness and Safetyof a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study” Diabetes Therapy April 2018, Volume 9, Issue 2, pp 583–612
- 58. Improvement in Biomarkers -20% 0 +20 % +40 % -40% Weight Body FatVisceral Fat Insulin Resistance (~18 lbs) -5.1% -43.7% -30% Published: 16 March 2019
- 59. Improvement in Biomarkers 0 -80% HOMA IRFasting INS MoCA Cognitive -89% -60% -40% -20% -85% Trig/HDL -55% HbA1c -30% -20% -40% +26% Published: Jan 2019
- 60. Array of ChronicDiseases Hyperinsulin Signal Present Cardiovascular Disease / Atherosclerosis 12 / 12 studies Diabetes / Polycystic Ovary Syndrome 12 / 13 studies Central Obesity / Sleep Apnea / Met Syn 15 / 15 studies Hypertension 9 / 10 studies Non-Alcoholic Liver Disease / Renal Failure 9 / 9 studies Dyslipidaemia / Met Syn 6 / 6 studies Certain Cancers 4 / 5 studies Data source: 2011–2014 National Health and Nutrition Examination Survey and 2015 U.S. Census Bureau ~65% of US adults over 45 …are pre-Diabetic or Diabetic. Pre-Diabetic ≈ Diabetic ≈ Insulin Resistant ≈ Hyperinsulinemic
- 61. The Wisdom ofthe Past? "Diabetic Cookery; Recipes and Menus" by Rebecca W Oppenheimer, 1917 Aw, c’mon now! } 2013 Ivor Cummins BE(Chem) MIEI
- 65.
Editor's Notes
- #5 Mr. Potato head in Singapore (what’s that – I still have a potato head? Thanks Jeff!)
- #9 Distracts from the main issues - Contributes to a “lie of omission” I believe it is truly dependent in vast majority of cases e.g.. heterozygous FH is one in hundreds only - and arguably environmental triggers make it a problem homozygous maybe doesn’t need environmental drivers - but it is 1 in a million Recent genetic paper – 10 times more genetic-related CVD than the old FH !
- #40 39
- #55 Distracts from the main issues - Contributes to a “lie of omission” I believe it is truly dependent in vast majority of cases e.g.. heterozygous FH is one in hundreds only - and arguably environmental triggers make it a problem homozygous maybe doesn’t need environmental drivers - but it is 1 in a million Recent genetic paper – 10 times more genetic-related CVD than the old FH !