See the Seminar at http://www.youtube.com/watch?v=xrsHqIKtXNw
A comprehensive analysis of the Metabolic Syndrome, Diabetes and Obesity Epidemic, exploring causal factors of appetite control derangement and descent into obesity, diabetes and coronary heart disease.
1. The Metabolic Sydrome
Engineering Root Cause…. and
Solution?
(Is it the Sugar/Carb or the Fat…..?)
Ivor Cummins BE (Chem)
October 11th 2013
2013 Ivor Cummins BE(Chem) MIEI
2. Introduction
Myself:
UCD, BE Chemical Engineering (Biochemical Stream)
5 Years Medical Device Manufacturing / R&D (hemodialysis & perfusion)
1 Year Precision Machine Design (Coronary Stent Manufacture)
16 Years here (Process, Product, Development…. Complex Problem-Solving focus)
Currently R&D Manager (Gen I)
This Body of Work:
IS
IS NOT
My personal analysis of broad root cause
An aligned view in the orthodoxy…
An Engineering Analysis based on Data
A Medical Study or medical guidance
A study of the Biochemistry of Life
A study of Nutrition Stuff and latest fads
A personal experiment with N = 1
A Prospective Clinical Trial(!)
Leveraging a vast canon of expert’s work
My own experiments and trials (bar 1)
Based on established science and literature
Based on any of the BS books out there
2013 Ivor Cummins BE(Chem) MIEI
3. A Selection of Experts from My Journey…
Robert H. Lustig: M.D. Professor of
Pediatrics in the Division of
Endocrinology at University of
California, San Francisco
Dr. Lustig is a Neuroendocrinologist,
with basic and clinical training relative
to hypothalamic development,
anatomy, and function
Dr Peter Attia: mechanical engineering
and applied mathematics at Queen’s
University.
Graduate Stanford Medical School; two
years as a post-doctoral fellow at NIH in
the National Cancer Institute as a surgical
oncology fellow, followed by surgical
residency
Kimber Stanhope: M.S. in Nutrition
Science and a Ph.D. in Nutritional Biology
from the University of California at Davis.
Project Scientist in the Department of
Molecular Biosciences.
20 years of nutrition research experience
working on over 150 projects
Dr. Neville Wilson M.D.
University of Cape Town Medical
School, The College of Medicine,
S.A.
After stints of service as Doctor
and Surgeon all over the world, he
is currently in charge of Medical
Services at Leinster Clinic Health
Services Maynooth.
Jeff S. Volek Ph.D., R.D.: associate
professor in The Human Performance
Laboratory at The University of
Connecticut, Storrs, CT. He is an R.D.
and has a Ph.D. in Kinesiology
(Pennsylvania State University). He
has published over 200 scientific
articles and chapters.
Andreas Eenfeldt M.D. Swedish
medical doctor specializing in family
medicine; his particular strength is in
comparing and contrasting
carbohydrate and fat metabolism in
their respective ability to drive the
diseases of modernity…he runs
DietDoctor.com
2013 Ivor Cummins BE(Chem) MIEI
4. Root Cause Methodology
Our Engineering Practice
Problem Definition
Comparative Analysis (IS / IS NOT)
•What, When, Where, Extent + Trends
General / Other Disciplines
Problem Definition
Correlation Analysis
• Epidemiological Studies
•Loose application of Is / Is Not
Root Cause Analysis
•Cause Effect chain – Root Cause Diagram
•Physics based mechanism for all Linkages
Hypothesis Generation
Mechanistic Evidence
•Explore mechanisms
•Focus on suspected factors
•For / Against Analysis
•Generate Targeted Experiments
Design & Analysis Of Experiments
•Screening Experiments, then fractional
•Statistical Inference informs next steps
Experimentation
•Prospective Studies
•Statistical Inference
2013 Ivor Cummins BE(Chem) MIEI
5. Root Cause Methodology
Our Engineering Practice
General / Other Disciplines
Problem Definition
Comparative Analysis (IS / IS NOT)
•What, When, Where, Extent + Trends
Problem Definition
Correlation Analysis
A
• Epidemiological Studies
•Loose application of Is / Is Not
B
Mechanistic Evidence
Root Cause Analysis
•Cause Effect chain – Root Cause Diagram
•Physics based mechanism for all Linkages
Hypothesis Generation
•Explore mechanisms
•Focus on suspected factors
•For / Against Analysis
•Generate Targeted Experiments
Design & Analysis Of Experiments
•Screening Experiments, then fractional
•Statistical Inference informs next steps
C
Experimentation
•Prospective Studies
•Statistical Inference
2013 Ivor Cummins BE(Chem) MIEI
6. The Trends – Linear for Weight….
USA
Proportion Overweight
England
Australia
France
Korea
(OECD Data)
2013 Ivor Cummins BE(Chem) MIEI
7. …and Exponential for Diabetes
Number with Diabetes
Number with Diabetes
Percent with Diabetes
Percent with Diabetes
2013 Ivor Cummins BE(Chem) MIEI
8. So is it Simply the Calories?
Why are we consuming so much?
% Obese
kCal/d
2013 Ivor Cummins BE(Chem) MIEI
9. Weight Control / Obesity is largely a
subset of
The Metabolic
Syndrome
To understand the drivers of both,
is the key to recovery…..
2013 Ivor Cummins BE(Chem) MIEI
11. Metabolic Syndrome Cost Impact?
My back-of-the-envelope calculation suggests somewhere in the
region of $1 Trillion + per annum in the coming decade for the
top 20 GDP countries….
2013 Ivor Cummins BE(Chem) MIEI
12. Metabolic Syndrome Definition:
Low HDL “Good
Cholesterol”
<1.0 mmol/L
Waist
>~38” Men
>~35”
Women
Blood Pressure
Elevated
>135/85 mmHg
High Blood
Triglycerides
>1.5 mmol/L
METABOLIC
SYNDROME
(3 or more of
the 5 factors)
High Blood
Sugar
>5.6 mmol/L
(Obesity)
Stroke
Atheroschlorosis
Coronory Heart
Disease
Gout
Type 2
Fatty Liver
Diabetes
Disease
Alzheimers
Arthritis
Asthma
13. Metabolic Syndrome Definition:
Low HDL “Good
Cholesterol”
<1.0 mmol/L
Waist
>~38” Men
>~35”
Women
Blood Pressure
Elevated
>135/85 mmHg
High Blood
Triglycerides
>1.5 mmol/L
METABOLIC
SYNDROME
(3 or more of
the 5 factors)
High Blood
Sugar
>5.6 mmol/L
How many people have it then? It’s
not too common, right?
(Obesity)
Stroke
Atheroschlorosis
Coronory Heart
Disease
Gout
Type 2
Fatty Liver
Diabetes
Disease
Alzheimers
Arthritis
Asthma
14. Metabolic Syndrome Definition:
Low HDL “Good
Cholesterol”
<1.0 mmol/L
Waist
>~38” Men
>~35”
Women
Blood Pressure
Elevated
>135/85 mmHg
High Blood
Triglycerides
>1.5 mmol/L
METABOLIC
SYNDROME
(3 or more of
the 5 factors)
High Blood
Sugar
>5.6 mmol/L
How many people have it then? It’s
not too common, right?
How does >50% of US population
strike you?
(Obesity)
Stroke
Atheroschlorosis
Coronory Heart
Disease
Gout
Type 2
Fatty Liver
Diabetes
Disease
Alzheimers
Arthritis
Asthma
20% of the
“Fat” are
“Fit”
40% of the
“lean” are
unhealthy
15. Metabolic Syndrome Definition:
Low HDL “Good
Cholesterol”
<1.0 mmol/L
Waist
>~38” Men
>~35”
Women
Blood Pressure
Elevated
>135/85 mmHg
High Blood
Triglycerides
>1.5 mmol/L
Key
METABOLIC
SYNDROME
(3 or more of
the 5 factors)
(Obesity)
Stroke
Atheroschlorosis
Phenomenon:
INSULIN
RESISTANCE
High Blood
Sugar
>5.6 mmol/L
How many people have it then? It’s
not too common, right?
How does >50% of US population
strike you?
Coronory Heart
Disease
Gout
Type 2
Fatty Liver
Diabetes
Disease
Alzheimers
Arthritis
Asthma
20% of the
“Fat” are
“Fit”
40% of the
“lean” are
unhealthy
16. B
Mech
A Crash Course in Endocrinology 1…..
Insulin / Glucagon / Ghrelin /
Leptin – know your control
system hormones!
sugar / simple
carbohydrate
ingestion primarily
High Blood
Sugar
1. Insulin
and
Glucagon
2013 Ivor Cummins BE(Chem) MIEI
17. B
Mech
A Crash Course in Endocrinology 2
• Ghrelin
and
Leptin
2013 Ivor Cummins BE(Chem) MIEI
18. And so, The KEY to the Cycle of Disease
Insulin (The Master Hormone):
• Gets glucose into Liver/Muscle AND FAT(!)
• In healthy people, drives brain appetite drop but…
• If driven too hard by Sugar and Carb in diet, leads to
INSULIN RESISTANCE - “Body says NO!”
• Brain Insulin Resistance: Appetite dysfunction results!
2013 Ivor Cummins BE(Chem) MIEI
19. The KEY to APPETITE CONTROL
Insulin (The Master Hormone):
• Gets glucose into Liver/Muscle AND FAT(!)
• In healthy people, drives brain appetite drop but…
• If driven too hard by Sugar and Carb in diet, leads to
INSULIN RESISTANCE - “Body says NO!”
• Brain Insulin Resistance: Appetite dysfunction results!
# 1: Insulin
Resistance
2013 Ivor Cummins BE(Chem) MIEI
20. And so, The KEY to APPETITE CONTROL
Insulin (The Master Hormone):
• Gets glucose into Liver/Muscle AND FAT(!)
• In healthy people, drives brain appetite drop but…
• If driven too hard by Sugar and Carb in diet, leads to
INSULIN RESISTANCE - “Body says NO!”
• Brain Insulin Resistance: Appetite dysfunction results!
# 1: Insulin
Resistance
#2: Appetite
Dysfunction
2013 Ivor Cummins BE(Chem) MIEI
21. And so, The KEY to APPETITE CONTROL
Insulin (The Master Hormone):
• Gets glucose into Liver/Muscle AND FAT(!)
• In healthy people, drives brain appetite drop but…
• If driven too hard by Sugar and Carb in diet, leads to
INSULIN RESISTANCE - “Body says NO!”
• Brain Insulin Resistance: Appetite dysfunction results!
Leptin:
• Is released by Fat Cells (Adipocytes)
• Signals brain that fat stores are fine – STOP EATING
• But Leptin Is Blocked by INSULIN RESISTANCE and…
• If driven too hard (Excess Fat) then LEPTIN RESISTANCE
# 1: Insulin
Resistance
#2: Appetite
Dysfunction
2013 Ivor Cummins BE(Chem) MIEI
22. And so, The KEY to APPETITE CONTROL
Insulin (The Master Hormone):
• Gets glucose into Liver/Muscle AND FAT(!)
• In healthy people, drives brain appetite drop but…
• If driven too hard by Sugar and Carb in diet, leads to
INSULIN RESISTANCE - “Body says NO!”
• Brain Insulin Resistance: Appetite dysfunction results!
Leptin:
• Is released by Fat Cells (Adipocytes)
• Signals brain that fat stores are fine – STOP EATING
• But Leptin Is Blocked by INSULIN RESISTANCE and…
• If driven too hard (Excess Fat) then LEPTIN RESISTANCE
# 1: Insulin
Resistance
#2: Appetite
Dysfunction
#3 Leptin
Signal Block
2013 Ivor Cummins BE(Chem) MIEI
23. And so, The KEY to APPETITE CONTROL
Insulin (The Master Hormone):
• Gets glucose into Liver/Muscle AND FAT(!)
• In healthy people, drives brain appetite drop but…
• If driven too hard by Sugar and Carb in diet, leads to
INSULIN RESISTANCE - “Body says NO!”
• Brain Insulin Resistance: Appetite dysfunction results!
Leptin:
• Is released by Fat Cells (Adipocytes)
• Signals brain that fat stores are fine – STOP EATING
• But Leptin Is Blocked by INSULIN RESISTANCE and…
• If driven too hard (Excess Fat) then LEPTIN RESISTANCE
# 1: Insulin
Resistance
#2: Appetite
Dysfunction
#3 Leptin
Signal Block
#4 Leptin
Resistance
2013 Ivor Cummins BE(Chem) MIEI
24. And so, The KEY to APPETITE CONTROL
Insulin (The Master Hormone):
Appetite
• Gets glucose into Liver/Muscle AND FAT(!)
• In healthy people, drives brain appetite drop but…
• If driven too hard by Sugar and Carb in diet, leads to
INSULIN RESISTANCE - “Body says NO!”
• Brain Insulin Resistance: Appetite dysfunction results!
Leptin:
• Is released by Fat Cells (Adipocytes)
• Signals brain that fat stores are fine – STOP EATING
• But Leptin Is Blocked by INSULIN RESISTANCE and…
• If driven too hard (Excess Fat) then LEPTIN RESISTANCE
# 1: Insulin
Resistance
#2: Appetite
Dysfunction
#3 Leptin
Signal Block
Obesity
Inflammation
Fatty Liver
“Bad Cholesterol”
Atherosclerosis
Heart Disease
Diabetes
Alzheimers
Cancers etc
“The Diseases
of Modernity”
#4 Leptin
Resistance
2013 Ivor Cummins BE(Chem) MIEI
29. B
Mech
Perhaps unsurprisingly, Insulin
Resistance Leads to the Metabolic
Maladies….
…..but, substantially, is it the chicken or the egg??
Excess Weight
Self-Reinforce
Loop Warning!
Self-Reinforce
Loop Warning!
2013 Ivor Cummins BE(Chem) MIEI
30. B
Mech
So, time to fix 4 decades of “Hypothesis
Resistance”, and move on…
Excessive Insulin Demand
exhausts Pancreatic Cells
Irrecoverable Cell Death
2013 Ivor Cummins BE(Chem) MIEI
31. B
Mech
So, time to fix 4 decades of “Hypothesis
Resistance”, and move on…
Greed +
}
Excessive Insulin Demand
exhausts Pancreatic Cells
Irrecoverable Cell Death
2013 Ivor Cummins BE(Chem) MIEI
32. B
Mech
So, time to fix 4 decades of “Hypothesis
Resistance”, and move on…
Greed +
} + appetite
derangement
Excessive Insulin Demand
exhausts Pancreatic Cells
Irrecoverable Cell Death
2013 Ivor Cummins BE(Chem) MIEI
33. B
Mech
So, time to fix 4 decades of “Hypothesis
Resistance”, and move on…
Greed +
SelfReinforce
Loop
Warning!
SelfReinforce
Loop
Warning!
} + appetite
derangement
SelfReinforce
Loop
Warning!
Excessive Insulin Demand
exhausts Pancreatic Cells
Irrecoverable Cell Death
2013 Ivor Cummins BE(Chem) MIEI
35. Fructose Vs Glucose Sources
Sucrose (Table Sugar):
50%glucose / 50% fructose
High Fructose Corn Syrup (HFCS):
55% fructose / 45% glucose
Glucose-glucose-glucose......chains
So-called ”Simple Carb”, added sugar too though..
Fruit: 4% to 8% Fructose
(but with lots of Fibre & Good Stuff!)
36. Metabolic Syndrome / Obesity
POTENTIAL ROOT CAUSE #1:
SUGAR
Fructose / HFCS
“Mega Sources”:
* Soft Drinks / Sports Drinks *
Most All Processed Food
Low Fat Products
Fruit Juices / Smoothies
Most Breakfast Cereals
Etc Etc Etc
2013 Ivor Cummins BE(Chem) MIEI
37. A
Corr
From one of the best, 1957
DIET AND CORONARY THROMBOSIS
HYPOTHESIS AND FACT
*
JOHN YUDKIN
M.A., Ph.D., M.D. Camb., M.R.C.P., F.R.I.C.
1.
2.
3.
4.
5.
USA
Australia
Canada
Finland
New
Zealand
6. UK
7. Denmark
8. Sweden
9. Norway
10. Netherlands
11. Switzerland
12. W. Germany
13. France
14. Italy
15. Japan
PROFESSOR OF NUTRITION IN THE UNIVERSITY OF LONDON AT
QUEEN ELIZABETH COLLEGE
NO Significant Correlation for
Fat and Heart Disease Rates
R2 = 0.1, P > 0.05
Significant Correlation for
Sugar and Heart Disease Rates
R2 = 0.41, P < 0.05
38. A
Corr
Let’s get up to date here….
Sugar g/day
%BMI > 25
Diabetes
Sugar g/day: Composite, multiple sources
BMI/Diabetes Data: http://www.cdc.gov/nchs/data/hus/hus12.pdf#063
2013 Ivor Cummins BE(Chem) MIEI
42. B
Mech
And now, a Crash Course in
Fructose Metabolism…..
Grateful thanks to Dr. Robert Lustig for the following slides
which I have augmented somewhat for clarity
•Professor of Endocrinology / Pediatrics, UCSF
•Director of Weight Assessment for Teen and Child Health
Please do see him professionally deliver this content
more comprehensively in “Sugar, the Bitter Truth”
http://www.youtube.com/watch?v=dBnniua6-oM
43. 120 kcal Glucose
24 kcal goes to liver
120 kcal Alcohol
94 kcal goes to liver
60 kcal
(+ 12 kcal
glucose)
120 kcal Sucrose
(50:50 Fruc/Gluc)
ALL Fructose
must go to liver
B
Mech
Glucose, Alcohol,
Fructose – One of
these things is not
like the others…..!
The Mitochondria Your Cellular Energy
Production Line
67. 1965 – 1972, Excellent Engineering Style
Studies – Not easy to find now
Low Sugar
High Sugar
Low Sugar
Lower is Better in
all plotlines here
High Sugar
Expt
Normal Diet
C
2013 Ivor Cummins BE(Chem) MIEI
68. 1965 – 1972, Excellent Engineering Style
Studies – Not easy to find now
Low Sugar
High Sugar
Lower is Better
in all plotlines
Low Sugar
Expt
Normal Diet
C
2013 Ivor Cummins BE(Chem) MIEI
70. C
Expt
2011: Fructose Drives Visceral Obesity
Glucose:
LOW
Visceral
Obesity
SAT =
Subcutaneous
Or “Safe”
Body FatFat
Body Type
Fructose:
HIGH
Visceral
Obesity
VAT =
Visceral
Or “Toxic”
Body Fat Type
2013 Ivor Cummins BE(Chem) MIEI
71. 2011: Fructose Drives Post-Prandial TG
Triglyceride (AUC)
Expt
Area
Under
Curve i.e.
The Common Fasting Trigs test :
Glucose > Fructose, but note
lower scale, ~0.18mmol/L
Average
Trig
Impact
Glucose Fructose
Sucrose
Triglyceride 22-24h
C
Glucose Fructose
Sucrose
Fructose:
HIGH (0.60 mmol/L)
Post-Meal Trigs….
where damage is done…
2013 Ivor Cummins BE(Chem) MIEI
72. ΔFasting ApoB (g/L)
Expt
2011: Fructose Drives ApoB Lipoprotein
(“The real BAD Cholesterol”)
Glucose:
Low
ApoB
Glucose
Fructose:
HIGH
ApoB
Sucrose
Fructose
Sucrose
% ApoB/ApoA
C
Glucose
Fructose
Sucrose
Note: As can be seen, the sucrose (50% Fructose and 50% Glucose)
seems synergistic in effect; my assumption is that the simultaneous Insulin
response triggered by the Glucose exacerbates the issue – but this is TBD
– the research team noted and deferred an explanation too…..
2013 Ivor Cummins BE(Chem) MIEI
74. POTENTIAL ROOT CAUSE #2:
FAT
Natural
????
A Topic for
another
Seminar(!)
Natural
Natural
Triglyceride – 3 Fatty Acids
with a Glycerol Backbone
2013 Ivor Cummins BE(Chem) MIEI
75. A
Corr
Fat Versus Sugar: Correlative Data
FAT g/day
%BMI > 25
Diabetes
Sugar g/day: Composite, multiple sources
Fat/BMI/Diabetes Data: http://www.cdc.gov/nchs/data/hus/hus12.pdf#063
2013 Ivor Cummins BE(Chem) MIEI
80. A
Corr
The Contemporaneous Controversy…
DIET AND CORONARY THROMBOSIS
HYPOTHESIS AND FACT
*
JOHN YUDKIN
M.A., Ph.D., M.D. Camb., M.R.C.P., F.R.I.C.
1.
2.
3.
4.
5.
USA
Australia
Canada
Finland
New
Zealand
6. UK
7. Denmark
8. Sweden
9. Norway
10. Netherlands
11. Switzerland
12. W. Germany
13. France
14. Italy
15. Japan
PROFESSOR OF NUTRITION IN THE UNIVERSITY OF LONDON AT
QUEEN ELIZABETH COLLEGE
NO Significant Correlation for
Fat and Heart Disease Rates
Significant Correlation for
Sugar and Heart Disease Rates
R2 = 0.1, P > 0.05
R2 = 0.41, P < 0.05
2013 Ivor Cummins BE(Chem) MIEI
81. A
Corr
And the Dreadful SATURATED Fat?
Increasing Heart
Disease with lower
fat
Orthodox
View
TrendLine
Eh, excuse
me?
An
Engineer’s
TrendLine
Decreasing
Heart Disease
with higher fat
2013 Ivor Cummins BE(Chem) MIEI
82. A
Corr
Another Recommended Paper
Men from
studies who
had NO Heart
Attacks
Men from the
studies
Who HAD
Heart
Attacks
Michael Gurr, Ph.D., renowned expert on lipids and author of the
authoritative textbook on lipid biochemistry, criticizes:
”…the degree of self delusion in research workers wedded to
a particular hypothesis despite the contrary evidence”
Dietary lipids and coronary heart desease: Old evidence, new perspective Review Article
Progress in Lipid Research, Volume 31, Issue 3, 1992, Pages 195-243
Michael I. Gurr, Professor in Food Science & Technology, University of Reading, UK.
Professor in Human Nutrition, Oxford Brookes University, UK.
2013 Ivor Cummins BE(Chem) MIEI
83. A
Corr
2010: The Metastudy of all studies
Meta-analysis of 21 prospective
cohort studies evaluating the
association of saturated fat with
cardiovascular disease
Conclusion: There is no
NO Effect of
Dietary
Saturated Fat
Seen Overall
significant evidence for
concluding that dietary
saturated fat is associated
with an increased risk of CHD
or CVD.
More data are needed to
elucidate whether CVD risks are
likely to be influenced by the
specific nutrients used to replace
saturated fat….(Ivor note: like
sugar or refined carb perhaps….)
2013 Ivor Cummins BE(Chem) MIEI
84. B
Mech
Fat Mechanistic Data
• Let’s make up some time here
and move on to experimental –
go on, you know you want to!
2013 Ivor Cummins BE(Chem) MIEI
85. C
Expt
FAT – Experimental – Krauss et Al 2008
Experiment Design: 3 weeks isocalorific,
remainder with -1000 calories per day (starve)
Trig Reduction
Serum Triglyceride –
Lower is Better
2013 Ivor Cummins BE(Chem) MIEI
86. C
Expt
FAT – Experimental – Krauss et Al 2008
Experiment Design: 3 weeks isocalorific,
remainder with -1000 calories per day (starve)
Lower is Better
l ohC ” doog“ L DH
Trig Reduction
Serum Triglyceride –
HDL –
Higher is Better
2013 Ivor Cummins BE(Chem) MIEI
87. C
Expt
FAT – Experimental – Krauss et Al 2008
Experiment Design: 3 weeks isocalorific,
remainder with -1000 calories per day (starve)
Tot Chol/HDL
TOTAL CHOL / HDL
Lower is Better
2013 Ivor Cummins BE(Chem) MIEI
88. C
Expt
FAT – Experimental – Krauss et Al 2008
Experiment Design: 3 weeks isocalorific,
remainder with -1000 calories per day (starve)
Apo B / Apo A
Tot Chol/HDL
TOTAL CHOL / HDL
ApoB / Apo A Lipoprotein
Lower is Better
Lower is Better
2013 Ivor Cummins BE(Chem) MIEI
89. C
Expt
FAT – Experimental – Krauss et Al 2008
r et e mi D e ci tr a P L DL
a l
Experiment Design: 3 weeks isocalorific,
remainder with -1000 calories per day
(starve)
LDL Particle Diameter
Higher is Better
2013 Ivor Cummins BE(Chem) MIEI
90. C
Expt
FAT – Experimental – Krauss et Al 2008
Experiment Design: 3 weeks isocalorific,
remainder with -1000 calories per day
(starve)
r et e mi D e ci tr a P L DL
a l
Ivor Conclusion:
• Low Sugar/Carb, high Fat diet
dramatically improves Key
MetS disease markers
LDL Particle Diameter
Higher is Better
2013 Ivor Cummins BE(Chem) MIEI
91. C
Expt
FAT – Experimental – Krauss et Al 2008
Experiment Design: 3 weeks isocalorific,
remainder with -1000 calories per day
(starve)
r et e mi D e ci tr a P L DL
a l
Ivor Conclusion:
• Low Sugar/Carb, high Fat diet
dramatically improves Key
MetS disease markers
LDL Particle Diameter
Higher is Better
Study Author’s Conclusion:
• A LOW FAT diet with
restricted calories sort of kinda
gets within range of the High
Fat diet in Key MetS disease
markers….???
•Come again???
•Are you Serious – call an
engineer, please……..!
2013 Ivor Cummins BE(Chem) MIEI
92. Can do this again
and again……
and again.
by Jeff S. Volek, Ph.D., R.D.
C
Expt
2013 Ivor Cummins BE(Chem) MIEI
95. Coup De Grace? 2013: The Rat Proxy…
“…this study aims to develop a rat model
which closely depicts MS in humans…”
“Replacing whole wheat with refined wheat flour in rat
chow in 60% fructose-fed Sprague-Dawley rats resulted
in:
hypertension (p 0.01)
hyperglycemia (p 0.03)
hyper-triglyceridemia (p 0.001)
HDL Reduction (p 0.002)
2013 Ivor Cummins BE(Chem) MIEI
In only
FOUR Weeks!
Fiber-free white flour with fructose offers a better model of metabolic
syndrome:
Amin and Gilani Lipids in Health and Disease 2013 12:44
doi:10.1186/1476-511X-12-44
96. More Rat Tales….
In results published online Feb. 26 2010 by the journal Pharmacology,
Biochemistry and Behavior, the researchers from the Department of Psychology
and the Princeton Neuroscience Institute reported on two experiments
investigating the link between the consumption of high-fructose corn syrup and
obesity.
"When rats are drinking high-fructose corn syrup at levels well below those in
soda pop, they're becoming obese -- every single one, across the board. Even
when rats are fed a high-fat diet, you don't see this; they don't all gain extra
weight."
The second experiment -- the first long-term study of the effects of high-fructose
corn syrup consumption on obesity in lab animals -- monitored weight gain, body
fat and triglyceride levels in rats with access to high-fructose corn syrup over a
period of six months. “Compared to animals eating only rat chow, rats on a diet
rich in high-fructose corn syrup showed characteristic signs of a dangerous
condition known in humans as the metabolic syndrome, including abnormal
weight gain, significant increases in circulating triglycerides and augmented fat
deposition, especially visceral fat around the belly. Male rats in particular
ballooned in size: Animals with access to high-fructose corn syrup gained 48
percent more weight than those eating a normal diet.”
2013 Ivor Cummins BE(Chem) MIEI
97. % Daily Calorific
Intake
Guidelines
Schmidelines…..
Make your minds
up guys…
25
X
Labelmania - What’s YOUR poison?
Brown sugar, Fruit juice concentrate, Lactose ,
Corn sweetener, Glucose, Malt syrup, Galactose,
Corn syrup, High-fructose corn, Rice Syrup,
Maltose, HFCS, Dextrose, Syrup, Honey,
Molasses, Fructose, Invert Sugar, Maltodextrin,
Raw sugar, etc, etc
Answer: All of it…welcome to
“Synynom Shenanigans”
2013 Ivor Cummins BE(Chem) MIEI
98. But I don’t eat that much Sugar…?
That means 6/9 teaspoons TOTAL INTAKE
per day for a female/male human
- NOT 6/9 that you add yourself to existing
food or drink, which is often loaded already!
Brekky
Time!
80g
250 ml
250 ml
Cereal
OJ
Smoothi
e
Total
Spoons
~4
~6
~8
~19
=
Over 2-3 times your daily
AHA adult guidelines…..
and more than a dozen
times the estimated human
evolutionary intake of ~1.5
teaspoons/day)…..
before you leave the
breakfast table
2013 Ivor Cummins BE(Chem) MIEI
114. B’fast
or
Lunch
Snack
Dinner
Supper
MINIMISE
etc
•Effectively NO Sugar
or
or
•Effectively NO Wheat
•Minimal Simple Carbs
•NO “Diet” Foods (sugar!)
•NO “Low Fat” stuff (sugar!)
•Olive not Vegetable Oils
•Butter not Margerine
•Plenty Healthy Meat and
Fish, leave the skin on!
•Loads of Veg with dinner
+
or
•Lots of eggs/cheese +
•Moderate Nuts
•Moderate Fruit
85% !!
•85% Choc, or Milk Choc
NO
•Olives, Avocados
•Tomatoes and salad veg
IDEAL
2013 Ivor Cummins BE(Chem) MIEI
115. SUMMARY FINDINGS
•Excessive Dietary Sugar and simple carbs are the primary root
cause of the Metabolic Syndrome and associated “Diabesity”
Epidemic (i.e No Sugar, and stick to Vegetables only for your carb input)
•Excessive Sugar and simple carbs promote insulin response and
appetite dysfunction, creating multiple self-reinforcing loops
•Sugar / simple carbs are the primary development agent of Insulin
Resistance Syndrome through proven mechanisms, and are a
primary driver of Lipid Generation (“Bad Cholesterol”) and
eventual dyslipidemia
•The driven weight gain consists of adipose tissue (esp. Visceral)
which exacerbates Insulin Resistence, drives Leptin Resistance and
reinforces the disease process
•Natural Dietary Fat is NOT a core root cause of the metabolic
syndrome and associated disease/obesity – and it does NOT cause
“Bad Cholesterol” !!!! Time to end 40 years of Bad Science….
2013 Ivor Cummins BE(Chem) MIEI
116. A Sample of Approachable Science
•
“Sugar, The Bitter Truth” Professor Robert Lustig
–
•
http://www.youtube.com/watch?v=dBnniua6-oM
“The Skinny on Obesity” (8 parts)
– http://www.youtube.com/watch?v=nOl5promItc
•
“High Sugar Diets and Disease” Dr. Kimber Stanhope
– http://www.youtube.com/watch?v=_AJka21yfyE
•
“Wheat Belly” Dr. William Davis
– http://www.youtube.com/watch?v=UbBURnqYVzw
•
“The Straight Dope on Cholesterol” Dr. Peter Attia
– http://www.youtube.com/watch?v=dAWdHYSrh7M
•
“How Bad Science and Big Business created the Obesity Epidemic” David
Diamond PhD
–
•
http://www.youtube.com/watch?v=3vr-c8GeT34
“The Blog of Dr. Neville Wilson”
– http://drnevillewilson.com/
117. B’fast
or
Lunch
Snack
Dinner
Supper
MINIMISE
etc
•Effectively NO Sugar
or
or
•Effectively NO Wheat
•Minimal Simple Carbs
•NO “Diet” Foods (sugar!)
•NO “Low Fat” stuff (sugar!)
•Olive not Vegetable Oils
•Butter not Margerine
•Plenty Healthy Meat and
Fish, leave the skin on!
•Loads of Veg with dinner
+
or
•Lots of eggs/cheese +
•Moderate Nuts
•Moderate Fruit
85% !!
•85% Choc, or Milk Choc
NO
•Olives, Avocados
•Tomatoes and salad veg
IDEAL
2013 Ivor Cummins BE(Chem) MIEI
118. Current Working Thesis:
1. Excessive Dietary Sugar (directly ingested or in as found in most processed
food/drinks) is the 1st order primary root cause of the Metabolic Syndrome and
associated “Diabesity” Epidemic through the following elements:
1.1 Insulin Resistance is the driving force of appetite dysfunction, excessive fat storage and the constellation
of metabolic disease.
1.2 Sugar is the primary aggravator of Insulin Resistance through proven mechanisms, and is a direct driver
of Lipid Generation and eventual dyslipidemia (Serum Triglyceride, VLDL etc)
1.3 An elevated proportion of simple, high-glycemic carbohydrate in the diet (Glucose rapidly released by
Amylase, no fibre to attenuate), works in tandem with the simple sugars to promote Insulin Resistance.
1.3 Fructose is particularly pathogenic thru many pathways – lack of satiety signalling, promotion of Hepatic
fat generation and hepatic IR, lack of Ghrelin suppression, impact to Leptin levels, etc
1.4 The driven weight gain consists of adipose tissue (esp. Visceral) which is itself an organ, releasing body
toxic cytokines and hormones, exacerbating Insulin Resistence and accelerating the disease process
2. The disproportionate / non-linear rise of disease relative to the increase in sugar consumption can
be attributed to amongst other things:
2.1 Gestational Insulin Resistance and predisposition towards obesity in the next generation (2 nd order effect)
2.2 Co-incident lowered level of physical activity in society exacerbates the high sugar / simple carb damage
3. Dietary Fat is NOT a core root cause of the metabolic syndrome, but excess sugar / simple carbs
through the action of the insulin elevation will drive dietary fat into storage (obesity) and further
negative pathways will result as seen
2013 Ivor Cummins BE(Chem) MIEI
122. The So-Called “Cholesterol”
http://www.slideshare.net/ancestralhealth/attia-ahs-talk-pcfriendly
"High triglycerides alone increased the risk of heart attack nearly three-fold.
And people with the highest ratio of triglycerides to HDL -- the "good"
cholesterol -- had 16 times the risk of heart attack as those with the lowest
ratio of triglycerides to HDL in the study of 340 heart attack patients and 340
of their healthy, same age counterparts.
The ratio of triglycerides to HDL was the strongest predictor of a heart attack,
even more accurate than the LDL/HDL ratio. (Harvard-lead study - Circulation
1997;96:2520-2525)."
2013 Ivor Cummins BE(Chem) MIEI