Cancer as a metabolic disease 2

Cancer
as a Metabolic
Disease 2
Dr. Fathi Neana, MD
Chief of Orthopaedics
Dr. Fakhry & Dr. A. Al-Garzaie Hospital
September,10 - 2018

‫و‬ِ‫ب‬‫ا‬َ‫ن‬‫أ‬‫ع‬َ ‫أ‬‫اْل‬َ‫و‬ ِ‫ل‬‫ي‬ ِ‫خ‬َّ‫ن‬‫ال‬ ِ‫ت‬‫ا‬َ‫ر‬َ‫م‬َ‫ث‬ ‫ن‬ِ‫م‬ُ‫ه‬‫أ‬‫ن‬ِ‫م‬ َ‫ون‬ُ‫ذ‬ ِ‫خ‬َّ‫ت‬َ‫ت‬َ‫ك‬َ‫س‬‫ا‬ً‫ر‬َ‫ل‬ َ‫ك‬ِ‫ل‬ََٰ‫ذ‬ ‫ي‬ِ‫ف‬ َّ‫ن‬ِ‫إ‬ ۗ ‫ا‬ً‫ن‬َ‫س‬َ‫ح‬ ‫ا‬ً‫ق‬‫أ‬‫ز‬ ِ‫ر‬َ‫و‬ً‫ة‬َ‫ي‬
َ‫ون‬ُ‫ل‬ِ‫ق‬‫أ‬‫ع‬َ‫ي‬ ٍ‫م‬ ‫أ‬‫و‬َ‫ق‬ِِّ‫ل‬(67)‫النحل‬ ‫سورة‬

Cancer disease
is it a genetic or a metabolic
disease with metabolic solutions ?
Thomas N. Seyfried

New Lifestyle diseases
Non-communicable diseases (NCDs)
• Obesity
• Metabolic syndrome
• Coronary artery disease
• Diabetes type 2
• Hypertension
• Arteriosclerosis
• Stroke
• Cancer
• Depression - anxiety
• Arthritis
• Osteomalacia
• Osteoporosis
• Swimmer's ear – loss of hearing
• Ch. obstructive pulmonary disease
• Liver Cirrhosis
• Nephritis
• Etc, etc, etc…
Emerged as bigger killers than infectious or hereditary ones.
The leading cause of death worldwide.
63% of all annual deaths.
> 38 million people are killed /year.
1- Cardiovascular diseases (17.5 million)
Complications of hypertension (9.4 million)
2- Cancers (8.2 million) – (8.8 m 2015)
3- Respiratory diseases (4 million)
5- Diabetes (1.5 million)
These 4 diseases account for 80 % of all NCDs deaths (> 38 million)
4- USA’s 4th Leading Cause of Death – Pharma’s Drugs
Posted on June 25, 2012 by Child Health Safety
Causes:
• Stress-Depression
• Diet
• Sleep-awake
• Lack of Exercise
• Sun avoidance
• Wireless WiFi devices
• Leaky gut syndrome
• Other pollutants
Including Medicines

Abstract
Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the
United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data
were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the
North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics.
In 2017,
USA 2017
1,688,780 new cancer cases
600,920 cancer deaths
For all sites combined, the cancer incidence rate is 20% higher in men than in women
Cancer death rate is 40% higher in men. However, sex disparities vary by cancer type.
For example, thyroid cancer incidence rates are 3-fold higher in women than in men (21 vs 7 per 100,000 population), despite
equivalent death rates (0.5 per 100,000 population), largely reflecting sex differences in the "epidemic of diagnosis."
Over the past decade of available data, the overall cancer incidence rate (2004-2013) was stable in women and declined by
approximately 2% annually in men, while the cancer death rate (2005-2014) declined by about 1.5% annually in both men and
women. From 1991 to 2014, the overall cancer death rate dropped 25%, translating to approximately 2,143,200 fewer cancer
deaths than would have been expected if death rates had remained at their peak.
Although the cancer death rate was 15% higher in blacks than in whites in 2014, increasing access to care as a result of the
Patient Protection and Affordable Care Act may expedite the narrowing racial gap; from 2010 to 2015, the proportion of blacks who
were uninsured halved, from 21% to 11%, as it did for Hispanics (31% to 16%).
Gains in coverage for traditionally underserved Americans will facilitate the broader application of existing cancer control
knowledge across every segment of the population. CA Cancer J Clin 2017;67:7-30.
© 2017 American Cancer Society.
CA Cancer J Clin. 2017 Jan;67(1):7-30. doi: 10.3322/caac.21387. Epub 2017 Jan 5.
Cancer Statistics, 2017.
Siegel RL1, Miller KD2, Jemal A3.

The Root cause and Culprit behind
Chronic Diseases, Cancer and Aging
1- A state of chronic low grade
inflammation
Dr. Richard K. Bernstein
Diabetes & Inflammation—the Vicious Cycle
(Hyperglycemia – Omega 6 - Obesity) - Leukotriene B(4) (LTB(4)
Lindsay Christensen
Lindsay Christensen is a health writer and researcher with her B.S. in
Biomedical Science and an Emphasis in Nutrition
(Pathogens, unhealthy diet, lack of exercise).
2- Mitochondrial dysfunction
(not the genetic make up)
Dr. Ron Rosedale
Breakthrough views on clinical metabolic biochemistry
1- Harmful Effects of too much Sugar
->> Insulin and leptin receptor resistance
->> Free radicals (ROS) 90% Mitochondria
2- Harmful Effects of too much Protein
->> Activation of the (mTOR) metabolic signaling pathway
3- Physical inactivity (lack of exercise) - (PGC-1α)
4- Pollutants - (free radicals –oxidative stress)
5- Drugs causing mitochondrial toxicity
(iatrogenic)
Mitochondrial dysfunction
Energy (ATP - ADP)
Leukotriene B(4) (LTB(4)
acts as a signal to relay
information from cell to
cell over long distances.

Dr Josef mercola:
I never learned anything about the root cause of chronic disease in med
school
Surprisingly, my seven years of medical school and family practice
residency never addressed the root cause of common chronic illness.
All I was taught was how to manage symptoms through the use of
pharmaceuticals and medical procedures.
Then, in 1995, my understanding of chronic disease took a quantum leap.
I was introduced to Dr. Ron Rosedale and his breakthrough views on
clinical metabolic biochemistry.
What I Learned in 1995 Forever Shaped My View on Cancer and
Chronic Disease
Cancer Is One of the Most Manageable Diseases “Once we
realize that cancer is a metabolic disease
The Root cause and Culprit behind Chronic Diseases, Cancer and Aging
Clinical metabolic biochemistry - breakthrough

In order for our organs to function properly, they
require energy, and that energy is produced by the
mitochondria (the power engine).
Since mitochondrial function is at the very heart of
everything that occurs in our body,
Optimizing mitochondrial function and preventing
mitochondrial dysfunction is extremely important for
health and disease prevention
Important nutrients and co-factors for mitochondrial
function include:
all B vitamins, magnesium, omega-3 fat, CoQ10,
acetyl L- carnitine, D-ribose, and alpha-lipoic acid.
Exercise is also important for mitochondrial health
and function
The Mitochondria

1- Mitochondria are tiny organelles in our cell
- Thousands comprising 15 to 50% of the cell volume
-Red blood cells and skin cells have very little to none
- Germ cells have 100,000
- Most cells have one to 2,000 of them
2- It is our body’s lifeline. It is a Power plant
3- They're the primary source of energy for our body. They
supply over 90% of our body’s energy
4- Converting the food we eat and the air we breathe into
usable energy
The Mitochondria
How Your Mitochondria Influence Your Health
January 24, 2016
5- It have enormous potential to influence our health, specifically cancer, and optimizing
mitochondrial metabolism may be at the core of effective cancer treatment

Acetic acid acetyl group, derived from acetic
acid, is fundamental to the biochemistry of
virtually all forms of life. When bound to
coenzyme A it forms acetyl-CoA
The citric acid cycle is a key metabolic pathway that unifies carbohydrate, fat, and protein metabolism.
The reactions of the cycle are carried out by 8 enzymes that completely oxidize acetate, in the form
of acetyl-CoA
ِ‫ب‬‫ا‬َ‫ن‬‫أ‬‫ع‬َ ‫أ‬‫اْل‬َ‫و‬ ِ‫ل‬‫ي‬ ِ‫خ‬َّ‫ن‬‫ال‬ ِ‫ت‬‫ا‬َ‫ر‬َ‫م‬َ‫ث‬ ‫ن‬ِ‫م‬َ‫و‬ُ‫ه‬‫أ‬‫ن‬ِ‫م‬ َ‫ون‬ُ‫ذ‬ ِ‫خ‬َّ‫ت‬َ‫ت‬
‫ا‬ً‫َر‬‫ك‬َ‫س‬ََٰ‫ذ‬ ‫ي‬ِ‫ف‬ َّ‫ن‬ِ‫إ‬ ۗ ‫ا‬ً‫ن‬َ‫س‬َ‫ح‬ ‫ا‬ً‫ق‬‫أ‬‫ز‬ ِ‫ر‬َ‫و‬‫أ‬‫ع‬َ‫ي‬ ٍ‫م‬ ‫أ‬‫و‬َ‫ق‬ِِّ‫ل‬ ً‫ة‬َ‫ي‬ َ‫ل‬ َ‫ك‬ِ‫ل‬َ‫ون‬ُ‫ل‬ِ‫ق‬
(67)‫النحل‬ ‫سورة‬
‫وسلم‬ ‫عليه‬ ‫هللا‬ ‫صلى‬ ‫قال‬:(َ‫خ‬‫ال‬ ُ‫م‬‫دا‬ِ‫اإل‬ َ‫م‬‫أ‬‫ع‬ِ‫ن‬ُّ‫ل‬)
‫مسلم‬ ‫رواه‬(2051)
‫الكحو‬ ‫ل‬ ّ‫تحو‬ ‫توضح‬ ‫التالية‬ ‫الكيميائية‬ ‫المعادلة‬‫إلى‬ ‫ل‬
‫األكسجين‬ ‫غاز‬ ‫مع‬ ‫بالتفاعل‬ ّ‫ل‬‫خ‬:
CH3CH2OH + 2 O2 --- >
2 CH3COOH + 2 H2O
Alcohol + Oxygen ---->
Acetic Acid + Water
‫كحول‬+‫أوكسجين‬----->‫حمض‬‫الخل‬+‫ماء‬
Mitochondria
CoA
How the human life is maintained

AIR
O2
FUEL
Carb-Protein-Fat
How the human life is maintained
WATER
﴾ٍِّ‫ي‬َ‫ح‬ ٍ‫ء‬‫أ‬‫ي‬َ‫ش‬ َّ‫ل‬ُ‫ك‬ ِ‫اء‬َ‫م‬‫أ‬‫ل‬‫ا‬ َ‫ن‬ِ‫م‬ ‫ا‬َ‫ن‬‫أ‬‫ل‬َ‫ع‬َ‫ج‬َ‫﴿و‬[‫اْلن‬ ‫سورة‬‫الية‬ ‫بياء‬:30]
And We have made from water every living thing.
ENERGY
Cell survival
Waste (ROS)
Free radicals
Cell apoptosis
Control system: (Signaling pathway - Feed back) - Nervous
(hypothalamus) – Hormonal – Enzymatic
Aged cells
Cancer cells
Mitochondria

Reactive Oxygen Species (ROS)
Possess multiple functions in cellular biology,
involving cell death, proliferation, and differentiation.
Moderate Amount of (ROS)
Regulates cell death (Apoptosis) , proliferation, and
differentiation.
(Apoptosis) of aged cells, cancer cells, damaged
cells
Too much (ROS)
Harm the mitochondria DNA itself
We adjust the dose of medicines to kill the
pathogens not to harm the host
The free radicals - Reactive Oxygen Species
(ROS)

The common factor in Chronic Diseases, Cancer and Aging
Oxidative cell stress
Metabolic (ROS) Environmental,
Drugs, Chemicals, virus, Radiation,
Infection, Starvation, etc..
nDNA & mtDNA abnormality
(Damage or Mutation)
Degenerative Diseases
Pulmonary fibrosis - Neuronal
degeneration - Heart failure -
Kidney failure
Metabolic dysfunction
Obesity - Diabetes
Cancer
Warburg effectAging & Apoptosis
Abnormal inflammation & Immunity
Mitochondrial
dysfunction
(Less Bioenergetic
metabolism)
mtDNA
Damage
Mutation

The common factor in Chronic Diseases, Cancer and Aging

Cell commits suicide by apoptosis. Cellular homicide is necrosis
Apoptosis (from Ancient Greek word “falling off”)
is a process of programmed cell death that occurs in
multicellular organisms.
Biochemical events lead to characteristic cell changes
(morphology) and death.
Programmed cell death
(APOPTOSIS)
Dr. Anurag Jain
Pathological causes :
1) Cell death produced by a variety of mild injurious stimuli like
– heat, radiation, cytotoxic cancer drugs, infection, etc.
that cause irreparable DNA damage that in turn triggers cell suicide pathways.
2) Cell injury in certain viral diseases such as viral hepatitis.
3) Cell death in tumors.
Physiologic causes:
1) The programmed destruction of cell during embryogenesis. It is programmed
because it is death of specific cell types at defined times during development.
2) Hormone-dependent physiologic involution, such as involution of the
endometrium during the menstrual cycle.
3) Cell deletion in proliferating cell population, such as intestinal crypt epithelium
4) Death of cells that have served there useful purpose, such as neutrophils in
an acute inflammatory respone.
5) Elimination of potentially harmful self reactive lymphocytes.

Mitochondrial Fuel
Which Fuel You Burn In Your Mitochondria for Energy Determines How Long Your Mitochondria Last
and That Determines How Long You Live!
Just As Gasoline Engines Run Best With Gasoline and Not
Diesel or Aviation Fuel, So Too,
Our Mitochondrial Cellular Engines Run Best
With Fat As Fuel, Instead of Sugar!
According to Dr. Ron Rosedale - “If I were to summarize in a single sentence what practice
would best promote health, it would be this”:
“Health and life span are determined by the proportion of fat
versus sugar people burn throughout their lifetime
The more fat that one burns as fuel, the healthier a person will be,
and the more likely he or she will live a long time;
The more sugar a person burns, the more disease ridden and the
shorter a life span a person is likely to have.”
(The above sentence is perhaps the most IMPORTANT statement you will ever read in regard
to health and longevity).
The mitochondria can only burn fat or sugar for
energy.
Which fuel is burned in the mitochondria for energy
determines how long the mitochondria stay in good shape.

Creating energy, by burning fuel in the mitochondria, is necessary, but it is destructive to our
bodies, just like burning gasoline or diesel is necessary, but destructive to the engine of the
automobile.
•Burning fat in the mitochondria produces more energy than does burning sugar.
•Fewer free radicals are released when burning fat than when burning sugar
•However, burning sugar is very fast compared to burning fat, and so, sugar burning is very
USEFUL DURING TIMES OF EMERGENCY.
You could almost say that our cells were designed to burn sugar only temporarily in times of
great exigency, when the damage from free radicals is not as important as dealing with the
emergency
If our bodies had been designed to primarily burn sugar as a fuel, then we would store sugar
cubes within our bodies, but we don’t, we store fat. We store only minor amounts of sugar
(in the form of glycogen) — enough to last for 30 to 60 minutes of emergency exertion.
Main Mitochondrial Fuel Concept
Fat is the Best Fuel

The Hypothalamus Sends Signals to the Body
Instructing Fat Burning or Sugar Burning.
In Many People the Hypothalamus is
Erroneously Sending the ‘Burn Sugar Signal’
The hypothalamus is a gland in the brain that dictates to
the entire body which fuel the cells of the body are to use:
fat or sugar.
The hypothalamus decides which mode to put the body in
based on the amount of leptin it can measure in the body.
A great number of people’s bodies are being “forced,
unnecessarily” to burn sugar instead of fat because that
tiny hypothalamus gland believes the body is starving,
and, therefore, sends a signal to the cells of the body that
sugar should be burned instead of fat (in order to conserve
fat).
This is unnecessarily causing the mitochondria
to “deteriorate faster”.
Why Does the Hypothalamus Unnecessarily Force
a Sugar Burning Mode in Our Bodies?
One of the most important functions of the
hypothalamus is to link the nervous system to
the endocrine system via the pituitary gland.
Thehypothalamus is located below the
thalamus and is part of the limbic system. In
the terminology of neuroanatomy, it forms the
ventral part of the diencephalon.

•Too much stored fat (Obesity).
Too much stored fat produces large amounts of circulating leptin which desensitizes the hypothalamus’s ability
to detect leptin (Leptin resistance). When leptin levels are not able to be detected, because the receptors in the
hypothalamus have been desensitized, the hypothalamus believes the body is starving and instructs sugar
burning in order to conserve and build up fat stores. This is ironic because essential the body’s pantries are full
of fat, but these pantries are inaccessible and so the cells are instructed to ignore fat and look for sugar to burn
for energy ( Craving).
There are only three reasons for the body
to be in sugar burning mode:
•Too much stress.
Stress creates the adrenal gland to relase
adrenaline. Adrenaline overrides the
hypothalamus signal and instructs sugar
burning.
•Too much blood sugar.
Blood sugar (over time) damages receptors in the
hypothalamus. When these receptors are damaged
then the hypothalamus cannot correctly sense
leptin... and believe there is no fat (i.e. starvation is
occurring).
Why Does the Hypothalamus Unnecessarily Force
a Sugar Burning Mode in Our Bodies?

Mitochondrial fission, fusion, and stress
Youle RJ1, van der Bliek AM.
Mitochondrial fission and fusion:
play critical roles in maintaining functional
mitochondria when cells experience metabolic or
environmental stresses.
Fusion:
helps mitigate stress by mixing the contents of partially
damaged mitochondria as a form of
complementation.
Fission:
is needed to create new mitochondria, but it also
contributes to quality control by enabling the removal
of damaged mitochondria and can facilitate
apoptosis during high levels of cellular stress.
Disruptions in these processes affect normal development, and they have been
implicated in neurodegenerative diseases, such as Parkinson's

PPARGC1A
PGC-1α )PPARGC1A):
is a protein encoded by the PPARGC1A gene. known as human accelerated
region 20 (HAR20).
PGC-1α is a transcriptional co activator that regulates the genes involved
in energy metabolism. It is the master regulator of mitochondrial biogenesis.
plays a central role in the regulation of cellular energy metabolism.
It stimulates 1- mitochondrial biogenesis 2- promotes the remodeling of
muscle tissue to a fiber-type that is metabolically more oxidative and less
glycolytic in nature.
It participates in the regulation of both carbohydrate & lipid metabolism.
It is involved in obesity, diabetes, & cardiomyopathy.
PGC-1α activating host factors:
1- Free Radicals
Reactive oxygen species (ROS) and reactive nitrogen species (RNS),
both formed intracellularly as by-products of metabolism but upregulated during
times of cellular stress.
2- Cold Exposure
adaptive thermogenesis
3- Endurance Exercise
PGC-1α determines lactate metabolism, preventing high lactate levels in
endurance athletes & making lactate as an energy source

Improving Your Mitochondria Function to Reduce Cancer Risk
By Dr. David Jockers DC, MS, CSCS
Mitochondria are unique because they contain their own copy
of DNA. The 3% of DNA responsible for producing cellular
energy generates 90% of a cell’s energy in the form of ATP
Mitochondria Sustain Life’s Functions:
1- Mitochondria are not only energy generators but are key
organelles in supporting everyday metabolic processes such
as:
2- Maintaining lipid levels
3- Provide the energy needed for blood circulation
4- Buffers ion concentrations required for physiological
communication
5- Supporting glucose and insulin transportation
6- Removing health hazards including damaged cells which
can wreak destruction on health
The destruction or weakening of mitochondria can lead to severe health
complications including: multiple sclerosis, autism, bipolar disorder, chronic fatigue
syndrome, type-2 diabetes, heart disease, and cancer.

Cancer as a Metabolic Disease: On the Origin,
Management, and Prevention of Cancer
by Thomas N. Seyfried
The book addresses controversies related to the origins of cancer
and provides solutions to cancer management and prevention.
It expands upon Otto Warburg's well-known theory that all cancer is
a disease of energy metabolism.
However, Warburg did not link his theory to the "hallmarks of
cancer" and thus his theory was discredited.
This book aims to provide evidence, through case studies,
that cancer is primarily a metabolic disease requiring
metabolic solutions for its management and prevention.
Support for this position is derived from critical assessment of
current cancer theories. Brain cancer case studies are presented as a
proof of principle for metabolic solutions to disease management,
but similarities are drawn to other types of cancer, including breast
and colon, due to the same cellular mutations that they
demonstrate.
Cancer is a Metabolic Disease with metabolic solutions
Mitochondrial dysfunction is the culprit

Cancer as a Metabolic Disease: On the Origin,
Management, and Prevention of Cancer
by Thomas N. Seyfried
Cancer is a Metabolic Disease with metabolic
solutions
Is Cancer a genetic disease?
Why it is not transferred through the nuclear DNA (genome)?

Is Cancer a genetic disease?
Why it is not transferred through the nuclear DNA (nGenome)?
Why mitochondrial DNA (mtGenome) promote or inhibit metastasis ?
Mitochondrial DNA Plays a Role in Metastasis
Experiments in mice show that mitochondria, both
within the tumor and beyond, can make the
difference between promoting or inhibiting cancer
spread.
Apr 18, 2018
KERRY GRENS
Mitochondrial genome was tied to the speed of
cancer growth and metastasis
2017 report in Cancer Research by Welch’s group
Danny Welch, a cancer biologist at the University of
Kansas Medical Center

Dr. Otto Warburg was a physician with a
Ph.D. in chemistry and was close friends
with Albert Einstein.
Most experts recognize Warburg as the
greatest biochemist of the 20th century.
He received a Nobel Prize in 1931
for his discovery that cancer cells use
glucose as a source of energy production
(anaerobic Glycolysis)
This is called the "Warburg Effect"
Sadly, to this day it is essentially ignored
by nearly every expert.

Some Features of Warburg Effect
Rule of hypoxia, mitochondrial dysfunction and sugar
Glucose uptake and glycolysis
proceed about ten times faster in most solid tumours than in non-
cancerous tissues.
Smaller numbers of mitochondria & mitochondrial
dysfunction in tumour cells
thus resulting in less ATP generation and higher consumption of
Energy (ATP).
Hypoxia of Tumour cells
(limited oxygen supply), because they initially lack an extensive
capillary network to supply the tumour with oxygen.
HIF-1 (Hypoxia-Inducible Factor -1)
is a protein that stimulates the activity of eight glycolytic enzymes
and it gives tumour cell capacity to survive Anaerobic conditions.
Glycolytic enzymes, overproduced by tumour cells
including an isozyme of Hexokinase-II and it results in committing
the cell to continued glycolysis.

Causes of Warburg Effect :
• Mitochondrial Defects:
mtDNA mutations lead to malfunction in respiration
and oxidative phosphorylation.
• Hypoxia :
Possible adaptation owing to lack of Oxygen
availability in the Environment.
• Oncogenic Signals :
Point Mutations in genes such as Ras family can
result in proliferation of cells and signal initiation.
• Altered Metabolic Enzymes:
Overproduction and mimicking of metabolic
enzymes such as Hexokinase-II result in
increased Glycolytic activity
Significance of Warburg Effect:
Scientists after extensive research came to the conclusion that most Tumour cells exhibit high glycolytic
uptake.
Taking cue from this mechanism, numerous Glycolytic Inhibitors have been developed. These
compounds are acting as potential anti- canceragents.
Alpha-cyano-4-hydroxycinnamic acid is a glycolytic inhibitor that has been successfully used in Brain
Cancer.
Recently, a molecule named Di Chloro Acetic or DCA acid was devised by University of Alberta, claiming
that it’s introduction would result in normal functioning of Mitochondria. The testing of this
compound’s claims are
underway.

4- ketogenic diet, forces cancer cells to use its mitochondria (cut off sugar) with a
burst of reactive oxygen species ROS.
ketogenic diet which radically improves mitochondrial health, could help most cancers,
especially if used in conjunction with glucose fermentation poisons like 3-bromopyruvate.
1- Serious mitochondrial dysfunction with decreased
numbers of functional mitochondria.
The mitochondria can still function in cancer cells
2- The metabolic switch:
Hypoxia in the presence of sugar cancer cells become
immediately dependent on glucose (Anaerobic glycolysis)
and not using their mitochondria (no reactive oxygen
species ROS any longer)
3- Forcing it to use its mitochondria (cut off sugar)
we get a burst of reactive oxygen species ROS that lead to
death, because that cancer cell is already primed for that
death. It's ready to die.
Mitochondria's Role in Cancer
The metabolic switch of Cancer cells

The metabolic switch of Cancer cells
Anaerobic Glycolysis
1- Mitochondrial dysfunction 2- Hypoxia 3- Sugar
Cancer cells
1-
2-
3-

Cut of this metabolic
switch
1- Mitochondrial
Biogenesis
2- Hyperbaric oxygen
3- Cut the Sugar off
The logical and sensible salvage
is to Cut off this metabolic switch

What causes
Mitochondrial
dysfunction ?

Dr. Ron Rosedale : Defective metabolic processes in mitochondria, not the genetic make up That cause
cancer and nearly all other chronic diseases, including accelerated aging
What causes Mitochondrial dysfunction?
The causes of Defective metabolic processes in mitochondria ?
1- The Harmful Effects of too much Sugar
A- Diet (HCLF)
Insulin and leptin receptor resistance
Free radicals (ROS) 90% in Mitochondria
B- Stress.
Adrenaline – hypothalamus ->> sugar
C- Obesity
Leptin resistance - hypothalamus ->> sugar
2- The Harmful Effects of too much Protein
Activation of the mTOR metabolic signaling pathway
3- Lack of exercise and Physical activity
Inhibition of PGC-1α (PPARGC1A)
4- Pollutants
free radicals – oxidative stress
5- Drugs
causing mitochondrial toxicity (iatrogenic)

Sugar is a “dirty” fuel, excessive free radicals caused by
reactive oxygen species (ROS).
Wile fat burns much cleaner. So by replacing carbs with
healthy fats,’ mitochondria are less likely to suffer damage
90 % or more of the total ROS (Reactive oxygen species)
are produced within the mitochondria, causing devastating
damage.
It was thought excessive ROS could be addressed by taking
antioxidants, but we now know that this was a flawed
strategy and it is far better to prevent their production by
eating an optimal fuel mixture.
LCHF - MMT - KD can help our cells’ mitochondria reach
the “Goldilocks” zone for producing ROS — not too much
and not too little, but just the “right” amounts for healthy
cellular and mitochondrial function.
Harmful Effects of too much Sugar
Chronic low grade inflammation - Mitochondrial dysfunction

Harmful Effects of too much Sugar
Chronic low grade inflammation - Mitochondrial dysfunction
1- State of chronic inflammation
2- Lipoprotein Oxidation & Glycation
3- Hyper insulinemia syndrome - Metabolic syndrome
-> Insulin resistance (type 2 DM)
-> increased triglycerides VLDL (Very-low-density lipoprotein)
-> Cholesterol (small dense LDL type B particles)
4- HFCS (High-fructose corn syrup) is found in almost all
types of processed foods and drinks (Sugar: toxic,
addicting, and deadly)
5- feeds” the cancer cells fructose is readily used by cancer
cells (not using mitochondria – no ROS to kill it)
6- Gaining weight (insulin and leptin signaling resistance)
7- Increases uric acid levels - risk for heart & kidney
8- Overloads and damages the liver much sugar or fructose
likened the effects of alcohol
9- Other diseases linked to metabolic syndrome include:
Type 2 diabetes, Heart disease, Hypertension, Polycystic
ovarian syndrome, Lipid problems, Dementia and
Alzheimer's disease

Harmful Effects
of too much
protein

Harmful Effects of too much Protein
Paleo diet
Activation of the The mammalian Target Of Rapamycin (mTOR) metabolic
signaling pathway by too much protein
The figure highlight and summarize the current
understanding of how mTOR nucleates distinct multi-
protein complexes, how intra- and extracellular
signals are processed by the mTOR complexes, and
how such signals affect cell metabolism, growth,
proliferation and survival.
mTOR function in skeletal muscle a focal point for overnutrition and exercise . A. Rivas,a Sarah J. Lessard,b Vernon G. Coffeya
aExercise Metabolism Group, School of Medical Sciences, RMIT University, Bundoora, Victoria 3083ailartsuA ,‫ز‬ The. Research Division, Joslin Diabetes
Center and Department of Medicine, Harvard Medical School, Boston, MA 02215ASU ,.‫ز‬ Corresponding author (email: vernon.coffey@rmit.edu.au) .
Published on the web 6 October 2009. . Received March 29,2009yaM detpeccA .26,2009.

Harmful Effects of too much Protein
Paleo diet
The mammalian target of rapamycin (mTOR) -
Discoveries that have been made over the last
decade
phosphatidylinositol 3-kinase-related kinase family of protein
kinases. signaling pathway integrates both intracellular and
extracellular signals
The mTOR pathway serves as a central regulator of
cell metabolism, growth, proliferation and survival.
The mTOR pathway is activated during:
1- Tumor formation, angiogenesis, insulin resistance,
adipogenesis and T-lymphocyte activation etc
2- Deregulated in diseases as cancer and type 2 diabetes.
Nutrients and Exercise modify mTOR function
Growing therapeutic use of mTOR inhibitors (rapamycin and
rapalogues) in solid tumors, organ transplantation, coronary
restenosis and rheumatoid arthritis.
The figure highlight and summarize the current
understanding of how mTOR nucleates distinct
multi-protein complexes, how intra- and
extracellular signals are processed by the
mTOR complexes, and how such signals affect
cell metabolism, growth, proliferation and
survival.

Hypoxia-inducible factor 1alpha (HIF-1)
is regulated by the mammalian target of
rapamycin (mTOR) via an mTOR signaling
motif.
J Biol Chem. 2007 Jul 13;282(28):20534-43. Epub 2007 May 14.
Land SC1, Tee AR.
1Institute of Medical Genetics, Wales College of Medicine, Cardiff
University, Heath Park, Cardiff, Wales, United Kingdom.
Abstract
Abstract
Tumors that form as a result of heightened mammalian target of rapamycin (mTOR) signaling are highly vascularized. This
process of angiogenesis is regulated through hypoxia-inducible factor (HIF)-mediated transcription of angiogenic factors. It is
recognized that inhibition of mTOR with rapamycin can diminish the process of angiogenesis. Our work shows that activation of
mTOR by Ras homologue enriched in brain (Rheb) overexpression potently enhances the activity of HIF1alpha and vascular
endothelial growth factor (VEGF)-A secretion during hypoxia, which is reversed with rapamycin. Mutants of Rheb, which do not
bind guanine nucleotide (D60K, D60V, N119I, and D122N) and are unable to activate mTOR, inhibit the activity of HIF when
overexpressed. We show that regulatory associated protein of mTOR (Raptor) interacts with HIF1alpha and requires an mTOR
signaling (TOS) motif located in the N terminus of HIF1alpha. Furthermore, a mutant of HIF1alpha lacking this TOS motif
dominantly impaired HIF activity during hypoxia and was unable to bind to the co-activator CBP/p300. Rapamycin treatments do
not affect the stability of HIF1alpha and modulate HIF activity via a Von Hippel-Lindau (VHL)-independent mechanism. We
demonstrate that the high levels of HIF activity in cells devoid of TSC2 can be reversed by treatments with rapamycin or the
readdition of TSC2. Our work explains why human cancers with aberrant mTOR signaling are prone to angiogenesis and
suggests that inhibition of mTOR with rapamycin might be a suitable therapeutic strategy.

World Health Organization MONICA
study
(MONICA : multinational MONITORING
trends and determinants in
CADIOVASCULAR disease)
14 European countries
+ urban Australian Aborigines
10 years
7 million people
40 studies collected
The ten year data collection was
completed in the late 1990s,
A diet low in saturated fat 'will not prevent
heart disease or prolong life'
"The Great Cholesterol Myth". Dr. Malcolm Kendrick
MD . July 2011.
As any person (no medical experience needed) with eyes can
see, the Aborigines had the lowest cholesterol and the highest
death rate from heart disease.

49
The typical atherosclerotic plaque comprises of the lipid
core and the fibrous cap, and is the most commonly
classified histologically by the American Heart Association
Atherosclerotic plaque
Causes:
1- Endothelial damage & permeability
2- Small dense particles LDL type B
3- Smooth muscle cells migration and proliferation
4- Monocyte adhesion, migration and foam cell
development.
Caused by:
1- State of chronic inflammation
->> Oxidative stress
2- Hyperglycemia
->> Lipoprotein Oxidation & Glycation
3- Hyper insulinemia – Hyper leptinemia
-> increased triglycerides VLDL
-> Cholesterol (small dense LDL type B particles)
Treat the cause is the logical thinking:
1- Anti-inflammatory lifestyle
2- Control Hyperglycemia-
3- Control Insulin - Leptin resistance
Hyper insulinemia – Hyper leptinemia
(Diet too high in sugars & Obesity)

Figure 1: Oxidative stress affects four fundamental mechanisms that contribute to
atherogenesis (i) oxidation of LDL to form ox –LDL (ii) endothelial cell dysfunction
(increased release of MCP-1, MMPs, increased expression of VCAM-1, ICAM-1 and LOX-1,
decreased activity of NO, platelet aggregation) (iii) vascular smooth muscle cells migration
and proliferation (iv) monocyte adhesion and migration and foam cell development. [15]

In Summary, Saturated Fats Are
Healthy
•Increase your LDL levels, but they increase the
large fluffy particles that are not associated with an
increased risk of heart disease
•Increase your HDL levels. This more than
compensates for any increase in LDL
•Do NOT cause heart disease as made clear in all
the above-referenced studies
•Do not damage as easily as other fats because they
do not have any double bonds that can be damaged
through oxidation
•Serve to fuel mitochondria and produce far less
damaging free radicals than carbs
Could Eating the Right Fats Save 1 Million Lives per Year?
D. Mercola - March 06, 2016

In many epileptic patients, anticonvulsant drugs either fail adequately to control
seizures or they cause serious side effects.
An important adjunct to pharmacologic therapy is the ketogenic diet, which often
improves seizure control, even in patients who respond poorly to medications.
The mechanisms that explain the therapeutic effect are incompletely understood.
Evidence points to an effect on brain handling of amino acids, especially glutamic
acid, the major excitatory neurotransmitter of the central nervous system.
The diet may limit the availability of oxaloacetate to the aspartate aminotransferase
reaction, an important route of brain glutamate handling.
The ketogenic diet and brain metabolism of amino acids: relationship to
the anticonvulsant effect.
Yudkoff M1, Daikhin Y, Melø TM, Nissim I, Sonnewald U, Nissim I.
Annu Rev Nutr. 2007;27:415-30.
As a result, more glutamate becomes accessible to the glutamate decarboxylase reaction to yield gamma-
aminobutyric acid (GABA), the major inhibitory neurotransmitter and an important antiseizure agent.
In addition, the ketogenic diet appears to favor the synthesis of glutamine, an essential precursor to GABA.
This occurs both because ketone body carbon is metabolized to glutamine and because in ketosis there
is increased consumption of acetate, which astrocytes in the brain quickly convert to glutamine.
The ketogenic diet also may facilitate mechanisms by which the brain exports to blood compounds such as
glutamine and alanine, in the process favoring the removal of glutamate carbon and nitrogen.

Alterations in the metabolism of excitatory amino acids
and γ-aminobutyric acid (GABA) during the high-fat, low-
carbohydrate ketogenic diet. Metabolism of acetyl-CoA
generated from fats leads to high consumption of
oxaloacetate (see Fig. 1). L-Aspartate, a nonessential
amino acid, is formed by the transamination of
oxaloacetate with an amino group from glutamate.
Reduced availability of oxaloacetate along with robust
availability of αketoglutarate from high activity of the first
part of the Krebs cycle leads to low aspartate levels. It
has been hypothesized that more glutamate is thus
accessible to glutamic acid decarboxylase for production
of GABA [33]. Not all Krebs cycle intermediates are
shown in the schematic.
The brain, energy is everything. The brain needs a crapload of
energy to keep all those membrane potentials maintained - to
keep pushing sodium out of the cells and pulling potassium into
the cells.
In fact, the brain, which is only 2% of our body weight, uses 20%
of our oxygen and 10% of our glucose stores just to keep
running.
(Some cells in our brain are actually too small (or have tendrils
that are too small) to accommodate mitochondria (the power
plants). In those places, we must use glucose itself (via
glycolysis) to create ATP.)
When we change the main fuel of the brain from glucose to
ketones, we change amino acid handling. And that means
we change the ratios of glutamate and GABA.
The best responders to a ketogenic diet for epilepsy end up with
the highest amount of GABA in the central nervous system.
glutamine, an essential precursor for GABA.
If you recall, GABA is the major inhibitory neurotransmitter in the
mammalian nervous system. Turns out, GABA is made from
glutamate, which just happens to be the major excitatory
neurotransmitter. You need them both, but we seem to get into
trouble when have too much glutamate. Too much excitement in
the brain means neurotoxicity, the extreme manifestation of
which is seizures. But neurological diseases as varied
as depression, bipolar disorder, migraines, ALS, and dementia
have all been linked in some way to neurotoxicity.

Cancer is One of the Most Manageable Diseases
Once we realize that cancer is a metabolic disease
Dr Josef Mercola - 2016
We can take charge of those kinds of things , with Eating too many
sugars and carbs without fiber, along with too much protein, we
ignite a cascade of metabolic events that includes:
•Widespread inflammation and cellular damage, especially our
mitochondria, or cells’ power factories
•Faster aging and a greater risk of all cancers from the activation of
body’s most important signaling pathway mTOR from eating excess
protein
•An increase in insulin resistance that can progress to prediabetes or
Type 2 diabetes because cells have lost their ability to respond to insulin
effectively
•Overeating due to leptin resistance with loss of control over appetite
and knowing when you’re “full”
•An inability to lose weight because body is holding on to fat instead of
burning it for fuel

Cancer_in_australia_summary_pages_2017-55
Now we know why the new life style diseases are high rocketed
after the high carb low fat (HCLF) guidelines 1980
our world in data cancer

Harmful Effects of
Lack of exercise and
Physical inactivity

PPARGC1A
PGC-1α )PPARGC1A): the master regulator of mitochondrial
biogenesis
is a protein encoded by the PPARGC1A gene. known as human accelerated
region 20 (HAR20).
PGC-1α is a transcriptional co activator that regulates the genes involved
in energy metabolism. It is the master regulator of mitochondrial biogenesis.
plays a central role in the regulation of cellular energy metabolism.
It stimulates:
1- Mitochondrial biogenesis
2- Promotes the remodeling of muscle tissue to a fiber-type that is
metabolically more oxidative and less glycolytic in nature.
3- It participates in the regulation of both carbohydrate & lipid metabolism.
4- It is involved in obesity, diabetes, & cardiomyopathy.
PGC-1α activating host factors:
1- Free Radicals
both formed intracellularly as by-products of metabolism but upregulated during
times of cellular stress.
2- Cold Exposure
PGC-1α determines lactate metabolism, preventing high lactate levels in
endurance athletes & making lactate as an energy source

1- low carb High fat Diet Regime (LCHF) –
Mitochondrial Metabolic Therapy (MMT) 2017 -
Ketogenic diet (KD)
2- Mitochondrial Metabolic Therapy (MMT) 2017 is
Similar to a ketogenic diet (epilepsy 30-50%)
3-MMT is a high fat, moderate protein,
low carb eating plan
Unlike a ketogenic diet, it emphasizes on high-
quality, (unprocessed whole foods )
Unlike Paleo diet it does not consume far too
much protein (moderate protien)
Mitochondrial Biogenesis
Salvage 1- The Harmful Effects of too much Sugar

Mice with metastatic cancer lived 103% longer with a combination of the ketogenic diet (KD),
ketone supplements (KE) and hyperbaric oxygen therapy (HBOT), compared to mice fed a
standard diet (SD), according to Dominic D’Agostino’s research.
LCHF - MMT - KD
can help our cells’ mitochondria reach the
“Goldilocks” zone for producing ROS — not too much
and not too little, but just the “right” amounts for
healthy cellular and mitochondrial function.

Cancer is a metabolic disease that can be
prevented and treated with the low-carb,
high-fat ketogenic diet, according to a
growing body of scientific research.
Studies show the ketogenic diet may beat
chemotherapy for some forms of cancer
Because cancer is a metabolic – not a
genetic – disease
Travis Christofferson, author of Tripping Over the Truth:
The Metabolic Theory of Cancer.
Tripping over the Truth The Metabolic Theory of Cancer
by Travis Christofferson - 2014

Intermittent fasting
Beside longevity and health issues, it also provide powerful cancer
prevention and treatment benefit.
And the mechanism for that is related to the effect fasting has on our
mitochondria.
Reactive oxygen ROS. Some free radicals are actually good and your
body requires them to regulate cellular function (fat burning),
but problems develop when you have excessive free radical production
(sugar burning) .
There are two possible solutions to this problem:
• Increase your antioxidants
• Reduce mitochondrial free radical production by (calorie
restriction) .
This is one of the reasons why intermittent fasting works, as it limits the
window that you are eating and automatically reduces your calories.
It is particularly effective if you avoid eating several hours before
going to sleep as that is your most metabolically lowered state.
Interventional strategy
where in individuals are
subjected to varying periods
of fasting.

Interventional strategy where in
individuals are subjected to varying
periods of fasting.
Fasting Promotes Healthy Mitochondrial Function, Our body has to rely
on lipids and stored fats for energy, which means our cells are forced
to use their mitochondria. mitochondria are the only mechanisms by which
our body can make energy from fat. So, fasting helps activate our
mitochondria.
Intermittent fasting, ketogenic diet and certain drugs can kill
cancer cells, by activating the mitochondria. It creates a burst of reactive
oxygen species ROS, the damage from which tips the scale and causes the
cancer cells to die.
Fasting clears away damaged cells through a process called autophagy, which basically
means when a cell that's damaged, it can die. But if it doesn't die, sometimes it becomes what's called
senescent and this happens a lot with aging. What that means is that the cell is not dead but it's not
really alive either. It's not doing its function.
It's just kind of sitting around in your body secreting pro-inflammatory molecules, things that are
damaging other nearby cells thereby accelerating the aging process because inflammation drives
aging in so many different ways.
Autophagy clears away those cells that are just sitting there creating damage and not doing much
else, which is nice because that's also a very important biological mechanism for staying healthy."

Why Does the Hypothalamus Unnecessarily Force a
Sugar Burning Mode in Our Bodies?
1- Overcoming too much stress.
Reducing stress is the antidote to adrenaline causing sugar burning. To do so, one
must eliminate fear, anxiety, and/or sleep deprivation. Sleeping sufficiently,
meditation and eliminating causes of stress are the keys.
2- Reducing blood sugar.
The best way to reduce blood sugar is to drastically reduce one’s consumption of
foods that contain sugar and other carbohydrates. The absolute best way to prevent
sugar fluctuations is to eat 5 to 6 small meals per day (every 2 to 3 hours), of non
sugar/carbohydrate containing foods.
3- Overcoming Leptin Insensitivity.(Obesity)
Overcoming leptin insensitivity (i.e. repairing the hypothalamus) isn’t so easy. The
rather long explanation of why it isn’t so easily overcome is that the bodies of sugar
burning people (primarily fat people) have large pantries of stored fat which creates
large amounts of the messenger molecule leptin which will push the leptin levels
above 9.0 ng/ml and damage the receptors. After a while, the hypothalamus cannot
detect leptin at all and thinks that its level is zero, and therefore, instructs sugar
burning mode. In a sugar burning mode, it is difficult to entice the body to burn fat
stores and therefore very difficult to get rid of fat so that leptin levels will go down to
a “fat burning”range of between 4.0 and 9.0. For a fairly in-depth discussion about
doing this, please request our Becoming Leptin Sensitive Booklet.

Managing Your Mitochondria, By Mark Sisson October 20, 2011
The single most fundamental – and simple – way to
improve mitochondrial function
is to turn away from relying on sugar-burning and
transform yourself into a fat-burning beast.
See, mitochondria burn fatty acids cleaner than they burn carbohydrates. Generating ATP
via fats/ketones produces fewer free radicals, because it’s more efficient, whereas generating ATP via carbs
produces more. As a result, glutathione can do its job and our ketone-burning mitochondria have to divert less
attention to cleaning up free radicals. This doesn’t just make mitochondrial ATP production from ketones more
efficient; it has the potential to render it downright anti-inflammatory, too. When we dip into a full-fledged
ketogenic diet, cut back on bad carbs, or intermittently fast, we are switching over to fat-burning. When we
switch over to fat-burning, our mitochondria do the same. Heck, that’s what we mean by “fat-burning.” There’s
even evidence that ketosis can spur mitochondrial biogenesis, albeit thus far only in rats.
In my new book I present my Primal prescription for becoming a fat-burning beast. In fact, one of the reasons I
wrote the 21-Day Total Body Transformation is because untold millions of people are languishing in sugar-
burning land and their mitochondria aren’t burning quite as cleanly as they could. The “transformative” aspect of
the 21-Day Total Body Transformation is the epigenetic switch from sugar-burning to fat-burning. And improving
mitochondrial function and (if that rat study pans out in humans) increasing mitochondrial biogenesis are at the
heart of this switch.

Salvage 2- The Harmful Effects of too much Protein
Mitochondrial Metabolic Therapy (MMT) 2017
is a high fat, moderate protein, low carb eating
plan
Unlike a ketogenic diet, it emphasizes on high-quality,
unprocessed whole foods
Unlike Paleo diet which allow consumption of far too
much protein
The mammalian target of rapamycin (mTOR) pathway is Central
regulator of cell metabolism, growth, proliferation and survival.

Salvage 3- Lack of exercise and Physical activity
Exercise Helps Keep Our Mitochondria Young
Exercise
Promotes mitochondrial health, as it forces your mitochondria to work harder. one of
the side effects of mitochondria working harder is that they're making reactive oxygen
species ROS , which act as signaling molecules. One of the functions they signal is to
make more mitochondria (fission). So, when you exercise, your body will respond by
creating more mitochondria to keep up with the heightened energy requirement.
Aging
Is inevitable. But your biological age can be quite different from your
chronological age, and your mitochondrial health have a lot to do with your
biological aging.
As noted by Patrick, "youthfulness" is not so much about your chronological age, but rather how old you feel, and
how well your body works:
"I want to learn how to optimize my own cognitive performance and my athletic performance. I want to also
increase the youthful part of my life. I want to be 90. I want to be out there, surfing in San Diego just like I was
when I was 20. I would like to not degenerate as rapidly as some people do. I like to stave off that degeneration
and extend the youthful part of my life as long as I possibly can so I can enjoy life."

Role of Regular Physical Exercise
A- Burn of fat
(as MMT & Ketogenic diet)
B- Improve insulin sensitivity
(depleting glycogen & fat stores)
C- Peak rise of hormones
Human growth hormone(HGH-GH) – Endorphins ,
Dopamine, Norepinephrine, Serotonin) - exercise intensity
D- Mitochondrial Biogenesis

Mitochondrial Biogenesis:
Exercise is one of the most powerful signals for PGC
1-alpha
A protein encoded by PPARGC1A gene (Peroxisome
proliferator-activated receptor gamma coactivator 1-alpha
(PGC-1α) )
PGC-1α )PPARGC1A): the master regulator of
mitochondrial biogenesis
PGC 1-alpha:
Is the primary signal for Mitochondria to Reproduce and
Multiply, a process called Mitochondrial biogenesis
PPARGC1A
(PGC-1α( is a protein encoded by the PPARGC1A gene. known as human accelerated
region 20 (HAR20).
PGC-1α is a transcriptional co activator that regulates the genes involved in energy
metabolism. It is the master regulator of mitochondrial biogenesis.

PPARGC1A
PGC-1α activating host factors
1- Free Radicals
both formed intracellularly as by-products of metabolism but
upregulated during times of cellular stress.
2- Cold Exposure
PGC-1α determines lactate metabolism, preventing high lactate levels
in endurance athletes & making lactate as an energy source
plays a central role in the regulation of cellular energy metabolism. It stimulates 1- mitochondrial biogenesis 2- promotes the
remodeling of muscle tissue to a fiber-type that is metabolically more oxidative and less glycolytic in nature
It participates in the regulation of both carbohydrate & lipid metabolism.
It is involved in obesity, diabetes, & cardiomyopathy.

Exercise (Mitochondrial Biogenesis) for
Cutting Cancer Risk:
The mammalian target of rapamycin (mTOR) -
Discoveries that have been made over the last decade
The mTOR pathway is Central regulator of cell
metabolism, growth, proliferation and survival.
Nutrients (less protein) and Exercise
modify mTOR function
1- Activated during tumor formation, angiogenesis, insulin resistance, adipogenesis and T-lymphocyte activation etc
2- Deregulated in diseases as cancer and type 2 diabetes.
3- Growing therapeutic use of mTOR inhibitors (rapamycin and rapalogues) in solid tumors, organ transplantation,
coronary restenosis and rheumatoid arthritis.

Exercise slashed the risk of cancer in 13 out
of the 26 cancers
for example
Kidney cancer by (23 %)
Lung cancer by (26 %)
Liver cancer by (27 %)
Esophageal adenocarcinoma by (42 %)
Large Study 2016 Underscores Value of Exercise for Cutting Cancer Risk
Journal of the American Medical Association Internal Medicine 2016; 176(6): 816-
825=
The research involved a mega-pool of
1.44 million men and women from a dozen
large European and U.S.
prospective cohort studies (groups of
participants who’d been followed for
several years).
Participant age, body mass index, gender,
self-reported data on exercise, smoking
status and, if applicable, any cancer
diagnoses, were analyzed to determine
the effect exercise had on various
cancers.
A total of 186,932 primary cancers were
diagnosed during the follow-up period,
which had a median length of 11 years.
Regardless of the person’s weight or
smoking history, the data suggested
physical activity cut their risk of cancer.

Salvage 4- Feeding Your Mitochondria
The following nutrients; co-factors needed for mitochondrial enzymes
to function properly:
•CoQ10 or ubiquinol (the reduced form)
•L-Carnitine, which shuttles fatty acids to the mitochondria
•D-ribose, which is raw material for ATP molecule
•Magnesium
•Omega-3 fatty acids
•All B vitamins, including riboflavin, thiamine, and B6
•Alpha-lipoic acid (ALA) - Thiotacid
Get as many micronutrients as you can from whole foods

Salvage 5- Avoid Environmental Toxins
Free radical create oxidative stress which inhibits antioxidants from defending
the body from cancer.
Reactive oxygen species (ROS) are a potent type of free radical which can
deplete vitamin C levels and stimulate systemic inflammation.
As inflammation in the body increases, the central nervous system has been shown to
leak signals to the brain and gastrointestinal tract.
This results in an autoimmune response from the body. Available antioxidant sources
become depleted as the immune system attempts to defend the body from an unknown
threat.
Individuals with mitochondrial dysfunction have been found to have low levels of
antioxidant support including carnitine, glutathione, and thioredoxin.
Cancer is characterized by numerous factors which lead to depression, a weakened
immune system, and chronic oxidative stress. Mitochondrial dysfunction is associated
with promoting every one of these factors.

1- Diet
A- High fat – moderate protein – cut off the sugar
1- low carb High fat Diet Regime (LCHF)
2- Ketogenic diet (KD)
3- Mitochondrial Metabolic Therapy (MMT) 2017
B- Intermittent fasting
(fat burner (less ROS) – low calorie intake (less ROS))
C- Avoid stress - obesity
2- Exercise and physical activity
Regular – endurance - PGC 1-alpha
3- Feeding Your Mitochondria
•CoQ10 or ubiquinol (the reduced form)
•L-Carnitine, which shuttles fatty acids to the mitochondria
•D-ribose, which is raw material for ATP molecule
•Magnesium
•Omega-3 fatty acids
•All B vitamins, including riboflavin, thiamine, and B6
•Alpha-lipoic acid (ALA) – Thiotacid
Get as many micronutrients as you can from whole foods
4- Avoid Environmental Toxins
Summary

Cancer as a metabolic disease 2

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