Biological Aging VS. Chronological Aging - How to Build a Healthy Longevity - An Important Role for the Mitochondria Part I Professor Serge Jurasunas, M.D. (hc) N.D. M.D (Hom) Topics in Part 1: A Longer Lifespan No Longer Means a Healthier Lifespan What are the Causes of Normal Aging or Premature Aging? Mitochondria, Oxidative Stress, and Premature Aging What are Mitochondria? Brain Neurons The Brain and Alzheimer’s

1. Biological Aging VS. Chronological Aging - How to Build a Healthy
Longevity - An Important Role for the Mitochondria
Part I
Professor Serge Jurasunas, M.D. (hc) N.D. M.D (Hom)
Figure #1: Older vs. Younger
Introduction
During my professional career, I have concentrated my research on cancer
treatment using a variety of innovative protocols, and dietary
supplementation and published many articles in the Townsend Letter.
However, biological aging and mitochondria are also a subject of great
interest to me, since in my work I am dealing with both cancer patients and
the elderly. It’s been years since I read a book by the famous Swiss doctor,
Bircher Benner about the Hunza land and longevity. This was associated

2. with their food style and it became a way for me to teach people some
rules to facilitate a healthy lifespan. Years later, Dr. Bernard Jensen
personally visited the Hunza land and told me all about his trip which
further convinced me about the value of natural food in the process of
healthy longevity. Over the past 5 decades, I considered myself fortunate
since I had the opportunity with most of my patients to observe year after
year how they aged according to my dietary and lifestyle advice. Others
have not followed my dietary advice and lifestyle, just coming in from
time to time when feeling bad for some help. They kept on eating the
wrong food. One man I saw recently now has a serious cognitive disorder,
having lost his sense of orientation, not to mention a list of other physical
disturbances. This week a regular patient came in for a consultation, a 71-
year-old woman, very good looking, she was 23 years old when she first
came to me, some 48 years ago. I also observed how individuals aged
prematurely and changed their physical morphology, complaining of
cognitive disorders long before their chronological age, including a patient
as young as 26 years old.
Once I had a 55-year-old man with Alzheimer's and dementia, who looked
20 years older. His 14-year-old son already looked like he was much older
and already showed a cognitive disorder. (1) It all started when in 1969
while traveling to Germany I met two research assistants of Otto Warburg,
including Paul Seeger, one of the great innovative scientific thinkers of the
past century. He spent four decades investigating mitochondria,
accumulating profound knowledge about mitochondrial function
associated with cancer. (see reference 3). Thus I discovered something
very new about the nature of mitochondria and the central role they play in
both the theory and treatment of cancer. As result, in 2008 and again in
2012 I published articles about mitochondria and cancer in the Townsend
Letter. (2-3) Today mitochondrial dysfunction and excessive free radical
activity are not only seen as a cause and treatment of cancer (4) but largely
implicated in the origin of early aging and neurodegenerative disease such
as Alzheimer’s. (5-6) For the past 3 decades, both the US and Europe have
seen a dramatic increase in neurodegenerative diseases chiefly Alzheimer's
disease (AD) Parkinson's Disease (PD), and other neurological diseases
and physical debility conditions in seniors from age of 60 years.

3. A Longer Lifespan No Longer Means a Healthier Lifespan
While human life expectancy has greatly increased over the past few
decades in most western countries, today it no longer coincides with a
similar increase in their health. In countries like the US which are
supposed to be at the leading edge of science and medicine, statistics have
shown that 86 percent of Americans suffer from some degenerative disease
that the situation is even deteriorating with poor health conditions in
elderly people. As another example, in France recently it has been shown
that 3 million seniors (over 60 years) are in a situation of extreme
dependence. A high percentage live in their homes, not being able to walk
out and come back. It is not better in retirement homes. Alzheimer’s
disease affects approximately 5.5 million people in the US and is projected
to grow to 11 to 16 million by 2030. 65% of women above the age of 60
years are affected by AD and according to the WHO, the number is
projected to quadruple by 2030. In the US every year more than $100
billion is spent for health care to treat AD in primary care settings alone.
Today it is estimated that there are about 50 million cases of AD in the
world. We are not talking anymore about only physical diseases but
neurodegenerative diseases and processes that over a lifetime deteriorate
the brain and physical body in a way that humans are now getting old
before their chronological age. Aging and change in our bodies appear
long before the age of 62 years and even many degenerative processes
begin in a person in their 20s. (7) While some people according to their
lifestyle and food style appear younger than their real chronological age,
others look much older with physical deterioration and cognitive disorders
associated with lifestyle and dietary style. In comparison, Centenarian
societies of various countries such as Okinawa are still physically active,
healthy, and happy long into their 80s and 90s even being very active
working in the field for up to 100 years. They have shown little if any
western degenerative disease even at these advanced ages. It seems that
other factors independent of food style and lifestyle may drive aging.
What are the Causes of Normal Aging or Premature Aging?
First aging is a normal process that occurs over the years in our lifetime
resulting in a decline in physical activity, accumulation and degradation of
oxidized proteins, a breakdown in muscle mass, skeleton, and blood

4. vessels, excessive free radicals activity that damages brain neurons, the
gradual decline of the senses, hearing, vision, wrinkle accumulating in the
skin, deterioration of our brain function and age-related diseases including
neurodegenerative disease, cardiovascular disease, etc. Aging may also
affect the function of the bowel, bladder, kidney, etc. From a naturopathic
standpoint, some theories stipulate that we may age from the colon, from
bad bowel function, and autointoxication. Thirty years ago, the Soviet
scientist Dr. Popov suggested that constipation and poor elimination of
toxic waste may lead to the aging process and I agree. This theory was
followed by several pioneers including Dr. W. Walker Dr. Sc., a well-
known nutritional researcher of aging in the US, and the author of the book
“Become Younger” In fact, it matches my theory of auto-intoxication that
I explain in my book, “Health and Disease Begin in the Colon” together
with my decades of clinical experience and iridology examination which
can easily focus on the condition of the colon. So the colon is important,
auto-intoxication is probably causing a disturbance in our cells but I
always give great importance to mitochondria function related to disease,
fatigue, heart failure cancer, and premature aging, Now Scientists noted
that mitochondria dysfunction is one of the major cause of aging but not,
of course, the only one. Shortening of telomeres from chronic oxidative
stress is also a well-known factor associated with aging A new study
published by the team of Elissa. S. Epel of the University of California
where the researcher measured the length of telomeres with healthy
females aged between 20 and 50 years under strong psychological stress.
Women with the highest levels of oxidative stress have their telomere
shorter and show at least 9 to 17 years of additional aging compared to
low-stressed women. (8)
Mitochondria, Oxidative Stress, and Premature Aging
Mitochondrial function is very much affected by three major factors
which are:
1- The aging process and the production of excessive free radicals.
2- By environmental factors such as insecticides, and herbicides.
Radiation etc... Pesticides are one main damaging factor to
mitochondria. Paraquat is one example since it has been shown to

5. inhibit the ETC enzyme complex and produce reactive oxygen
species. Organochlorine pesticides can reduce mitochondria counts,
membrane potential, and ATP production. Organophosphorus
insecticides have been shown to reduce the number of mitochondria
and can seriously damage the mitochondria. Several antibiotics like
fluoroquinolones, Statins, anti-depressants, NSAIDs (former
Ibuprofen), birth control pills, Viagra and even some vaccines, etc.,
are all factors that may affect the mitochondria respiratory chain and
ATP production. Some antineoplastic treatments, doxorubicin, and
tamoxifen also may impair the respiratory chain of the mitochondria.
It is important to mention that 70% of the antibiotics in the US go to
farm animals and agriculture thus in food.
3- By genetic dysfunction. mutation of mitochondrial DNA inherited
from the mother can hasten the offspring’s aging process. A team
from the Max Planck Institute for The Biology of Aging in Cologne
Germany has shown that aging is determined not only by the
accumulation of mtDNA damage that occurs during our lifetime
but also by damage (mutation) that we acquired from our
mother. (9) We inherit our mitochondrial DNA only from our
mother from the oocytes and anything that may have affected our
mother or grandmother, good or bad passes on to us. Mutation of
maternally inherited mtDNA influences the offspring so the aging
process may start from birth. Pregnant women have the greatest
responsibility to improve their diet and lifestyle, defend themselves
from pollution and avoid drugs including vaccines.
What are Mitochondria?
The name mitochondrion comes from the Greek ‘mitos’ (filaments) and
‘hondros’ grains. Mitochondria are subcellular organelles of 0.5-20u in
length, either filamentous or oval, and are bounded by a double membrane
and found in all aerobic (eukaryotic) mammalian cells both animal and
plant cells and vary considerably in size, structure, and number which can
be from several hundred up to several thousand. They are the descendants
of an ancestral anaerobic bacteria incorporated about 2-3 billion years ago
into the eukaryotic cell after the release of billions of tons of oxygen on the
planet becoming poisonous to anaerobic life. Some species die, while

6. others penetrate the host cell and became symbiotic, intracellular parasites,
that evolved, adapted, and developed some systems to use oxygen as fuel
to burn foodstuff to generate high-energy molecules of adenosine
triphosphate (ATP) critically important for all the cell’s function including
cellular differentiation, regulating the cell cycle and cell death. When
released ATP energy is transferred to cytosols and this is why we call
mitochondria the powerhouses of the cells. This is the basis of aerobic life
on this planet. We are all aware of how dependent we are on oxygen
however at the same time mitochondria have developed effective
antioxidant enzyme systems against the corrosive effect of oxygen itself a
deadly gas and the production of ROS. The mitochondrial antioxidant
enzyme, manganese superoxide dismutase (MnSOD acts as the chief ROS
scavenger enzyme), sometimes known as the Guardian of the
Powerhouses.
Animals with the longest life spans, such as man have the highest levels of
SOD when it is expressed as a function of the oxidative metabolic rate.
Lifespan is directly proportional to the level of SOD produced in a
mammalian species or man. Thus SOD is associated with aging since it is
the only antioxidant enzyme synthesized in the mitochondria, to detoxify
the first free radicals generated the superoxide radical damaging by
themselves, that if not scavenged contribute to produce other free radicals
such as the destructive hydroxyl radical associated with degenerative
disease. (10-11)

7. Figure 2: Electron Micrograph of Human Liver Cell. Mitochondria (M)
on Left Nucleus (N)
Mitochondria are the major source of superoxide radicals mainly in
complexes I, and II followed by complex III, and responsible for oxidative
damage and mitochondrial dysfunction if not scavenged by MnSOD. Due
to its strategic location in the mitochondria, MnSOD is essential for the
survival of aerobic life (12) and to increase the life span of species. (13)
Mice lacking MnSOD die shortly after birth indicating its crucial role to
maintain lifespan in humans and animals. Normally about 90-95% of the
oxygen we breathe is utilized in the process of oxidative phosphorylation
to produce ATP energy and for this reason, are more susceptible than any
other organ to produce oxygen free radicals. As explained, a decline in
MnSOD is associated with aging since logically it increases the production

8. Figure 3: Mitochondria - Hallmark of Aging
of reactive oxygen species and correlates with mitochondria oxidative
damage and mtDNA mutation (14) One other example is the study done
by Gregory, EM, and Fridovitch, I, who have provided substantial
evidence that MnSOD is necessary for survival in all oxygen metabolizing
cells. Knockout of MnSOD activity by creating inactive mutants or the
complete elimination of MnSOD led to early death in mice. (15) One other
characteristic; mitochondria have their own DNA and ribosomes. They can
make their own proteins, exactly 13 proteins encoded in the mitochondrial
genomes localized within the matrix out of 1500 different types imported
from the cell nucleus which are essential for the electron transport and
oxidative phosphorylation, which occur in cellular respiration. They
replicate differently and at a different time than molecular DNA showing
their independent biological origin. While nuclear DNA is well protected
by histone proteins that act like a shield to protect DNA from high energy
radiation and reactive oxygen species mtDNA does not have such
protection and is thus more subject to damaging effects. For instance, the

9. mutation rate of mtDNA is up to 15-fold higher as compared to the DNA in
the cell nucleus itself. MtDNA is much more sensitive than nuclear DNA
to oxidative attack and damage. mtDNA has only rudimentary DNA repair
capability, contrary to nuclear DNA since none of the proteins made in
mitochondria are designed for DNA repair. This is why mitochondria are
very sensitive to oxidation and damage since the repair mechanism is
limited while mitochondria turnover is rapid (about 30 days). Impairment
of mitochondrial function and ETC due to overproduction of ROS,
decreasing antioxidant enzyme levels of ATP production that affect organs
such as the brain, the heart, and the skeletal muscles was reported (16-17)
causing accelerated aging. However, it may also be responsible for several
disorders or serious clinical features such as dementia, myopathy,
cardiomyopathy, liver failure, and kidney pathologies. In addition, the link
between mitochondrial DNA mutation dysfunction and age-related
diseases as well as Alzheimer's disease is well established, (18) Now
damaged mitochondria produce more ROS and thus accelerate more toxic
ROS generation and more damage. But of course, the normal lifespan of
both mice and humans is also associated with a decrease in the number of
mitochondria and changes in mitochondrial morphology. (19) Species with
high metabolic rates have shorter lifespans. (20) Rats, for instance, live
only about 40 months because of the high rate of free radicals such as
10,000 attacks per day, per cell while in humans only 1000 attacks per day,
per cell.
Brain Neurons
The brain is rich in unsaturated fatty acids, and approximately 60 percent
consists of lipids. This is why brain neuron membranes are more
susceptible to oxidative stress, these membranes being sensitive to oxygen
radicals. Neurons contain a high concentration of mitochondria and require
a large flux of oxygen because the central nervous system (CNS) has an
extraordinarily high metabolic rate as it consumes about 20% of oxygen
inspired at rest, and account for only 2% of body weight. Inevitably they
are the main source of free radicals and more vulnerable to the damaging
effects on mtDNA which oxidizes much faster than other cells, inducing
mutations associated with aging (21-22). For instance, damaged mtDNA

10. Figure #4: A - As normal neurons begin to age they accumulate
a dense granular material, the lipofuscin. B-C: The dendrites
begin to degenerate disrupting connections with other neurons.
C- The neuron is practically near death (Alzheimer’s).
appears up to three-fold higher in brain samples from Alzheimer’s patients
and is substantially increased in very old patients without any clinically
detectable disease. The number of mitochondria reflects the energy
demand of the cell type, such as in the liver containing about 2000-4000
mitochondria, since higher ATP energy is necessary. Did you know that a
healthy person produces from 40kg to 65 kg ATP per day on average?
Therefore mitochondria have a Herculean task to fulfill as the most
efficient production sites for the cell’s current ATP. The reason is that ATP
energy is not stored, but only approximately 85 gr. accumulates
permanently in the form of ATP molecules, offering the organism a quick 5
to 8-second release in the caloric form. One example is seen in cardiac
tissue. Mitochondria turnover produces each time, 700mg of ATP that lasts

11. for 10 seconds or about 10 heartbeats. 86,000 beats/day = 6 million mg.
ATP is utilized daily. Now myocardial ATP turns over 10,000 times/day so
imagine how the mitochondria need to constantly produce energy. Heart
muscle cells contain from 5000 to 8000 mitochondria to power heart
pumping while the kidney has the second highest mitochondrial content
after the heart and also requires high levels of SOD due to a higher
superoxide radical production. Do we think about it?! Thus the importance
of Coenzyme Q10, an electron carrier, is necessary to stimulate the
respiratory chain. We will discuss the process further in part II. The
increasing number of deaths from heart failure in middle age and younger
could be very well associated with mitochondria ATP collapse (23). Now
as explained before a person can inherit a mutation with no disease and
accumulate a somatic mutation that in such person will accelerate aging.
For instance in Alzheimer's disease somatic mutation and inherited
mutation when compared to healthy tissue accumulated long before the
disease is diagnosed. About one out of 200 women carry a mitochondrial
mutation which can drive the child to earlier degenerative disease and
heart failure as we assist now with juveniles in various countries including
Portugal and the US. In our Society, about 35% to 50% of people over 35
years show early dysfunction in ATP production. They already start to age
with no disease yet. At age 67 you have twice as less mitochondria than at
40 years of age. Much less ATP energy is produced. During our lifetime,
our normal capacity to synthesize ATP energy decreases by about 8% per
decade. (24) Our body produces more free radicals from stress or oxygen
itself than oxidized lipids and proteins found in cells. With age, the body
produces more free radicals from oxygen alone. For instance, in a healthy
individual, 20% of oxygen inhaled produces free radicals, while in an
elderly unhealthy person, 80% of oxygen inspiration forms free radicals.
Definitively the link between mitochondrial dysfunction and age-related
diseases is well-established with Alzheimer's disease. (25)
Aging and Alzheimer's is also Determined by the Damage We Acquire
from our Mother
It is interesting to point out what I have been documenting for many years
in my practice, noting that in the same family several members may suffer
from the same pathology such as diabetes and obesity, including the
mother and grandmother. The 40-year-old female patient I saw looked

12. already like a 55-year-old woman, especially from the skeleton. Now her
daughters, respectively 19 years and 15 years follow the same path with
diabetes and obesity. According to Roy Wolford a well know biologist,
diabetic patients reflect an aging pattern that is 15 to 20 years ahead of
their chronological age, which here is the case for the mother and the two
daughters. Remember mitochondria pass only from the mother to her child
and if her girl will be the same in the future for her children. Another
interesting fact is the excessive oxidative stress condition of the mother
and the two daughters from the results I obtained with the observation of
the Oxidative Dried Blood Test. (26) It confirmed the decreasing
antioxidant enzymatic defense in diabetic patients or other patients such as
ones with Alzheimer's disease since the test usually shows with this
particular patients at stage 3 (See my book, “Cancer Treatment
Breakthrough”, pages 34-35) but I do manage to decrease it with dietary
supplementation and some molecular antioxidant compound having a
SOD-like activity, quickly absorbed by the body for immediate healing.
Therefore, aging can start already in the embryo. In fact, the number of
mitochondria we have in cells is highly associated as explained, with
inherited mitochondria from our mother including mtDNA mutation.
Oocytes contain from 100,000 to 600,000 mitochondria while only 10 in a
germinal cell and 1000 in the blastocysts. The embryo requires an
enormous supply of energy to develop an abnormal functioning of oocyte
mitochondria leading to a decrease in oxphos can cause abnormal embryo
development in humans.
The Brain and Alzheimer’s
I mentioned that aging can start in the embryo and why not Alzheimer's
disease as well? Speaking again about oxidative stress and free radicals we
need a stable balance between the pro-oxidant and the antioxidant to
prevent excessive free radical activity and damage done to our
mitochondria. Oxidative damage contributes to the degradation of neurons
as it has been supported by numerous studies in experimental animals, For
instance, as they age, cells tend to accumulate material not found in
younger cells. As an example, excessive ROS activity in the brain neurons
contributes to the formation of an abnormal material or toxic waste known
as lipofuscin-meaning dark fat in Greek and Latin that appears to be the
by-product from the oxidation of unsaturated fatty acid from damaged

13. neuron membranes or damage to the mitochondria. Lipofuscin is made of
cross-bound oxidized proteins (30%) and oxidized lipid degradation
products (50%) formed from lipid peroxidation and other oxidative
damage, being considered a Hallmark of Aging. (27) By middle age the
brain is already overloaded with a large amount of this insoluble material
Figure 5: Mean Lipofuscin Content in Nerve Cells
or toxic waste that seems to be the end result of the cell’s capacity to
eliminate this waste. A major constituent of lipofuscin is malondiadehyde
(MDA) which is often used as a marker of lipid peroxidation. As we age
mitochondria progressively lose the capacity to eliminate MDA. In
experiments done with rats, at 24 months of age, their capacity was
reduced by 40 % to eliminate MDA compared to the level of 6-month-old
rat Lipofuscin that accumulates in neurodegenerative diseases including
Alzheimer’s disease, dementia, and Parkinson's disease. (28) However,
lipofuscin may also contain other materials such as heavy metals including
mercury, aluminum, iron, copper, zinc, etc... Several studies have related
elevated aluminum concentration in drinking water as well as
environmental aluminum increasing the incidence of AD in rats

14. and human. (29) With no surprise Alzheimer’s patients exhibit four to six
times more aluminum deposits in the brain tissue than a normal person. In
humans, lipofuscin may accumulate in neurons up to 80 percent of the
cellular volume before killing it. The bad news is when the pigment of
lipofuscin accumulates in the apex of the nerve cell communication, a
process leading to a gradual deterioration of brain function, blocking the
flow of vital nutrients, and may eventually destroy all. As consequence, the
dendrites begin to degenerate disrupting connections with other neurons
and mental function starts to deteriorate. This is what happens with
Alzheimer's disease. (see the figure) What is more tragic is the fact that
today lipofuscin pigment may appear very early in life, even in even in
children. Some research has observed lipofuscin in fetal nerve cells and as
bad new offspring’s aging process can start already in the embryo and
immediately at birth. Consequently, our interest is to focus on the various
factors associated with the physical and neurological degradation leading
to premature aging and age-related disease as Alzheimer's. It includes
environmental pollution, electromagnetic pollution, lifestyle, exercise,
meditation, and especially dietary style. Thus several potential targets that
have effects on mitochondria and brain mitochondria, eliminate toxins,
reducing MDA levels for prolonging health and lifespan will be discussed
in part 2 of the article.
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17. The Author – Professor Serge Jurasunas
Serge Jurasunas is an internationally well-known practitioner and
researcher in complementary oncology and molecular medicine, besides
being a naturopath and a fervent believer in nutrition and detox since he
met with Dr. Bernard Jensen in 1962. Member of the New York Academy
of Science Serge Jurasunas is a former professor at Capital University of
Integrative Medicine in Washington D.C. and has devoted over five
decades to treating all kinds of diseases and cancers of all types and
grades. He is the author of 8 books including Cancer Treatment
Breakthrough. Immuno-Oncology using Rice Bran Arabinoxylan
compounds. He has a large blog with many stories, articles include in
Slideshare. Serge Jurasunas is a frequent contributor to Townsend Letter
since 1999 and maintains a private part-time practice only for cancer
patients.
Contact information: sergejurasunas@gmail.com

18. Blog: Https://naturopathiconcology.blogspot.com
Slideshare. Https://www.slideshare.net/sheldonstein