Biological Aging vs. Chronological Aging: How to Build a Healthy Longevity – An Important Role for the Mitochondria, Part I

Professor Serge Jurasunas, MD(hc), ND, MD(Hom)


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 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 and lifestyle in the process of healthy longevity. 

Over the past five 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.

Even taking some supplements when feeling bad changed their life. This week a regular patient came in for a consultation, a 71-year-old woman, very good looking for her age; she was 23 years old when she first came to me, some 48 years ago, and she remains healthy.

I also observed how individuals aged prematurely and changed their physical morphology, complaining of cognitive disorders long before their chronological age, including patients 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  

In 1969, 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 2). 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 cancer4 but largely implicated in the origin of early aging and neurodegenerative disease such as Alzheimer’s.5,6 For the past three 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.


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 the US, which is supposed to be at the leading edge of science and medicine, statistics have shown that 86 percent of Americans suffer from some degenerative diseases. 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 no better in retirement homes.

Alzheimer’s disease (AD) affects approximately 5.5 million people in the US and is projected to grow to 11 to 16 million by 2030. Sixty-five percent 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 so 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; breakdown in muscle mass, skeleton, and blood vessels; excessive free radicals activity that damages brain neurons; gradual decline of the senses (eg, hearing, vision); wrinkling in the skin; deterioration of 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. Norman W. Walker, DSc, a well-known nutritional researcher of aging in the US and author of the book Become Younger.

More recently in Portugal, a well-known medical doctor, Manuel Pinto Coelho, published a book about how to age young and healthy; to my surprise he explained how auto-intoxication of the colon is a source of disease and early aging. In fact, it matches my auto-intoxication theory that I explained in my book, Health and Disease Begin in the Colon, first published in 2009, 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, which need to be detoxified through food diet and colon hydrotherapy. I always do this in my practice, but I always give great importance to mitochondria function related to disease, fatigue, heart failure cancer, and premature aging,

Now scientists note that mitochondria dysfunction is one of the major causes 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 study published by the team of Elissa S. Epel of the University of California measured the length of telomeres in healthy females, aged between 20 and 50 years, under strong psychological stress. Women with the highest levels of oxidative stress have shorter telomeres 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: the aging process itself and the production of excessive free radicals, environmental factors, and genetic dysfunction.

Environmental factors include insecticides, herbicides, pharmaceuticals, radiation, etc. Pesticides are one of the main damaging factors to mitochondria. Paraquat is one example since it has been shown to 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, antidepressants, NSAIDs (eg, 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. 

By genetic dysfunction I mean that mutation of mitochondrial DNA (mtDNA) 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 0.5-20 μm in length, either filamentous or oval, and are bounded by a double membrane. They are found in all aerobic (eukaryotic) 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 became poisonous to anaerobic life. Some species died, while others penetrated the host cell and became symbiotic, intracellular parasites that evolved, adapted, and developed some systems to use oxygen as fuel to burn foodstuff and generate high-energy molecules such as ATP.

ATP is critically important for the cellular process, transport signal transduction, 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 (reactive oxygen species). The mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) acts as the chief ROS scavenger enzyme and is sometimes known as the Guardian of the Powerhouses.

Animals with the longest lifespans, such as man, have the highest levels of SOD (superoxide dismutase) 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, being the first line of antioxidant defense to detoxify the first free radicals generated in our body. These superoxide radicals can be damaging by themselves, if not converted, and contribute to the production of other ROS such as the destructive hydroxyl radical associated with degenerative diseases.10,11

Mitochondria are the major source of superoxide radicals—mainly in complexes I, and II followed by complex III—that are 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 life12 and to increase the lifespan of species.13 Mice lacking MnSOD die shortly after birth indicating its crucial role in maintaining 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 free radicals. As explained, a decline in MnSOD is associated with aging since logically the decline increases the production of reactive oxygen species and correlates with mitochondria oxidative damage and mtDNA mutation.14 

Another example of the MnSOD’s importance is the study done by E.M. Gregory and I. Fridovitch. They 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 

Mitochondria have their own DNA and ribosomes. They can make their own proteins, exactly 13 proteins are 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 that occur in cellular respiration. Mitochondria 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 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, 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 electron transfer due to overproduction of ROS was reported to cause accelerated aging that affects organs using high levels of energy demand such as the brain, the heart, and the skeletal muscle.16,17 Decline of mitochondria function together with the decline of antioxidant enzyme levels and ATP production may be responsible for several disorders or serious clinical features such 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

Damaged mitochondria produce more ROS and thus accelerate more toxic ROS, such as hydroxyl radical and peroxynitrite 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 accounts for only 2% of body weight. Inevitably neurons are a main source of free radicals and more vulnerable to the damaging ROS effects on mtDNA, inducing mutations associated with aging.21,22 For instance, damaged mtDNA 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 daily the equivalent of 40 kg of ATP23 while it is also said that the human body can recycle its own weight equivalent of ATP each day.  According to Chris Shubert, a professor and researcher at Harvard, an average human of 70 kg consumes approximately 69 kg of ATP per day, which equals nearly the amount of his or her weight (See online: The Fuel of life by Chris Shubert). 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, 700 mg of ATP that lasts 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 that 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.24  

Now as explained before a person can inherit a mutation with no disease and accumulate a somatic mutation that will accelerate aging. For instance in Alzheimer’s disease, somatic mutation and inherited mutation when compared to healthy tissue accumulate long before the disease is diagnosed. About one out of 200 women carry a mitochondrial mutation that 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 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.25

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.26  


Aging and Alzheimer’s Is Also Determined by the Damage We Acquire from Our Mothers

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. As an example, a 40-year-old female patient I saw already looked like a 55-year-old woman, especially seeing her skeleton. Then her daughters, respectively 19 years and 15 years that I had examined, also had a poor physical condition. They were following the same path with diabetes and obesity. According to Roy Wolford, a well-known biologist, diabetic patients reflect an aging pattern that is 15 to 20 years ahead of their chronological age, which here was exactly the same the case for the mother and two daughters. Remember mitochondria pass only from the mother to her child and, if a 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.27It 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 these particular patients at stage 3 (See my book, Cancer Treatment Breakthrough, pages 34-37); 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, and 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 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.28 By middle age the brain is already overloaded with a large amount of this insoluble material 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 rats. Lipofuscin accumulates in neurodegenerative diseases, including Alzheimer’s disease, dementia, and Parkinson’s disease.29  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 and humans.30 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. Consequently, 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 5).

What is more tragic is the fact that today lipofuscin pigment may appear very early in life, even in children. Some research has observed lipofuscin in fetal nerve cells, and a new offspring’s aging process can start already in the embryo and immediately at birth. Therefore, our interest is to focus on the various factors associated with the physical and neurological degradation leading to premature aging and age-related disease such 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, and reduce MDA levels in order to prolong health and lifespan will be discussed in Part 2 of the article (see March 11, 2023 e-Letter).


References

  1. Serge Jurasunas. Biological Aging-Signs in the Iris. Explore. Volume 13, Nov 6.2004.
  2. Serge Jurasunas. The Clinical Evidence of Cellular Respiration to Target Cancer. Townsend Letter. Aug\Sept 2012.
  3. Serge Jurasunas. Mitochondria and Cancer. Townsend Letter. August/Sept 2007.
  4. J.S Modica-Napolitno and KK Singh. Mitochondrial dysfunction in cancer. Mitochondrion. Vol4. N.56 pp 755-762. 2004.
  5. Hirai K, Aliev G, Nunomura A, et al. Mitochondrial Abnormalities in Alzheimer’s disease. Journal of NeuroScience. 2001-21 (4) 3017-3023.
  6. Lunnon K, Keohane A, et al. Mitochondrial genes are altered in blood early in Alzheimer’s disease. Neurobiol Aging. 2017.53, 36-47.
  7. Cheryl Buxberry. Aging and the Threshold of disease. University of Waterloo. CA. Course Notes Biology and Human Aging.
  8. Elissa Epel, Elizabeth H, Blackburn, Jue Lin, et al. Accelerated Telomere shortening in response to life stress. Biological Sciences. Dec 1. 2004; 1001 (49): 17312-17315.
  9. Prof Dr Nils, Goran Larsson.  A mother’s genes influence her child’s aging. Max Plank Institute for Biology of Aging (Germany) August 212013.
  10. Li Y, Huang TT, Carlson EJ, Wallace DC, Epstein CJ. Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase. Nat Genet.1995. (11)376-381.
  11. Fridovitch I. Superoxide radical and superoxide dismutase. Ann Rev Biochem. 1995;64:97-118.
  12. Carlioz A, Touati D. Isolation of superoxide dismutase mutants in Escherichia Coli is superoxide dismutase necessary for aerobic life? EMBO journal. 1986.5. 623-630.
  13. J Sun. D Folk. TS Bradley and J Tower. Induced overexpression of mitochondrial Mn superoxide dismutase extends the life span of adult drosophila melanogaster. Genetics. Vol 161. N2. Pp 661-672.
  14. Yau-Huel Wel. Hsin Chen Lee. Oxidative stress, Mitochondrial DNA mutation, and impairment of antioxidant enzymes in Aging. Experimental Biology and Medicine. Volume 227. issue 9. Oct.2002.
  15. Gregory EM, Fridovitch I. Oxygen toxicity and the superoxide dismutase. Journal Bacterial. 1973; 14. (3): 1193-1197.
  16. KR, Short, MI, Bigelow J, Kahl, et al.   Decline in skeletal muscle mitochondrial function with aging in human. Proceedings of the National Academy of Sciences of the United States of America. 2005;Vol 12. n15:pp 5618-5623.
  17. G Barja and A Herroro. Oxidative damage to mitochondrial DNA is inversely related to the maximum life span in the heart and brain of mammals. FASEB Journal, 2000; Vol 4. N2: pp 312-318.
  18. Linnane AW, Marzikis, Ozawa T, Tonaka M. Mitochondrial DNA mutations as an important contributor to aging and degenerative disease. Lancet. 1989;1:642-645.
  19. Ian R, lanza and K Sreekumaran Nair. Mitochondrial function as a determinant of life span. Pfluger Arch. 2010. 459. (2) 277-284.
  20. Adelman R, Saul RI and Ames B.N. Oxidative damage to DNArelation to species metabolic rate and life span. Pro Natl Acad Sci. USA. 1988;85:2706-2708.
  21. Bua E, Johson J. Herlist A, and Aiken JM, Mitochondrial DNA deletion, mutations accumulate intra-cellularly to detrimental levels in aged human skeletal muscle fibers. Am. J Hum Genet. 2006;79:469-480.
  22. Alexeyev, MF. Is there more to aging than mitochondria DNA and reactive oxygen species. FEBS Journal. 2009; 276: 5768-5787.
  23. Sudina Bhuju, Nita Thapa and Histesh Kumar Bhattaral. ATP synthase.Structure, Function and Inhibition. Journal of Biomolecular Concepts. March 7, 2019
  24. Lesnefsky EJ, Moghaddas S, Tandler B, Kerner J, Hoppel CL. Mitochondrial dysfunction in cardiac ischemia, reperfusion, aging, and heart failure. Journal of Molecular and Cellular cardiology. June 2001;33 (6):1065-1089.
  25. Short KR, Bigelow ML, Kahl J, Raghavakaimal S, Nair KS. Decline in skeletal muscle mitochondrial function with aging, Proc. Natl Acad. Sci. USA. 2005;102:5618-5623.
  26. LunnanK, Kdohan A, et al. Mitochondrial genes are altered in blood early in Alzheimer’s disease. Neurobiol Aging. 2017.53. 36-47.
  27. Serge Jurasunas. The Oxidative Dried Blood Test in the Assessment of Metabolic dysfunction and inflammatory conditions. Townsend Letter. June 2018: 28-33.
  28. Brunk UT, Therman A. Lipofuscin mechanism of age-related accumulation and influence cell function, Free Radic. Biol Med. 2002; 33: 611-619.
  29. Lipofuscin hypothesis of Alzheimer’s Disease, Dementia, and Genetic Disorder. Extra. Sept 2011.
  30. Virginie Rondeau, Daniel Commenges, Helene Jacquim, Gadda Jean, Francois Dartignes. Relation between aluminum concentration in drinking water and Alzheimer’s Disease – An 8 years follow up study. American Journal of Epidemiology. July 2000;Vol 152. issue 1: 59-6


About the Author

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 his meeting with Dr. Bernard Jensen in 1962. A 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 eight books, including Cancer Treatment Breakthrough: Immuno-Oncology Using Rice Bran Arabinoxylan Compounds. He has a large blog with many stories and articles/presentations on Slideshare. Serge Jurasunas has been a frequent contributor to Townsend Letter since 1999 and maintains a private part-time practice only for cancer patients.

Contact information: sergejurasunas@gmail.com