Cancer and Yoga

This document will be divided into parts.

First about cancer, its causes and what to watch out for.
This section will be divided into easy and moderate level of understanding.
Then we will get into how yoga can contribute to help the body heal itself and prevent it.

Easy Level

Why did cancer start?

Anaerobic metabolism, mitochondria became tired and became dysfunctional

Functional apoxia, mitochondria stops using oxygen (effectively).

Cancer cell, once emerge into this act (theater) no longer tolerates oxygen to the point where it dies
if the milieu is restored (Otto Warburg effect 1931).

To starve the cancer cell, removal of food source is necessary. Cancer cell “eat” exclusively glucose
and glutamine. Hence, important to remove all carbs to prevent feeding the cancer cell.

95 % of the time when cancer comes back, it comes back stronger and more aggressive. Chemo
kills the weakest cell, the most tenacious one become even stronger after chemo.

Statistic of chemo in case of prostate cancer (which is the one with the most efficiency): 48 %
success rate, follow up after 5 years.
30 – 40 % in Infant Leukemia

Info on survival rate after 5 years with chemo

When a man's knowledge is not in order, the more of it he has the greater will be his confusion.
- Herbert Spencer

Current model of medicine is inadequate for treatment of cancer due to over-abundance of

unstructured knowledge (no pragmatic, concise, universally agreed methodology which works)

Most of the time patient dies, in rare case of “cure”, it is more accurate to call remission.
5 years without cancer is considered “cured” of the cancer in many places. The statistics end at the
end of those five years and if the person who had the cancer gets it after 7 years of remission, it is
consider (in statistics) a new cancer even if same source/cancer.

3 stages of cancer which covers the arch type of how the cancer goes about in the body. They are in
other as:

Division

Invasion

Migration

GcMAF – Dr. Nobuto Yamamoto

If High, does not matter if cancer cell present, it deals with them

6000 – 12000 cancer cell per day, what kills them among many thing is GcMAF
It is a protein activator of macrophages, which protects against cancer
420 amino acids - threonine

Gc-Protein (Vitamin D3 Binding protein)

Vitamin D3 50- 80 ng per ml in patient with cancer to keep GcMAF in body high

Without the N sugar of GcMAF stops being a macrophages activator, there is a weakening/decrease
in the efficiency of the immune system.

This can happen if Nagalase is high. A substance secreted by cancer cell to block the Gc-protein to
turn in GcMAF

Google Scholar : More than 660 articles on the subject of GcMAF

Immuno therapy against cancer thanks to the GcMAF

Also used in autism, HIV and of course cancer

What causes cancer: 3 causes

Dis-nutrition, Intoxication, emotional conflict

2 years prior to the cancer which strong emotional event happen in your life?

In order to manifest (cancer) it requires at least 2 of the 3 components above. Most of the time, all 3
are present.

The therapeutic approach to all cancer must be multi-factorial, hence why many things must be
taken into consideration to heal.

99.99% of mutation in the body do not cause cancer.

Cancer is a cytoplasmatic disease!
It is not a nuclear disease.
Why? Because the mitochondria is in the cytoplasm,

Virus and Cancer

The virus below are know to cause cancer in some cases.
Epstein-Barr Virus (EBV) - Burkitt's lymphoma
Hepatitis B Virus (HBV) - Liver Cancer
Hepatitis C Virus (HCV) - Liver Cancer
Human Papillomavirus (HPV)
(KSHV) - Kaposi's Sarcoma
Human T-cell Lymphotropic Virus 1 (HTLV)
Cancer causing infections, such as hepatitis and human papilloma virus (HPV), are responsible for
up to 25% of cancer cases in low- and middle-income countries. (3)
Chemo has no effect in these case since if virus still not killed.
The above leads to mitochondria dysfunction, which leads to oncogenes, which lead to a
suppression of suppressor genes.

Oncogenes are like accelerator in a car, suppressor genes is the break. If you don’t press on the
break, collision occurs. They (oncogenes) are present in the body but not engage by default
(genetically), it is due to the mitochondria dysfunction.

Of course, epigenetic variation can occurs and you can have by hereditary.
BRCA1 and BRCA2 are example of such. They compose 5 – 8% of all women who have cancer.
Those who have the genes above have 8 times more likely to develop breast cancer compare to
those who do not.

============================

Moderate Level

You have cancer!

This phrase is repeated 4549 times per day in the States.
1,660,290 new cases in the US in 2014
Brazil: 580,000 new case in 2014

There are over 200 different types of cancer that may be found in the human body.

Causes Cancer

5 – 10% genetic
15% Virus
75 – 80% Lifestyle/Environment

Des-nutrition, Intoxication, emotional conflict leads to dysfunctional mitochondria. Which in turns

lead to genetic mutation (epigenetic)

HIF1A - Hypoxia-inducible factors 1 alpha – HIF-1 is over expressed in many human cancers.[52]
[53] HIF-1 over-expression is heavily implicated in promoting tumor growth and metastasis through
its role in initiating angiogenesis and regulating cellular metabolism to overcome hypoxia.[54]
Hypoxia promotes apoptosis in both normal and tumor cells.[55] However, hypoxic conditions in
tumor microenvironment especially, along with accumulation of genetic alternations often
contribute to HIF-1 over-expression.[10]

Significant HIF-1 expression has been noted in most solid tumors studied, which include cancers of
the colon, breast, pancreas, kidneys, prostate, ovary, brain, and bladder.[56][57] Clinically, elevated
Hif-1a levels in a number of cancers, including cervical cancer, non-small-cell lung carcinoma,
breast cancer (LV-positive and negative), oligodendroglioma, oropharyngeal cancer, ovarian cancer,
endometrial cancer, esophageal cancer, head and neck cancer, and stomach cancer, have been
associated with aggressive tumor progression, and thus has been implicated as a predictive and
prognostic marker for resistance to radiation treatment, chemotherapy, and increased mortality.[23]
[58][59][60][61][62][63]

Virus and Cancer in More Depth

Viruses can disrupt cell behavior in several different ways.

They can directly cause DNA damage (mutations) by inserting their genomes into the DNA
of the host cell. The integration can disrupt important regulatory genes.

The viruses may contain their own genes that disrupt the regulation of the cell. This process
may be beneficial to the virus if it allows for rapid production of progeny but can be seriously
detrimental to the host.

Some viruses actually carry altered versions of genes that they have picked up from previous
host cells. These altered genes no longer function properly, and when they are inserted into a new
host cell, they cause disregulation and can lead to cancerous growth.

Through their mutagenic activity or their effects on cell behavior, viruses play a significant role in
the development of particular cancers in many different animals, including humans.
Viruses have also been a major target of scientific investigation with respect to cancer. Some of the
earliest work on the identification of oncogenes and tumor suppressors utilized viruses. (1)

Epstein-Barr Virus (EBV) - Burkitt's lymphoma

Associated Cancer: Lymphoproliferative disease, most commonly Burkitt's Lymphoma. There is
increasing evidence EBV is also associated with Hodgkin lymphoma.

Prevalence: It's estimated that more than 90% of the World population is infected with EBV. EBV is
responsible for infectious mononucleosis (the 'kissing disease')

Transmission: Mechanism of transmission generally unknown, possibly through saliva.

Infection: EBV Infection usually begins in the epithelial cells of the oropharynx, posterior
nasopharynx and parathyroid glands. From there EBV infects B cells and persistent infection is
established. Almost all cases of EBV infection are controlled by the immune system and infected
individuals are asymptomatic (have no symptoms of infection).

Carcinogenic Potential: B cell Infection is necessary for EBV mediated carcinogenesis. Only a
small percentage of infections lead to cancer, most cases arising in immunocompromised or
transplanted individuals. These patients are especially susceptible because they lack sufficient
immune function to inhibit the growth of infected B cells. EBV-mediated carcinogenesis is most
likely caused by the actions of viral gene products. Two proteins in particular are thought to play a
major role in B cell immortalization; latent membrane proteins (LMP's) and EBV nuclear antigen
(EBNA's). LMP1 is inserted into the host cell membrane and acts as an activated growth factor
receptor, resulting in unregulated growth. EBNA's affect the cell in many different ways; one
pathway leads to altered activity of tumor suppressors including Rb, p53, and Arf.

Hepatitis B Virus (HBV) - Liver Cancer

Associated Cancer: Human Hepatocellular Carcinoma (HCC)
Prevalence: HBV is prevalent on every continent, but is especially high in sub-Saharan Africa and
Southeast Asia. It is estimated that over 400 million people worldwide are infected.
Transmission: HBV is transmitted via contact with contaminated blood, sweat, or tears. It can also
be spread through sexual contact and from mother to child.
Infection: HBV Infection occurs mainly in the liver, but viral antigens can be detected in the blood
throughout the body. Chronic Infection is indicated by the presence of viral antigens in the blood for
longer than 6 months. Chronic Infection can lead to cirrhosis of the liver and development of HCC.
Carcinogenic Potential: Hepatitis viruses (B and C) are responsible for 70-85% of primary liver
cancers. Viral integration into the host genome is regularly found in chronic liver infection and
cancer. This suggests it plays an important role in carcinogenesis. HBV encodes a protein (HBX)
that may promote cell proliferation and interfere with DNA repair. HBV mediated carcinogenesis is
likely due to a number of factors; the oncogenic properties of HBX, chronic liver damage, chronic
inflammation, and the continuous tissue regeneration needed to maintain the liver during an
infection.

Hepatitis C Virus (HCV) - Liver Cancer

Associated Cancer: Human Hepatocellular Carcinoma (HCC)
Prevalence: HCV is prevalent on every continent, but it is especially high in sub-Saharan Africa and
Southeast Asia. It's estimated over 170 million people are infected with HCV worldwide.
Transmission: HCV is transmitted primarily through blood-blood contact.
Infection: HCV Infection occurs mainly in the liver and produces a more severe inflammation than
HBV. Over 80% of those infected with HCV will develop cirrhosis of the liver or HCC.
Carcinogenic Potential: Hepatitis B and C are responsible for 70-85% of primary liver cancers.
HCV is not known to integrate into the host genome. In vitro HCV has been shown to affect a wide
range of cellular mechanisms that may promote carcinogenesis, but these have not been reproduced
in vivo. The carcinogenic potential of HCV lies in its ability to cause chronic immune response-
mediated hepatic damage, inflammation, and tissue regeneration.

Human Papillomavirus (HPV) - Cervical Cancer, Anal, Oral, Pharyngeal, and Penile Cancers
What is the Human Papillomavirus (HPV)?
There are over 200 known genetically different strains of human papillomavirus. Some strains of
the virus are responsible for common warts and plantar warts (warts on the bottom of the feet).
Other strains can infect the inner lining of the cervix; these strains are divided into low risk and high
risk strains. The high risk strains are those strongly associated with cervical cancer. Two high risk
strains, 16 and 18, are thought to be responsible for over 70% of cervical cancer cases. Low risk
strains 6 and 11 are responsible for a large percentage of genital warts.8

Other than the appearance of genital warts, infection with the human papillomavirus is
asymptomatic (doesn't have symptoms). In most cases HPV doesn't cause any problems and is
cleared by the immune system.9

Prevalence
A 2007 study in United States found approximately 26.8% of all women examined (aged 14-59)
were infected with the human papillomavirus. It is important to note that most HPV infections are
cleared within two years (i.e. most infections are not lifelong).10

14-19 ~ 24.5%
20-24 ~ 44.8%
25-29 ~ 27.4%
30-39 ~ 27.5%
40-49 ~ 25.2%
50-59 ~ 19.6%

Transmission
The human papillomavirus is transmitted via skin-skin contact. Sexual intercourse is not necessary
for transmission, but is the most common route. The virus can infect the genital, anal, and oral
regions of the body. Infection occurs when viruses enter into small breaks in the skin or mucous
membranes. The probability of acquiring HPV from a single sexual encounter is not known, but is
probably high.11

HPV and Genital Warts

Some types of HPV can cause warts on or around the genitals or the anus. The two types that cause
most cases of genital warts are 6 and 11. These are low-risk strains and are not associated with
cervical cancer.

HPV and Cervical Cancer

The human papillomavirus is the primary risk factor for cervical cancer. It is responsible for at least
90% of cases. High risk HPV type 16 is the most common high-risk type and is found in over 50%
of cervical cancers. The second most common high-risk type is 18 and it is responsible for 10-12%
of cervical cancers. Although HPV responsible for virtually all cases of cervical cancer, 80% of
women clear an infection within 1-2 years.

There are 3 steps necessary for cervical cancer development:12

 HPV Infection. HPV infection is quite common; a recent study estimates over 26% of women in
the United States are infected.
HPV Persistence. Less common. In most women (~80%), HPV infections are cleared or
suppressed by the immune system within 1-2 years of exposure. Therefore, most cases of HPV
infection do NOT cause cervical cancer. If HPV infection is not cleared and persists for a long
period of time a condition called cervical intraepithelial neoplasia (CIN) can develop. See below for
more about cervical intraepithelial neoplasia.
Cell Transformation and Invasion. Rare in comparison to the number of women infected by HPV.
Invasion usually occurs after a long period of infection. It is thought that severe dysplasia does not
occur without certain co-factors. (e.g. Smoking, HIV co-infection, Immunosuppression)

HPV and Other Types of Cancer

It is well known that HPV is a direct cause of cervical cancer, but its role in cancer may be much
larger. Recently, studies have strongly linked HPV with cancers of the vulva, penis, anal canal, and
head-and-neck.13

73% of oral cavity tumors tested positive for HPV-16 DNA.14

80% of anal cancers positive for either HPV-16 or 18 DNA.

In 2012, a population (epidemiologic) study showed an association between HPV subtypes that
infect skin (called cutaneous infections) and the development of squamous cell skin cancer (SCC).
The role of the virus in the development of the disease is not yet clear.15

(KSHV) - Kaposi's Sarcoma

Associated Cancer: HHV8 primarily causes Kaposi's Sarcoma (KS), a type of cancer that affects the
skin and soft organs. HHV8 is also associated with several blood disorders.

Prevalence: HHV8 is uncommon in most of the world, only 1-5% of people in North America and
Northern Europe are infected. Mediterranean populations have a higher infection rate (5-20%) and
Sub-Saharan Africa has the highest rate (>60%). In the U.S., gay men also have a higher infection
rate (~40%).

Transmission: HHV8 is most commonly spread through sexual contact and via saliva. Transmission
also may occur via organ transplantation or blood transfusion.
Infection: HHV8 infects B cells, epithelial cells, endothelial cells and possibly monocytes. HHV8
infection is high in populations with high incidence of KS and low in populations with low
incidence of KS.

Carcinogenic Potential: HHV8 DNA is found in all cases of KS, but infection is not enough to cause
cancer. The exact method by which HH8V induces cancer is still under investigation. KS probably
starts as an inflammatory process to which circulating cells (including HHV8 infected cells) are
recruited, leading to further inflammation, tissue damage, and viral infection. HHV8 then
establishes a persistent infection which may send signals promoting angiogenesis and inflammation.
This cycle may ultimately lead to tumor development. Untreated AIDS confers a 20,000 fold higher
risk of developing KS, but other than immunosuppression the role of AIDS is generally unknown.

Human T-cell Lymphotropic Virus 1 (HTLV)

Associated Cancer: Adult T-cell Leukemia (ATLL)

Prevalence: Approximately 10 to 20 million people are infected worldwide. HTLV-1 is endemic in

southwest Japan, in and around the Caribbean islands, in parts of Central Africa and South America.
Transmission: HTLV1 can be transmitted via sexual or blood-blood contact. It can also be passed
through breast milk and from mother to fetus.

Infection: HTLV-1 is an RNA virus (a retrovirus) that can infect T-cells, B-lymphocytes, monocytes,
and fibroblasts.

Carcinogenic Potential: About 3-5% of people with HTLV1 will develop adult T-cell leukemia, with
most cases occurring in middle aged people. At least one of HTLV1's regulatory proteins, (Tax), is
thought to be involved with ATLL development. Tax may contribute to carcinogenesis by inducing
cellular proliferation, activating cell survival proteins, and also may contribute to chromosomal
instability.2021

Several other retroviruses are also associated with cancer and the use of retroviral vectors in cancer
treatment has to take into consideration the possibility that the treatments could cause major
problems.2223

PISCHINGER SYSTEM

According to the conference, lungs, liver and kidneys lose his filtering capacity in consequence
of the current way of life. Then waste cellular accumulates in the ECM in acid form, diminishing
the cellular nutrition and producing diseases. This process is known as Pischinger system. Cells to
defend itself use three strategies
Anacostia River Washington, D.C. (2015 pic)
The city recently announced that they plan to make the putrid Anacostia River swimmable by
2022,
Over 50% of the fish in this river have hepatic tumors

What is the use of treating the tumor, if you put the fish back into this river?

The same thing applies to humans, if you merely treat the tumor and the person returns to his daily
lifestyle of eating badly, drinking, unresolved emotional issues, etc. A new tumor is bound to come
or return.

Excretion from the cell becomes food as well wont be entering

Thus detox is an essential part of remission of the cancer

The immortality of the cancer cell is due to the cell, after using all means available to keep
functioning, acquires anti-apoptotic mechanism and second, mutating and stimulating the
telomerase her (cancer) telomere no longer shrinks after cell division.

9 to 14 years to get 1 g of cancer (1 Billion cancer cells) (breast/prostate cancer average)

Misoneism: a hatred, fear, or intolerance of innovation or change (Most doctors are like that)

1/33 were to have cancer in 1910 vs 1/3 in 2010 (people over 75 old)

The ambient we live has changed.

A new born umbilical cord had over 100 chemical substance which does not belong to a child
currently.
Number of death per day have remained almost virtually the same in the past 30 years.

Other factors such as antibiotics, contribute to the development of some cancer as is the case of
breast cancer

Ketones, through ketogenic diet have a tremendous impact on cancer, Alzheimer, diabetes and
diabesity. The book bellow illustrates this well.
People who don’t like coconut oil can make use of MCT (Medium Chain Triglycerides) or Ghee
(sattvic)
With this brief information comes the end of causes and what to what out for in cancer. The next
section will be focus on yoga and what it can do for you both as a preventative and therapeutic
means of health in case of cancer.

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Yoga Contribution in Overall Health

Easy Level

Yogic practices in normal subjects lead to improvement in cardio-respiratory performance (increase

in overall oxygen intake),[6] lipid and carbohydrate metabolism[7] and psycho logic well being,[8]
through body-and-breath-control, including relaxation techniques.[1]

Regular yogic practices have shown profound improvement in thermoregulatory and psychological
functions such as mental performance, improvement of memory and creation of a sense of well
being (which in turn affects emotional aspects one one self).[8]

Intense stretching and muscle conditioning during yoga postures also improve oxidative capacity of
skeletal muscles, decrease glycogen utilization via oxidative enzymes and or increased number of
mitochondria.[1] As stated previously, cancer comes as a result of anaerobic metabolism after the
mitochondria became tired and became dysfunctional. Hence, it acts as preventative measure
against future cancer.
Pranayamas improves the ventilatory function of the lungs by using fullest capacity of lungs,
reducing the oxygen debt, improving the gaseous exchange and preventing exhaustion.[11] Slow
increase in the lung capacity associated with well practiced yoga breathing recruits the normally
unventilated lungs, thereby increasing oxygen delivery to muscles.

The slow breathing rates associated with yogic breathing also substantially reduce chemo reflex
response to hypoxia, probably through the improved oxygen delivery to tissues and possibly the
result of acquired “tolerance” to hypoxia that is produced by change in the chemo reflex
threshold[1].

Ray US (2001) also demonstrated improved aerobic capacity and decreased perceived exertion after
maximal exercise after practice of Hatha yogic exercise.[11]

Schell (1994) demonstrated significant difference in the personality inventory in the yoga group
showing markedly higher scores in life satisfaction, ability to cope up with stress and lower scores
in aggressiveness and emotional complaints.[14]

Moderate Level

Some terms:
Bohr effect: haemoglobin’s oxygen binding capacity is inversely related to carbon dioxide
concentrations, meaning that without CO2 oxygen cannot be released into tissues, as it cannot be
released from the haemoglobin molecule.
Haldane effect: deoxygenation of the blood increases its capacity for carbon dioxide.
Mitochondria: cellular organelle, often considered the “energy factory” / “power plant” of the cell.

When someone hyperventilates they breathe out large amounts of carbon dioxide and inhibit the
Bohr effect, paradoxically over breathing results in decreased cellular respiration, even though the
blood may be carrying significant quantities of oxygen.

This results in increased rates of glycolysis, an inefficient form of energy (ATP) production,
resulting in the formation of lactic acid, this further exacerbates the situation as lactic acid appears
to compete with carbon dioxide in the blood resulting in increased losses of carbon dioxide,
whereas carbon dioxide inhibits lactate production, some of these effects are likely mediated
through acid-base homeostasis (Cohen et al 1990).

This is in many respects the respiratory pathology that Otto Warburg noted as the defining feature
of cancer, aerobic glycolysis, the production of lactate in presence of oxygen.

This aerobic glycolysis is a fundamental respiratory defect, and occurs whenever the mitochondrial
oxidation of pyruvate is inhibited, and there are multiple agents capable of inhibiting this efficient
energy production, however they all appear to function in fairly common manner, that is they
stimulate inflammation, or cellular swelling and oedema. These agents include estrogen, histamine,
bacterial endotoxin, polyunsaturated fatty acids, serotonin, and lactate itself.
Anaerobic glycolysis occurring as a result of intense physical exertion is adaptive with those actions
of lactate that could be considered pathological in other circumstances acting to assist in the
organism’s adaptation to the stress, for example lactate’s stimulation of angiogenesis (Hunt et al
2008) can be seen as a functional signal assisting in bring increased blood to an area undergoing
adaptive growth, of course in other circumstances the signals involved, vascular endothelial
growth factor (VEGF), transforming growth factor beta (TGF beta), interleukin-1 (IL-1), and
hypoxia-inducible factor (hif-1alpha) are all associated with such pathological conditions as
cancer.

Many of the pranayamas used in hatha yoga share a common factor they work in some way to slow
and reduce standard unconscious breathing, for example nadi shodanna, alternates the breathing
between each nostril and whilst this may produce additional subtle effects it acts to reduce airway
size so slowing the rate at which air can be inhaled and exhaled, the gentle contraction of the base
of the throat used in Ujayi also serves to restrict airway size, breath retention in general will
obviously reduce breathing.

This hypoventilation will induce a mild hypercapnic condition (increased Carbon dioxide),
this increased carbon dioxide will improve oxygen delivery throughout the body, through the
Bohr effect as well as through carbon dioxide’s vasodilatory effects, stabilize nerve cells, decrease
inflammation through a number of mechanisms including stabilizing mast cells inhibiting histamine
and serotonin release.

Further if Ray Peat is correct potentially increasing mitochondria and hence increasing the
Generative Energy available to an individual, this increased metabolic energy is available both
physically and mentally, with greater energy available an individual is capable of a higher level of
function.

Emotional Dimension and Yoga

Cancer is a leading cause of death worldwide. The disease accounted for 7.4 million deaths (or
around 13% of all deaths worldwide) in 2004 [1]. Patients with cancer often have to deal with
severe side effects and psychological distress during cancer treatment, which have a substantial
impact on their quality of life (QOL) [2]. Among the most common symptoms of cancer and the
results of treatments for cancer are pain [3], depression [4], and fatigue [5]. These symptoms may
appear or persist, even after treatment ends.

In addition to physical symptoms, people with cancer nearly always experience considerable levels
of psychological distress. Psychological health in cancer patients is defined by the presence or
absence of distress as well as the presence or absence of positive wellbeing and psychological
growth. It is determined by the balance between two classes of factors: the stress and burden posed
by the cancer experience and the resources available for coping with this stress and burden [6].

Yoga, as a main component of the Mindfulness-Based Stress Reduction (MBSR) program [11], is a
combination of breathing techniques, physical postures, and meditation that have been practiced as
various styles of hatha yoga for over 5,000 years [12]. It has been used to lower blood pressure,
reduce stress, and improve coordination, flexibility, concentration, sleep, and digestion [13]. It has
also been used as a supplementary therapy for such diverse conditions as cancer [8], diabetes [14],
asthma [15], and AIDS [16].

Some studies have specifically demonstrated potential psychological benefits of yoga in various
clinical populations, including patients with depression [27–29], stress [30], and anxiety [31, 32].
Eight studies had at least one outcome measure for depression [17, 18, 20, 21, 23–26]. The outcome
measures used to assess depression in the cancer populations were Hospital Anxiety and Depression
Scale (HADS) [18, 21], Center for Epidemiologic Studies-Depression Scale (CES- D) [17, 20, 25],
Profile of Mood States (POMS) [23, 26], and Symptoms Checklist Revised (SCL-90-R) [24]. The
results showed significant improvements in the yoga groups ( ), and the standardized mean
difference was −0.95 (−1.55 to −0.36).

Three of the 10 studies measured QOL [17, 22, 23]. The 3 studies with outcome measurement data
for quality of life outcomes used different measures, including the Functional Assessment of Cancer
Therapy-Breast (FACT-B) [17], European Organization for Research and Treatment of Cancer
Quality of Life Questionnaire Version 3.0 (EORTC QLQ-C30) [23], and Functional Assessment of
Cancer Therapy: General (FACT-G) [22]. The quality of life of the yoga groups showed a trend
toward more improvement ( ) than the control groups, and the standardized mean difference was
−0.29 (−0.58 to 0.01).
In summary, our findings show potential benefits of yoga for people with cancer in improvements
of psychological health.

Preliminary findings also provide practitioners with important information that yoga may be a
possible adjunctive therapy for cancer patients to help manage psychological distress and to
improve quality of life. Nevertheless, more attention must be paid to the physical effects of yoga
and the methodological quality of future research, as well as to improve these areas in the future.

Effect on immune system:

Fifteen RCTs (randomized controlled trials)were eligible for the review. Even though the existing
evidence is not entirely consistent, a general pattern emerged suggesting that yoga can
downregulate pro-inflammatory markers. In particular, the qualitative evaluation of RCTs revealed
decreases in IL-1beta, as well as indications for reductions in IL-6 and TNF-alpha. These results
imply that yoga may be implemented as a complementary intervention for populations at risk or
already suffering from diseases with an inflammatory component.

To conclude, yoga has great potential both as a preventative measure and as a

compliment in people with cancer and undergoing chemo therapy. It boost immune
system, decrease inflammatory factors, improves body detox through sweating,
increase overall oxygen utilization and has an effect on the emotional dimension of
ones being.

Virus and Cancer Reference:

1. Cooper G. Oncogenes. Jones and Bartlett Publishers, 1995. 151-152, 175-176.

 2. Urry, L. A., Cain, M. L., Wasserman, S. A., Minorsky, P. V., & Reece, J. B. (2017).
Campbell Biology (11th ed.). Pearson.
 3.a. b. c. d. e. E. Boccardo and LL Villa. Viral Origins of Human Cancer. Current Medicinal
Chemistry. 2007; 24: 2526-39. [PUBMED]
 4. Brady G, Macarthur GJ, Farrell PJ. Epstein-Barr virus and Burkitt lymphoma. Postgrad
Med J. 2008 Jul;84(993):372-7. [PUBMED]
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 7. B. Ensoli, C. Sgadari, et al. Biology of Kaposi's sarcoma. European Journal of Cancer.
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 8. Schiffman M, Castle PE, Jeronimo J, Rodriguez AC, Wacholder S. "Human
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 11. Burchell AN, Winer RL, de Sanjosé S, Franco EL. Chapter 6: Epidemiology and
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 13. Chaturvedi AK. Beyond cervical cancer: burden of other HPV-related cancers among
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