HIV-AIDS Causes: Low Body Oxygen due to Ineffective Breathing
What causes progression of
HIV-AIDS? Critically low body or cell oxygen level (tissue hypoxia) as the
central HIV-AIDS cause have been suggested and confirmed by numerous medical
studies (Wang et al, 1993; Mootsikapun et al, 1996; Khare & Sharland, 1999;
Pellicelli et al, 2001; Zhang et al, 2002; Deshmane et al, 2009; Long et al,
2009). In particular, more recent studies conducted in the Laboratory of
Clinical and Experimental Pathology of the Louis Pasteur Hospital (Nice, France) observed higher expression of the
hypoxia-inducable factor -1 was associated with Kaposi sarcoma progression (Long
et al, 2009).
Other medical studies found that severely sick HIV-AIDS patients (STAGE 4
: Progression from HIV to AIDS) have very large respiratory rates. Their average breathing frequency at rest was 29 to 49 breaths per minute in one
study (Zhongguo et al, 2004), and about 30 breaths/min in another (Montaner
et al,1993), while the medical norm for adults is
10-12 breaths/min. A high respiratory rate was a normal clinical finding for
59 HIV-AIDS patients with interstitial infiltrates on chest radiographs (Knauer
et al, 2005). This group of the severely sick patients had tuberculosis, Pneumocystis pneumonia (PCP), bacterial pneumonia (20.3%) and fungal
pneumonia (10.2%).
Another cardiorespiratory parameter (the heart rate) was measured in 2 of
these studies. The Chinese study (Zhongguo et al, 2004) found that the pulse
of their HIV-AIDS patients ranged from 89 to 145 beats/min, while the
Canadians doctors reported that their patients had the average pulse of 100
beats per minute (Montaner et al,1993). All this evidence points out the main
physiological cause of HIV-AIDS
progression.
It is known that chronic hyperventilation leads to elevated heart rates in many groups of patients (e.g., asthma, heart disease, cancer, diabetes, and may other conditions). Generally, advance of any respiratory and/or inflammatory condition is manifested in higher heart rates, as it is reflected in the Buteyko Table of Health Zones. Hence, the results testify about presence of severe hyperventilation in all these patients.
Hence,
the cause of HIV-AIDS is ineffective breathing and classical symptoms of
hyperventilation have been known to medical professionals for many decades. They
include: poor perfusion of all vital organs due to hypocapnia, reduced cell
oxygen content due to CO2-induced vasoconstriction and suppressed Bohr
effect, immune dysfunction caused be cell hypoxia, mental symptoms due to
low CO2 and O2 levels in the brain, and hundreds of other abnormalities that
affect virtually all chemical reactions and processes in the human body, as
well as all vital organs.
The HIV virus does not cause the development of AIDS and death. All symptoms, including changes in the lungs, development of yeast infections (Candida), skin rashes and many others take place naturally in other people due to presence of hyperventilation. Hence, the HIV virus simply reinforces pathological effects caused by hyperventilation. In order to check these findings, a patient should find his respiratory parameters and see how these parameters relate to his symptoms.
Results of the clinical trial with HIV/AIDS patients reveal the cause of HIV-AIDS
Russian doctors practicing the Buteyko breathing method had a
clinical trial for a group of HIV patients with very encouraging
results. For these doctors the body oxygen level (CP test - see instructions
below) is the main
measuring tool of personal health. They discovered that with higher body oxygen
content or CP (due to
breathing exercises and lifestyle changes), typical
manifestations of HIV-AIDS disappear. Thus, the participants had their standard
medication and practiced breath work, as a supplementary technique to fight
HIV-AIDS and effects of hypoxia. I translated the official report
about this HIV-AIDS clinical trial.
Abnormal breathing causes HIV-AIDS
What are the usual results for the body oxygen test for HIV-AIDS patients? The results, according to Russian clinical research, are linked with these typical symptoms and effects:
| Body oxygen test | Symptoms in people with HIV-AIDS virus |
| 1-10 seconds | Advance of opportunistic infections: Pneumocystis jirovecii Pneumonia (PCP), Tuberculosis (TB), Kaposi's Sarcoma (KS), Herpes simplex, Kaposi's sarcoma, Varicella Zoster, Cryptosporidiosis, Candida, Cytomegolavirus (CMV), Isosporiasis, Kaposi's Sarcoma, Cytomegolavirus, Toxoplasmosis, Cryptococcosis, Non Hodgkin's lymphoma, Varicella Zoster, and Herpes simplex, which affect respiratory system, gastro-intestinal system, central/peripheral nervous system, and skin leading to HIV wasting syndrome, chronic herpes simplex infection, recurrent severe bacterial pneumonia, pneumocystis pneumonia, Kaposi sarcoma, candidasis of trachea, bronchi and/or lungs, extrapulmonary cryptococcosis including meningitis, HIV encephalopathy, progressive multifocal leukoencephalopathy, disseminated non-tuberculous mycobacteria infection, chronic isosporiasis, chronic cryptosporidiosis, lymphoma (cerebral or B cell non-Hodgkin), extrapulmonary histoplasmosis, coccidiomycosis, recurrent septicaemia (including non-typhoidal Salmonella), symptomatic HIV-associated nephropathy or HIV-associated cardiomyopathy, invasive cervical carcinoma |
| 11-20 seconds | Fatigue, skin rashes, night sweats, mouth ulcers, moderate digestive complaints, and fungal skin infections. Typical problems are chronic oral and/or vaginal thrush (a fungal rash or spots), recurrent herpes blisters on the mouth (cold sores) and/or genitals, ongoing fevers and persistent diarrhea, and some weight loss. The disease will progress to clinical stage 4 or end-stage, especially with the transition to mouth breathing, sleeping on one's back at night and/or chest breathing. |
| 20-40 seconds | No need for medication and no major HIV-AIDS symptoms, with mild symptoms related to worsened sleep, intestinal candidasis, and light morning fatigue |
| Over 40 seconds | Excellent health, including blood tests, parameters of the immune system, and mental well being. |
The natural and stress-free body oxygen test is also valuable in numerous situations to check the effects of various factors, including sleep, exercise, diet, etc. on the HIV-AIDS cause. To increase body oxygen test results and slow down breathing rates are the central goals of the Buteyko method. What reduces body oxygen level? The main physiological factors include lack of physical activity, exercise with mouth breathing, sleeping too long and/or on the back, overeating, overheating, stress, poor posture and many others.
Hence, breathing retraining or normalization of breathing parameters is necessary for faster health restoration. Furthermore, any HIV-AIDS treatment program must have breathing techniques as a necessary part for health restoration and elimination of the main physiological cause of HIV-AIDS.
All HIV-AIDS web pages:
HIV-AIDS Cause - Suppression of the immune
system can take place only due to low oxygen levels in body cells. Therefore,
tissue hypoxia, due to abnormal breathing in people with HIV-AIDS, is the cause
HIV-AIDS Therapy - Improve body
oxygenation with breathing retraining (you need to change your automatic
breathing patterns in order to have more oxygen in the body 24/7)
HIV-AIDS Clinical Trial - Breathing
exercises reverse typical signs and symptoms of advanced HIV-AIDS.
References: CO2 Effects Web Pages
Vasodilation: CO2 expands arteries and arterioles facilitating perfusion
(or blood
supply) to all vital organs
The Bohr effect
How and why oxygen is released by red blood cells in tissues
Cell Oxygen Levels and oxygen transport are controlled by
alveolar CO2 and breathing
Oxygen Transport depends on
breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr
effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2
content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes
place due to anaerobic cell respiration caused by cell hypoxia. Hence,
antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by
breathing since hypoxia leads to or intensifies chronic inflammation through over-expression
of the hypoxia-inducible factor 1, while normal
breathing reduces these processes
Nerve stabilization takes place due to calmative or
sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells
is normal at high CO2, while hypocapnia causes muscular tension, poor posture
and, sometimes, aggression and violence
Brochodilation - dilation of
airways (bronchi and bronchioles) by carbon dioxide, and their constriction due
to hypocapnia
CO2: Best Natural Cough Suppressant
and "home remedy" since it calms urge-to-cough nerve receptors located in the
tracheobronchial tree and larynx
Blood
pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon
dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine
in the Brain, CO2 fixation, and other chemical reactions
CO2 myth
"CO2 is a toxic waste gas" myth
Breathing control
How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic?
Reference Web Pages: Breathing norms, Medical Graphs and Tables about Breathing Rates (Minute Ventilation) and
Body Oxygen in Healthy, Normal and Sick People
Breathing
norms Parameters, graph, and description of the normal
breathing pattern
6 breathing myths 6
myths about breathing and body oxygenation (prevalence: over 90%)
Hyperventilation Definitions of
hyperventilation: their advantages and weak points
Hyperventilation Syndrome in the
Sick. Table
1. Western scientific evidence about prevalence of CHV
(chronic hyperventilation) in patients with various chronic conditions
(34 medical studies)
Normal Minute Ventilation in
Healthy Subjects: Easy and Light Breathing (14 Studies)
Hyperventilation Prevalence Present in Over 90% of
Normal People (24 medical publications)
HV and hypoxia
How and why deep breathing reduces oxygenation of cells and tissues of
all vital organs
Body oxygen test
How to measure your own breathing and body oxygenation (a simple DIY test)
Body oxygen in healthy
Table 4. CP (body oxygen level) in healthy people (27 medical
studies)
Body oxygen in sick Table 5.
CP (body oxygen level) in sick people (14 medical studies)
Buteyko
Table of Health Zones with clinical description of most common zones
Morning HV Morning
hyperventilation effect or how and why critically ill people are most
likely to die during early morning hours
References
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2004 May;16(5):284-6.
[Study of infusion of oxygen-enriched liquid to correct severe hypoxemia
in infectious diseases: a report of pilot clinical study]
[Article in Chinese]
He Q, Xu C, Wang S, Cui JJ, Duan G, Ye TS, Yang DG, Zhou BP, Zhao LS.
Donghu Hospital of Shenzhen, Shenzhen 518020, Guangdong, China.
OBJECTIVE: To investigate a new therapy for effectively correcting severe
hypoxemia in patients with infectious diseases by infusion of
oxygen-enriched liquid, in order to raise the partial pressure of blood
oxygen without passing through pathologically damaged alveoli of such
patients.
METHODS: Intravenous drip with oxygen-enriched liquids was given to 6 cases
suffering from severe acute respiratory syndrome (SARS), and 3 cases of
acquired immune deficiency syndrome (AIDS) in the course of treatment for 1
to 5 days, 500-700 ml per day.
RESULTS: For all the 9 SARS cases, their hypoxemia was gradually corrected
to normal in 20 minutes' or 4 hours' intravenous drip with oxygen-enriched
liquid. Respiratory rate decreased from 29-49 breath/min to 18-22
breath/min, heart rate decreased from 89-145 beats/min to 60-79 beats/min,
two faint patients regained consciousness, hypoxemia was redressed, partial
pressure of oxygen in artery increased from 56 mm Hg (1 mm Hg=0.133 kPa) to
87 mm Hg, saturation of oxygen increased from 0.89 to 0.96.
CONCLUSION: Intravenous drip of the oxygen-enriched liquid effectively
helped correct the hypoxemia of SARS and other infectious diseases cases by
bypassing the diseased alveoli through which oxygen would not pass into the
blood by conventional oxygen inhalation. This therapy of oxygen-enriched
liquid infusion could be quite life-saving in the combined treatment for
SARS and other infectious diseases.
Wien Klin Wochenschr. 2005;117 Suppl 4:49-55.
Clinical features, aetiology and short-term outcome of interstitial
pneumonitis in HIV/AIDS patients at Bamrasnaradura Hospital, Nonthaburi,
Thailand.
Knauer A, Das AK, Tansuphasawadikul S, Supanaranond W, Pitisuttithum P,
Wernsdorfer WH.
Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.
This prospective study was conducted at Bamrasnaradura Hospital from
November 11, 2002, until January 5, 2003, in order to describe the clinical
manifestations and determine the aetiologies as well as to assess the
short-term outcome of interstitial pneumonitis in HIV/AIDS patients. 59
patients with interstitial infiltrates on chest radiographs were included in
the study. Tuberculosis (TB) was the most common diagnosis (44%), followed
by Pneumocystis pneumonia (PCP) (25.4%), bacterial pneumonia (20.3%) and
fungal pneumonia (10.2%). In TB, compared to other diagnoses, a mild cough
(p = 0.031), pallor (p = 0.021), lymphadenopathy (p < 0.001), an absence of
skin lesions (p = 0.003), a higher mean body temperature (p = 0.004) and an
absence of dyspnoea on exertion (p = 0.042) were significant findings. In
PCP, compared to other diagnoses, dyspnoea on exertion (p = 0.014),
nonpurulent sputum production (p = 0.047), a higher mean respiratory rate
(p < 0.001), and an absence of lymphadenopathy (p < 0.001) were
significant factors. In bacterial pneumonia, compared to other diagnoses,
production of purulent sputum (p = 0.014), haemoptysis (p = 0.006), skin
lesions (p = 0.002) and severe cough (p = 0.040) were significantly
associated factors. In fungal pneumonia, compared to other diagnoses,
headache and papulonecrotic skin lesions were common findings, but no factor
showed a significant association. After four weeks, 59.3% patients were
alive and 13.6% had died. Among those alive, 88.6% had clinically improved.
The cumulative survival after 28 days was highest among PCP patients,
followed by bacterial pneumonia, TB and fungal pneumonia, but these
differences were statistically not significant (p = 0.453).
Virchows Arch. 2009 Aug;455(2):159-70. Epub 2009 May 30.
LANA-1, Bcl-2, Mcl-1 and HIF-1alpha protein expression in HIV-associated
Kaposi sarcoma.
Long E, Ilie M, Hofman V, Havet K, Selva E, Butori C, Lacour JP, Nelson AM,
Cathomas G, Hofman P.
Laboratory of Clinical and Experimental Pathology, Louis Pasteur Hospital,
Nice 06002, France.
Human herpesvirus 8 (HHV8) is necessary for Kaposi sarcoma (KS) to develop,
but whether the tissue viral load is a marker of KS progression is still
unclear. Little is known about the level of expression of
apoptosis-regulating proteins and of hypoxia-inducible factors (HIFs) in KS
tumour cells relative to HHV8 expression. We therefore investigated the
expression of the latency-associated nuclear antigen (LANA-1) of HHV8,
Bcl-2, Mcl-1, Bax, Bcl-xL, caspase 3 and HIF-1alphain KS tissue specimens at
different stages of the disease. The expression of these proteins was
evaluated immunohistochemically using tissue microarrays (TMAs) in tissue
specimens from 245 HIV-positive patients at different stages of the disease.
Both LANA-1 and HIF-1alpha were expressed in KS biopsies taken at different
stages, but their level increased throughout tumour progression.
Additionally, the levels of Bcl-2 and Mcl-1 were higher in visceral KS
lesions compared to levels observed in cutaneous and mucosal KS. This study
demonstrates that late tumour stages of KS in tissues from HIV-positive
patients are associated with high levels of LANA-1, HIF-1alpha and of the
anti-apoptotic proteins, Bcl-2 and Mcl-1. Finally, the expression of these
proteins can be potentially used as a tissue biomarker in defining patients
with a higher risk of disease progression.
J Biol Chem. 2009 Apr 24;284(17):11364-73. Epub 2009 Feb 9.
Activation of the oxidative stress pathway by HIV-1 Vpr leads to induction
of hypoxia-inducible factor 1alpha expression.
Deshmane SL, Mukerjee R, Fan S, Del Valle L, Michiels C, Sweet T, Rom I,
Khalili K, Rappaport J, Amini S, Sawaya BE.
Department of Neuroscience and Center for Neurovirology, Temple University
School of Medicine, Philadelphia, Pennsylvania 19122, USA.
The detection of biomarkers of oxidative stress in brain tissue and
cerebrospinal fluid of patients with human immunodeficiency virus, type 1
(HIV)-associated dementia indicates the involvement of stress pathways in
the neuropathogenesis of AIDS. Although the biological importance of
oxidative stress on events involved in AIDS neuropathogenesis and the HIV-1
proteins responsible for oxidative stress remain to be elucidated, our
results point to the activation of hypoxia-inducible factor 1 (HIF-1) upon
HIV-1 infection and its elevation in brain cells of AIDS patients with
dementia. HIF-1 is a transcription factor that is responsive to oxygen.
Under hypoxic conditions, HIF-1alpha becomes stable and translocates to the
nucleus where it dimerizes with aryl hydrocarbon receptor nuclear
translocator and modulates gene transcription. Activation of HIF-1 can also
be mediated by the HIV-1 accessory protein Vpr. In addition, cellular
components, including reactive oxygen species, contribute to the induction
of HIF-1alpha. Our results show that Vpr induces reactive oxygen species by
increasing H(2)O(2) production, which can contribute to HIF-1alpha
accumulation. Interestingly, increased levels of HIF-1alpha stimulated HIV-1
gene transcription through HIF-1 association with HIV-1 long terminal
repeat. These observations point to the existence of a positive feedback
interplay between HIF-1alpha and Vpr and that, by inducing oxidative stress
via activation of HIF-1, Vpr can induce HIV-1 gene expression and
dysregulate multiple host cellular pathways.
Med Hypotheses. 2002 Jun;58(6):439-43.
Human-bacteria nitric oxide cycles in HIV-1 infection.
Zhang H, Boring D, Haverkos H.
Food and Drug Administration, Center for Drug Evaluation and Research,
Division of Antiviral Drug Products, Rockville, USA.
...In
HIV infection, however, the NO(3)(-) is converted into NO and nitrite
NO(2)(-) and recirculated in the body, perhaps as a result of concomitant
opportunistic bacterial infections and cellular hypoxia...
Ann N Y Acad Sci. 2001 Nov;946:82-94.
Pathogenesis of HIV-related pulmonary hypertension.
Pellicelli AM, Palmieri F, Cicalini S, Petrosillo N.
Istituto Nazionale per le Malattie Infettive, Lazzaro Spallanzani, IRCCS,
Rome, Italy.
...Chronic hypoxia is observed with
increased frequency in HIV patients...
Indian J Pediatr. 1999 Nov-Dec;66(6):895-904.
Pulmonary manifestations of pediatric HIV infection.
Khare MD, Sharland M.
Pediatric Infectious Diseases Unit, St. George's Hospital, London, United
Kingdom.
Vertically acquired HIV infection is becoming increasingly common in India.
The main clinical manifestations of HIV in childhood are growth failure,
lymphadenopathy, chronic cough and fever, recurrent pulmonary infections,
and persistent diarrhea... The commonest AIDS
diagnosis in infancy is PCP, presenting in infancy with tachypnea, hypoxia,
and bilateral opacification on chest-X-ray (CXR)...
J Med Assoc Thai. 1996 Aug;79(8):477-85.
Pulmonary infections in HIV infected patients.
Mootsikapun P, Chetchotisakd P, Intarapoka B.
Department of Medicine, Faculty of Medicine, Khon Kaen University, Thailand.
We retrospectively reviewed causes, clinical presentations and chest
radiographs of pulmonary infections in symptomatic HIV infected patients
diagnosed in Srinagarind Hospital from February 1992 to 1994. We found 95
episodes of pulmonary infections in 88 HIV infected patients enrolled in our
review. The three most common pathogens were Mycobacterium tuberculosis
(37.2%), Pneumocystis carinii (23.8%), and Cryptococcus (15.2%). Coexistent
pulmonary infections were seen in 10.5 per cent, mostly due to P. carinii
and Cryptococcus neoformans. Extrapulmonary infections were also common,
particularly with M. tuberculosis (49%) and C. neoformans (100%). The common
clinical presentations were fever, dyspnea, and cough which frequency varied
among the organisms. Chest radiographs were nonspecific, the most common
finding was bilateral pulmonary infiltrates except that bacterial pneumonia
usually presented with unilateral infiltrates. All patients wit PC had
significant hypoxia (PaO2 < 70 mmHg)...
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