HIV-AIDS Virus Defeated by Body O2: Breathing Methods
Any HIV-AIDS
therapy, in order to be successful and efficient, should include breathing
retraining, in addition to accepted practices of medication use, so as to
improve body-O2 content
using breathing exercises and lifestyle correction (learning diaphragmatic
breathing, prevention of mouth breathing during sleep, physical exercise with
nose breathing only, etc.). Such an approach allows faster improvements in the parameters of
the immune system to fight the HIV virus and improve digestion, sleep, and desire and tolerance to exercise.
Clinical evidence of doctors, as well as available physiological studies, found that advance of HIV-AIDS is always manifested in reduced cell oxygenation. Decades of medical research revealed hundreds of pathological effects of chronic hyperventilation that is present even in modern normal subjects.
Is there any western published evidence that HIV-AIDS sufferers breathe heavier during the progression of the disease? I could not find any studies that had measured minute ventilation numbers provided, but there are other publications were respiratory frequency and heart rates were reported.
In one study, Canadian doctors from St Paul's Hospital (University of British Columbia, Vancouver) discovered that corticosteroids reduced initial breathing rates from 30 to 22 breaths/min at rest (Montaner et al, 1993). Hence, the initial breathing frequency in these HIV-AIDS patients was about 30 breaths per minute (the normal range is 10-12 breaths per min at rest). It corresponds to about 5 s for the body-oxygen test and the last stage of the disease (the terminal stage). After application of cortisol, their breathing became slower (22 breaths/min), which according to the Buteyko Table of Health Zones is over 15 s, which corresponds to mild forms of the disease.
In another study, a group of Chinese MDs used oxygen-enriched liquid to
reduce low blood oxygenation in patients with SARS and HIV-AIDS virus. Their
initial respiratory rate ranged from 29 to 49 breaths per minute (less than
6 s for the body-oxygen test). Hence, HIV-AIDS patients do indeed suffer
from very heavy breathing during the last stage of the disease.
Therefore, heavy breathing is the cause of HIV-AIDS, and medical studies indeed point out that hypoxia is a normal clinical feature in HIV-AIDS patients (follow the link for research studies). Chronic hyperventilation immediately leads to a cascade of pathological changes in the lung tissue due to alveolar hypocapnia (CO2 deficiency) and equally injurious effects in all vital organs and body cells. These effects are summarized on web pages devoted to CO2 uses in the human body.
Furthermore, such respiratory disturbances (e.g., very fast breathing, quick and forceful exhalations, absence of the automatic pause after the exhalation, etc.) should cause reduced nitric oxide production and absorption, as it was reported by US scientists from the Oregon Health Sciences University in Portland (Loveless et al, 1997).
Clinical Trial: Application of the Buteyko breathing therapy for HIV-AIDS patientsIn the early 1990s, a large group of Russian and
Ukrainian MDs organized a clinical trial for 7 people with advanced HIV-AIDS
disease. Here are the main trial's conclusions: |
Usual CP (body-oxygen content) numbers in HIV-AIDS patients What are the usual CP numbers (oxygenation index) for HIV-AIDS
patients and their clinical features? |
Note
that the CP fluctuates throughout the day and the most important result
is immediately after waking up in the morning. This is exactly the most
miserable time for patients with HIV-AIDS virus, while other severely sick
patients (those with stroke, coronary heart disease, epilepsy, COPD, diabetes, asthma,
etc.) are most likely to die during early morning hours due to severe
overbreathing and critical oxygenation numbers.
The natural and stress-free CP test is invaluable in numerous situations. One can check the effects of various factors, including allergies, nutritional deficiencies, exercise, etc. To increase tissue oxygen content and the CP (stress-free breath holding time after exhalation) are the central goals of the Buteyko breathing method.
What reduces body-oxygen content? The main physiological factors include: sleeping too long and/or on the back, overeating, overheating, stress, lack of physical activity, exercise with mouth breathing, poor posture and many others. All these factors make respiration more frequent and heavier causing losses of CO2 and this is the key factor that triggers negative effects of chronic diseases, including cell hypoxia and suppressed immune system.
More resources and details about healthy and risk lifestyle factors can be
found on these web pages:
-
Hyperventilation Causes
- Learning the Buteyko breathing exercises by modules.
An even faster and easier technique for higher body-oxygen content is to use the Amazing DIY Breathing Device or the Frolov breathing device. The breathing exercises with the device are much more efficient (by around 50%) for those patients, who have less than 30 s for their CPs during initial stages of breathing retraining.
Reference pages: Breathing norms and medical facts:
-
Breathing
norms: Parameters, graph, and description of the normal
breathing pattern
- 6 breathing myths: Myths and superstitions about breathing
and body oxygenation (prevalence: over 90%)
- Hyperventilation: Definitions of
hyperventilation: their advantages and weak points
- Hyperventilation syndrome:
Western scientific evidence about prevalence of chronic hyperventilation in patients with chronic conditions
(37 medical studies)
- Normal minute ventilation: Small and
slow
breathing at rest is enjoyed by healthy subjects (14 studies)
- Hyperventilation prevalence: Present in
over 90% of
normal people (24 medical studies)
- HV and hypoxia:
How and why deep breathing reduces oxygenation of cells and tissues of
all vital organs
- Body-oxygen test (CP test)
: How to measure your own breathing and body oxygenation (two in one) using a simple DIY test
- Body oxygen in healthy:
Results for the body-oxygen test for healthy people (27 medical
studies)
- Body oxygen in sick
: Results for the body-oxygen test for sick people (14 medical studies)
- Buteyko
Table of Health Zones: Clinical description and ranges for breathing zones:
from the critically ill (severely sick) up to super healthy people
with maximum possible body oxygenation
- Morning hyperventilation: Why people feel
worse and critically ill people are most
likely to die during early morning hours
References: pages about CO2 effect:
- 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: How alveolar CO2 influences
oxygen transport
- Oxygen transport: O2 transport is controlled by
vasoconstriction-vasodilation and the Bohr effects, both of which rely on CO2
- Free radical generation:
Reactive oxygen species are produced within cells due to anaerobic cell respiration caused by cell hypoxia
- Inflammatory response: Chronic inflammation
in fueled by the hypoxia-inducible factor 1, while normal breathing reduces
and eliminates inflammation
- Nerve stabilization: People remain calm due to calmative or
sedative effects of carbon dioxide in neurons or nerve cells
- Muscle relaxation: Relaxation of muscle cells
is normal at high CO2, while hypocapnia causes muscular tension, poor posture
and, sometimes, aggression and violence
- Bronchodilation: Dilation of
airways (bronchi and bronchioles) is caused by carbon dioxide, and their constriction
by hypocapnia (low CO2)
- Blood
pH: Regulation of blood pH due to breathing and regulation of other bodily fluids
- CO2: lung damage: Elevated carbon
dioxide prevents lung injury and promotes healing of lung tissues
- CO2: Topical carbon dioxide can heal skin and tissues
- Synthesis of glutamine
in the brain, CO2 fixation, and other chemical reactions
- Deep breathing myth:
Ignorant and naive people promote the idea that deep breathing and breathing
more air at rest is beneficial for health
- Breathing control: How is our
breathing regulated? Why hypocapnia makes breathing uneven, irregular and erratic.
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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