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HIV-AIDS Virus vs. Body Oxygen: Breathing Therapy

HIV-AIDS Virus in BloodAny HIV-AIDS therapy, in order to be successful and efficient, should include breathing retraining, in addition to accepted practices of medication use, so that to improve body oxygen content using breathing exercises and lifestyle correction (learning diaphragmatic breathing, prevention of mouth breathing during sleep, physical exercise with nose breathing only, etc.). Such 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 breathe heavier during 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, that corresponds to mild forms of the disease.

HIV-AIDS virus attacking a human cell 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 patients

In 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:
- 1. The use of the Buteyko method has resulted in improvements in clinical symptoms.
- 2. No side-effects or complications have been observed in patients with AIDS during the Buteyko therapy.
- 3. It is sensible to continue careful observations and laboratory investigations of AIDS patients and recommend the Buteyko method for further testing.
- 4. Regular psychotherapy that had been used earlier proved ineffective, and the health state of four patients even worsened.
Here are the translation of the clinical trial and an official letter to the Deputy Minister of Health of Ukrainian SSR about this HIV-AIDS clinical trial.

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?
1-10 s of oxygen in body cells - HIV wasting syndrome, pneumocystis pneumonia, Kaposi sarcoma, candidiasis of trachea, chronic herpes simplex infection, recurrent severe bacterial pneumonia, progressive multifocal leukoencephalopathy, disseminated non-tuberculous mycobacteria infection, bronchi and/or lungs, extrapulmonary cryptococcosis including meningitis, HIV encephalopathy, chronic isosporiasis, chronic cryptosporidiosis, lymphoma (cerebral or B cell non-Hodgkin), invasive cervical carcinoma, extrapulmonary histoplasmosis, coccidiomycosis, recurrent septicaemia (including non-typhoidal Salmonella), symptomatic HIV-associated nephropathy or HIV-associated cardiomyopathy
10-20 s - Fatigue, mouth ulcers, skin rashes, night sweats, moderate digestive complaints, and fungal skin infections. Typical problems are recurrent herpes blisters on the mouth (cold sores) and/or genitals, chronic oral and/or vaginal thrush (a fungal rash or spots), ongoing fevers, persistent diarrhea, and weight loss
Over 25 s - No need for medication and no major symptoms
Over 40 s CP 24/7 - Normal health, including blood tests, various parameters of the immune system, digestion and mental well being.

Young man sleeping, sickNote 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 (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.

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.

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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