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Des "bienfaits" des trithérapies ...

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Invité rock-en-rock

Hé bien vieux frère de Pierre ... je suis content ... ben oui que ta vas remonter la pente !

... et que tu vas reprendre ta plume ...

Moi en ce moment, c'est Benoit qui m'inspire ... 4-piout.gif

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Rock-en-Rock,

"à ce sujet, je me pose des questions sur jimmy le rebel dont on est sans nouvelles...ainsi que la disparation spectaculaire de pierre candidiasis icon_biggrin.gif ....qui aurait des infos??".En voilà un peu! icon_biggrin.gif

Jaimerais bien avoir des nouvelles deJimmy le rebel également!

Ne Tinquiètes pas!, je suis toujours en vie ! albator7k.gif

Ma grippe sest améliorée durant toute la semaine dernière icon_biggrin.gif .Comme javais choisi les médecines les plus douces (essentiellement de la phyto, des tisanes). Je ne mattendais pas à un résultat rapide. Je métais donné de 4 à 6 semaines pour sortir de la grippe.Celà à lair de correspondre a ce que jobserve.

Je suis exténué par ces 4 semaines de grippe et il me faudra encore plusieurs semaines pour rretrouver mes différents équilibres (alimentaire, hydratation et sommeil ). icon_cry.gif

A+,

Pierre

Merci de têtre inquiéter de moi icon_bravo.gif

Cela fait plaisir de te retrouver parmi nous ^pierre^

Retape toi pbien, nous sommes impatients de te relire

Rock, pour Benoît, finalement, mieux vaut tiare que jamais 4-ptdrasrpt.gif

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Invité kdt

Question bête : qu'est-ce qu'il se passe si l'on est "détecté" positif et que l'on refuse les tri-thérapies en France ?

J'ai lu des sites où l'on expliquait qu'aux States, on obligeait des femmes enceintes à les prendre.

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Invité rock-en-rock

Question bête : qu'est-ce qu'il se passe si l'on est "détecté" positif et que l'on refuse les tri-thérapies en France ?

A ma connaissance, il ne se passe rien encore (le système est perfectible) ... si ce n'est d'être considéré comme un sale con ... et un crétin ...

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http://www.ncbi.nlm.nih.gov/entrez/query.f...3772&query_hl=5

AIDS. 2005 Sep 2;19(13):1407-14. Related Articles, Links

Anal intraepithelial neoplasia in the highly active antiretroviral therapy era among HIV-positive men who have sex with men.

Palefsky JM, Holly EA, Efirdc JT, Da Costa M, Jay N, Berry JM, Darragh TM.

From the Departments of aMedicine bStomatology cEpidemiology and Biostatistics dPathology, University of California, San Francisco, California, USA.

OBJECTIVES:: The incidence of anal cancer among men who have sex with men (MSM) has continued to increase since the introduction of highly active antiretroviral therapy (HAART). The prevalence of the putative anal cancer precursor, anal intraepithelial neoplasia (AIN) was high among HIV-positive MSM prior to the availability of HAART but little is known about AIN since HAART was introduced. We characterized the prevalence of AIN among HIV-positive MSM and examined the association between AIN and various factors including use of HAART. DESIGN AND METHODS:: A baseline point-prevalence analyses in a prospective cohort study of AIN was performed at a university-based research clinic. A total of 357 HIV-positive MSM with no history of anal cancer completed a questionnaire detailing behaviors and medical history, anal cytology and human papillomavirus (HPV) testing, and high-resolution anoscopy with biopsy for detection of AIN. RESULTS:: Eighty-one percent of participants with available CD4+ cell counts at baseline had AIN of any grade; 52% had AIN 2 or 3; and 95% had anal HPV infection. In multivariate analysis, detection of >/= 6 HPV types [odds ratio (OR), 36; 95% confidence interval (CI), 7.4-171) and use of HAART (OR, 10; 95% CI, 2.6-38) were associated with AIN after adjustment for length of time participants were HIV-positive, CD4+ cell count and HIV viral load. CONCLUSIONS:: The prevalence of AIN has remained high among HIV-positive MSM after the introduction of HAART. Our data indicate that HAART is not associated with a reduced prevalence of AIN and support measures to prevent anal cancer among HIV-positive MSM whether or not they are using HAART.

PMID: 16103772 [PubMed - in process]

http://groups.msn.com/aidsmythexposed/gene...538332006771774

Well at least the body.com seem to report straight here about that incredible data.

http://www.thebodypro.com/newsroom.shtml

HAART Associated With Higher Risk of Anal Cancer Precursor

HAART use appears to be associated with an increased, though not necessarily a direct, risk of grade 2 or 3 anal intraepithelial neoplasia (AIN) among HIV-infected men who have sex with men (MSM), according to a study by University of California-San Francisco researchers. More than half of the 357 study participants, all of whom were MSM in San Francisco, were found to have grade 2 or 3 AIN, and 95% were infected with anal human papillomavirus. No significant association was found between AIN and CD4+ cell count or viral load, but use of antiretrovirals -- and particularly of HAART -- was significantly associated with a greater risk of AIN. The risk appeared to increase with greater duration of HAART and number of antiretrovirals used.

I am abit concerned by this and are they sought of twisting around there own quite scary data ?

Copy and paste url.

http://www.aidsmap.com/en/news/44E54C4A-27...0E7C70499B8.asp

Edwin J. Bernard, Monday, August 29, 2005

A study of HIV-positive gay men in San Francisco has found that 95% have anal HPV (human papilloma virus) infection, and more than 50% have grade 2 or 3 anal intraepithelial neoplasia (AIN), precursors of anal cancer. The study, which appears in the September 2nd edition of AIDS, confirms other studies which suggest that highly active antiretroviral therapy (HAART) is not protective of AIN, and found that the men on HAART actually had an increased risk of AIN. Although the study does not suggest that HAART itself increases the risk of AIN, it does, at the very least, support the conclusion that HAART does not reduce the risk, and that the prevalence of anal cancer amongst HIV-positive gay men on HAART continues to increase.

Dr Joel Palefsky and colleagues from the University of California, San Francisco (UCSF), have published extensively on the incidence and treatment of HPV infection, AIN and anal cancer in HIV-positive gay men. Their latest study sought to determine the factors associated with, and prevalence of, AIN in a cohort of HIV-positive gay men, and to determine whether HAART use was associated with lower prevalence.

Gay men were recruited into this cohort study through newspaper advertisements and community outreach at the UCSF between February 1998 and January 2000. A total of 357 HIV-positive gay men were enrolled, and stratified according to their current antiretroviral regimen: no antiretrovirals (n=50, 14%), non-HAART regimen (n=40, 11%) and HAART regimen (n=267, 75%), the latter of which was defined as three or more antiretrovirals including at least one protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI). There were no significant differences in baseline characteristics apart from the mean age of men using a non-HAART regimen which was, at 44, three years higher than the men not on antiretrovirals (age = 41, p<0.05).

Only 25 (7%) had never taken any antiretroviral regimen, and most had used between two and five nucleoside reverse transcriptase inhibitors (NRTIs) in their lifetime, although 8% had used between six and ten; 36% had ever taken at least one NNRTI; and whilst 31% had only ever taken one PI, 15% had taken four or five PIs. Lamivudine (3TC, Epivir; 59%) was the most commonly used, currently taken antiretroviral, followed by stavudine (d4T, Zerit; 52%), indinavir (Crixivan 26%) and zidovudine (AZT, Retrovir; 25%). In total, 137 different antiretroviral combinations were currently being used.

All the men were tested for CD4 cell counts and viral load. They also answered extensive lifestyle and medical history questioning, and underwent clinical examination. PCR testing defined 26 different HPV types; anal cytology via PAP smears were classified as normal, atypical squamous cells of undermined significance (ASCUS), AIN 1, 2 or 3; and anal biopsies were classified as normal, atypical, AIN 1, 2 or 3. The more serious of either the cytology or biopsy results were used (the higher the number the more serious the risk of anal cancer), unless the biopsy proved to be normal, in which case the result was considered indeterminate and the data excluded from analysis.

AIN & CD4 cell counts and viral load

The researchers found no significant association between CD4 cell count or viral load and AIN. AIN of any grade was found in 81% of the men with available CD4 cell counts: 29% had AIN 1 or condyloma; 39% had AIN 2 and 13% had AIN 3. There was a non-significant trend towards an increased risk of AIN with decreasing CD4 cell counts (p<0.07), and there was no association between AIN and viral load.

In comparison, a recent four city US study found a 20% prevalence of anal cancer precursor cells in 1262 HIV-negative gay men (Chin-Hong 2005).

AIN & HPV infection

As expected from previous studies, the researchers found a significant association between HPV and AIN. Of the 354 men with an anal swab available for HPV testing, 31 (8.8%) tested negative for beta-globulin resulting in 323 evaluable men. Of these, 308 (95%) had anal HPV infection. The men with anal HPV infection had a 15-fold increased risk (95% CI 4.0-57) of AIN of any stage and a 19-fold increased risk (95% CI 3.7-101) of AIN 2 or 3, compared with HPV-negative men. The investigators also found a statistically significant trend (all p<0.001) for the risk of AIN with increasing number of HPV types. Of the 128 men with six or more HPV types, 120 (94%) had any AIN, and 85 (66%) had AIN 2 or 3. Conversely, among the 163 men diagnosed with AIN 2 or 3, HPV was detected in 160 (98%).

AIN & HAART

The researchers found that the men who were taking antiretrovirals had an increased risk for any grade of AIN (OR 6.1; 95% CI, 2.6-14), and of AIN 2 or 3 (OR 6.3; 95% CI, 2.5-16), compared with those men who were not taking antiretrovirals. Although the men on HAART had an equivalent risk of any grade of AIN (OR 6.0; 95% CI, 2.5-14 vs. 6.1; 95% CI, 1.4-26) to those men taking antiretroviral therapy not classed as HAART, the risk of AIN 2 or 3 was higher for the men on HAART (OR 6.3, 95% CI 2.5-16) compared with the men taking a non-HAART regimen (OR 5.2; 95% CI, 1.0-26; p<0.001). The risks for any AIN, or AIN 2 or 3, also increased significantly with increasing time on HAART (p<0.001), and the number of antiretroviral drugs ever used (p<0.001).

AIN & other risk factors

Men who had a history of PCP, oral or oesophageal Candidiasis, shingles, Molluscum contagiosum or aciclovir use (as a marker of herpes infection) also had an increased risk of any AIN or AIN 2 or 3, even when adjusted for CD4 cell count. However, the researchers found that that was no association between any grade of AIN, or AIN 2 or 3, and race, education, time since HIV diagnosis, changes of medications in the past three years, drug holidays, antiretroviral adherence, time on current regimen, sexual activities, use of alcohol, tobacco, or recreational drugs, or other medical conditions or therapeutic drugs.

HPV & HAART use increases AIN risk

When a model that included the number of HPV types, CD4 cell count, HIV viral load and current viral load was adjusted for length of time since HIV-positive diagnosis, CD4 cell count and HIV viral, both the number of HPV types and current use of HAART were associated with an increased risk of any AIN or AIN 2 or 3. Having six or more HPV types increased the risk of any AIN 36-fold (95% CI, 7.4-171) and AIN 2 or 3, 108-fold (95% CI, 15-763) compared with no HPV infection. The men currently taking HAART had a 10-fold increased risk (95% CI, 2.6-38) of any AIN and a 12-fold increased risk (95% CI, 2.4-64) compared with the men not currently taking antiretrovirals.

"At a minimum HAART does not reduce the risk of AIN"

The investigators write that although their findings suggest that HAART appears to increase the risk of AIN, they "do not suggest that use of HAART directly increases the risk of AIN," but rather, "at a minimum they do support the conclusion that HAART use does not reduce the risk for AIN." They explain their findings by suggesting that the "men on HAART are different from those not on HAART in several ways and it is possible that the increased risk for AIN in this study reflected unmeasured differences between the two groups." This might include lifetime cumulative immunosuppression, a risk factor which is suggested by the association between an increased risk of AIN and "lifetime usage of antiretrovirals, history of pneumocystic and candidiasis, and the total number of different antiretroviral drugs ever used."

A role for earlier HAART?

The authors discuss the idea, supported by pre-HAART AIN studies, that immune suppression may be more important early in the natural history of AIN, but that other factors, including chromosomal changes, may be more important when it comes to the persistence of high-grade AIN and progression to cancer. They hypothesise that earlier use of HAART at higher CD4 cell counts than current treatment guidelines recommend may affect the natural history of AIN, but this would be difficult to prove unless studies were set up to specifically examine this issue. Nevertheless, they suggest that a possible benefit of HAART has been seen once cervical intraepithelial neoplasia has been treated in HIV-positive women, and so the relationship between HAART use and response to treatment for AIN should also be the subject of further investigation.

More studies "urgently needed"

The investigators conclude by stating that "unlike most other HIV-related malignancies, the incidence of anal cancer has been increasing since the introduction of HAART. Studies to document the utility of treatment of AIN 2 or 3 to prevent anal cancer are urgently needed."

Reference

Palefsky J et al. Anal intraepithelial neoplasia in the highly active antiretroviral therapy era among HIV-positive men who have sex with men. AIDS 19 (13):1407-1414, 2005.

Chin-Hong PV et al. Age-related prevalence of anal cancer precursors in homosexual men: the EXPLORE study. J Natl Cancer Inst 97: 896-905, 2005.

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Conseiller Message 2 sur 15 dans la discussion

De : GlutathioneSurvival1 Envoyé : 04/09/2005 03:50

I think these two stories are linked.

Highly active antiretroviral therapy may increase a patient's risk of developing oral warts, according to a study conducted by researchers at the University of California-San Francisco and published in the current issue of the Lancet. Dr. Deborah Greenspan and colleagues retrospectively studied 1,280 patients at an HIV dental clinic between July 1990 and June 1999 and found a three-fold increase in oral warts among patients taking antiretroviral therapy excluding protease inhibitors and a six-fold increase among those who were on HAART, a two- or three-drug combination therapy including a protease inhibitor.

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http://www.aidsmap.com/en/news/53C08FA7-99...3AF79C00C06.asp

Herpes and genital warts most common symptoms of immune reconstitution inflammatory syndrome (IRIS)

Edwin J. Bernard, Tuesday, October 28, 2003

Immune reconstitution inflammatory syndrome (IRIS) is the name given to a diverse group of symptoms that can occur soon after the initiation of HAART. This can include the first appearance or the recurrence of previously-treated opportunistic infections, like TB, CMV, PCP or MAI, or the flare-up of viral infections that include hepatitis and herpes.

Even though the syndrome has been identified for more than four years, remarkably little is known about why it occurs or how to identify it. Only one study has been published, by an Australian team in 1999, which found that low CD4 counts at HAART initiation were the only independent predictor of IRIS. This finding has led to two schools of thought regarding the cause: either that a greater immune restoration leads to more IRIS events, or that it is caused by a deferred or partial CD4 response after HAART is initiated.

The findings of a team of British reseachers from Kings College Hospital in south east London appear to support the second view, since they found that baseline CD4 counts were not an independent factor in their case review study. In fact, the only difference they found between those people who began HAART and experienced an IRIS-associated adverse event and those who did not, was that IRIS cases were significantly younger by two years (p=0.021), although in univariate analysis a lower CD4 count at 12 weeks (suggesting a partial or deferred rise in CD4 counts) was found to be a predictor of IRIS.

However, these findings are particularly significant because they identify the most common IRIS events, which may be very useful to clinicians who are uncertain as to whether the appearance of certain set of symptoms within six months of starting HAART are due to disease progression or IRIS. This will be of particular relevance in resource-limited settings where virologic or immunologic monitoring is not available.

The study reviewed the case notes of 199 HIV-positive individuals who commenced HAART between January 2000 and August 2002 at Kings College Hospital. The genders were evenly distributed, 59% were African, 29% were white, and 10.5% Caribbean. Median baseline CD4 count was 174 cells/mm3, although 13.6% began HAART with less than 50 cells/mm3 and median viral load was 36,878 copies/ml. The vast majority (83%) were on NNRTI-based HAART.

They found that 44 (22%) had IRIS events, which occurred at a median of 12 weeks (range 3 - 24 weeks) following the initiation of HAART, and that the majority (78%) were due to the occurence - or the more frequent and/or more severe recurrence - of dematological problems: genital herpes simplex (HSV) made up 50% of the cases; genital warts caused by human papilloma virus (HPV), 24%; molluscum contagiosum, 9.5%; and varicella zoster virus, 9.5%.

Non-dermatological manifestations of IRIS were much less common: 2% had TB symptoms, 2% had new liver problems related to hepatitis B (HBV), and there was one case each of KS or PCP symptoms.

A prior history of certain infections appeared to be more likely to recur as part of IRIS. Two thirds of those with genital warts and one third of those with genital herpes simplex had IRIS flare-ups. One quarter had recurrences of hepatitis B-related liver problems, and one fifth had new TB symptoms.

The researchers concluded that although IRIS appears to most commonly manifest as new or more severe or recurrent genital herpes or other dermatological infections, they suggest that those with HSV, HPV, TB and HBV be monitored closely for IRIS when intiating HAART.

Reference

Thevarajan I. et al. Epidemiology Of immune reconstitution inflammatory syndrome (IRIS) in an ethnically diverse HIV infected cohort Ninth European AIDS Conference, Warsaw, abstract F4/4, 2003.

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http://www.rethinking.org/aids/cite/topic_279.html

Effect of highly active antiretroviral therapy on frequency of oral warts.

Greenspan D et al.

There was...a striking increase in [oral] warts: three-fold for patients on antiretroviral therapy and six-fold for those on HAART (p = 0.01). This pattern of oral disease in a referral clinic suggests that an increase in oral warts could be occurring as a complication of HAART.

Lancet. 2001 May 5;357:1411-2. 2001

Ask The Expert: Outbreaks of Oral Warts Coinciding With HAART?

1

A "striking increase in oral warts" has been noted among people taking anti-HIV meds according to several reports published in the mainstream medical literature. One study found oral warts were three times more frequent in HIV positives taking "antiretroviral therapy" and six-fold more common among those on the drug combinations known as HAART. A doctor¹s letter to Medscape mentions a patient with multiple, severe outbreaks of oral warts that coincided with the initiation of a triple drug regimen. The doctor observed the warts "disappear when he is off medications outbreaks of oral warts that coincided with the initiation of a triple drug but reappear when his therapy is restarted." Another study found oral warts in patients also experiencing "reductions in viral load." Medscape¹s advising physician on the wart issue, Dr. Graeme Moyle, Associate Director of HIV Research at Chelsea & Westminster Hospital in London, interprets this as evidence that oral warts may be related to "immune reconstruction," turning wart outbreaks into something to celebrate.

Medscape HIV/AIDS 8(2), 2002, posted 07/10/2002 2002

xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

Ask The Expert: Outbreaks of Oral Warts Coinciding With HAART?

1

A "striking increase in oral warts" has been noted among people taking anti-HIV meds according to several reports published in the mainstream medical literature. One study found oral warts were three times more frequent in HIV positives taking "antiretroviral therapy" and six-fold more common among those on the drug combinations known as HAART. A doctor¹s letter to Medscape mentions a patient with multiple, severe outbreaks of oral warts that coincided with the initiation of a triple drug regimen. The doctor observed the warts "disappear when he is off medications outbreaks of oral warts that coincided with the initiation of a triple drug but reappear when his therapy is restarted." Another study found oral warts in patients also experiencing "reductions in viral load." Medscape¹s advising physician on the wart issue, Dr. Graeme Moyle, Associate Director of HIV Research at Chelsea & Westminster Hospital in London, interprets this as evidence that oral warts may be related to "immune reconstruction," turning wart outbreaks into something to celebrate.

Medscape HIV/AIDS 8(2), 2002, posted 07/10/2002 2002

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Conseiller Message 3 sur 15 dans la discussion

De : GlutathioneSurvival1 Envoyé : 04/09/2005 04:21

Oral Health Prev Dent. 2003;1(1):73-9. Related Articles, language=JavaScript1.2> </SCRIPT> language=JavaScript1.2> </SCRIPT> Links

Oral mucosal lesions in a UK HIV/AIDS oral medicine clinic. a nine year, cross-sectional, prospective study.

Zakrzewska JM, Atkin PA.

Barts and The London School of Medicine and Dentistry, Queen Mary College, University of London, UK. j.m.zakrzewska@qmul.ac.uk

PURPOSE: To investigate changes in presentation of oral mucosal lesions in patients with HIV/AIDS attending a dedicated oral medicine clinic over a nine year period. MATERIALS AND METHODS: 358 Patients with HIV/AIDS attending a dedicated oral medicine clinic, contained within a genitourinary medicine clinic. Data was collected prospectively for all patients attending the oral medicine clinic, and entered into a database. Lesions were recorded according to the EEC-WHO diagnostic criteria 1991/1993. RESULTS: In 358 patients with 542 lesions, over 54% of the lesions belong within one of the five categories of ulcers, warts, candidiasis, OHL and Kaposi's sarcoma. The major differences in the presentation of the lesions over time were between the ulcers and the warts, but in this series the introduction of HAART did not make a statistical difference. CONCLUSIONS: There has been a large reduction in the presentation of oral ulcers, and there appears to be a relative increase in viral papillomata, and a decrease of other mucosal diseases over the period of study. Many of the warts biopsied showed dysplastic changes, and continued follow-up of these patients will be important to determine whether these patients are at increased risk for developing oral squamous carcinoma. Also, proposals are put forward suggesting a need for alteration of the three groups of HIV/AIDS lesions classification suggested by the EEC-WHO consensus.

PMID: 15643751 [PubMed - indexed for MEDLINE]

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Lancet. 2001 May 5;357(9266):1411-2.

Effect of highly active antiretroviral therapy on frequency of oral warts.

Greenspan D, Canchola AJ, MacPhail LA, Cheikh B, Greenspan JS.

Department of Stomatology and the Oral AIDS Center, University of California at San Francisco, San Francisco, CA, USA. dgre@itsa.ucsf.edu

To investigate changes in the pattern of oral disease associated with highly active antiretroviral therapy (HAART), we assessed the frequency of these lesions in our clinic over 9 years. We retrospectively studied 1280 patients seen between July, 1990, and June, 1999, and related oral findings to medication use, immune function, and viral load. We found significant decreases in oral candidosis, hairy leucoplakia, and Kaposi's sarcoma over time, but no change in the occurrence of aphthous ulcers. There was an increase in salivary-gland disease and a striking increase in warts: three-fold for patients on antiretroviral therapy and six-fold for those on HAART (p=0.01). This pattern of oral disease in a referral clinic suggests that an increase in oral warts could be occurring as a complication of HAART.

PMID: 11356441 [PubMed - indexed for MEDLINE]]

PS notons que je connais un gay decede des suites d un cancer anal qui s est declaré deux ans aprés ARRET

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ERREUR : donc deux ans aprés arret de la tri therapie........notons que la vaseline est cancerigene..........( presente dans les preservatifs )

http://www.biam2.org/www1/Sub3701.html#SubEII

donc ma qestion :

est ce que les tri therapies ne sont pas les nouveaux anti cancereux du futur ??...

est ce que les personnes dites seropositives ne sont pas plus à risque de cancer que d autres ???...est ce que la PCP n aurait pas en diagnostic differentiel cancer des poumons au stade debutant ??....

NOTONS QUE :

les chimios anti cancereuses classiques ont pour effets secondaires le sida.

supposons que les t4 interviennent dans des processus cancereux

avec les tri therapies, on fais avec une pierre deux coups !

J ai plusieurs fois evoqué cette hypothese qui n a jamais eu d echo.......pourtant celle ci me semble la plus logique.......je n arrive pas à me faire à l idee que l etre humain soit aussi bete pour depenser des milliards dans le tout et le n importe quoi.....surtout à ce niveau !.

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Invité Le_Celte

A l'origine la molécule qui sert de base au tri-thérapie avait été dévellopée pour soignerles cancers et leucémies, vu qu'elle avais été reconnue dangereuse cet usage a été arrêté, mais dès le début de "l'épidémie" de SIDA les labo se sont empréssé de l'essayer sur les séro-positifs avec pour argument "on n'a pas de traitement pour le SIDA, essayons ca a tout hasard".... 4-spamafote.gif

20 ans plus tard ca continue, certe en "cocktail" avec d'autre molécules mais bon...

La vaseline est cancérigène??? Tu sort ca d'ou??? icon_eek.gif

Le Celte 4-guerrier.gif

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pour la vaseline voir lien indique ci dessus, celui de la biam.

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Invité Le_Celte

Le lien que tu donne concerne l'huile de vaseline/paraffine, prise par voie orale et/ou nasale.

Pas la meme chose que la vaseline en tube utilisée comme lubrifiant intime.

Le Celte

4-guerrier.gif

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Le lien que tu donne concerne l'huile de vaseline/paraffine, prise par voie orale et/ou nasale.

Pas la meme chose que la vaseline en tube utilisée comme lubrifiant intime.

Le Celte

4-guerrier.gif

pas la même chose? Eh ben zut alors!!!

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Terry,

si vous lisez bien les références données par James W. , vous constaterez que les personnes prenant la trithérapie - à la place de l'AZT seul ou d'autres thérapies comme le bactrim..., je précise - ont plus de cancer et de condylomes (warts) que la normale.

Tout ceci, n'en déplaise d'ailleurs James, qui n'est pas tout-à-fait d'accord avec moi sur le 3TC, va pourtant bien dans le sens suivant, décrit par Stefan Lanka et Heinrich Kremer :

les oxydants, qui favorisent le suicide cellulaire, font diminuer le cancer (pour lequel ce suicide cellulaire estdiminué). Les anticancéreux sont donc quelque part des oxydants...

mais les oxydants favorisent le sida...qu'on traite maintenant avec des substances antioxydantes (3TC et IP : voir les références de James sur un autre topic de Aidsmythexposed)...donc les cancers augmentent.

Tout simplement parce que notre "médecine moderne" ne sait faire que contrer les manifestations qu'elle trouve gênantes, alors qu'il eût fallu d'abord remettre le système en équilibre (homéostasie). Mais cela, elle ne sait pas le faire.

Le cancer et le sida sont simplement l'expression des limites de cette "médecine"

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*Le lien que tu donne concerne l'huile de vaseline/paraffine, prise par voie orale et/ou nasale.

Pas la meme chose que la vaseline en tube utilisée comme lubrifiant intime*

Le Celte

alors celle là on ne me l avait jamais faite....!

autre sujet :

est ce que l on utilise toujours le talc chez les enfants atteint de varicelle ??.......certains verront surement le rapprochement !

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Cheminot a ecrit :

les oxydants, qui favorisent le suicide cellulaire, font diminuer le cancer (pour lequel ce suicide cellulaire estdiminué). Les anticancéreux sont donc quelque part des oxydants...

mais les oxydants favorisent le sida...qu'on traite maintenant avec des substances antioxydantes (3TC et IP : voir les références de James sur un autre topic de Aidsmythexposed)...donc les cancers augmentent.

donc apparement nous sommes ok.....il y a bien bel et bien un lien direct et indirect entre sida et cancer......

comme vous le dite il y a donc un equilibre trés precis entre oxydation et anti oxydation.....tout excés dans un sens ou dans l autre favorisent donc la survenue de cancer.....

donc il est evident que de se bourrer d anti oxydants ( vitamine c à fortes doses ) peux conduire, chez certains, à des cancers.......etc etc.....

ce qui serait interressant c est de savoir comment quantifier/doser cette balance.....ne serais ce pas cela en fait ce que mesure la charge virale des VIH ????

y a

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greuu fausse manip :

je me demandais si il y avait des etudes de faites sur la pcr chez des patients cancereux negatifs au vih.......mon petit doigt me dit que oui......dans ce cas là il serait bon de savoir si certains derivés des tri therapies ( zoovirax par exemple ) font descendre la charge virale aussi....je pense aussi aux ipp ( inhibiteurs des pompes à protons, style mopral, lanzor )....car je reste persuadé que pleins de medicaments ont ete tirés de l azt et autre et que ceux ci sont donnés à des seronegatifs pour d autres pathologies ( ou identiques selon les diagnostics differentiels bien sur ! et surtout).....

j ai bien aimé le dernier message de cheminot....pour une fois que l on entre dans le vif du sujet.......

en ce qui concerne les t4.....rare sont les recits sur le net disant que certains seropos donc ( vu que l on les compte que chez eux, du moins ce que l on nous dit aussi ! ) aient reussis a les faire remonter sans tri therapies de manière durable.....

alors cd 4 = decompte cellulaire = horloge biologique ?

hormis les seropos, chez qui trouve t on le moins de cd4 ?? = chez les personnes agés denutries, malades ou pas.......qui a des etudes disant que la majorité des gens agés de plus de 70 ans ont plus de 800 t4 au compteur.....?....

si toute la science vih/sida ne voulait vraiment rien dire...depuis bientot 30 ans.....croyez vous tous que l on serait encore là entrain d en parler ??.....

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en ce qui concerne les t4.....rare sont les recits sur le net disant que certains seropos donc ( vu que l on les compte que chez eux, du moins ce que l on nous dit aussi ! ) aient reussis a les faire remonter sans tri therapies de manière durable.....

alors cd 4 = decompte cellulaire = horloge biologique ?

hormis les seropos, chez qui trouve t on le moins de cd4 ?? = chez les personnes agés denutries, malades ou pas.......qui a des etudes disant que la majorité des gens agés de plus de 70 ans ont plus de 800 t4 au compteur.....?....

si toute la science vih/sida ne voulait vraiment rien dire...depuis bientot 30 ans.....croyez vous tous que l on serait encore là entrain d en parler ??.....

Voilà vraiment une approche de la séropositivité et de la maladie Sida qui retient mon attention.

Comme tu le dis : Et si les tests ne mesuraient que le degré de vieillissement de certaines fonctions vitales ?

Les implications de cette approche sont énormes....et la premiére question est : comment fait on pour provoquer ce phénoméne....et comment une personne de 20 ans (par exemple) peut se retrouver avec certains paramétres vitaux d'une personne de 70 ans .

Cela lui laisse donc une espérance de vie d'une vingtaine d'années quels que soient les traitements.

Mais la deuxiéme implications est encore plus intéressante.....que signifierait guérir de la séropositivité , sinon passer de l'age de 70 ans à l'age de 20 ou 30 ans...!

Voilà bien sur une vision qui ne s'intégre pas dans la logique médicale du vieillissement .

Il est communément admis que la courbe du vieillissement évolue dans le même sens que la courbe du temps.

Un jour ces dogmes finiront par s'ecroulaient , et l'on prendra peut être conscience que dans des conditions normales de vie , l'organisme posséde toutes les ressources pour maintenir toutes les fonctions vitales à un niveau optimum , jusqu'au seuil de la mort ....

Le terme du voyage ? ....C'est quand on est arrivé là ou l'on devait allé ....alors qu'aujourd'hui on pense que .....c'est là ou la "voiture" tombe en panne.

Modifié par sicnarfa

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Pas mal votre discussion, c'est intéressant d'avoir des points de vue aussi "exotiques" (dans le bon sens du terme!)

Quand vous dites "les oxydants, qui favorisent le suicide cellulaire, font diminuer le cancer (pour lequel ce suicide cellulaire estdiminué). Les anticancéreux sont donc quelque part des oxydants..." d'accord et pas d'accord car le propre d'une cellule cancéreuse c'est qu'elle n'a pas réussi à s'autodétruire ou à ^étre détruite avant ce processus donc trop d'oxydant vont pouvoir augmenter les cancers. Les anticancéreux vont exercer une action plutôt "tueuse de cellules " malheureusement pas très spécifique en bloquant des processus vitaux pour la cellules : arrêt de la division cellulaire, séquestration de facteurs indispensables à sa survie etc.....

C'est marrant la phrase " il est evident que de se bourrer d anti oxydants ( vitamine c à fortes doses ) peux conduire, chez certains, à des cancers.......etc etc.." parce que la vit C est éliminée directement quand plus de 1g par jour mais effectivment si t'en bouffe 50g je ne sais pas !!!!!! De toute façon l'exès de quoi que ce soit est nocif non ? Le tout est d'apporter ce quil faut à l'organisme quand il en a besoin

Originale l'hypothèse CD4 = horloge biologique mais vu le nombre de paramêtres diminués chez les personnes agées, difficile de dire celui qui est le plus pertinant surtout si tu considère que les personnes avec moins de 500 T4 par ex ne sont pas plus malades que ça.

"Un jour ces dogmes finiront par s'ecroulaient , et l'on prendra peut être conscience que dans des conditions normales de vie , l'organisme posséde toutes les ressources pour maintenir toutes les fonctions vitales à un niveau optimum , jusqu'au seuil de la mort ....

Le terme du voyage ? ....C'est quand on est arrivé là ou l'on devait allé ....alors qu'aujourd'hui on pense que .....c'est là ou la "voiture" tombe en panne. " alors si on poursuit le raisonnement à un moment ou à un autre tout s'arrète comme ça d'un coup, on passe de ça va bien à on est mort ???? Notre organisme veillit parce que notre corps s'oxyde progressivement, on se détruit petit à petit jusqu'au jour où ça ne marche plus non ? Qu'est ce qui te fait penser le contraire ?

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Ce vieillissement prématuré serait tout simplement du à un usage de produits oxydants !(?)...antibios, drogues etc.....voir les écrits de cheminot......avec les tri therapies surement que les scientifiques essaient de retablir la balance oxydants/anti-oxydants, donc par la meme, recule le vieillissement.....tout simplement........mais là où ca va pas c est que d'une ca ne marche pas sur tout les sujets ( les ex toxicos tirent plus profit des tri therapies que les gays : d apres ce que je vois )....et deux les produits sont trés toxic......je note tout de meme qu une personne proche de chez moi a eu un changement de traitements ( ftc norvir et deux autres dont je ne me souviens pas le nom)....un an aprés cette personne n a pas bougé physiquement, sa lypodystrophie s est bloquée net..........et sans faire de sport sa musculature s est devellopée encore plus qu avant..........alors ??? que pensez vous de cela ??.....poar contre en lisant toutes ces analyses j ai vu que pendant 3 mois son taux de lymphocytes totaux est passé de 1200 a 3600 ( t4 150 à 330 ).....que s est il passé pendant ces 3 mois ?:

arret de la tri therapie pour un lavage comme le disent les retrovirologues, avant d entamer un nouveau traitement.....mais surtout, cette personne est resté sans toucher une cigarette pendant 3 mois .

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Invité crepator4

Il est peut etre important de differrentier ANTI-OXYDANT DE SYNTHESE ??? pour ceux qui foutent le "patacaisse" (cancer)dans les thérapies...???

Anti-Oxydant (de synthese donc icon_biggrin.gif ) que le corps ne sait peut etre pas trop gérer...comme cela arrive generalement avec tout ce qui est de synthese...

Modifié par crepator4

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