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Author Topic: good news count up to 510 and no meds yet on Niacinamide****  (Read 1435 times)

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Offline bimazek

  • Member
  • Posts: 781
good news count up to 510 and no meds yet on Niacinamide****
« on: April 18, 2007, 08:33:12 PM »
good news my count went up to 510 and no meds yet
i have been poz for two years and two months
my numbers went down last test to 410 and 16% now they went up to 510 19%
they had been 450-592 and 24% for a year

what am i doing?

swim and exercise everyday, i notice if i do not swim and get extra oxygen-ated every day i feel tired and fatigued   i swim with snorkelling swim fins and just kick for an hour, i dont like my hair wet also do dolphin kick

i take   

Selenium and

ECGC green tea extract avail at trader joes cheap and i take

Niacinamide****  I had to order this as bulk powder... it is suppose to help and here is the science behind it...

anti-HIV studies performed from 1991 to the present. This review brings together these 2 bodies of inquiry and raises the possibility that, with more study, this small molecule could emerge at the beginning of the 21st century either as a therapeutic agent in itself or as the lead compound for a new class of agents with activity against both M. tuberculosis and HIV.   

Here is the article.  nicotinamide (niacinamide)
http://www.sandiegomilliondollarwebpage.com/niacinamide.html

 The story of nicotinamide's antimycobacterial capacity is unknown to many, because the literature predates the careers of most people currently involved in the treatment of these infections as well as the National Institutes of Health PubMed database [1]. In 1945, the first trials of streptomycin that involved humans were taking place in the United States [2], and a worldwide search for other effective antiMycobacterium tuberculosis therapies was underway. That year, in Paris, Ernst Huant [3] reported a serendipitous discovery regarding the use of nicotinamide for the treatment of patients undergoing radiation therapy for "lung tumors." He found that nicotinamide therapy, which he had initiated in an attempt to protect patients' mucous membranes from the effects of radiation, shrunk those lung infiltrates that were caused by M. tuberculosis. This report complemented another report from France by Chorine [4], who suggested a new role for nicotinamide, distinct from its known vitamin effect, as an antiM. tuberculosis therapy. McKenzie et al. [5], who apparently were screening compounds without knowledge of either Huant or Chorine's work, independently confirmed these findings.
     Two structurally related compounds, pyrazinamide and isoniazid, were found to be effective antiM. tuberculosis therapies in the period from 1945 through 1951; these discoveries were made, in part, through the use of nicotinamide as a lead compound (figure 1) [6, 7]. Nicotinamide monotherapy resulted in clinical improvement for up to 64% of M. tuberculosisinfected patients described in published reports [8]. However, interest in nicotinamide as a treatment for M. tuberculosis faded rapidly when one of the foremost research groups of the day reported antagonism between nicotinamide and isoniazid when they were used together as a 2-drug therapeutic regimen

2003 Feb 1
    Nicotinamide: an oral antimicrobial agent with activity against both Mycobacterium tuberculosis and human immunodeficiency virus.    Department of Medicine, Brigham and Women's Hospital, Harvard University, Boston, MA 02115, USA. mmurray@partners.org

    Coinfection with Mycobacterium tuberculosis and human immunodeficiency virus (HIV) is responsible for one-third of all deaths due to acquired immunodeficiency syndrome. More than 99% of cases of HIV-M. tuberculosis coinfection occur in the developing world, where limited resources add urgency to the search for effective and affordable therapies. Although antimicrobial agents against each of these infections are available, single agents that have activity against both M. tuberculosis and HIV are uncommon. The activity of nicotinamide has been evaluated in 2 different eras: in anti-M. tuberculosis studies performed during 1945-1961 and in anti-HIV studies performed from 1991 to the present. This review brings together these 2 bodies of inquiry and raises the possibility that, with more study, this small molecule could emerge at the beginning of the 21st century either as a therapeutic agent in itself or as the lead compound for a new class of agents with activity against both M. tuberculosis and HIV.



     By the 1990s, all of this information had fallen into relative obscurity. In fact, a comprehensive review of nicotinamide's pharmaceutical effects, published in 1991 (the year of the first reported use of nicotinamide in HIV research), makes no mention of its effects against M. tuberculosis [10].
     In the past decade, 3 different hypotheses have prompted the testing of nicotinamide for use as therapy for HIV. First, several groups studied the effects of treatment with nicotinamide for HIV, giving attention to its inhibitory activity against the nuclear enzyme poly-ADP ribose polymerase (PARP) [11, 12]. Second, in 1995, when we reported that nicotinamide was an inhibitor of HIV [13], our hypothesis was generated out of interest in potential correlations between pellagra and AIDS [14]. Third, Cossarizza et al. [15] pursued studies of nicotinamide in the context of its antioxidant properties, and they reported inhibition of HIV-induced cellular damage. Of interest, these hypotheses were all pursued without reference to the antiM. tuberculosis data that preceded them by  years.       Single agents with activity against both HIV and M. tuberculosis are rare.

 Although some of the nucleoside reverse-transcriptase inhibitors have been shown to have antibacterial inhibitory effects in addition to their known antiretroviral effects, this antibacterial activity does not extend to mycobacteria [16]. A number of cytokines have been shown to be significant in both infections, and therapeutic cytokine delivery for these infectious diseases is an area of active investigation [17, 18]. Nicotinamide is neither a reverse-transcriptase inhibitor nor a cytokine. Although nicotinamide is an inexpensive and orally available agent without significant side effects that has been in use for 65 years, there remain many unanswered questions regarding its unusual antimicrobial spectrum.

HIV-1 AND NICOTINAMIDE
     The first study of nicotinamide against HIV was published in 1991 [11]. This study showed the efficacy of nicotinamide and other PARP inhibitors as antiretroviral agents. Also, in 1991, Yamagoe et al. [12] reported that nicotinamide could inhibit the HIV long terminal repeat in an inducible in vitro system. Furlini et al. [40] demonstrated that HIV infection was associated with an increased intracellular ADP ribosylation of proteins. PARP activity recently was shown to be critical to efficient HIV integrase action, and inhibition of this enzyme with nicotinamide may cause inhibition at the point of proviral integration [41], although nicotinamide's activity in a postintegrational HIV model system suggests that other points in the virus's life cycle are also affected.
     We have postulated that HIV induces niacin depletion. This is based on 4 observations: a pentad of features common to HIV and pellagra (table 2), the existence of a model for clinically significant infection-induced vitamin deficiency (i.e., measles and vitamin A) [42], the existence of other inducible nondietary niacin deficiency states (table 3), and the lack of any specific dietary niacin deficiency in HIV-positive patients [43]. Plasma tryptophan deficiency, which is 1 of 5 shared features of HIV and pellagra, has been demonstrated in HIV-positive patients by several groups. In a test of the use of pharmacological doses of nicotinamide for HIV-infected persons, we found a specific and significant increase in plasma tryptophan levels after 2 months of treatment with high-dose nicotinamide [22]. Further study is needed to determine whether this therapy has effects on virus load, immune function, or clinical outcomes.
 Table 2.          Pentad of shared features of classical dietary pellagra and HIV infection.
 Table 3.          Dietary and nondietary causes of pellagra.

     Observational studies of niacin (i.e., pooled nicotinic acid and nicotinamide) intake among HIV-infected persons in the United States have suggested that even modest increases in niacin intake are associated with beneficial outcomes. Abrams et al. [44] observed that higher niacin intake was associated with higher CD4 cell counts. When Tang et al. [45] studied the Multicenter AIDS Cohort Study cohort with use of time to death as the clinical endpoint, they observed that a daily niacin intake equaling 34 times the US recommended daily allowance correlated, as an independent variable, with slower progression and improved survival. These data imply that increasing the niacin intake from the US recommended daily allowance of 20 mg/day (0.3 mg/kg/day) to >64 mg/day (1 mg/kg/day), independent of other interventions, may prolong the life of HIV-infected patients (figure 4). Although this dosage of niacin would not be expected to yield plasma concentrations comparable to the observed in vitro antiviral threshold, the effects of niacin observed by Tang et al. [45] and Abrams et al. [44] may be the result of benefits other than direct antiviral effects, such as the repletion of intracellular NAD concentrations in uninfected nonT lymphocyte "bystander cells"

The beneficial effects of nicotinamide for the treatment of HIV infection appear to be linked to cellular utilization of NAD. Nicotinamide appears to be void of any cell-free reverse-transcriptase inhibition or virucidal activities [13]. However several cell-associated observations link HIV, nicotinamide, and NAD. HIV-infected cells demonstrate an increase in the ADP ribosylation of proteins, a phenomenon in which NAD is used as the ADP-ribose donator to covalently modify proteins [40]. As a general feature, nicotinamide inhibits ADP ribosylation reactions. Protein ADP ribosylation can occur in the nucleus, in the cytoplasm, and on the cell surface of lymphocytes. PARP is a nuclear enzyme that catalyzes the formation of ADP-ribose polymers that attach to multiple different proteins. The activity of PARP is critical to the integration of foreign DNA, including proviral DNA; inhibition or absence of this enzyme interrupts the HIV life cycle [41]. Along with poly-ADP ribosylation, monoribosylation steps also involve proteins in cells, including the ADP ribosylation of both HIV Tat protein [61] and cellular defensins [62, 63]. The antimicrobial action of nicotinamide might also work through the modulation of certain histone deactylase reactions (i.e., Sir2 proteins) that use NAD in the silencing of chromosomal DNA expression [64].

There is interest in nicotinic acid as a lipid-modulating agent for HIV-infected patients receiving HAART, and several clinical trials have been initiated [21, 70]. Nicotinic acid used in pharmacological doses would be expected to raise circulating nicotinamide concentrations in participating patients via conversion in the liver and red blood cells. Although it is possible that these clinical trials may shed light on the use of niacin compounds for the treatment of HIV-infected patients, drawing conclusions from the secondary analysis of any study always requires caution.
     The death toll associated with HIVM. tuberculosis coinfection was estimated to be 1 million deaths in 1999 [71]. Although nicotinamide, compared with most pharmacological agents, is a relatively weak inhibitor in both infections, there are several reasons to pursue evaluation of its potential use: it is nontoxic, orally available, and inexpensive, and it appears to have prohost effects. Nicotinamide exists in food, but, unlike other vitamins, it can also be synthesized in the human body; therefore, it can be viewed as a vitamin or nutritional supplement in low concentrations or a drug when used in pharmacological concentrations. As with any drug, the use of nicotinamide needs to be monitored for potential associated side effects. Nicotinamide, a "pellagra-preventive" agent first used in 1937, may eventually contribute to therapeutic approaches of the 21st century as part of regimens used as "AIDS-preventive" agents [72] and "tuberculosis-preventive" agents.

Here is the article. Take a multivitamin and nicotinamide (niacinamide)
 
http://www.sandiegomilliondollarwebpage.com/niacinamide.html

stephen martin told me about it

 


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