176 replies to this topic

[ajnast4r]

son of a bitch! i just bought a bottle today haha...

so is it just 600+mg doses that are a problem?

woud 300mg/day avoid the problems w/ NAC and still allow you to obtain the benefits?

[zoolander]

whoops

[methodice]

How about we keep NAC and find something to deal with the SNOAC problem. Reduce conversion to SNOAC or mop up SNOAC once it is made.

Who knows maybe it's a dose issue and a lower dose is fine.

Do we take anything that causes our blood to appear hyperoxygenated (hyperoxic-mimetic effect).

Who knows, maybe the SNOAC modecule will be found to have new benefits, and we will be able to buy SNOAC in supp form in the future.

[s123]

How about we keep NAC and find something to deal with the SNOAC problem. Reduce conversion to SNOAC or mop up SNOAC once it is made.

Who knows maybe it's a dose issue and a lower dose is fine.

I know that endothelial nitric oxide synthase inhibitors exists but I don't know of these are safe to take and if they are avoidable.
Probably, most things are dose related think about what Paracelsus told us: "dosis sola facit venenum". Only the dose causes the toxicity.

[liorrh]

take it with some kind of NO supplement and I'm guessing you'll be fine

[inawe]

According to Gaston when hypoxia is sensed pulmonary arteries narrow and PAH develops. This goes contrary to common sense. One would expect that to counter hypoxia pulmonary arteries would open up. Are we so badly designed?
The key to understand this would be in a more basic analysis of the reaction of the pulmonary vasculature to hypoxia. Could be in the paper PMID: 15483284, which I don't have.

[ortcloud]

The purpose of taking NAC is to boost glutathione. So other avenues of accomplishing that prob needs to be explored that would bypass this problem. Some options of the top of my head.


1.) determine if using a different cysteine precursor would prevent this, undenatured whey, cysteine peptide (not be be confused with l-cysteine which can even more toxic than NAC)

2. ) cutting back the cysteine precursor and compensating with glutathione recyclers, boosters. Vitamin c, turmeric, sam-e, selenium, alpha lipoic acid.(most people prob take these already, there are limits on the selenium and lipoic acid but you could add more vitamin c or also take ascorbyl palmitate, that might recycle glutathione intracellularly better than water soluble ascorbate) this might be a better strategy regardless as I suspect a diminishing roi or boost in glutahtione production with increased levels of nac consumption. Has anyone seen dose escalation studies of cysteine precursors and intracellular glutahtione levels ? As the synthesis enzyme that makes glutathione probably gets saturated at some point. Also redox balance of glutathione intracellularly seems just as important as total glutathione levels.

3.) Skip the precursors all together and use liposomal glutathione, liposomal glutathione seems to be the only way to slip glutathione through the gut and the cell wall. This might also enable one to achieve optimal levles of glutathione if some synthesis pathway is impeded or even attain supraphysiological levels of glutathione, (which may or may not be a good thing)


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[scottl]

According to Gaston when hypoxia is sensed pulmonary arteries narrow and PAH develops. This goes contrary to common sense. One would expect that to counter hypoxia pulmonary arteries would open up. Are we so badly designed?
The key to understand this would be in a more basic analysis of the reaction of the pulmonary vasculature to hypoxia. Could be in the paper PMID: 15483284, which I don't have.

My explanation that I posted was incorrect, see later post.

Edited by scottl, 11 September 2007 - 10:25 PM.

[liorrh]

PS one more thing is that NAC's bioavailability is drastically affected by other stuff you eat.

I've research on it being absorbed well with animal proein I think, whey, glutamine and I think glycine.

so taking 600mg on an empty stomach with nothing else will amount to very little.

[inawe]

According to Gaston when hypoxia is sensed pulmonary arteries narrow and PAH develops. This goes contrary to common sense. One would expect that to counter hypoxia pulmonary arteries would open up. Are we so badly designed?
The key to understand this would be in a more basic analysis of the reaction of the pulmonary vasculature to hypoxia. Could be in the paper PMID: 15483284, which I don't have.

You need to understand some basics of flow....

for example take a spigit that carries water attach a garden hose. water flows with a certain pressure. Substitite a narrower hose and the pressure forcing water out the end of the hose goes up. substitue a wider hose and the pressure goes down. Sooo if you are hypoxic, narrowing the pulm artery will increase the pressure pushing blood into the system.

Well, I was under the impression that the pulmonary artery carries to the lung blood to be oxygenated. Less blood will be oxygenated in a narrower artery.
Let us look at your illustration: "take a spigit that carries water attach a garden hose. water flows with a certain pressure. Substitite a narrower hose and the pressure forcing water out the end of the hose goes up. substitue a wider hose and the pressure goes down". This would more properly apply to the pulmonary vein, not the artery.

[zoolander]

How about we keep NAC and find something to deal with the SNOAC problem

you have to undertsand that the regulation of respiration at the brainstem is controlled by S-nitrosothiols (SNO). These SNO's include GSNO and SNOAC. Inhibiting the enzyme (gamma-GT) will also block the production of other SNO's. No good. Unfortunately the SNO formed from NAC (SNOAC) bypasses regulation and this is where the problem occurs.

Re. continuing with NAC....i would advise that you do at your own risk. Thinking that 600mg a day should be ok is a dangerous assumption in light of this recent research. Keep in mind that an increases in PAH are not looked at when they are at sub-clinical level i.e no signs and symptoms. Thickening of the RV wall could take many years in response to small increases in PAH.

Anyhow....we could see a study in the next year or so in humans that trumps the current study in mice

[scottl]

Well, I was under the impression that the pulmonary artery carries to the lung blood to be oxygenated. Less blood will be oxygenated in a narrower artery.
Let us look at your illustration: "take a spigit that carries water attach a garden hose. water flows with a certain pressure. Substitite a narrower hose and the pressure forcing water out the end of the hose goes up. substitue a wider hose and the pressure goes down". This would more properly apply to the pulmonary vein, not the artery.

My explanation was incorrect (though I know which is the pulmonary artery and vein--I used the word...I guess it was system confusingly).

In any case, the reason things work as they do is as follows:

If you have an area of the lung where there is no gas exchange i.e. no opportunity for the blood to become oxygenated, the body would prefer not to supply the pulmonary arteries in that area of the lung with blood. Thus hypoxia causes reflex vasoconstriction. This shunts blood away from that area of the lung and to other areas of the lung where there is lower resistance.

[inawe]

[QUOTE=scottl
If you have an area of the lung where there is no gas exchange i.e. no opportunity for the blood to become oxygenated, the body would prefer not to supply the pulmonary arteries in that area of the lung with blood. Thus hypoxia causes reflex vasoconstriction. This shunts blood away from that area of the lung and to other areas of the lung where there is lower resistance.[/quote]

OK then. Naively, hypoxia can be seen as blood deprived of oxygen and thus needing to be oxygenated. However, our body interprets a perceived hypoxia as a failure of of the oxygenation mechanism and shuts down the store. As i said before, we could be better designed.

[krillin]

Quoted from the original paper:

Similarly, NAC increased HIF 1 activity in whole-lung extracts in vivo (Figure 5A), though NAC suppresses upregulation of HIF 1{alpha}, the oxygen-labile subunit of HIF 1, by both substance P (31) and by oxidized low-density lipoprotein (32) in vitro

So if we block HIF-1, maybe we're safe. Vitamin C can do it. Feverfew might help.

Free Radic Biol Med. 2007 Mar 15;42(6):765-72.
Modulation of hypoxia-inducible factor-1 alpha in cultured primary cells by intracellular ascorbate.
Vissers MC, Gunningham SP, Morrison MJ, Dachs GU, Currie MJ.
Free Radical Research Group, Pathology Department, Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand. margret.vissers@chmeds.ac.nz

Control of the transcription factor hypoxia inducible factor (HIF)-1 is mediated by hydroxylation by proline and asparagine hydroxylases. These enzymes require ascorbate for optimal activity, but little attention has been given to the effect of ascorbate on HIF-1 activation. Furthermore, cells in culture are ascorbate deficient. We investigated the effect of intracellular ascorbate on HIF-1alpha protein levels and on HIF-1-mediated gene expression in two human primary cell lines (umbilical vein endothelial cells and skin fibroblasts) and one human cancer cell line (A431 epithelial cells). Under normal culture conditions the cells contained no ascorbate and adding ascorbate to the medium increased intracellular concentrations in a dose-dependent manner. A basal level of HIF-1alpha detected in nonsupplemented cells under normoxic conditions disappeared when 10 microM ascorbate was added to the medium. Induction of HIF-1alpha by hypoxia (1% O(2)) or by CoCl(2) was markedly inhibited by ascorbate and loading with physiological levels resulted in almost complete reversal of HIF-1alpha stabilisation. Gene expression was similarly affected, with VEGF mRNA and GLUT-1 up-regulation being inhibited by ascorbate. Hence intracellular ascorbate is a major regulator of the hypoxic response in normal cells and optimal levels of this vitamin will have a profound effect on HIF-1-regulated processes.

PMID: 17320759

Cancer Cell. 2007 Sep;12(3):230-8.
HIF-Dependent Antitumorigenic Effect of Antioxidants In Vivo.
Gao P, Zhang H, Dinavahi R, Li F, Xiang Y, Raman V, Bhujwalla ZM, Felsher DW, Cheng L, Pevsner J, Lee LA, Semenza GL, Dang CV.
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

The antitumorigenic activity of antioxidants has been presumed to arise from their ability to squelch DNA damage and genomic instability mediated by reactive oxygen species (ROS). Here, we report that antioxidants inhibited three tumorigenic models in vivo. Inhibition of a MYC-dependent human B lymphoma model was unassociated with genomic instability but was linked to diminished hypoxia-inducible factor (HIF)-1 levels in a prolyl hydroxylase 2 and von Hippel-Lindau protein-dependent manner. Ectopic expression of an oxygen-independent, stabilized HIF-1 mutant rescued lymphoma xenografts from inhibition by two antioxidants: N-acetylcysteine and vitamin C. These findings challenge the paradigm that antioxidants diminish tumorigenesis primarily through decreasing DNA damage and mutations and provide significant support for a key antitumorigenic effect of diminishing HIF levels.

PMID: 17785204

Cell Biochem Biophys. 2007;47(1):33-44.
Functions of serotonin in hypoxic pulmonary vascular remodeling.
Esteve JM, Launay JM, Kellermann O, Maroteaux L.
IGBMC, F-67400 France; INSERM, U596, Illkirch, F-67400 France; CNRS UMR7104, Illkirch, F-67400 France; Univ Strasbourg, Illkirch, F-67400 France.

In lung vasculature, reversible constriction of smooth muscle cells exists in response to acute decrease in oxygen levels (hypoxia). Progressive and irreversible structural remodeling that reduces blood vessel lumen takes place in response to chronic hypoxia and results in pulmonary hypertension. Several studies have shown a role of serotonin in regulating acute and chronic hypoxic responses. In this review the contribution of serotonin, its receptors and transporter in lung hypoxic responses is discussed. Hypoxic conditions modify plasma levels of serotonin, serotonin transporter activity, and expression of 5-HT1B and 5-HT2B receptors. These appear to be required for pulmonary vascular cell proliferation, which depends on the ratio between reactive oxygen species and nitric oxide. A heterozygous mutation was identified in the 5-HT2B receptor gene of a patient who developed pulmonary hypertension after fenfluramines anorexigen treatment. This C-terminus truncated 5-HT2B mutant receptor presents lower nitric oxide coupling, and higher cell proliferation capacity than the wild-type receptor. Under low oxygen tension, cells increase the transcription of specific genes via stabilization of the transcription factor hypoxia-inducible factor (HIF)-1. Factors such as angiotensin II or thrombin that can also control HIF-1 pathway contribute to pulmonary vascular remodeling. The 5-HT2B receptor via phosphatidylinositol-3 kinase/Akt activates nuclear factor-kappaB, which is involved in the regulation of HIF-1 expression. Acontrol of HIF- 1 by 5-HT2B receptors explains why expression of pulmonary vascular remodeling factors, such as endothelin-1 or transforming growth factor-beta, which is HIF-1-alpha regulated, is not modified in hypoxic 5-HT2B receptor mutant mice. Understanding the detailed mechanisms involved in lung hypoxic responses may provide general insight into pulmonary hypertension pathogenesis.

PMID: 17406058


Acta Pharmacol Sin. 2000 Dec;21(12):1106-14.
5-Hydroxytryptamine-inhibiting property of Feverfew: role of parthenolide content.
Mittra S, Datta A, Singh SK, Singh A.
Panacea Biotec Limited, P O Lalru 140501, Punjab, India.

AIM: To study the mechanism of antimigraine activity of Tanacetum parthenium (Feverfew), its extracts and parthenolide, a component of Feverfew, by observing their effect on 5-HT storage and release, and stimulation of 5-HT2B and 5-HT2A receptors. Also to standardize a dosage form of Feverfew with respect to its parthenolide content. METHODS: Isometric responses to 5-HT and an indirect acting serotonergic, d-fenfluramine, were obtained on rat fundus and ileum. In one set of experiments the effect of dichloromethane extract of Feverfew and parthenolide was observed on the above. The extract was then thermally degraded upto 10%, 23%, and 33% with respect to its parthenolide content by keeping at 60 degrees C and 75% relative humidity and the experiments were repeated. In another set of experiments rats were fed with 20 mg/kg Feverfew powder (equivalent to a human dose of 500 micrograms parthenolide per day) for 30 d or were i.p. injected with parthenolide (23.4 micrograms/day) for 7 d. In the same set of experiments one group of rats were fed with 15% and 77% degraded Feverfew powder in the same dose as mentioned above. After 30 days the effects of the above were observed on 5-HT and d-fenfluramine. Feverfew was specially formulated and tested for stability under accelerated conditions. RESULTS: Parthenolide (1 x 10(-5) mol/L) non-competitively antagonised the effects of d-fenfluramine but had no significant effect on 5-HT2B and 5-HT2A receptors in rat fundus and ileum at 30 min which turned significant on increasing the incubation time to 1.5 h, in rat fundus. Parthenolide (5 x 10(-5) mol/L) followed the same trend. However, Feverfew extract (1 x 10(-5) mol/L) potently and directly blocked 5-HT2B and 5-HT2A receptors and neuronally released 5-HT. At 5 x 10(-5) mol/L the extract potently and irreversibly blocked the above. Both parthenolide and Feverfew extract showed a time-dependency in their action. The extract when degraded thermally upto 10% could significantly block the 5-HT receptors and neuronal release of 5-HT, however, on further degradation it lost its inhibitory capacity markedly. Similar results were observed in rats fed orally with undergraded and degraded Feverfew powder and injected i.p. with parthenolide. Feverfew powder was more effective than any of its extracts or pure parthenolide. CONCLUSION: Feverfew powder is more potent than any of its extract or parthenolide alone in its antiserotonergic activity. Degraded Feverfew extracts show a marked decrease in their antiserotonergic activity. With thermally degraded Feverfew powder containing less contents of parthenolide no built-up antiserotonergic responses were observed after one month. This ascertains that Feverfew should be dispensed in a properly stabilized form wherein its parthenolide content is not degraded to less than 90% of the original content.

PMID: 11603284

[zoolander]

hang on one second. People are suggesting that we try and inhibit enzymes/reactions that are vital to the central control of respiration. Don't you see that this could lead to problems that are worse than the original problem.

What we have is one byproduct (SNOAC) involved in the same reaction as other SNO's but somehow SNOAC does not react the in the same manner as the others. It's sort of like the cancer cell that decides to ignore the stop phase in the replication cycle. You don't go and stop all cells from replicating just to stop the cancer cell do you. It's easier to remove the precursor that started or will start the cell going into uncontrolled replacation in the first place i.e the carcinogen

[ajnast4r]

im with zoo on this one

[health_nutty]

Me too. NAC is out. I'll rely on ALA to boost my glutathione.

[mike250]

I'm going to wait a bit until those human studies are done.

[zoolander]

The important thing is that as much information as we can find on the subject be provided here for people to review. That way everyone can make their own informed choice yay or nay

[inawe]

Sildenafil has been used as a palliative of pulmonary hypertension.
Wonder if is any good in preventing it.

[health_nutty]

I'm going to wait a bit until those human studies are done.

While you are waiting you going to take NAC or not? It wasn't clear.

[mike250]

I'm going to wait a bit until those human studies are done.

While you are waiting you going to take NAC or not? It wasn't clear.

I've been taking 600mg up until now. I will probably lower my dosage and keep using it until more research can confirm this.

[efosse]

A question: my mom has been smoking cigarettes for 40+ years. I urged her to take NAC due to its effects on pulmonary diseases often associated with smoking.

Question: should someone who has a high risk for lung-related diseases avoid NAC in light of this recent study?

Thanks and much appreciated,
efosse

[ortcloud]

I wonder if they will pull it from the lef mix ?

[trh001]

hang on one second. People are suggesting that we try and inhibit enzymes/reactions that are vital to the central control of respiration. Don't you see that this could lead to problems that are worse than the original problem.

What we have is one byproduct (SNOAC) involved in the same reaction as other SNO's but somehow SNOAC does not react the in the same manner as the others. It's sort of like the cancer cell that decides to ignore the stop phase in the replication cycle. You don't go and stop all cells from replicating just to stop the cancer cell do you. It's easier to remove the precursor that started or will start the cell going into uncontrolled replacation in the first place i.e the carcinogen

"hang on one second. People are suggesting that we try and inhibit enzymes/reactions that are vital to the central control of respiration. Don't you see that this could lead to problems that are worse than the original problem."

Great point. [thumb]

What I worry about: REDOX reactions, as information, or in this case misinformation, is a central theme in the risk of supplementing. Bruce Ames documented adaptive gene expression to "antioxidants" (quotes, to underscore the context-based nature of any such attribute) as early as the 80's.

A fairly recent example of this:

Mech Ageing Dev. 2006 Dec;127(12):897-904. Epub 2006 Nov 7. Links
Life-long vitamin C supplementation in combination with cold exposure does not affect oxidative damage or lifespan in mice, but decreases expression of antioxidant protection genes.Selman C, McLaren JS, Meyer C, Duncan JS, Redman P, Collins AR, Duthie GG, Speakman JR.
Aberdeen Centre for Energy Regulation and Obesity (ACERO), School of Biological Sciences, University of Aberdeen, Aberdeen AB24 2TZ, UK. c.selman@ucl.ac.uk

Oxidative stress is suggested to be central to the ageing process, with endogenous antioxidant defence and repair mechanisms in place to minimize damage. Theoretically, supplementation with exogenous antioxidants might support the endogenous antioxidant system, thereby reducing oxidative damage, ageing-related functional decline and prolonging life- and health-span. Yet supplementation trials with antioxidants in animal models have had minimal success. Human epidemiological data are similarly unimpressive, leading some to question whether vitamin C, for example, might have pro-oxidant properties in vivo. We supplemented cold exposed (7+/-2 degrees C) female C57BL/6 mice over their lifespan with vitamin C (ascorbyl-2-polyphosphate), widely advocated and self administered to reduce oxidative stress, retard ageing and increase healthy lifespan. No effect on mean or maximum lifespan following vitamin C treatment or any significant impact on body mass, or on parameters of energy metabolism was observed. Moreover, no differences in hepatocyte and lymphocyte DNA oxidative damage or hepatic lipid peroxidation was seen between supplemented and control mice. Using a DNA macroarray specific for oxidative stress-related genes, we found that after 18 months of supplementation, mice exhibited a significantly reduced expression of several genes in the liver linked to free-radical scavenging, including Mn-superoxide dismutase. We confirmed these effects by Northern blotting and found additional down-regulation of glutathione peroxidase (not present on macroarray) in the vitamin C treated group. We suggest that high dietary doses of vitamin C are ineffective at prolonging lifespan in mice because any positive benefits derived as an antioxidant are offset by compensatory reductions in endogenous protection mechanisms, leading to no net reduction in accumulated oxidative damage.

PMID: 17092545 [PubMed - indexed for MEDLINE]

If the above assessment is correct, then, similar to what Ames said 20-30 years ago, "it's not nice to" [try to] "fool mother nature" (sorry, I have fond memories of those commercials about the butter substitute, given the vast increase in colon cancer rates in response to polyunsaturates that saturated the market.) Or we could note de Grey's cautionary remarks, as well.

Historically I've always sided with something like, "show me a compound that purports to be an antioxidant, and doing something in vivo, and one generally can expect to see a later paper showing a non-REDOX effect that seems to account for it."

NAC, seems to be an exception here.

However, this only serves to underscore the danger, rather than the (in general) futility of assigning the "antioxidant" attribute: occasionally one gets efficacy.

Still, the authors of the NAC study note "10 mg/ml NAC in the drinking water for 3 weeks (achieving serum NAC levels of 16.2 ± 4.3 µM as measured by liquid chromatography/MS). " Assuming a mouse drinks an ml of water per day, more or less continuously accessing the water bottle in 0.1ml doses, that's 50mg/kg (assuming a mouse is ca. 0.02kg) x 10 doses per day. So, aside from lack of continuous exposure in the case of the 600mg dose that most have indicated they take, we have, perhaps, a ca. 10mg/kg dose for a light person (60kg) taken once per day. I've seen mice really hit the bottle, too, so perhaps their dose estimate might be a bit higher?

Net-net: Probably not much similarity in the pharmacokinetic plots.

On the other hand, there were, as much as 10-20 years ago, other reasons to avoid NAC.

I recall a paper that showed GSH increases in response to NAC in all tissues examined, with exception of bone marrow.....where it dropped precipitously post dosing of NAC. This is a decade-old recollection, and I'll try and dig up the reference. Still, again, I recall looking at the doses used and wondering if my small dose would amount to much. I seem to recall thinking it unlikely, then.

Additionally, if one *really* wanted to worry, one could start to generalize to other sulfhydryl cpds, such as those found in garlic.

A recent paper that made me concerned about my daily salad with fresh garlic:

J Interferon Cytokine Res. 2007 May;27(5):377-82. Links
Systemic production of IFN-alpha by garlic (Allium sativum) in humans.Bhattacharyya M, Girish GV, Karmohapatra SK, Samad SA, Sinha AK.
Sinha Institute of Medical Science & Technology, 288 Kendua Main Road, Garia, Calcutta 700 084, India.

The effect of foods on the production of interferon-alpha (IFN-alpha) is currently unknown. Garlic (Allium sativum) used as a folk medicine is reported to stimulate nitric oxide (NO) production. We investigated the systemic increase of NO due to the ingestion of garlic on the plasma IFN-alpha level in normal volunteers. Normal volunteers (10 groups, 10 in each group) ate 2 g fresh garlic, and plasma NO and IFN-alpha levels were determined after 2 and 4 h. The participants were also asked to eat garlic for various periods of time, and plasma NO and IFN-alpha were similarly assayed. Ingestion of 2 g fresh, but not boiled, garlic was found to increase the basal plasma level of NO from 2.7 +/- 0.1 microM to 8.76 +/- 0.21 microM at 2 and 4 h, respectively. The basal plasma IFN-alpha level increased from 9.51 +/- 0.26 nM to 46.3 +/- 1.2 nM in normal volunteers (n = 10) at the same time. The chronic eating of garlic was found to maintain IFN-alpha at high levels for at least 7 days. The exposure of neutrophils to garlic in vivo or in vitro, which also stimulated synthesis of NO in these cells, was found to stimulate IFN-alpha synthesis as measured by the stimulation of IFN-alpha mRNA synthesis. Thus, consumption of garlic resulted in stimulated synthesis of NO and, in turn, IFN-alpha in humans, which could be beneficial in viral or proliferative diseases.

PMID: 17523869 [PubMed - indexed for MEDLINE]


Great if one has a cold, but does one really want chronic upregulation of inflammatory mediators given the role of chronic inflammation in aging and various disease states?

Finally, what sort of collective reductant effect might an entire host of "antioxidants" have additively or synergistically, assuming they were all effective as indicated (e.g they really did function as antioxidants in vivo)?

Difficult to assess and impossible to speculate (productively) on all this (at this hour, anyway). [glasses]

Edited by trh001, 12 September 2007 - 06:36 AM.

[scottl]

I do not wish to contribute to thehysteria, but feel I should correct some false assumptions about pulmonary artery hypertension.

http://www.emedicine...d/topic1962.htm

Early symptoms are nonspecific. Often, neither the patient nor physician recognizes the presence of the disease, which leads to delays in diagnosis. Complicating matters, PPH requires an extensive workup in an attempt to elucidate an identifiable cause of the elevated pulmonary artery pressure.

[chipdouglas]

I do not wish to contribute to thehysteria, but feel I should correct some false assumptions about pulmonary artery hypertension.

http://www.emedicine...d/topic1962.htm

Early symptoms are nonspecific. Often, neither the patient nor physician recognizes the presence of the disease, which leads to delays in diagnosis. Complicating matters, PPH requires an extensive workup in an attempt to elucidate an identifiable cause of the elevated pulmonary artery pressure.

Scottl,

Will you personnally keep taking NAC at same dosage you've for years, or rather you'll keep it at 600 mg/day just in case ?

[chipdouglas]

This is weird. NAC has been found to protect against hypoxia-induced PH in previous studies. And, if this was going to happen in humans, I would think it would have already been reported as this should affect high-level athletic performance.

Something which has crossed my mind, is the so-called conspiracy against dietary supplements--is it possible that some study results are knowingly skewed to fit a predetermine outcome ? It crossed my mind, but I do not personally think this is what is going on.

I think this conspiracy against dietary supplements is probably blown out of proportion by some, although we all know that money rules our world. But on the other hand, I don't think that the instance of NAC has anything to do with such a theory, since NAC is used in hospitals.

I do not want people to think that I'm buying this rumor going around for some time, unless someone who's closely involved in this sector comes and tells me otherwise.

[inawe]

NAC might be dangerous. Don't gamble with your health
http://www.clinicalt...how/NCT00273702

[chipdouglas]

I asked Roger Mason, who's a biochemist from this website : http://youngagain.com/ Yes I know he's selling supps. but I think this man is very honest given the low prices of his supps. and only sells supplements with good science behind them.


Anyway, I asked him to share his take on the NAC study and this is what he wrote :

you really need to be more discriminating here. if there are 100 studies that
say NAC is a valid supplement, and 1 study that says it isn't, who are you
going to believe? have you read the study? of course you haven't. did you
notice it was done on mice? do you have any idea how much they were
given or if they were injected? of course you don't. you read one article
on the internet by a MEDICAL DOCTOR who eats garbage, never take
supplements or hormones, poisons people and butchers them, and you're
ready to throw your NAC in the trash. not very rational, huh?
do you think i do this part time after i get home from my real job? i have
an entire file on NAC. every month we get more clinical proof of the
effectiveness. why do you think we sell NAC when we only sell 65
supplements?
i will bet money the mice were injected and totally overdosed to the
point of ridiculousness. what kind of "study" is that?