NAC (cysteine) Increases Melanoma Spread

Dr. B

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It is useful too break up mucus because it breaks the di-sulfide bonds in the mucus, allowing it to thin out, hence more easily flowing to be removed.
I would like to see studies on the stomach assumption, I have the feeling that dose plays a big part in that assertion. My stomach has felt better since using NAC. It may have drawbacks, but then everything does, so if something mitigates a problem that nets worse outcomes, the harm is less than the cure, if there is even a harm.
I havenr seen studies but it was actually the legion supplement companys research director who cautioned me on NAC, even though their multivitamin i believe contained some. And yes he did mention dose. But I wonder if nac becomes more risky for people who already have leaky gut or slow metabolism?
 

Dave Clark

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I havenr seen studies but it was actually the legion supplement companys research director who cautioned me on NAC, even though their multivitamin i believe contained some. And yes he did mention dose. But I wonder if nac becomes more risky for people who already have leaky gut or slow metabolism?
I know some people use high doses, and this may be the problem. I only use 600 mg at night before bed, which seems to keep allergies attenuated, especially this time of year. Too much NAC may strip away mucus lining protection, but I have not heard that at low doses. As always, I keep tuned in to on going research and anecdotal reports. Right now it is working for me, but nothing is written in stone when it comes to health science, and while NAC may be very valuable to some, it may cause problems for others.
 
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The Baylor study is very compelling. They analyzed various biomarkers of aging and they all seem to improve dramatically during the short study period. But the benefits disappear or at least reduce after stopping.


GlyNAC supplementation improves mitochondrial dysfunction​

Mitochondria generate energy to support life. Aging is associated with mitochondrial dysfunction, which could result in impaired energy availability. In this study, compared to fasting YA, fasting OA had two key defects in fasting MFO – impaired mitochondrial fatty-acid oxidation and elevated mitochondrial glucose oxidation (MGO). In an earlier study in OA, we found and reported that GlyNAC supplementation for 2 weeks improved mitochondrial fatty-acid oxidation.20 However, the effect of long-term GlyNAC supplementation on MFO in OA was unknown, especially in relation to the possibility of tachyphylaxis. This study supplemented GlyNAC in OA for a longer duration of 24 weeks and found that the impaired mitochondrial fuel oxidation improved after taking GlyNAC for 12 weeks, without any evidence of tachyphylaxis after 24 weeks of taking GlyNAC. However, the improvements in mitochondrial function were lost on stopping GlyNAC for 12 weeks. These data are consistent with our prior publication that GlyNAC supplementation in aged mice corrected mitochondrial function measured by tracer methodology and molecular techniques.20 These results are important and relevant because effective interventions to improve or correct mitochondrial dysfunction in OA (or any human condition) are currently lacking, and GlyNAC supplementation could offer a novel nutritional approach to improve and correct mitochondrial dysfunction in older humans and possibly other human conditions. Additional evidence that GlyNAC supplementation could improve mitochondrial dysfunction in other human conditions comes from our recent report in HIV patients where supplementing GlyNAC at identical doses fully corrected mitochondrial dysfunction.50 Although data from this pilot study suggest that GlyNAC can improve mitochondrial function in older humans, this should be confirmed in a randomized clinical trial in older humans.

GlyNAC supplementation improves inflammation and endothelial dysfunction​

Chronic, elevated inflammation, and endothelial dysfunction are linked to OxS and to many diseases of aging,51, 52 but underlying contributory mechanisms are not well understood, and interventions are limited. Consistent with the published literature, this study found that OA had severely elevated inflammation and endothelial dysfunction, but found that these defects improved with GlyNAC supplementation. Data from this trial indicate that GlyNAC supplementation could combat inflammation by its dual actions on lowering elevated levels of pro-inflammatory cytokines (IL6, TNFα and CRP) and simultaneously increasing the anti-inflammatory response. It is also interesting to note the measured markers of inflammation and endothelial function do not return to pre-supplementation values after 12 weeks of withdrawing GlyNAC – this suggests a long-term persistence of benefits due to GlyNAC. The mechanisms to account for this are not clear and should be investigated in future studies.

Because inflammation, endothelial dysfunction, insulin resistance, mitochondrial dysfunction, and increased waist circumference are linked to an elevated risk of metabolic syndrome and cardiovascular disease in aging humans, improvements in these defects with GlyNAC supplementation suggest the possibility of promoting cardiovascular and cardiometabolic health. Evidence to support this comes from our recent publication where GlyNAC supplementation in aged mice was found to correct defective cardiac mitochondrial energetics, lower cardiac inflammation, and improve diastolic dysfunction.53 Further studies are needed to understand the impact and implications of GlyNAC supplementation on lowering inflammation, endothelial dysfunction, and cardiometabolic risks in aging humans.

GlyNAC supplementation lowers insulin resistance​

GlyNAC supplementation significantly lowered insulin resistance in OA. Elevated OxS has adverse effects on insulin signaling54 and Glut4 transcription,55 and promotes inflammation56 and mitochondrial dysfunction.57-59 The improvement in OxS, inflammation and mitochondrial dysfunction in this study could have contributed to the observed significant decrease in insulin resistance.

GlyNAC supplementation improves cognition​

Aging is the greatest risk factor for cognitive decline and dementia affecting millions of OA and results in impaired learning, memory, executive function, attention, language, perceptual motor function, and social cognition,60 but effective interventions are either limited or lacking.

Glucose is the primary fuel for the brain. In this study, we found two paradoxical observations regarding whole-body MGO and cognition as measured by testing performance: (1) prior to starting GlyNAC supplementation, OA had impaired cognition (compared to YA) despite increased whole-body MGO and (2) after GlyNAC supplementation their whole-body MGO decreased, but cognition improved. The most parsimonious explanation for these opposing and paradoxical findings is as follows: In the fasting state, glucose provides energy for the brain, and fatty-acids provide energy for non-brain tissues. GSH adequacy is essential for optimal mitochondrial fatty-acid oxidation.20 OA in this study had GSH deficiency, impaired whole-body mitochondrial fatty-acid oxidation and higher whole-body MGO prior to GlyNAC supplementation suggesting that non-brain tissues were using glucose instead of fatty-acids for energy needs. However, tracer studies indicated that the glucose production rates in OA were not increased compared to YA and did not change with GlyNAC supplementation, suggesting that the available glucose pool remained constant. In this situation where the glucose pool available for energy needs has not expanded, any increase in glucose consumption by non-brain tissues will lead to diminished glucose availability for the brain. We term this the "glucose-steal phenomenon" where non-brain organs by virtue of switching to glucose oxidation are competing for glucose with the brain. This "glucose-steal" could explain the paradox of increased whole-body MGO, but lower cognitive performance. With GlyNAC supplementation, the non-brain tissues revert to using fatty-acids as a source of fuel and relinquish utilization of glucose – this results in a fall in the magnitude of whole-body MGO, and more glucose is now available for the brain (a reversal of the "glucose-steal phenomenon"), and cognitive improves. Elevated insulin resistance could also impact cognition by limiting glucose entry into the brain, and improvement in insulin resistance has been linked to improved cognition.61 OA in this study had severely elevated insulin resistance which improved significantly with GlyNAC supplementation and could have contributed to cognitive improvement. The dual impacts of glucose-steal and elevated insulin resistance in this study could help explain why FDG-PET scans show low glucose uptake in cognitively impaired OA.62 Because cognitive impairment is also associated with elevated brain inflammation and endothelial dysfunction,63 improvements in these defects with GlyNAC supplementation could also have contributed to cognitive improvement in this study. GlyNAC could also be having a direct effect in the brain as seen by a significant increase in the diminished levels of the brain biomarker BDNF. BDNF is involved in the preservation of memory, synaptic plasticity, and maintenance of neuronal networks,64, 65 and lower plasma levels of BDNF are associated with lower cognitive test scores and mild cognitive impairment.66 In this study, OA with lower cognitive scores had lower levels of BDNF, which improved significantly in parallel with the cognitive improvement with GlyNAC supplementation, and fell on stopping GlyNAC. The results of the study do not support that cognitive improvements may occurred due to practice effects as a result of repeated testing. The basis of the practice effect is that test scores improve with repeated test taking. The cognitive test scores of OA did improve between the first time it was administered (0 weeks), midpoint (12 weeks) and end of supplementation (24 weeks). However, when it was taken a 4th time, 12 weeks after stopping supplementation (at 36 weeks), several scores declined, which argues against a learning/practice effect. Changes in BDNF concentrations which track closely with cognitive changes in this study as a result of GlyNAC supplementation and withdrawal also argue against a practice effect. Collectively, these observations offer early exciting leads which suggest that GlyNAC supplementation could potentially improve cognitive function in OA. Although this is a pilot trial, these findings could be relevant because cognitive impairment in OA is not well understood, and there are no effective interventions, and results support the need for future trials focused on GlyNAC to understand its impact on cognition as well as underlying mechanistic defects linked to cognition in terms of OxS, GSH deficiency, mitochondrial impairment, inflammation, insulin resistance, and endothelial function.

GlyNAC supplementation improves muscle protein breakdown – implications for sarcopenia​

Maintaining optimal muscle mass depends on a balance between muscle protein synthesis and breakdown. In the fasting state, muscle protein breakdown exceeds synthesis,67 which results in net protein loss. Sarcopenia in OA involves both declining muscle mass and declining muscle strength. Combating sarcopenia is restricted to boosting muscle protein synthesis, due to lack of interventions to lower muscle protein breakdown. Therefore, our finding that GlyNAC supplementation decreases muscle breakdown could have important implications for sarcopenia. However, muscle mass did not improve with GlyNAC, suggesting that combining dual strategies to boost muscle synthesis and also decrease breakdown may be necessary for combating muscle loss in sarcopenia. Although there was no increase in muscle mass, GlyNAC supplementation was associated with a significant improvement in muscle strength and physical function, and this is discussed next.

GlyNAC supplementation improves gait speed, strength, and exercise capacity​

Increasing age is associated with physical decline and diminished exercise capacity, both of which are components of sarcopenic obesity in OA. Although a key meta-analysis in OA has shown that lower gait speed is linked to decreased survival,68 restoring gait speed in OA to levels seen in YA has been difficult to achieve. This study found that GlyNAC supplementation for 24 weeks increased gait speed in OA to match YA while simultaneously improving muscle strength and exercise capacity, suggesting that GlyNAC supplementation improves physical function in OA. While the underlying mechanisms contributing to the improvement in physical function are not clear, it is known that mitochondrial function is linked to strength and walking speed.69 Therefore, mitochondrial dysfunction could have contributed to the decline in muscle strength and physical function observed in OA prior to GlyNAC supplementation, and the improvement in mitochondrial dysfunction with GlyNAC could have played a role in the observed improvement in muscle strength and physical function.

GlyNAC supplementation improves body composition​

Although impaired MFO is a risk factor for weight gain,70 it is unclear whether improving MFO can induce weight loss. This study found that improving MFO was associated with a significant reduction in total body fat and waist circumference, which suggests that the fat loss may have preferentially occurred in the abdomen.
 

Dave Clark

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The question is: do we need to use the amounts they used in the study to get similar benefits? I would like to think that lower more reasonable doses would be beneficial.
 

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