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Old 11-03-2012, 05:07 PM #85
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Are there any disadvantages to taking NO? Bought Black Powder yesterday and I'm impressed so far.
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Old 11-03-2012, 07:13 PM #86
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Old 11-30-2012, 10:01 PM #87
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http://chua2.fiu.edu/faculty/kalmand...%2010-2006.pdf

People supplementing whey isolate gained 11lbs of LBM over 10 weeks WHILE losing BF.





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Old 12-03-2012, 05:42 AM #88
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Old 01-02-2013, 08:02 PM #89
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Thoughts on WPI vs WPC/WPI mixes?
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Old 01-02-2013, 10:35 PM #90
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Old 01-03-2013, 06:29 AM #91
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Old 01-07-2013, 08:35 AM #92
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Just trying to get a better understanding of the possible long-term risks that may accompany their use.

In Alzheimer's disease, it is proposed that elevated background concentrations of glutamate between the pre and postsynaptic neurons causes the postsynaptic membrane to become more frequently depolarized, thus resulting in the displacment of the voltage-dependent Mg2+ ion that normally blocks the NMDA ion channel, followed by excitotoxic Ca2+ influx. This in turn negatively impairs physiological signaling mechanisms/synaptic plasticity/learning/memory ect.

The literature indicates that postsynaptic glutamate transporters remove glutamate from the synaptic cleft in a rapid fashion under normal physiological conditions. However, my concern is that NMDA supplementation [may] alter glutamate transport homeostasis, resulting in the inadequate removal of glutamate from the synaptic cleft, as a result of prolonged supraphysiological exposure to glutamate.

Now the implication from other respected members was that the voltage-gated NMDAR requires previous activation of the AMPA receptor for membrane depolarization. However if that's the case, I'd like to hear some discussion on the following....



"Originally Posted by Espinosa et al, 2009 "

"we propose that the residual NMDA receptor component of spontaneous mEPSCs stems from continual incomplete Mg2+block of NMDA receptors at the resting membrane potential rather than unblock triggered by concurrent AMPA receptor activity."

"partial blockade of AMPA receptors does not affect the NMDA receptor-mediated component of mEPSCs arguing against the possibility that the NMDA component is due to relief of Mg2+ block via local depolarization mediated by AMPA receptors."

"These findings are consistent with our observations, and they strongly suggest that NMDA receptors are active at rest during spontaneous neurotransmission, despite their reduced ion conductance due to Mg2+ block."

"These findings indicate that mEPSC driven signaling is more widespread than previously thought and reinforce the premise that mEPSCs can drive biochemical signaling in addition to electrical activity."

"spontaneous glutamate release may constitute a bone fide pathway for interneuronal signaling independent of pre and postsynaptic activity."



Additionally, it has been suggested that NMDARs must bind to glutamate and to glycine prior to activation however, according to Papouin et al, 2012, D-serine displays preferential affinity for [synaptic] NMDARs, whereas glycine's affinity is [extrasynaptic]. The authors notate that excitotoxicity & LTP are exclusively governed by the coagonist D-serine in synaptic NMDARs.





Neuron-

"The NMDA receptor is a voltage-gated channel which requires previous activation of the AMPA receptor for membrane depolarization

since the compound "NMDA" cannot agonize the AMPA receptor, its ability to activate the NMDA receptor would be limited, and so a direct neurotoxic effect will not likely occur from oral supplementation

if you take a neuron in a vacuum (en vitro), its normal electrical homeostasis is disrupted, and the NMDA receptor no longer is voltage gated. if you bath this neuron in NMDA, excitotoxicity will occur, whereas en vivo it can't"



Cyrus-

"The bottom line is that we don't know what dose of oral NMDA can cause excitoxicity. Oral doses are far safer than injections into the brain because one of the primary functions of the BBB is to prevent excitoxic insult. I do not know how much NMDA penetrates the BBB per mg taken orally, but I do know that it will be less than an equivalent amount of DAA due to the active transport of AAs at the barrier. Assuming some methylation of DAA and conversion to NMDA in the brain (mediated endogenously of course), it's likely that the dose of NMDA provided by intimidate will be met through basic DAA supplementation (this assumes a 1% conversion rate). So, in my opinion, excitotoxicity is unlikely with intimidate.(NMDA product)"



Magnetotropic-

"This is a study of miniature excitatory postsynaptic currents (mEPSCs), not evoked EPSCs. The former is due to random release of unprovoked pre-synaptic neurotransmitter release, and the latter is due to the classical action potential induced sequence.

What this study says is that magnesium isn't permanently docked on the NMDAr, and that their may be times where the NMDA receptor is activated when magnesium is displaced. This is fairly obvious since the intracellular/extracellular polarity is not completely electrically static.

And since the AMPA receptor has its utilitiy in depolarizing the intracellular compartment allowing magnesium displacement, and thereby NMDA activation, if magensium is not docked on the NMDA receptor in the first place, then AMPA has lost its function (extremely temporarily).

AMPA receptor pre-activation is still required for the vast majority of glutaminergic NMDA signaling, and so the significance of this study is unknown.

It is worth noting that the article mentioned this:

Finally, partial blockade of AMPA receptors does not affect the NMDA receptor-mediated component of mEPSCs arguing against the possibility that the NMDA component is due to relief of Mg2+ block via local depolarization mediated by AMPA receptors.
However, we could detect clear NMDA receptor-mediated mEPSCs only in one of eight recordings in the presence of 10 μM NBQX to block AMPA currents (data not shown).

Ultimately, I would say this study is interesting, but certainly does not alter the classical paradigm in any way.

Here is the authors final thoughts. Keep in mind that the context is key:

Collectively these results indicate that NMDA receptors significantly contribute to signaling at rest in the absence of dendritic depolarizations or concomitant AMPA receptor activity."



The prevailing conception [at least within a community that utilizes supplemental NMDA] is that it poses no risk, as the NMDAR is voltage-gated, and that due to the fact that NMDA does not directly agonize the AMPA receptor, there is no forseeable risk to it's supplementation. Now this may, or may not be the case however, discussions like these reguarding theoretical implications on the subject are beneficial for educational purposes, at least to some degree.

So following the creation of this thread, we've established the fact that the NMDA compound does [not] have to directly agonize the AMPA receptor for postsynaptic depolarization to take place. Additionally, it appears as though both spontaneous and evoked neurotransmission can activate certain sets of NMDA and/or AMPA receptors.

Astrocytic PAR1-triggered glutamate efflux [may] be another mechanism by which depolarization relieves the Mg+2 block to potentiate NMDA receptor-mediated excitatory postsynaptic currents, however addmittedely, I haven't done much research on the subject.

Nonetheless, these factors at least open the possibility of excitotoxic insult - be it low risk or not.



--"These results support the notion that spontaneous and evoked neurotransmission activate distinct sets of AMPA receptors and bolster the hypothesis that synapses harbor separate microdomains of evoked and spontaneous signaling." - Yildirim et al, 2011

"Collectively, these results support the premise that spontaneous and evoked neurotransmissions activate distinct sets of NMDA receptors and signal independently to the postsynaptic side." - Deniz Atasoy et al, 2008



--Andy-

"Sustained, pathologically excessive Ca2+ influx is necessary for an apoptotic/necrotic cascade, and that requires a glutamate dump. If anything, calcium transients as a result of excess NMDA in the synapse would end up being beneficial, depending on the region and type of neuron, in new memory formation."



--So if the Ca2+ influx is transient, it won't likely be pathologically deleterious, even with prolonged use."



Andy-

"That's the physiologically sound consideration, yes.

Also regarding aggression, there's significant reason to believe LH and FSH can contribute to behavioral effects. I've been thinking about this for a long time because testosterone administration alone does not induce behavioral effects but anecdotal evidence abounds for some natural testosterone boosters, and it's been going on for too long for me to believe it's purely psychosomatic in every case."



Condescending Guy Dumbs It Down-

"Specific conditions must be met in order for NMDA activation (Mg2+ displacement)/excitotoxicity to occur, i.e. presynaptic NMDAR glutamate binding, and depolarization (which occurs with AMPAR glutamate binding, and an influx of Na+).

NO HYPE is questioning if NMDA activation/Mg2+ displacement can occur through alternative means, such as mEPSCs, or astrocytic PAR1-triggered glutamate efflux.

tms;du (too much science, didn't understand) Certain conditions must be met in order for excitotoxicity to occur, NO HYPE is questioning whether such toxicity may occur by other means."
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Old 01-07-2013, 08:36 AM #93
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Studies-

1.)

http://www.ncbi.nlm.nih.gov/pubmed/19261712

Under physiological conditions N-methyl-D-aspartate (NMDA) receptor activation requires coincidence of presynaptic glutamate release and postsynaptic depolarization due to the voltage-dependent block of these receptors by extracellular Mg(2+). Therefore spontaneous neurotransmission in the absence of action potential firing is not expected to lead to significant NMDA receptor activation. Here we tested this assumption in layer IV neurons in neocortex at their resting membrane potential (approximately -67 mV). In long-duration stable recordings, we averaged a large number of miniature excitatory postsynaptic currents (mEPSCs, >100) before or after application of dl-2 amino 5-phosphonovaleric acid, a specific blocker of NMDA receptors. The difference between the two mEPSC waveforms showed that the NMDA current component comprises approximately 20% of the charge transfer during an average mEPSC detected at rest. Importantly, the contribution of the NMDA component was markedly enhanced at membrane potentials expected for the depolarized up states (approximately -50 mV) that cortical neurons show during slow oscillations in vivo. In addition, partial block of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor component of the mEPSCs did not cause a significant reduction in the NMDA component, indicating that potential AMPA receptor-driven local depolarizations did not drive NMDA receptor activity at rest. Collectively these results indicate that NMDA receptors significantly contribute to signaling at rest in the absence of dendritic depolarizations or concomitant AMPA receptor activity.







2.)

"Neuroprotective effects of creatine administration against NMDA and malonate toxicity.

Malcon C, Kaddurah-Daouk R, Beal MF.
Source

Neurochemistry Laboratory, Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Abstract

We examined whether creatine administration could exert neuroprotective effects against excitotoxicity mediated by N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid. Oral administration of 1% creatine significantly attenuated striatal excitotoxic lesions produced by NMDA, but had no effect on lesions produced by AMPA or kainic acid. Both creatine and nicotinamide can exert significant protective effects against malonate-induced striatal lesions. We, therefore, examined whether nicotinamide could exert additive neuroprotective effects with creatine against malonate-induced lesions. Nicotinamide with creatine produced significantly better neuroprotection than creatine alone against malonate-induced lesions. Creatine can, therefore, produce significant neuroprotective effects against NMDA mediated excitotoxic lesions in vivo and the combination of nicotinamide with creatine exerts additive neuroprotective effects."
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Old 01-07-2013, 08:54 AM #94
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Thank you for doing this, even if it is an older thread. I've been reading this for about 3 days on and off.
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Old 01-07-2013, 01:20 PM #95
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Would occasionally using Iodized salt be necessary if you strictly use sea salt as your primary source of sodium?

Question part 2: Do you guys believe in supplementing iodine to begin with?
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Old 01-07-2013, 01:51 PM #96
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Sea salt opposed to iodized salt is almost picking hair. You should be getting enough regardless through your diet. Zinc, copper, and selenium can also help with that.
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Old 01-23-2013, 02:50 AM #97
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Old 01-23-2013, 07:36 PM #98
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^Is that something you've added to your so-called "sleep stack", or just to be used by it's lonesome?
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Old 01-23-2013, 08:30 PM #99
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Old 01-23-2013, 09:45 PM #100
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The Magnesium + Zinc + Melatonin stack seriously puts me out cold. If I'm not prepared to sleep for at least 8 hours, I can't take it otherwise it takes me half a day to wake up.
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Old 01-24-2013, 07:24 AM #101
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Melatonin and b6 before bed everyday. I forget enough times that I haven't developed much if a tolerance yet.
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Old 02-26-2013, 04:02 PM #102
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Some I3C information:

Quote:
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400mg Daily

3 Months On/1 Month Off

I would avoid the NOW Brand due to the flax component (estrogenic).

"I keep coming back to this one.

It just irks me so much that this info still surfaces. Dr. Zeligs owns a patent on a product containing DIM that combines DIM with d-alpha-tocopheryl polyethylene glycol-1000 succinate to make it absorbable by the gut. Polyethylene glycol is a detergent-like chemical that breaks down fat (not to be confused with propylene glycol which is used in anti-freeze). D-alpha-tocopheryl succinate is a synthetic, water-soluble form of vitamin E. According to Zeligs, this is the first time this combination has been used for a supplement.

Zeligs claims that I3C “disappears” after it’s ingested. What’s the truth about this?

It “disappears” because it’s converted to other products, including DIM. According to researchers, “At acid pH comparable to that found in the stomach, I3C forms to wide variety of condensation products ranging from linear and cyclic dimers, trimer and tetramers to extended heterocyclic compounds such as indolocarbazoles”. To put DIM’s contribution into perspective, DIM represents about 6% of the total condensation products of I3C. I3C itself is one of hundreds of phytochemicals in cruciferous vegetables.

Zeligs claims that I3C creates “questionable reaction products” in the gut.

One of those “questionable” products is DIM. When DIM is administered by itself, it can actually provoke the growth of human breast cancer cells and upregulate the estrogen receptor under certain laboratory conditions. Stressing the point that this does not occur when the full product, I3C, is taken under ordinary conditions.

While the break-down products of I3C may act unpredictably by themselves, when taken as I3C in their natural form, they are beneficial for preventing, and possibly treating, hormone-related cancers. The data is so compelling, it has provoked normally reserved researchers into such praise as, “I3C has tremendous potential in the treatment and prevention of cancer, particularly estrogen-enhanced cancer.” Although that comment was directed towards I3C’s estrogen-blocking potential, I3C has equally important actions against all types of cancer. The list includes powerful DNA protection, carcinogen detoxification, modulation of the growth and invasion of cancer cells, induction of apoptosis selectively in cancer cells, bone marrow protection during chemotherapy, neutralization of cancer-causing heterocyclic amines (i.e., from cooked meat), modulation of the estrogen receptor (which is also a player in non-hormone related cancers), and possible upregulation of tumor suppressor genes.

Zeligs says that “no direct benefits can be attributed to absorbed I3C.” The benefits of I3C have been proven in vitro, in rodents and in humans. Whether they are direct or indirect—I3C works.

According to Zeligs, DIM has been “extensively tested” in humans.

One of the biggest problems with DIM is that it hasn’t been extensively tested in humans. In fact, there are no published human studies at all. This is a critical difference between DIM and I3C. One of the problems with DIM is that because human studies haven’t been done, no one knows the proper dose. Is this important? You bet. In separate studies, using different amounts, researchers have gotten completely opposite results on DIM’s effect on the estrogen receptor in vitro.

Zeligs claims that DIM is more stable than I3C and therefore more desirable.

If I3C were stable, it would never form DIM or the myriad of other beneficial phytochemicals. I3C is inherently unstable in stomach acid which converts it to its multi-faceted products. As with all pro-active vitamins and supplements, I3C should be protected from heat and light. The product has been tested for 12 months at room temperature with no loss of potency.

According to Zeligs, the anti-cancer effects of I3C are due to DIM.

Far from it. DIM by itself has, in some cases, completely opposite effects of I3C on human breast cancer cells. Research indicates that there is a difference between the way I3C acts versus the way its
individual products act. For example, regarding a study on androgen metabolism and I3C, researchers at Queen’s University wrote that “the action of multiple inducers present in cruciferous and other vegetables might produce androgen metabolic profiles very different from those produced by individual components isolated from them.” There is a prevailing view that the effects of I3C are due to the combination of its condensation products together, not one single product. DIM may eventually prove to enhance the effects of I3C, but the research has not been done.

What are some of DIM’s “opposite effects” on breast cancer cells? I use this to simply combat the components of the piece, not that I expect you guys to be the 1% of males with breast Ca.

I3C studies show that I3C stops the growth of estrogen receptor-positive and negative breast cancer cells in culture. DIM reportedly either makes estrogen receptor positive breast cancer cells grow or inhibits them in culture. According to researchers at the University of California, DIM promotes the growth of human breast cancer cells about as half as well as estrogen when no estrogen is present in the culture. In addition, DIM’s inhibition of cancer cell growth was “weak” in the presence of estrogen. Remember, these are laboratory conditions only and probably don’t occur in real life. How DIM behaves, however, may depend on dose. Researchers at Texas A&M report that DIM significantly counteracts estrogen-induced growth of MCF-7 cells in culture at higher doses. However, unlike I3C which retards the growth of estrogen receptor negative breast cancer cells, DIM has no effect on estrogen receptor negative cells. Another question about DIM is whether it can increase aromatase in breast and other tissue. Aromatase is an enzyme that helps create estrogen. DIM reportedly enhances the enzyme in adrenocortical cancer cells.

Not only is DIM not responsible for the anti-cancer effects of I3C, it has fewer anti-cancer effects (due to fewer molecular mechanisms), when it’s isolated from the other phytochemicals that naturally occur with it.

Why does Zeligs say that DIM is the “active form” of I3C responsible for improved estrogen metabolism?

Good question, because the study Zeligs uses to back that up doesn’t say that. It points to another product, ICZ, as potentially having greater estrogen metabolizing potential than either DIM or I3C. Not only is DIM not the active form of I3C, it may not even be a desirable form of I3C. In the cited study, DIM had to be injected to reach the level of estrogen modulation obtained with oral I3C.

Zeligs claims that DIM promotes cervical health.

The women in the study he refers to took I3C, not DIM.

According to Zeligs, DIM makes estrogen replacement therapy safer in women and DHEA therapy safer in men.

It’s a plausible theory, but DIM’s ability to modulate hormone replacement therapy is unknown. The studies cited by Zeligs were done with I3C, not DIM. Studies on I3C show that it modulates hormones in addition to estrogen, including androsterone, androstenedione and testosterone. This, along with the fact that I3C prevents uterine-related cancers, suggests that I3C will be beneficial for people taking hormone replacement therapy. These kinds of studies have not been done with DIM.

According to Zeligs, “Supplemental use of DIM promotes higher levels of 2-hydroxy estrogens. This use in animals has been shown to be associated with the prevention of spontaneous, estrogen related cancer of the breast and uterus.”

It sounds good, but the problem is that, again, the research was done with I3C, not DIM.

Zeligs claims that DIM is unique in its ability to shift estrogen metabolism, and that DIM decreases the “activity” of the estrogen receptor “system”.

The study Zeligs says backs this up tested both I3C and DIM. DIM was less effective when taken orally. Only when it was injected, did DIM reach I3C’s level of estrogen modulation. Far from being “unique” in its ability, DIM was less effective than I3C when taken orally. As for the claim that DIM decreases estrogen receptor “system activity”, estrogen receptors were not evaluated in the study at all.

However, another study has evaluated the effect of DIM on the estrogen receptor. According to the results, DIM activates, not deactivates, the estrogen receptor. Activating the estrogen receptor enhances, rather than prevents, the growth of estrogen-dependent cancer cells. Again, this points up the problem of isolating DIM from its natural milieu. When DIM is taken in its natural form, I3C, the estrogen receptor is
downregulated.

Zeligs claims that people should buy DIM instead of I3C.

Only if they want to take something that’s untested versus something that’s proven. Part of I3C is naturally converted to DIM when I3C is taken as a supplement or eaten in vegetables. I3C forms dozens of other phytochemicals in addition to DIM which have proven anti-cancer effects. Anyone who metabolizes I3C will get DIM along with other naturally-occurring products.

The importance of co-factors in determining how these phytochemicals behave is illustrated by what vitamin C does to I3C. If vitamin C is not present when cruciferous vegetables are eaten, more I3C will naturally form. If vitamin C is added, less I3C will form, but more of a different product will result from digestion. It’s called ascorbigen, and it can produce 20 times more ICZ than I3C. No one knows the significance of this yet, although it’s been suggested that ICZ may be able to change estrogen metabolism better than I3C or DIM.




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Old 02-26-2013, 04:03 PM #103
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Quote:
The cancer fighting compounds in cruciferous vegitables clearly work synergistically. That’s why a person wanting to gain an extra edge over cancer should stick with I3C, which has valid scientific studies behind it."


Dr. Houser-

"(2) Estrogenic Channeling Agents

Indole-3-Carbinol (I3C)

EVIDENCE-BASED EFFICACY: I have written extensively in various posts on my support of this compound versus its DIM metabolite as well as any other compound in the post-cycle realm from the category of ?dietary supplement.? Perhaps the single-most important mechanism of action of I3C is modulating estrogen metabolism. That?s right, tell your friends ? ALL ESTROGEN IS NOT CREATED EQUAL. Estrogen receptors are located on the surface of virtually every type of tissue in the human body. Guys, you too, are not off the hook as this applies to you as well.

The body modifies (metabolizes) estrogens through two mutually exclusive pathways, which lead to compounds with dramatically different biological activities. Estradiol is the primary estrogen in circulation (as the example used above in Diversification Model) and one of the most active. It is metabolized to a number of other chemicals, all with some degree of estrogenic activity.

Key here, are the enzymes 2-hydroxylase and 16-alpha-hydroxylase. Several years ago, scientists hypothesized that a preference towards the 2-hydroxylase pathway and the subsequent generation of 2-hydroxyestrone (2-OHE1), results in less toxic metabolites in the circulation, which was subsequently gone on to support a decreased number of breast cancer outcomes if this were the dominant pathway (later, this proved true for prostate cancer as well). It was also around that same time that the hypothesis of greater estrogenic metabolism via the 16-alpha-hydroxylase enzyme would yield greater amounts of the more potent 16-alpha-hydroxyestrone (16alpha-OHE1) and a larger number of estrogen-dependent cancers would likely be the result.

Summary of ORDET study of 2000 (always nice fancy acronyms)
Participants: 10,000 Italian women
Duration: > 5 years
Measured Items: Diet, other breast cancer risks
Findings: Increased level 2-OHE1:16alpha-OHE1 at beginning of study associated with less risk of breast cancer development.

This simply set precedent, mind you ? although there is a 1% risk for men to develop breast cancer, posting this study is merely the landmark to establish the importance of greater 2-OHE1:16alpha-OHE1 ratios being desired for decreased estrogen-sensitive cancer risk. This is very important information to someone embarking on post-cycle supplementation.

Summary of Prostate Cancer Study
Although there was a failure to achieve statistically significant results in this study, elevated 2-OHE1 urinary levels indicated a decreased risk of prostate cancer, whereas an increased 16alpha-OHE1 urinary level showed an increase of prostate cancer 2-times that of men with the highest levels of 2-OHE1.

I3C modulates these pathways shifting the conversion of estradiol metabolism to favor the 2-hydroxylase pathway and the subsequent 2-OHE1:16alpha-OHE1 ratio is INCREASED, which correlates with a decreased risk of various estrogen-sensitive cancers. A potential caveat worth further exploration is the increase in production of yet another estrogen exhibited by some studies (4-hydroxyestrone ? this is very potent). These increases were NOT significant, however, and as you will see and have seen in my various posts, are put out by people with vested interest in other products. There are multitudes of studies that actually show a concurrent DECREASE in 4-OHE1, so the mixed results tend to leave me questioning those trying to prove their various products superior. Catch my drift?

In addition, and certainly not something studied, but the data seems to suggest shifts from the more potent (2-OHE1) to less potent (16alpha-OHE1) in a time when there is the potential for increased conversion (and this goes out to all of my aromatase-inhibitor-loving friends) ? namely, during the post-cycle period would also contribute to a shift in dose-response curves to the right (and that is for my pharmacologically-inclined friends). We?ll see in the pharmaceutic exploration (parts IV + V) that this is NOT the entire picture ? unfortunately, I can only address these items one by one in a certain time allotment.

FORMS & DOSAGES: 200mg to as high as 400mg has been studied and based on available evidence, this is what I would be hard-pressed not to suggest at this time. There is no upper-limit established, but even while in the post-cycle realm, I would beg you to adhere to a max of 400mg per day as this is simply what has been supported to date.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Although it may seem obvious that a substance consumed over 1000s of years by millions worldwide is inherently safe, it has been challenged recently by those with vested interest in its metabolite DIM. I have expressed my concern at the challenges DIM supporters have offered and it is just plain bad science. Numerous cell culture, animal, and human studies have demonstrated I3C?s safety and tolerability, along with its targeted ability to SUPPRESS estrogen-receptor-sensitive (breast, cervical, and important for this discussion ? prostate) cancer growth (sorry Dr. Z), and induce programmed cell death in a variety of tumors, including those associated with breast, prostate, endometrial, leukemia, and colon cancers.

As an aside, the cytochrome P450 enzymatic system discussed above in the AT / ATD section within both the liver and intestinal track is actually STRENGTHENED by use of I3C ? something that could prove especially beneficial to C17 alkylated users. "
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Old 04-07-2013, 08:31 PM #104
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http://www.nature.com/nm/journal/vao...l/nm.3145.html

Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis


TL;DR
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Old 04-08-2013, 02:03 PM #105
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Here are some things that cannot be concluded:

TMAO in humans causes heart disease. ApoE-/- mice are used since it is easy to research pro-artherogenic cholesterol metabolism, but these are mice with a specific genetic fault. This research would have to be replicated in regular mice (and then in humans). Additionally, the human correlational research does suggest there is a link but cannot state that it is a causative link, and past research on Choline does suggest that TMAO is fairly rapidly excreted via the kidneys (suggesting some effects that are differential dependent on species).

Carnitine causes heart disease, as the link between TMAO and heart disease is not fully established in humans.

TMAO is bad. To nip this in the bud, most molecules have good and bad associated with them (good example: Cortisol) and it would be improper to conclude that TMAO must be avoided at all cost. To reiterate as well, the correlation between TMAO and cardiovascular disease could very well be a biomarker of some other lifestyle habits; it cannot be ruled out yet.



TL;DR?

The study found that in genetically modified mice, a high (but not impossible) dosage of l-carnitine did double plaque build up. This may or may not be related to TMAO, we cannot say. This may or may not happen in humans, we cannot say. Overall? It's just preliminary research that should only interest other researchers, not the layperson.
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