The Sleep Thread
- 10-15-2011, 10:08 PM
The Sleep Thread
While the number of hours you sleep won't affect the number of pounds you'll lose while dieting, it will affect where those pounds come from, according to a relatively recent study in the Annals of Internal Medicine. When dieters got adequate sleep (about 8.5 hours), most of the weight they lost came from fat deposits. "Those who got less sleep (around 5.5 hours) lost more 'fat-free mass,' which includes mostly muscle but also other tissues such as liver, kidneys, etc...," says study co-author Plamen Penev, MD, of the University of Chicago.
Bottom Line: a good night's sleep is essential for maintaining muscle and blasting fat.
I am going to open this one up to discussion that would center on our hours of slumber...the good, the bad, and the ugly.
D_Anabolicminds.com Featured Author
- 10-15-2011, 10:21 PM
I usually have HORRIBLE sleep patterns as a result of my job (12 hour shifts that alternates from day to night shift). I usually average only about 5-6 hours of sleep a night! I know I need to work on it but it feels there just isn't enough time in the day"The only good is knowledge and the only evil is ignorance." - Socrates
- 10-15-2011, 10:30 PM
Not sure if this is off topic but would like to get your thoughts on this and a couple questions.
Currently my pre-bed protocol is a couple caps ALA, 5 caps HGHup and a scoop of BCAAs.
Evidence for an Inhibitory Effect of Physiological Levels of Insulin on the Growth Hormone (GH) Response to GH-Releasing Hormone in Healthy Subjects
It has been previously reported that in healthy subjects, the acute reduction of free fatty acids (FFA) levels by acipimox enhances the GH response to GHRH. In the present study, the GH response to GHRH was evaluated during acute blockade of lipolysis obtained either by acipimox or by insulin at different infusion rates. Six healthy subjects (four men and two women, 25.8 ± 1.9 yrs old, mean ± SE) underwent three GHRH tests (50 µg iv, at 1300 h) during: 1) iv 0.9% NaCl infusion (1200 - 1500 h) after oral acipimox administration (250 mg) at 0700 h and at 1100 h; 2) 0.1 mU·kg-1·min-1 euglycemic insulin clamp (1200 - 1500 h) after oral acipimox administration (250 mg at 0700 h and at 1100 h); 3) 0.4 mU·kg-1·min-1 euglycemic insulin clamp (1200 - 1500 h) after oral placebo administration (at 0700 and 1100 h).
Serum insulin (immunoreactive insulin) levels were significantly different in the three tests (12 ± 2, 100 ± 10, 194 ± 19 pmol/L, P < 0.05), plasma FFA were low and similar (0.04 ± 0.003, 0.02 ± 0.005, 0.02 ± 0.003, not significant), and the GH response to GHRH was progressively lower (4871 ± 1286, 2414 ± 626, 1076 ± 207 µg/L·120 min), although only test 3 was significantly different from test 1 (P < 0.05). Pooling the three tests together, a significant negative regression was observed between mean serum immunoreactive insulin levels and the GH response to GHRH (r = -0.629, P < 0.01).
Our results indicate that in healthy subjects, acipimox and hyperinsulinemia produce a similar decrease in FFA levels and that at similar low FFA, the GH response to GHRH is lower during insulin infusion than after acipimox. These data suggest that insulin exerts a negative effect on GH release. Because the insulin levels able to reduce the GH response to GHRH are commonly observed during the day, for instance during the postprandial period, we conclude that the insulin negative effect on GH release may have physiological relevance
On the other hand GH is also released in response to low blood sugar and is not controlled by GHRH, but by something else. (leptin, Ghrelin, or galanin) So while insulin does suppress Growth Hormone release (GHRH), hypoglycemia will stimulate a Ghrelin induced GH release right?? So when low blood sugar is induced by something other than insulin, in my case the ALA, it would give an even bigger spike than with insulin because there is no inhibitory effect?
Am I correct?
The formulator of glycobol, Dr.D had touched on this briefly in a post somewhere here on the board which basically said a combo of deep sleep + low blood sugar + hyperaminoacidemia would work towards boosting GH. I take BCAAs pre bed based off his recommendation but have been considering switching to straight leucine instead. What are your thoughts on using the BCAAs pre-bed in my above protocol? What kind of effect would they have?"The only good is knowledge and the only evil is ignorance." - Socrates
10-15-2011, 11:02 PM
Focusing on sleep has recently become a more important thing for me. I had a sleep study done 2 nights ago and should hopefully find out all the results, soon. I very likely have (obstructive) sleep apnea. I'll be paying close attention to this thread.
Psalm 34:10 - "The lions may grow weak and hungry, but those who seek the Lord lack no good thing."
EvoMuse Rep | Inspire to Evolve
10-19-2011, 09:06 AM
Now, what's also interesting is the theory contradicts ITSELF in that BCAAs are gluconeogenic (i.e. - raise blood sugar). The reason to include BCAAs and/or leucine or any other protein source for that matter (casein, et al...) prior to bed is to limit your period of "controlled catabolism," NOT to induce the opposite. They thwart cortisol for this very reason (and cortisol is at its highest in the morning - first thing ... it's probably the most stressful thing on the body to simply open your eyes in the morning). Cortisol is of the counter-regulatory set of hormones (with GH); you are not very successful in its control without sacrificing some of the GH stimulus off the bat. Now, the largest GH stimulus happens with INDUCTION of sleep, so if you're ingesting a lot of macros (proteins/aminos; fats/FAs; or CHOs of any sort) before bed; you are going to blunt the time when GH surge is highest.
Will any of these effects make a huge physique difference...I would suspect not; although it is very difficult to control for and see outward clinical change. That said, all of this theory is "interesting" but probably inconsequential to your existence as a lifter/physique athlete.
Anabolicminds.com Featured Author
10-19-2011, 09:07 AM
Oh, btw...this does NOT mean I think the product "Glycobol" has purpose; in fact, I love glucose disposable products overall and if timed correctly - they have pertinence; however, this scenario is not one of them.
Anabolicminds.com Featured Author
10-20-2011, 06:25 PM
Just curious as to what you think for people that have little trouble falling asleep, but cannot seem to sleep for longer then a couple hours at a time, and seem to just wake up and fall back to sleep over and over, night after night. I have found that the only method for me being able to sleep the whole night is to smoke a little bud before I go to sleep, but if I don't I just cannot get a good night of sleep. I haven't got a good night of sleep in the past four days because of this and its really starting to get to my head.
As a kind of prior background info, I have never really slept well or soundly, but it just seems more pronounced in recent memory. Clearly things such as stress could affect this and with being in 4h year university, I do certainly have stress, but none that is significantly more then any I have had before in my life. I have always just thought that I have an overactive mind that is unable to be shut off without the use of some kind of drug basically.
10-23-2011, 07:25 PM
let me begin by saying i think it is awesome to have a doctor around to run things by to get a professional opinion
i am a long time insomniac (no diagnosis or anything, i just cant ever sleep for sh*t)
wanted to know what you think of phenibut for sleep, im aware of the abuse potential/tolerance issues, those are not my concern.
1. does phenibut interfere with REM sleep? or is it simmilar to ghb and causes REM sleep?
2. is phenibut toxic to any organs?
3. would phenibut case supression of any hormones?
thanks, if i can think of any more ill let u know
10-23-2011, 07:33 PM
Is there a relation with bodybuilding and sleep. It seems like most of us have trouble sleeping...... What works best for me is to go to sleep and wake up at the same times everyday. Melatonin and chamomile tea help a little.
10-23-2011, 08:19 PM
And here you thought I would ok your use of bud I bet. HA! What kind of doc would I be? The problem with marijuana is that it can act as a stimulant in some cases and it is very psychoactive dependent upon what kind you are using.
If you have an issue STAYING asleep; I do recommend a product call Somnidren GH (http://www.nutraplanet.com/product/m...nidren-gh.html) and it isn't often I recommend products. It does have a pill equivalent now without the Phenibut (http://www.nutraplanet.com/product/m...-110-caps.html), which may assist with the hung-over feeling issues with some sleep aids secondary to phenibut. Let me start by saying if you have not used this product, it is a pretty intense sensation people describe with it; first you'll notice the feet get a bit heavy; your breathing slows and you are out before you know it. You wake up (and while I cannot guarantee 10 hours of sleep or anything), you are feeling refreshed and like you have experienced 8-10 hours in say 6. It is truly hard to explain. If you have tried this product and not experienced this, you are certainly in the minority. Please note that I have ZERO financial interest in this product; there just isn't anything (inclusive of pharmaceutic aids) that I have had more success with.
Keep in mind, you may want a day or two per week a planned alternative as your body WILL adapt to GABAergics (i.e. - GABA itself and/or Phenibut) readily easy and render the product useless. I use VERY heavy doses of L-theanine and some melatonin (I will get to why I don't recommend constant use of melatonin in a future response).
So; maybe a setup would look as follows....
M-F: Somnidren GH
S-S: L-theanine (500-1000mg) + Melatonin (3-10mg; have used a second dose of 10mg in some people with success; Life Extension Foundation puts out a nice 10mg melatonin pill in case you are one who doesn't like ingestion of 100s of pills)
Anabolicminds.com Featured Author
10-23-2011, 09:04 PM
There is suggestion of it; given the associations of other GABAergics and their relative interference with REM, but I am uncertain it is well supported by literature nor will it likely ever be. There is an entire school of thought on the net reporting REM-rebound effects as well. I think this is best fought against with a 5-on, 2-off approach and possibly putting together other agents in the interim for your weekend holiday should you choose to embrace it.
Now, keep in mind that in cases of sleep deprivation, even GABAergics will NOT overcome your body's tendency to not only get to REM quicker, but spend additional time there. So, this is probably more of an "it depends" answer.
In short, likely not - not even the liver which is often suggested on bb message boards. Phenibut has low acute toxicity (in fact, very low). Reported LD50s (dose required to kill 50% of laboratory animals) are 900 mg/kg i.p. in mice, 700 mg/kg i.p. in rats, and 1000 mg/kg in rats (method of administration not given). Chronic administration of 50 mg/kg did not have teratogenic effects in rats. In clinical studies, no signs of toxicity have been reported, and side effects are few. Some report drowsiness, but this effect is not nearly as likely or severe as with benzodiazepines.2. is phenibut toxic to any organs?
One should be aware of the potential for drug interactions when taking phenibut. In many cases, it will decrease the threshold dose and potentiate certain actions of a drug. It amplifies some of the effects of anesthetics (ether, chloral hydrate, and barbiturates), diazepam, alcohol, and morphine; it would also presumably have an interaction with related drugs, such as other opiates and GHB. In contrast, taking phenibut with some other drugs, such as stimulants, will more than likely just blunt their effect.
In humans, the plasma half-life after a 250 mg oral dose of phenibut is 5.3 hours, and most of the administered drug is excreted unchanged (which is likely why people experience a hangover effect; just due to the long biologic life; people pontificate all over the place that this is secondary to metabolites, blah, blah, blah...without any modification to the drug when looking at excretion data). Reported dosages used in clinical studies range from 250 to 1500 mg daily, usually divided among three doses. Feedback indicates that the ideal dose may be in the higher end of this range.
It is suggested as a GH-secretagogue (due mostly to data from close relatives GABA and Baclofen, the latter of which is a chlorinated version of phenibut marketed as a muscle relaxant). If this is truly the case to any significant degree, then long-term use will lead to SUPPRESSION by way of feedback mechanisms inherent to all hormonal systems.3. would phenibut case supression of any hormones?
Probably moreso than effects on hormonal systems is data on neurotransmitters. Because of the structural similarity to PEA, phenibut may share some similarities and differences with it. When phenibut is administered along with PEA, it antagonizes many of its effects, such as promotion of anxiety, promotion of seizures, and hyperthermia. This has led some to postulate that antagonism of PEA, rather than the GABA-mimetic activity, may be the important mechanism of action for the anxiolytic effect of phenibut.
Phenibut also increases dopamine levels, and it has been postulated that the structural similarity to PEA may play a role in this effect. If you think about this, you could potentially have suppression of prolactin with dopaminergic agonists, the same as any which would be a neat "side effect" property.
There is one report in the literature of serotonergic effects of phenibut, but it does not look as though this has been followed up on. I mention serotonin because any discussion would be incomplete without talk of the interplay between serotonin and melatonin, which this could play an interesting role in.
Anabolicminds.com Featured Author
10-23-2011, 09:05 PM
10-23-2011, 09:08 PM
I figured this would be a good time and place to include a former article's discussion about melatonin cascades as they pertain to the post- and peri-cycle periods.
What is known to us surrounding the post-cycle environment is that there is a high-frequency of changes associated with sleep patterns in many users. Sometimes this is an extension of increased testosterone levels and would be likely extinguished as hormonal harmony is regained, or is it? There are multiple pattern variations seen (i.e. - decrease in the number of hours of sleep, decrease in the time spent in REM, decrease in ability to induce sleep, etc...). Is this surprising? Not at all - HOWEVER, there is completely different rationale usually supporting what I call peri-cycle insomnia (PeCI) and post-cycle insomnia (PoCI) should they occur. [author’s note: a definition of the terms “peri” implies “next to” in the literal sense and “during” as read as I have chosen to use it in this piece]. It is imperative to note that exact timing of this side effect has a particular etiology and amendment of such allows appropriate addressing of the problem.
Etiology finds three-fold rationale depending on (1) aromatizing capability of the compound, (2) shifts in dose-response curve [i.e. - once again, volume of distribution plays a direct role], and (3) various negative feedback mechanisms directly proportionate to cycle length. Unfortunately, discussion of these is beyond the scope of this article and I would like to turn our attention to the post-cycle time frame.
If a patient notes “SOLITARY” post-cycle development of sleep loss, our attention turns to the pineal gland as the predominant etiologic rationale for our newfound deficiency. Trading in one hormonal deficiency for another may seem like a huge contradiction of terms, but it too is part of the hormonal chaos you create while on cycle. Understanding our deficiency means we have to visit semi-equivalent research done in the area of pineal gland tumors and deficiency and their association with abnormal pubertal development for answers. The original hypothesis to explain precocious puberty in boys with pineal tumors was that the tumors destroyed the capacity of the pineal gland to inhibit sexual development. In fact, much evidence suggests that precocity is due to production of the beta subunit of human chorionic gonadotropin (beta-hCG) by germ cell tumors of the pineal gland. This relationship has nevertheless stimulated much work on the possible role of the pineal gland through the secretion of melatonin as a means of timing human puberty. It has been shown that both precocious and delayed puberty have been associated with pineal tumors.
So what about PCT? Let’s see what happens in the dinoiii model. Oh yeah, those that get real scared to see science...turn away now.
Melatonin secretion is actually a response to various light input on retinal receptors and a complex cascade of events thereafter that follow:
Step 1) Light –> eye –> (+) Hypothalamic suprachiamatic nucleus / (+) Hypothalamic paraventricular nucleus –> hindbrain –> spinal cord –> superior cervical ganglion –> divergent outflow tracts [go to Step 2a OR 2b]
Step 2a) Superior Cervical ganglion –> Norepinephrine –> Beta-adrenergic receptor [go to Step 3a]
Step 2b) Superior Cervical ganglion –> Norepinephrine –> Alpha-adrenergic receptor [go to Step 3b]
Step 3a) (beta-adrenergic sequelae) ATP –> cAMP-dependent phosphorylation via AA-NAT promotor binding –> 5-HT N-Acetyl Transferase - 5-HT NAT [move on to Melatonin-processing cascade]
Step 3b) (alpha-adrenergic sequelae) C-kinase input into beta-adrenergic cAMP phosphorylation crossover
[Return to Step 3a]
1. Tryptophan –> 5-HTP
2. 5-HTP –> 5-HT
3. 5-HT –> N-Acetylserotonin (via 5-HT NAT from Step 3a)
4. N-Acetylserotonin –> Melatonin (via hydroxyindole-O-methyltransferase - HOMT)
The model is consistent with the suggestions offered in PCT: ACV III regarding hypOadrenalism in the “immediate” post-cycle realm contributing to a DECREASE in catabolic balance in roughly the first 2.5 weeks of post-cycle era, inclusive of not only cortisol, BUT also catecholamine (i.e. - NE) output. This is where the difference arises in PoCI - outisde of its intimate connection with serum gonadotropin-effects, you also have changes in enzymatic processing unique to PCT.
So Dana, melatonin supplementation would be the simple answer, right? NOT SO FAST! You really don’t think I spent all that time on the melatonin processing cascade to talk about simple melatonin supplementation, did you? Now, remember with our crossover pathway, melatonin has crossover feedback to follow suit and a subsequent DECREASE in serum gonadotropin [FSH + LH] via GNRH outflow during the sleep hours as shown in most current research. Decreased Melatonin is actually a good thing in PCT as the body’s own mechanism for restoring balance [though beyond our scope here it may be a GH deficiency you have then to worry about if sleep deprivation results - quite complex, huh? Though the hormonal chaos always gets oversimplified! ALL HOMRONES DO NOT ACT IN A VACUUM, THERE ARE ALWAYS ATTEMPTS AT HOMEOSTATIC BALANCE! Disrupt it, and its like tipping a scale where but another hormonal pathway will suffer]. In people experiencing PoCI, the likelihood of reaching serum gonadotropin suppression is nearly 100%.
What’s more...Melatonin 1 [MT1, not to be confused with M1T] receptor subtypes are also present in the pars tuberalis to increase prolactin output possibly potentiating post-cycle galactorrhea (nipple discharge).
[author’s note: melatonin conveys photoperiodic info influencing the pattern of something called mPer expression in the pars tuberalis for the control of seasonal variations of that MT1 receptor - which is way beyond the scope of this article, but explains even furthermore why simple supplementation here is NOT warranted in everyone].
These effects seem to dissipate, however, with long-term supplementation BUT it is likely NOT a good plan in the post cycle era to be trying melatonin or secretagogues (i.e. - 5-HTP, et al.] for the first time.
So, what you’re telling me is that should insomnia crop up in the post-cycle era, I am left to suffer, right? Nah, there are some potential alternatives which offer sedative effects that could override this melatonin system.
Anabolicminds.com Featured Author
10-23-2011, 10:00 PM
this is exactly what america needs..... genuine people to help educate consumers about supplements/drugs/steroids/compounds and what effects they may (or may not) have....
i dont think we need any further restriction or regulation from the govt. just more people like dinoii to help us out
one more question...
1 carboxy- i think its just glorified macuna pruriens.... ldopa whatever ....
1. does this compound increase GH?
2. am i actually sleeping deeper? or is it the conversion from ldopa to dopamine to epinephrine <or however that sh*t goes... doexycarbolase who whatnot (im sorry im not the most educated individual)
3. what would you recommend (well not recommend but suggest) one take to minimize the above conversion from happening, green tea? extract or straight green tea? or something else?
4. how safe is this product to use?
5. if this does help boost gh, to what degree, and what dosage ?
10-24-2011, 07:12 PM
10-24-2011, 07:48 PM
10-24-2011, 09:28 PM
I've pretty much given up on sleep. There are a lot of things I need to work on before we'll ever be friends, if ever.
I'm subbing for the info though.
ADVANCED MUSCLE SCIENCE
Strongest On The Market
RECOVERBRO: Est. Post #3222
10-25-2011, 02:49 PM
If so, there are NO anti-cortisol properties in a state of hypOglycemia (low-blood sugar)! Quite the opposite actually...it would be a state where counter-regulatory hormones (i.e. - cortisol, catecholamines, GH, etc...) run amok. So as far as I am concerned, AMPK and anti-cort effects are back order when we're using 250mg Na-R-ALA (most potent compound in this product).
As far as mucuna and GH...the reference is usually in response to L-Dopa standardizations BUT understand that most data on GH response to L-Dopa administration was in regards to Mucuna (not in isolation) but coupled with something else (i.e. - arginine infusion, pyridostigmine, the agent carbidopa in the pharmaceutic agent Sinemet to help with BBB issues, etc...) OR usually incorrect citation of IV infusions of L-dopa so it is very hard for me to translate.
What I can tell you is on a testosterone scale, the 15-20% extracts have a larger impact on T than do say 40-75% extracts or higher for reasons unbeknownst to the research world to date. If you'd like more on this mucuna literature, I direct you to "The Fertility Thread" and you can look for yourself.
We can be e-friends for sure, whether you sleep or not...it just gives you more time to post while pondering how to remedy everything.
Anabolicminds.com Featured Author
10-25-2011, 03:00 PM
10-25-2011, 07:56 PM
Actually - Na-R-ALA DECREASES hypothalamic AMPKNa-R-ALA increases AMPK thus whole body expenditure.
Anti-obesity effects of alpha-lipoic acid mediated by suppression of hypothalamic AMP-activated protein kinase.
Kim MS, Park JY, Namkoong C, Jang PG, Ryu JW, Song HS, Yun JY, Namgoong IS, Ha J, Park IS, Lee IK, Viollet B, Youn JH, Lee HK, Lee KU.
Department of Internal Medicine, University of Ulsan College of Medicine, 138-736 Poongnap-dong, Songpa-ku, Seoul 138-736, Korea.
AMP-activated protein kinase (AMPK) functions as a fuel sensor in the cell and is activated when cellular energy is depleted. Here we report that alpha-lipoic acid (alpha-LA), a cofactor of mitochondrial enzymes, decreases hypothalamic AMPK activity and causes profound weight loss in rodents by reducing food intake and enhancing energy expenditure. Activation of hypothalamic AMPK reverses the effects of alpha-LA on food intake and energy expenditure. Intracerebroventricular (i.c.v.) administration of glucose decreases hypothalamic AMPK activity, whereas inhibition of intracellular glucose utilization through the administration of 2-deoxyglucose increases hypothalamic AMPK activity and food intake. The 2-deoxyglucose-induced hyperphagia is reversed by inhibiting hypothalamic AMPK. Our findings indicate that hypothalamic AMPK is important in the central regulation of food intake and energy expenditure and that alpha-LA exerts anti-obesity effects by suppressing hypothalamic AMPK activity.
PMID: 15195087 [PubMed - indexed for MEDLINE]
Your bodies attempts to keep TIGHT blood sugar control (as stated above: 75/80-100 mg/dl)...LOW blood sugar TRUMPS anything that could block cortisol and it is very fortunate it does or you'd possibly fall into a fatal hypOglycemic state through the night.why arent there anti cortisol properties in hypOglycemia? if the product contains and anti cortisol agent how does tthis happen
Anabolicminds.com Featured Author
10-25-2011, 08:18 PM
"Therefore, we hypothesized that α-LA improves energy metabolism and mitochondrial biogenesis by enhancing AMPK-PGC-1α signalling in the skeletal muscle of aged mice."
I know in mice....
full text here
10-25-2011, 08:21 PM
i guess another topic for discussion lol
" Importantly, energy expenditure is increased not only by stimulation of AMPK activity in peripheral tissues but also suppression of it in the hypothalamus. Note that the hypothalamus coordinates signals from peripheral tissues to control energy homeostasis. It seems that LA-mediated increase in the whole-body energy expenditure might be mainly due to its modulation of the hypothalamic function. In addition to direct effects on the muscle, LA inhibited the hypothalamic activity of APMK to promote negative energy balance 54. However, further studies are warranted to define LA-mediated central vs. peripheral actions using tissue-specific AMPK deficiency mouse models. Therefore, LA-mediated metabolic effects in the present study might not only result from suppression of food intake, but also stimulation of energy expenditure, which is regulated by LA-mediated AMPK signaling in the hypothalamus and peripheral tissues (such as muscle, adipose tissue, and liver). Notably, there was a reduction in lean mass in LA-treated mice. Due to a greater loss in fat mass, however, lean mass expressed as the percentage of body composition actually increased in the LA-treated mice. It is unclear whether LA-mediated loss of lean mass resulted from increased rates of protein degradation and/or decreased rates of protein synthesis. The mammalian target of rapamycin (mTOR, a nutrient sensor) regulates cell growth and survival and controls protein synthesis. Phosphorylation of both mTOR and p70S6 kinase decreased in the skeletal muscle of the LA-treated mice, probably indicating decreased protein synthesis. In consistent with this, protein synthesis was suppressed in LA-treated C2C12 cells. Importantly, activation of AMPK by AICAR appears to suppress protein synthesis in rat skeletal muscle through down-regulating mTOR signalling 55, 56. Thus, LA might suppress protein synthesis in the skeletal muscle, probably resulting from activated AMPK-mediated suppression of the mTOR signalling pathway. Further studies are warranted to establish how LA down-regulates the mTOR signalling involved in protein and energy metabolism to optimise a LA-based treatment for the management of the metabolic syndrome, which might offer the maximum benefit on energy expenditure and glucose metabolism with the minimum loss of lean body mass."
06-27-2012, 11:29 PM
I have had good success with a product called ZenBev. It's organic pumpkin seed flour aka a natural source of trytophan.
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