I will take time to answer this, but this isn't a scientific response and it discarded numerous arguments to tease out the pieces that met your views. Be that as it may, I understand your concern...so let me address.
The selenium athletic study wasn't hidden by me. Most data is mixed in results. We're not making insane marketing claims. We use science and don't hide it. The fact is...there's a lot of science out there on every ingredient...most good, some not as good, which happens when there is tons of data...but mind you...
NIM...SAFE...1000's of studies...safe...means, safe...one study doesn't tear that down...it means merely...we need to do more studies to elucidate the real cause and effects relationships...there's so many factors. For example in that study of antioxidants, selenium is not the only ingredient and the data on alpha-tocopherol is mostly poor in these studies. There's no study using only selenium. Antioxidant effect is not at all what we're going for in this formulation and really selenium is only an indirect antioxidant.
Radiation "wastage"...ahhh...well...where to go with that...
I gave the example of exploiting a pathway can cause "wastage" by pushing the pathway in a certain direction by loading up on substrates...this can cause increased need at various points. 200-300mcg average is widely prescribed by physicians and medical community with lots of supportive data on mortality.
Lastly, we could have ingredients that no one could dispute because there is NO DATA or its grossly extrapolated from something in an herb that this version is not even standardized for...or it was given IV in the study...or it was given at an insane dose, force-fed to rats at like 300mg/kg. Then, there's companies that play the name game with ingredient or do proprietary blends.
We're open about the ingredient, the research, the dose, the testing and having a MD and RD back it. I'd feel as certain as one could about anything you ingest with our product. If new compelling data comes along...we'd reformulate...until then this is rock solid to us.
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11-24-2008, 10:30 AM #181
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Shawn Wells, MPH, RD, CISSN
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11-24-2008, 10:53 AM #182
This was the response I recieved from AORtech regarding their reducing the selenium dosage from 200mcg to 55mcg in their products. Take what you want out of it, but that was their reasoning... at least I am glad they did, even so I wouldn't have to worry about getting 200-400mcg from Ultima and another 200mcg or so from Ortho Core = 400-600mcg... although I don't usually go the full dosage.
Hi Peter,
The dose was reduced following the studies showing a risk for type 2 diabetes. Although the risk was shown in only one study so far, the study was by far the most elaborate with over 7 years duration in more than 1200 people. We felt it was necessary to reduce the dose of the selenium in our products to reflect these findings. Given the incidence of type 2 diabetes, we felt an increase of the risk from 8.4 to 12.6 cases per 1000 needed to be addressed.
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11-24-2008, 11:33 AM #183
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NOW I know the study you guys are talking about, from last year. It just clicked. Most of the life extension and medical community crowd have addressed that. It was felt that there were several variables at play in the study and the form used was of concern...much like the mixed (high gamma) tocopherol vs. alpha-tocopherol. I will post more on this...
Again, this is why data can often be so misinterpreted, a study is one snapshot...it can be blurry, out-of-focus, and have too many things going on it. Many snapshots helps form a near 3-d image...
I will post back. I am surprised AOR took that stance. Interesting. People take arginine and there's numerous studies...I will save that for another day. I am working on that article now.Shawn Wells, MPH, RD, CISSN
Director of Research and Development - Dymatize
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11-24-2008, 11:41 AM #184
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I found this done as of this month, Nov.8, from Europe...again...stating the exact opposite. Metabolic Syndrome/Diabetes II are decreased by selenium. I do remember the other study being about the form most people were debating, never whether selenium was worthy. I need to read back through that one though.
Researchers from the University of Navarra in Pamplona report that selenium status appears to be linked with serum complement factor 3 (C3), which has been reported to be a marker for increased risk of the metabolic syndrome.
Metabolic syndrome (MetS) is a condition characterised by central obesity, hypertension, and disturbed glucose and insulin metabolism. The syndrome has been linked to increased risks of both type 2 diabetes and CVD.
Study details
One hundred healthy young adults with an average age of 20.7 and an average BMI of 21.6 kg per m2 were recruited. Lifestyle features were analysed and blood pressure measurements taken, while finger nail samples were taken to measure selenium concentrations.
Using data from fasting blood samples, the researchers found that higher C3 levels had a positive association with several measures, including BMI, waist circumference, blood glucose levels, and triacylglycerol levels. On the other hand, selenium levels measured from the finger nails were negatively associated with C3 concentrations, they said.
?C3 seems to be related with selenium status and several anthropometrical and biochemical measurements linked to metabolic syndrome in apparently healthy young adults,? wrote the authors.
?These findings suggest a possible role for selenium intake in the modulation of C3, whose assessment may be an early marker of metabolic syndrome manifestations.?
Source: European Journal of Clinical Nutrition
Published online ahead of print, 5 November 2008, doi:10.1038/ejcn.2008.48
?Selenium intake reduces serum C3, an early marker of metabolic syndrome manifestations, in healthy young adults?
Authors: B. Puchau, M.A. Zulet, A. Gonzalez de Echavarri, I. Navarro-Blasco and J.A. MartinezShawn Wells, MPH, RD, CISSN
Director of Research and Development - Dymatize
www.dymatize.com
SWells@Dymatize.com
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11-24-2008, 12:11 PM #185
Here's a link to the full article Shawn referenced above:
http://www.nature.com/ejcn/journal/v...cn200848a.html
One of the issues I have with a lot of this is that too many people are taking the study authors' conclusions and there have been 4 studies on this suggested offering since the start of SELECT (interesting we have to defend against it, but it never ceases to amaze me, alas I digress)...2 have suggested similarity, 1 showed no difference, 1 showed decreased incidence and then there was the above which doesn't really fit as I don't tend to speak too often on foreign research as I am not the best read on things that don't appear in American peer reviews unfortunately (some things like ADVANCE and so on if there is an Endocrine focus, but even that Australian study had BS conclusions).
Why we never see the forest through the trees is beyond me. Interesting enough, the studies suggesting increased Diabetes risk did NOT bring up the issue of genetics (increased genetic ties in DMII) and didn't (perhaps conveniently) mention that BMIs are elevated in the particular individuals in the study populations - in other words, already at a higher risk - not necessarily atypia however in something seeking out prostate cancer with increased estrogenic offering (i.e. - higher aromatase levels in fatty tissues and IGF-1/Estradiol attachments if you understand the pathology settled on for prostate pathology development).
In any event, perhaps it is important to note that diet and exercise are far bigger benefit or deleterious offering for soemone fending off DMII and I would presume the population that is bb.com would already be following suggested lifestyle patterns.
Additionally, when I compare DMII and hyperhomocysteinemia (understand selenium is needed to drive particular reactions forward in said cascades), the latter should be more applicable to the exercising populace (in other words - YOU!)....that said, heightened levels of protein that likely exist in your diet and subsequently heightened levels of methionine, probably mean having all adequate substrates and cofactors in place a better idea.
If you are following the lifestyle you should be, it is imperative to suggest that you are NOT typical of the study population and making conclusions based on a subpar trial is certainly premature at best.
D_Dana Houser, MD, MHSA, CISSN
Industry Author & Product Development Consultant
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11-24-2008, 02:32 PM #186
I like that last paragraph esp. and I can see many of your points... I guess for many, including and possibly, esp. those who read the recommendations and warnings regarding selenium, it might be hard to simply accept taking a 400mcg dose/day on top dietary intake... I wonder why so much more is needed, as I would have thought a little would go a long way with this mineral and I guess that would be my main point with selenium... wouldn't even having 100mcg work with the formula to serve its purpose?
I'm open to your writeup and possible explanations for everything in Ultima and might ease my worry some... I made the point that it might not be an everyday supplement and then you can always adjust the dose individually if desired... the same ratio of ingredients will still be there.
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11-24-2008, 02:54 PM #187
More reason to love CDP-Choline
CDP-Choline as I stated previously, has been a favorite brain-nutrient of mine for quite awhile now... I just love its MOA, the supporting science and the proven safety.
Here's a recent study for ya: There's some interesting findings in there. It has lots of potential.
Citicoline enhances frontal lobe bioenergetics as measured by phosphorus magnetic resonance spectroscopy
M. M. Silveri 1 2 3 *, J. Dikan 1, A. J. Ross 1 2 3, J. E. Jensen 2 3, T. Kamiya 4, Y. Kawada 4, P. F. Renshaw 2 3, D. A. Yurgelun-Todd 1 2 3
1Cognitive Neuroimaging Laboratory, McLean Hospital, Belmont, MA, USA
2Brain Imaging Center, McLean Hospital, Belmont, MA, USA
3Department of Psychiatry, Harvard Medical School, Boston, MA, USA
4Healthcare Products Development Center, Kyowa Hakko Kogyo Co., Ltd, Tsukuba, Ibaraki, Japan
Abstract
Citicoline supplementation has been used to ameliorate memory disturbances in older people and those with Alzheimer's disease. This study used MRS to characterize the effects of citicoline on high-energy phosphate metabolites and constituents of membrane synthesis in the frontal lobe. Phosphorus (31P) metabolite data were acquired using a three-dimensional chemical-shift imaging protocol at 4 T from 16 healthy men and women (mean ? SD age 47.3 ? 5.4 years) who orally self-administered 500 mg or 2000 mg Cognizin? Citicoline (Kyowa Hakko Kogyo Co., Ltd, Ibaraki, Japan) for 6 weeks. Individual 31P metabolites were quantified in the frontal lobe (anterior cingulate cortex) and a comparison region (parieto-occipital cortex). Significant increases in phosphocreatine (+7%), -nucleoside triphosphates (largely ATP in brain, +14%) and the ratio of phosphocreatine to inorganic phosphate (+32%), as well as significant changes in membrane phospholipids, were observed in the anterior cingulate cortex after 6 weeks of citicoline treatment. These treatment-related alterations in phosphorus metabolites were not only regionally specific, but tended to be of greater magnitude in subjects who received the lower dose. These data show that citicoline improves frontal lobe bioenergetics and alters phospholipid membrane turnover. Citicoline supplementation may therefore help to mitigate cognitive declines associated with aging by increasing energy reserves and utilization, as well as increasing the amount of essential phospholipid membrane components needed to synthesize and maintain cell membranes.
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11-24-2008, 07:31 PM #188
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11-24-2008, 07:38 PM #189
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We did establish it would equal a 200mcg dose as people would work out 3-4 times a week using this product. 400mcg per serving...3-4 times a week. NSI uses 400mcg in their platinum multi, a physician formulation that formulated this year...the one that's about $300/month. LEF's multi-mix and booster, which is what they recommend on the phone or on the site as their basic place to start is 400mcg. and again physician formulated. The National Institute of Medicine backs that dose. Research backs that dose as being very safe and nearly every study being a positive or no effect under various parameters.
One study showed some level of correlation...not causality...read NOT CAUSALITY...as they weren't even looking for diabetes...didn't test serum selenium and correlate that...and I just find it an odd study to use as there are so, so many factors when its not set up to even study this "relationship". All it says to me is do more studies...until then the bulk of the data, the scientific community and the medical community back a dose we use as safe and further, as I stated the net is actually half of that when looked at using the servings as most would.
A newer study that was looking at diabetes/metabolic syndrome directly, that I showed...showed the exact opposite to be true...of which I would consider the stronger data. Selenium was associated with less metabolic syndrome/diabetes. A newer study that was looking at diabetes/metabolic syndrome directly, that I showed...showed the exact opposite to be true...of which I would consider the stronger data, but again one must look at the vast amounts of toxicology, safety, LD50 data with mice, rats, primates, humans, etc. There is tons of research that goes in to setting these limits...Tons.Shawn Wells, MPH, RD, CISSN
Director of Research and Development - Dymatize
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11-24-2008, 07:39 PM #190
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11-24-2008, 07:40 PM #191
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11-25-2008, 05:00 AM #192
You certainly won't deny that there is a principal difference between studies analyzing a correlation between selenium blood levels and certain conditions on the one hand and studies that show a correlation between supplemental selenium intake and certain conditions on the other hand.
Many studies have shown that people with higher blood vitamin levels have lower risk for cancer and/or cardiovascular events. But where are the studies that could show a benefit from supplemental vitamin use?
I hope you can see where I am coming from. Having a good blood selenium level is one thing - especially when the selenium stems from healthy foods.
The big question is: what does supplemental selenium intake do in the body?
There is increasing evidence that supplemental antioxidant vitamins (e.g.ACE) may not be as beneficial and even potentially harmful - in strong contrast to naturally ingested vitamins / trace minerals.
For example: Alpha-Tocopherol and Beta-Carotene intake have been associated with increased lung cancer rates in smokers.
And now, we have two (not just one) large studies that suggest an association between supplemental Selenium intake and Diabetes.
Here is a very insightful comment from the Annals of Internal Medicine in 2007:
Selenium and Diabetes: More Bad News for Supplements
Joachim Bleys, MD, MPH; Ana Navas-Acien, MD, PhD; and Eliseo Guallar, MD, DrPH
21 August 2007 | Volume 147 Issue 4
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In this issue, Stranges and colleagues (1) report findings from the Nutritional Prevention of Cancer (NPC) trial that show an increased risk for diabetes among participants randomly assigned to receive supplements with 200 ?g of selenium daily for 7.7 years compared with placebo. This effect was largely limited to participants in the top tertile of plasma selenium level at baseline (>121.6 ng/mL). In this group, the hazard ratio for incident diabetes in persons using selenium supplements compared with placebo was 2.70 (95% CI, 1.30 to 5.61). The NPC trial is the largest and longest available experimental study of selenium supplements compared with placebo. Although diabetes was not a primary end point of the trial and the investigators used self-report and medical records to assign the diagnosis, the results have credibility because of the randomized, double-blind design; the monitoring of baseline and follow-up plasma selenium levels; and other methodological strengths. The public health implications of these findings are substantial: More than 1% of the U.S. population take selenium supplements, and more than 35% take multivitamin and multimineral supplements (2) that often contain selenium.
Before it was found to be an essential nutrient (3, 4), selenium was considered highly toxic to animals and humans (5). The key breakthrough occurred in 1973, when Rotruck and colleagues discovered that selenium protected against oxidative damage by means of selenium-dependent glutathione peroxidase (3). Selenium is incorporated into selenoproteins as selenocysteine through a complex genetic mechanism encoded by the UGA codon (6). Selenoproteins, including glutathione peroxidases, thioredoxin reductases, iodothyronine deiodinases, and selenoprotein P, have important enzymatic functions. Through selenoproteins, selenium is involved in many biological functions, including protection against oxidative stress, immune function, and thyroid function (6, 7).
The concentration and activity of glutathione peroxidases and other selenoproteins increase with increasing intake of selenium until the dose?response relationship reaches a plateau. With the possible exception of selenoprotein P, this plateau of maximum activity is reached at plasma selenium levels of 70 to 90 ng/mL. At greater levels, additional selenium intake further increases the plasma selenium level because of nonspecific incorporation of selenomethionine into albumin and other proteins rather than increased concentration or activity of glutathione peroxidases (8, 9). In the United States, dietary intake of selenium is relatively high (80 to 165 ?g/d) (9). Indeed, 99% and 50% of adults have serum selenium levels greater than 95 ng/mL and 124 ng/mL (9), respectively. In short, the risk for selenium deficiency in the United States is negligible, and the use of selenium supplements in this country is unlikely to increase the antioxidant activity of glutathione peroxidases.
Not only are the benefits of selenium supplementation in the United States uncertain, but selenium has a narrow therapeutic range and may be toxic (5, 9). Overt symptoms of acute and chronic selenium toxicity include brittleness and loss of hair and nails, fatigue, neurologic damage, hepatic degeneration, gastrointestinal disturbances, enlarged spleen, and chronic dermatitis (9).
The Institute of Medicine set the Tolerable Upper Intake Level (UL) for selenium at 400 ?g/d to avoid visible symptoms of selenium toxicity in sensitive persons (9). In the NPC trial, participants in the active intervention group received daily supplementation with 200 ?g of selenium in addition to their usual selenium intake (1). The increased risk for diabetes in this group alerts us that asymptomatic yet pathologic changes related to chronic selenium toxicity could take place at intake levels lower than the currently defined UL. If the findings of Stranges and colleagues are confirmed, the Institute of Medicine should revise the current upper UL.
The apparent increase in risk for diabetes with selenium supplementation in persons with a dietary intake of selenium in the high-normal range may be biologically plausible. The potential diabetogenic effect of excess selenium could be explained paradoxically by the ability of some selenium compounds to generate reactive oxygen species (10). Selenium may also accumulate in the pancreatic tissue of several animals (5). Under conditions of oxidative stress, reactive oxygen species may increase insulin resistance and affect pancreatic ?-cell function (11).
Corroborative epidemiologic evidence is limited. In NHANES III (Third National Health and Nutrition Examination Survey), which was conducted in a representative sample of the U.S. population, participants in the highest quintile of serum selenium level (137.7 ng/mL) had an increased prevalence of diabetes compared with those in the lowest quintile (<111.6 ng/mL) (12). An observational analysis within the SU.VI.MAX (Supplementation with Antioxidant Vitamins and Minerals) trial also found a positive association between baseline plasma selenium levels and fasting plasma glucose levels at baseline and after 7.5 years of follow-up (13). However, a substudy of the Health Professionals Follow-up Study found an inverse association between toenail selenium levels and the prevalence of diabetes at baseline (14), and a small cross-sectional study of Asian persons residing in Singapore found similar mean serum selenium levels among participants with and without diabetes (15).
High-quality prospective cohort studies and randomized trials investigating the effects of dietary selenium and selenium supplements on the incidence of diabetes are needed. These studies should closely monitor diabetes incidence by measuring fasting plasma glucose and other indices of glucose metabolism in groups with a wide range of selenium intake. Ongoing trials (16, 17) could also be used to confirm the findings of Stranges and colleagues. These studies can help us to understand the dose?response relationship between selenium intake and health outcomes, the benefits and risks for selenium supplementation on diabetes and other chronic health outcomes, and the existence of vulnerable subgroups at risk for side effects. However, until further randomized, controlled trials show that selenium supplementation does not cause diabetes or establish that the potential risk for diabetes is outweighed by yet unproven health benefits, people with diets that provide the Recommended Dietary Allowance for selenium (55 ?g/d) (9) should avoid selenium supplements, except in the context of experimental studies.
Although obesity and lack of physical activity are the major factors responsible for the diabetes epidemic, environmental exposures may also be important. High selenium levels (12) or use of selenium supplements by persons with adequate selenium status (1) may contribute to this problem, although the extent of the role of these factors is unknown. Furthermore, the potential harmful effects of selenium supplementation in persons with high-normal selenium levels could extend beyond diabetes. A secondary analysis of the NPC trial identified some benefit of selenium supplementation for cancer prevention among participants with baseline plasma selenium levels less than 121.6 ng/mL but a possible small increase in total cancer risk among participants with higher levels (hazard ratio, 1.20 [CI, 0.77 to 1.86]) (18).
In the past decade, randomized, controlled clinical trials have shown that ?-carotene and vitamin E supplements, which were widely believed to be safe, increase mortality and morbidity (19, 20). No dietary supplement, including selenium, has proven useful so far for the prevention of cardiovascular disease or cancer in the general U.S. population. The balance of the potential benefits and harms of selenium supplementation depends on the dietary selenium intake in different countries. However, the U.S. public needs to know that most people in this country receive adequate selenium from their diet. By taking selenium supplements on top of an adequate dietary intake, people may increase their risk for diabetes.
Last edited by HottaChicka; 11-25-2008 at 05:06 AM.
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11-25-2008, 08:19 AM #193
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I agree, now, you are talking about forms...alpha-tocopherol has mixed data. The form we're using is the same found in food for selenium, much like eating brazil nuts, which has higher dose...roughly double in 1 oz. Mixed, natual tocopherols is a better choice of E...
I've repeatedly stated dose, timing, and form...studies often don't address all three.
I've beat this to death. If you're really worried...I am at the point where I'd say skip it. We've used every bit of research to make the best decisions. Again, the real dose of this "natural" form is 200mcg...is not used chronically for years, but for a few months and cycled off, if backed by research, HAS NEVER, NEVER, EVER in 100s of studies shown any toxicology or ill effect directly, the one study that shows correlation that wasn't even assessing diabetes that may lie with infinite other factors would be easily refuted when a new study (which this article that you mentioned didn't take in account) that is BRAND NEW that assesses your concern exactly...metabolic syndrome and diabetes...not only shows that there is no NEGATIVE relationship, but shows a positive one. Carbohydrate and lack of exercise can increase rick of diabetes...nobody using 2 grams less of maltodextrin...I mean the argument is silly. It isn't even correlated to mortality and certainly has nothing to do with causality...again it requires more studies...one of which was done and refutes it fully...showing anti-diabetic relationship.
I can find a negative study on every single vitamin and mineral out there...on some level...with some correlation. You must look at the body of research. Again, the NIM is massive. They look at all the data, an article by a doctor that may not even be in that field is not the same as a board of the top researchers and physicians with NIM deciding upper limits and safety. Selenium is prescribed safely.
Further, as I have stated, when pushing a reaction you'll use more substrate. Higher use. Like the carbohydrate - diabetes example...you exercise...you can use more and have less body fat, risk of metabolic syndrome. An athlete would be remiss to not use a higher amount of carbohydrate than a sedentary person.
I have beat this in to the ground. LEF and NSI have boards of physicians as well and have twice as much as us for chronic dosing purposes for the sedentary, lay population... and not pushing a certain pathway/reaction with more substrate needed.
You can put confidence in an unnamed herbal product that has no research, maybe laced with heavy metals, no toxicology data, etc? You guys continue to use supplemental arginine and there's many, many studies showing not so positive things...
This is beginning to baffle me. Seriously, there will be a write-up and from here I will mention it no more.
I've repeated myself countless times. So, that's becoming fruitless. I've read everything you've given me, prior to formulating...as did Dana. I work with cardiologists and endocrinologists that no thins data...DANA's working towards a fellowship in endocrinology (which covers metabolic syndrome/DM II). It's been discussed on countless life extension and medical boards I frequent and has been discarded readily.Shawn Wells, MPH, RD, CISSN
Director of Research and Development - Dymatize
www.dymatize.com
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11-25-2008, 08:23 AM #194
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11-25-2008, 08:29 AM #195
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The beta-carotene thing is grossly flawed as well with smokers. An antioxidant in the presence of subclinical or clinically diagnosed Cancer may in fact, protect the cancerous cells. Thereby, speeding the rate of effect for Cancer severity. They are smokers (clearly at higher risk for cancer anyway) and all most likely ALREADY had Cancer at some stage (possibly subclinical)...this tends to be consensus now with that study again showing correlation, not causality...again, beta-carotene is something I still supplement with and when we discussed it in my Master's program...no one, professors to students thought this had remarkable relevance. It is more of legal/ethical decision with these studies as the parameter behind funding require one to stop the study when even a casual correlation is shown like this...it doesn't mean what newspapers sensationalize.
Again......................moving on......................Shawn Wells, MPH, RD, CISSN
Director of Research and Development - Dymatize
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11-25-2008, 08:31 AM #196
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So back to CDP-choline...anyone use it? Also I am curious has anyone here used glucuronolactone solo? Actually any nootropic type supplement feedback I'd love to hear.
Shawn Wells, MPH, RD, CISSN
Director of Research and Development - Dymatize
www.dymatize.com
SWells@Dymatize.com
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11-25-2008, 08:35 AM #197
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Yes, I want to break in to Life extension markets with it and it is my desire, but the ingredient I want to use we may have to wait a few months, so as to not sacrifice taste. It may not be in the beta, but we're working on it. I want to give the details, but I can't.
The initial release will use, "safe" sweeteners...splenda and ACE-K. Which is better, by a long shot over nutrasweet or saccharin...but...I do want to go that direction if we can maintain great taste and the two "natural sweeteners" I want I think we can. I'll keep you informed on that.Shawn Wells, MPH, RD, CISSN
Director of Research and Development - Dymatize
www.dymatize.com
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11-25-2008, 08:37 AM #198
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11-25-2008, 08:56 AM #199
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11-25-2008, 08:57 AM #200
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11-25-2008, 09:08 AM #201
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Pathway...substrate...write-up. I will explain more, but seriously this topic is burning me out and is completely inane to me...seriously baffling with how much is given in the past few pages it has been exhausted. I don't mean to be offensive at all. We just need to move on. If you make a separate thread discussing that topic that's fine and I may add to it, but we need to move on. Please.
Shawn Wells, MPH, RD, CISSN
Director of Research and Development - Dymatize
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11-25-2008, 09:09 AM #202
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11-25-2008, 09:10 AM #203
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11-25-2008, 09:29 AM #204
Ha I appreciate the compliments Shawn though I was not a winner. As for science I actually just abandoned my political science degree two years in to switch to Applied Human Nutrition which unfortunately meant I had to take a semester off and take grade 12 chem/bio through the mail. In Canada the way it works is there are a few accredited universities that offer applied human nutrition with integrated internships meaning if my grades are high enough and I qualify for 3 rounds of interning I get my bachelor of science as well as my R.D. after 4 years. It's funny to think how much this board has had an impact on my actual life.
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11-25-2008, 10:22 AM #205
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11-25-2008, 11:23 AM #206
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11-25-2008, 01:59 PM #207
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11-25-2008, 02:34 PM #208
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11-25-2008, 08:58 PM #209
In one sense the competition is over but in terms of the market itself, it still exists. Of course with the patented ingredients one could theoretically divulge said product ingredients without much fear of copying due to the threat of litigation. Alas, we know the feasibility of such actions and it's not a greta deterrent. But I think they with hold disclosure so they can maintain a certain mystique concerning Ultima.
I think there were some valid concerns with selenium but I guess we'll have to wait for the write-up to see how justified they may be.Yes, there is indeed a deeper component to it all.
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11-25-2008, 10:07 PM #210
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I have not really ever used any form of choline, the only nootropic I have used to manipulate acetylcholine was huperzine, and only in a combo ingredient in the old Designer supplements adrenalean, though I thoroughly enjoyed it. Andro I was making a list today on various ways to prolong the life of effects of neurotransmitters, and this is all I came up with, I would appreciate anything you have to add:
1. Provide Substrate/Cofactors
2. Inhibit Degrading Enzyme
3. Inhibit reuptake (in the synapse)
4. Direct agonism/release
Sorry I've been absent from this thread. Been very busy. But very excited about ultima.CPT, CEO, R&D
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