Super Supps...the next wave..

Discussion in 'Anything and Everything about dietary supplements' started by seemore, Jul 29, 2007.

  1. seemore

    seemore Member

    Seeing as Aaron was so friendly about it....

    It was a poster presentation. I can't remember where from.

    I've got some other bits and pieces....

    Re: Flex Wheeler

    To whom it may concern:

    I am writing this letter per the request of Flex Wheeler.

    I would first like to briefly provide you with some background information regarding BALCO Laboratories. BALCO has been working with elite Olympic and professional athletes for over fifteen years. BALCO has provided testing and consultation for over 250 NFL players including the entire 1998 Super Bowl Champion Denver Broncos team and the entire Miami Dolphins team. BALCO works with professional athletes in many sports including teenis (Michael Chang, Jim Courier, etc.), hockey, bodybuilding (10 of the 16 1998 Mr. Olympia contestants), track and field, soccer and basketball (Seattle SuperSonics).

    BALCO Laboratories has been testing and monitoring Flex on a routine basis during the last year. We have performed tests including blood chemistry (SMAC), complete blood count (CBC), PSA, anabolic hormone levels, genotyping as well as comprehensive testing for nutritional elements. Flex's test results have been compared to twenty-four other professional bodybuilders and overall he has one of the healthiest profiles. Basically, Flex is in excellent health and has demonstrated the discipline necessary to maintain a peak level of conditioning.

    Flex was a participant in a study we recently conducted in collaboration with the Department of Human Genetics at the University of Pittsburgh involving 62 men who made unusually large gains in muscle mass in response to strength training (extreme responders). Flex was one of only nine extreme responders that had the very rare "myostatin mutation." Myostatin is the gene that "limits muscle growth." Specifically, Flex had the rarest form of myostatin mutation at the "exon 2" position on the gene. This simply means Flex has a much larger number of muscle fibers compared to the other subjects or the normal population. We believe that these are the very first myostatin mutation findings in humans and the results of this landmark study have already been submitted for publication. Flex was also found to have a very unusual type of the IGF-1 gene. In fact, Flex was the only participant in the study that did not have a "match." All of the other extreme responders had at least three other subjects with a matching IGF-1 gene. Based upon Flex's very unique genetic profile, we plan to expeditiously publish a scientific paper that reveals his complete genotype in specific detail. The publication of his remarkable genetic data should generate an enormous amount of media exposure.

    Hope this information will be helpful and please call if I can be of assistance.

    Sincerely,

    /s/ Victor Conte
    Victor Conte
    President
    BALCO Laboratories, Inc.

    1520 Gilbreth Road • Burlingame, CA 94010 • 1-800-777-7122 • FAX (650) 687-6576


    MATERIALS AND METHODS

    Sequencing of selected regions of the myostatin gene and genotyping
    of common variants were carried out in a comparison sample of
    96 randomly selected Caucasian and 96 African American subjects
    from the general population. An additional 72 individuals were
    screened for a common exon 2 variant. One hundred fifty-three
    subjects, including 127 men (32 African American, 91 Caucasian,
    and 4 Asian) and 26 women (9 African American, 16 Caucasian, and
    1 Asian), were categorized by the magnitude of increases in muscle
    mass they experienced from strength training. The subjects consisted
    of world-class bodybuilders (ranked in the top 100 worldwide)
    (N 5 18; 5 were ranked in the top 10), competitive bodybuilders not
    ranked in the top 100 (N 5 25), elite power lifters (N 5 7), university
    football players (N 5 9), previously untrained subjects who had their
    quadricep muscle volume measured by magnetic resonance imaging
    before and after 9 weeks of heavy resistance strength training of the
    knee extensors (N 5 33), and nonathletes, who were questioned
    about their ability to increase their muscle mass in response to
    intense and prolonged strength training (N 5 61). A rating of 5 was
    given to those who were world-class bodybuilders and to those who
    increased their quadriceps muscle mass by .400 cm3 after only 9
    weeks of strength training, whereas a rating of 0 was given to those
    who experienced no noticeable increase in muscle mass after vigorous
    strength training for at least 6 months. Eighteen subjects received
    a rating of 5, and 13 subjects received a rating of 0. The
    ratings of the remaining subjects fell somewhere between these two
    extremes. Subjects who were rated as either 4 or 5 were classified as
    extreme responders (N 5 62) and were compared to those who were
    rated as either 0 or 1 and were classified as nonresponders (N 5 48).
    Subjects were also grouped and compared by race. Information on
    muscle mass changes with strength training from the remaining
    subjects was obtained through either estimates of fat-free mass
    assessed by dual-energy X-ray absorptiometry or hydrodensitometry
    or in the case of competitive bodybuilders, power lifters, football
    players, and nonathletes, through questionnaire data on prior success
    in bodybuilding competition and/or reported changes in muscle
    mass with strength training. Informed consent was obtained from all
    subjects under protocols approved by the Institutional Review
    Boards of the University of Maryland and the University of Pittsburgh.
    Laboratory methods. Genomic DNA was prepared from EDTA
    anticoagulated whole blood or from cheek swabs by standard methods
    (Miller et al., 1988). DNA amplification primers for each exon and
    the 59-flanking region of the human myostatin gene were designed
    based on the cDNA sequence of human myostatin (GenBank Accession
    No. AF019627) and the genomic organization of the bovine
    myostatin gene (Grobet et al., 1997).


    it is interesting to note that three of the
    African American nonresponders were homozygous for
    the less common (Arg) allele at the exon 2 K153R site,
    while none of the responders were homozygous for this
    allele. Three of the five mutations causing the doublemuscle
    phenotype in cattle occur in exon 2 and are
    recessive, but two are chain termination mutations
    and one is a deletion, expected to produce a nonfunctional
    myostatin protein (Grobet et al., 1998). Whether
    variation in the myostatin gene influences muscle phenotypes
    other than the muscle mass increase in response
    to strength training requires further exploration.


    1: J Appl Physiol. 2007 Mar 8;
    Activin RIIB and Follistatin Haplotype Associations with Muscle Mass and Strength in Humans.
    Walsh S, Metter EJ, Ferrucci L, Roth SM.


    PURPOSE: Genetic variation in myostatin, a negative regulator of skeletal muscle, in cattle has shown remarkable influence on skeletal muscle resulting in a double-muscled phenotype in certain breeds; however, DNA sequence variation within this gene in humans has not been consistently associated with skeletal muscle mass or strength. Follistatin and Activin RIIB (ACVR2B) are two myostatin-related genes involved in the regulation/signaling of myostatin. We sought to identify associations between genetic variation and haplotype structure in both follistatin and ACVR2B with skeletal muscle related phenotypes. METHODS: Three hundred and fifteen males and 278 females aged 19-90 years from the Baltimore Longitudinal Study of Aging were genotyped to determine respective haplotype groupings based on HapMap data. Whole-body soft tissue composition was measured by dual-energy X-ray absorptiometry. Quadriceps peak torque (strength) was measured using an isokinetic dynamometer. RESULTS: Women carriers of ACVR2B haplotype group 1 exhibited significantly less quadriceps muscle strength (shortening phase) than women homozygous for haplotype group 2 (109.2 +/- 1.9 vs 118.6 +/- 4.1 N.m, 30 degrees /sec, respectively, p = 0.036). No significant association was observed in men. Male carriers of follistatin haplotype group 3 exhibited significantly less total leg FFM than non-carriers (16.6 +/- 0.3 vs 17.5 +/- 0.2 kg, respectively, p = 0.012). No significant associations between these haplotype groups were observed in women. CONCLUSION: These results indicate that haplotype structure at the ACVR2B and follistatin loci may contribute to inter-individual variation in skeletal muscle mass and strength, though these data indicate sex-specific relationships. Key words: genetics, skeletal muscle, myostatin, sex.

    PMID: 17347381 [PubMed - as supplied by publisher]


    Interview with the doctor from the study
     
  2. Aaron_F

    Aaron_F New Member

    Victor Conte

    enough said.
     
  3. seemore

    seemore Member

    I've tried attaching the scan of the presentation, but it keeps rejecting it, it's only 152kb.
     
  4. Bulldog

    Bulldog Active Member

    What type of file is the presentation? Try compressing it into a ZIP file and then try uploading it.
     
  5. seemore

    seemore Member

    Here's a new study. It shows that follistatan levels are important in determining muscle growth.

    John Hopkins

    <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Johns Hopkins Medical Institutions

    'Mighty mice' made mightier

    --------------------------------------------------------------------------------

    --------------------------------------------------------------------------------

    Comparison of body and muscle size between normal (left) and double mutant mice lacking myostatin and overproducing follistatin (right).

    Click here for more information.
    --------------------------------------------------------------------------------

    The Johns Hopkins scientist who first showed that the absence of the protein myostatin leads to oversized muscles in mice and men has now found a second protein, follistatin, whose overproduction in mice lacking myostatin doubles the muscle-building effect.

    Results of Se-Jin Lee’s new study, appearing on August 29 in the online, open-access journal PLoS ONE, show that while mice that lack the gene that makes myostatin have roughly twice the amount of body muscle as normal, mice without myostatin that also overproduce follistatin have about four times as much muscle as normal mice.

    Lee, M.D., Ph.D., a professor of molecular biology and genetics, says that this added muscle increase could significantly boost research efforts to “beef up” livestock or promote muscle growth in patients with muscular dystrophy and other wasting diseases.

    Specifically, Lee first discovered that follistatin was capable of blocking myostatin activity in muscle cells grown under lab conditions. When he gave it to normal mice, the rodents bulked up, just as would happen if the myostatin gene in these animals was turned off. He then genetically engineered a mouse that both lacked myostatin and made extra follistatin. If follistatin was increasing muscle growth solely by blocking myostatin, then Lee surmised that follistatin would have no added effect in the absence of myostatin.

    “To my surprise and delight, there was an additive effect,” said Lee, who notes these muscular mice averaged a 117 percent increase in muscle fiber size and a 73 percent increase in total muscle fibers compared to normal mice.

    “These findings show that the capacity for increasing muscle growth by targeting these pathways is much more extensive than we have appreciated,” adds Lee. “Now we’ll search for other players that cooperate with myostatin, so we can tap the full potential for enhancing muscle growth for clinical applications.”

    Lee adds that this issue is of particular significance, as most agents targeting this pathway, including one drug being currently tested in a muscular dystrophy clinical trial, have been designed to block only myostatin and not other related proteins.
    </div>
     
  6. xahrx

    xahrx New Member

    <div>
    (seemore @ Sep. 09 2007,08:34)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Here's a new study. It shows that follistatan levels are important in determining muscle growth.

    John Hopkins

    <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Johns Hopkins Medical Institutions

    'Mighty mice' made mightier

    --------------------------------------------------------------------------------

    --------------------------------------------------------------------------------

    Comparison of body and muscle size between normal (left) and double mutant mice lacking myostatin and overproducing follistatin (right).

    Click here for more information.
    --------------------------------------------------------------------------------

    The Johns Hopkins scientist who first showed that the absence of the protein myostatin leads to oversized muscles in mice and men has now found a second protein, follistatin, whose overproduction in mice lacking myostatin doubles the muscle-building effect.

    Results of Se-Jin Lee’s new study, appearing on August 29 in the online, open-access journal PLoS ONE, show that while mice that lack the gene that makes myostatin have roughly twice the amount of body muscle as normal, mice without myostatin that also overproduce follistatin have about four times as much muscle as normal mice.

    Lee, M.D., Ph.D., a professor of molecular biology and genetics, says that this added muscle increase could significantly boost research efforts to “beef up” livestock or promote muscle growth in patients with muscular dystrophy and other wasting diseases.

    Specifically, Lee first discovered that follistatin was capable of blocking myostatin activity in muscle cells grown under lab conditions. When he gave it to normal mice, the rodents bulked up, just as would happen if the myostatin gene in these animals was turned off. He then genetically engineered a mouse that both lacked myostatin and made extra follistatin. If follistatin was increasing muscle growth solely by blocking myostatin, then Lee surmised that follistatin would have no added effect in the absence of myostatin.

    “To my surprise and delight, there was an additive effect,” said Lee, who notes these muscular mice averaged a 117 percent increase in muscle fiber size and a 73 percent increase in total muscle fibers compared to normal mice.

    “These findings show that the capacity for increasing muscle growth by targeting these pathways is much more extensive than we have appreciated,” adds Lee. “Now we’ll search for other players that cooperate with myostatin, so we can tap the full potential for enhancing muscle growth for clinical applications.”

    Lee adds that this issue is of particular significance, as most agents targeting this pathway, including one drug being currently tested in a muscular dystrophy clinical trial, have been designed to block only myostatin and not other related proteins.
    </div></div>
    It's a pretty study. Are there any double blind studies done specifically using oral administration of Folstaxan that show significant increases in muscle mass over a control group in healthy adult males?
     
  7. seemore

    seemore Member

    That's in the pipeline apparently.

    I am thinking that unless they have added a special delivery system (which I doubt), you could probably get the follistatin the same way from eating fertilised eggs...no?
     
  8. Here's another study: Novel phytoandrogens and lipidic augmenters from Eucommia ulmoides (Gutta-Percha tree bark)

    Basically, its the opposite of Soy (phytoestrogen), check it out, looks very interesting.

    Its a non-sponsored study done at the National University of Singapore.

    link: http://www.biomedcentral.com/1472-6882/7/3

    what do you think?
     
  9. quadancer

    quadancer New Member

    The opposite of soy? I can see a &quot;supermilk&quot; on the horizon!
     
  10. seemore

    seemore Member

    This was a mass email sent out by the company, sounds like they are having trouble getting organised and a small business off the ground, or as the more cynical amongst us would say: they are master scam artists.

    <div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Dear Customer,

    Thank you for your patronage and support of Folstaxan. Scaling up from lab
    to commercial production has been a monumental task for us and we have been
    barraged with unforeseen set backs. The production of Folstaxan is a
    complicated process which includes the work of seven outsourced production
    steps as well as in-house work. There have been delays with outsourced
    work. We are committed to bring to you finished product with active proteins
    that will assist you in reaching your goals. We apologize for the delays.

    The purpose of this communication is to share with you some important
    updates regarding the ordering and delivery of Folstaxan.

    1. Delivery Positions

    There are no more delivery positions available. Anyone placing an order
    now, will be making an order for product delivery. For those of you who
    purchased delivery positions, we will be sending you an months supply as a
    good will gesture for your support in addition to any orders for product you
    have placed. You will receive a months supply even if you did not make
    additional purchases.

    Also, as promised, if you were a delivery position customer, you will
    receive a refund check of $30.00 US for each of the next three monthly
    supplies you purchase before the end of October. There is no way for our
    ordering system to include a discount at the time of order, so we must honor
    your discount through means of a refund check.

    2. Ordering

    We are having issues with credit card processing. This problem should be
    fixed by end of this week. You can place orders through Pay Pal or by
    calling our toll free number: (866)750-5168.

    We see no problem with international shipping and customs. If there is a
    problem, we will offer a refund.

    3. Toll free number

    The hours of operation are Monday thru Friday, 10:00 AM to 4:00 PM CDT. If
    you have any product related questions, please call the (866)750-5168 or
    send an email.

    4. Inquiries

    Please refrain from asking about delivery timing. As soon as we feel
    confident about delivery status we will let you know.
    If you placed an order, we got it. No need to confirm anything. If you
    changed your address through email or the toll free number, we have it
    noted. Again, no need to confirm.

    Do not use aim.com or any IM address. It will foul our email system.

    Please call (866)750-5168 for questions. Have your email address ready, for
    questions the call center cannot answer. Please do not call our corporate
    offices.

    5. Express delivery

    If you ordered recently and requested express delivery, we will refund the
    additional amount charged for express shipping. We presently recommend that
    customers do not request express shipping.

    6. Research

    Please do not ask about participation in, or outcomes of our research. We
    cannot update or let anyone know the results of any research until it is
    published. The studies are not complete and we cannot speculate about the
    timing of the close of studies.


    Again, thank you for your support. If there are no unseen delays we hope to
    ship within two to three weeks.



    Rick Green
    President and CEO
    Celldyne Biopharma, LLC
    12000 Network Blvd. Ste B-200
    San Antonio, TX 78249

    [email protected]
    No virus found in this outgoing message.
    Checked by AVG Free Edition.
    Version: 7.5.488 / Virus Database: 269.13.31/1031 - Release Date: 9/26/2007
    12:12 PM

    </div>
     

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