Allright, now these can all be found here:
Clinical Studies - Body of Science
This is a reference you MUST READ if Arachidonic Acid supplementation interests you.
EFFICACY: Benedictine AA Study
THE EFFECTS OF ARACHIDONIC ACID SUPPLEMENTATION ON MYOTUBE DEVELOPMENT
David Bisterfeldt, Howard Hughes Medical Institute Student Researcher Allison Wilson , Ph.D. Department Chair Biological Sciences Craig Broeder, Ph.D. FACSM, FNAASO
Director Activities of Daily Living Performance Enhancement Research Center Director of the Masters of Clinical Exercise Physiology Program
BENEDICTINE UNIVERSITY. DEPARTMENT OF BIOLOGICAL SCIENCES. LISLE, IL
The current cell-culture studies we are conducting are designed to determine what effects arachidonic acid (AA) may have on the development and molecular constitutions involved in the differentiated myoblast to skeletal muscle myotube cells in vitro. We are targeting three specific areas of muscle growth including actin-myosin cell development-cell fusion, androgen receptor expression, and how protein cell-signaling activities are affected by various AA concentrations. To date, we have focused on the myotube hypertrophy and cell fusion effects of AA using immunohistochemical staining of myosin and actin.
We are also in the final stages of setting up the optimum in-vitro model for identifying androgen receptor expression with and without AA added to our cell-culture medium.
Cell di erentiation, myosin hypertrophy and fusion studies using C C myoblasts Precursor muscle cells cells were conducted initially. These C C cells were replenished with either fresh 10% fetal bovine serum (FBS) or the appropriate 2% horse serum (HS) media (containing no AA or 12.5 μM, 25 μM, or 50 μM AA) and then incubated for 96, 120, or 144 hours. These results indicated that the best differentiation was noted for at 144 hour incubation time in 2% HS and when comparing 25 μM or 50 μM AA to control cultures. Thus, a 144 hour incubation times were used as the experimental condition for all measurements.
For the myosin hypertrophy and fusion studies, the same experimental conditions described above were used. Thus far, we have observed clear phenotypic changes in C2C12 cells to myotubes whose medium contains arachidonic acid. These changes occurred most notable in 25 μM and 50 μM concentrations. The myotubes have an increased lateral diameter, enhanced levels of myosin deposition, and a greater concentration of nuclei than controls
(Figures 1 and 2). These results suggest that arachidonic acid may play a role in enhancing protein synthesis and myotube development at the cellular level. Moreover, we observed increased levels of nuclear fusion suggesting arachidonic acid may augment a muscle’s hypertrophic response through enhanced cellular myotube growth in our mouse myoblast cell-culture model.
EFFICACY: Baylor Study Results #1
Proceedings of the International Society of Sports Nutrition (ISSN) Conference June 15-17, 2006.
Performance and body composition changes after 50 days of concomitant arachidonic acid supplementation and resistance training.
M Iosia, M Roberts, C Kerksick, B Campbell, T Harvey, C Wilborn, R Wilson, M. Greenwood, D Willoughby and R Kreider. Exercise & Sport Nutrition Laboratory, Center for Exercise, Nutrition & Preventive Health Research, Baylor University, Waco, TX 76798-7313.
Arachidonic acid (AA) is a polyunsaturated omega-6 (0-6) fatty acid that is stored within skeletal muscle phospholipids and has been purported to stimulate changes in strength and body composition while resistance training. The purpose of this study was to determine if 50 days of concomitant resistance training and AA supplementation affects performance and/or body composition adaptations in previously resistance-trained males. Thirty-one subjects (22.1 ± 5.0 yrs, 178.9 ± 3.4 cm, 86.1 ± 13.0 kg, 18.1 ± 6.4 % body fat) were randomly assigned to ingest either a corn oil placebo (P: n=16) or AA (n=15). All subjects ingested a total of four capsules each day by ingesting one 0.25 gram capsule every four hours for a total daily dose of 1 gram•d-1 and were given a supplemental protein powder in order attain a protein intake of 2 g•kg-1•d-1. Each subject completed two upper-body and two lower-body workouts each week in a split-body fashion. Total training volumes were calculated from training logs. Body mass, body composition using DEXA, bench press one-repetition maximum (1RM), leg press 1RM and Wingate anaerobic capacity tests were completed at 0, 25 and 50 days. Data were analyzed using repeated measures ANOVA and are presented as mean ± SD changes from baseline after 50-days. No significant differences (p>0.05) between groups were noted for training volume. Training significantly increased body mass (p<0.01), DEXA lean mass (p<0.001), bench press 1RM (p<0.001), leg press 1RM (p<0.001), Wingate average power (p<0.001) and Wingate total work (p<0.001) indicating that the subjects experienced positive training adaptations. No significant group x time interaction effects were observed among groups in changes in body mass (AA: 1.6 ± 2.3; P: 1.0 ± 2.1 kg, p=0.45), DEXA lean mass (AA: 1.2 ± 1.6; P: 1.0 ± 1.9 kg, p=0.71), or leg press 1RM (AA: 25.0 ± 24.7; P: 22.7 ± 34.0 kg, p=0.83). Statistical trends were seen in bench press 1RM (AA: 11.0 ± 6.2; P: 8.0 ± 8.0 kg, p=0.20), Wingate average power (AA: 37.9 ± 10.0; P: 17.0 ± 24.0 W, p=0.16), and Wingate total work (AA: 1292 ± 1206; P: 510 ± 1249 J, p=0.087). A significant group x time interaction effect was observed in Wingate relative peak power (AA: 1.2 ± 0.5; P: -0.2 ± 0.2 W•kg-1, p=0.015). In conclusion, AA supplementation during resistance-training promoted significant increases in relative peak power with other performance related variables approaching significance. These findings provide some preliminary evidence to support the use of AA as an ergogenic aid. More research is needed to explore the effects of AA supplementation on training adaptations.
EFFICACY: Baylor Study Results #2
Proceedings of the International Society of Sports Nutrition (ISSN) Conference June 15-17, 2006.
Hormonal and intramuscular adaptations over 50 days of concomitant arachidonic acid supplementation and resistance training.
Roberts, M, C Kerksick, L Taylor, M Iosia, B Campbell, C Wilborn, T Harvey, R Wilson, M. Greenwood, D Willoughby and R Kreider. Exercise & Sport Nutrition Laboratory, Center for Exercise, Nutrition & Preventive Health Research, Baylor University, Waco, TX 76798-7313.
Prostaglandins are derived from dietary arachidonic acid (AA) and up-regulate recovery mechanisms including inflammation and protein synthesis within skeletal muscle in response to resistance training. The purpose of this study was to determine if 50 days of concomitant resistance training and AA supplementation elicited changes in hormonal and/or intramuscular markers in resistance-trained males. Thirty-one subjects (22.1 ± 5.0 yrs, 86.1 ±1 3.0 kg, 178.9 ± 3.4 cm, 18.1 ± 6.4 % body fat) were randomly assigned to a placebo (P: n = 16; 1 g capsulated corn oil/day) or AA group (AA: n = 15; 1 g capsulated AA/day) and were given supplemental protein powder to ingest in order attain an adequate protein intake of 2 g/kg/day while participating in a 4 day/wk resistance training regimen (2 upper/ 2 lower). Fasting blood was taken on days 0, 25 and 50 and muscle biopsies were taken from the vastus lateralis on days 0 and 50. Prostaglandin E2 (PGE2), prostaglandin F2a (PGF2a), interleukin-6 (IL-6), free testosterone (fTEST), total testosterone (tTEST) and cortisol (CORT) were assessed with EIA while myosin heavy chain isoform (MHC I, -IIa, -IIx) and mRNA levels were detected using SDS-PAGE and real-time RT-PCR, respectively. Hormonal and MHC data were analyzed by ANOVA with repeated measures while independent t-tests were used to assess changes in MHC mRNA expression. Data are expressed as means ± SD changes from baseline after 50-days of supplementation for the AA and P groups, respectively. Statistical trends were found for PGE2 increases (98.5 ± 217; P -73.8 ± 273 pg/ml, p=0.063) and IL-6 decrements (-28.8 ± 47; 52.5 ± 45 pg/ml, p=0.067) in the AA group. A non-significant increase in PGF2a was also found in the AA group (AA: 45.2 ± 153; P: -33.6 ± 139 pg/ml, p=0.143). fTEST significantly decreased (p=0.03) in both groups over time with no differences among groups (AA: -2.99 ± 6; P -2.60 ± 8 pg/ml, p=0.88). There was no significant group or main effects for tTEST or CORT. MHC IIa levels significantly increased in both groups over time (p=0.009) with no differences among groups (AA: 120 ± 229; P 139 ± 262 ng/ml, p=0.84). There were no significant time or group x time effects for MHC I or MHC IIx levels. A significant decrement was observed in MHC IIx basal mRNA expression in the AA group (AA: -6.96 ± 24.28; P: -4.97 ± 10.88 %, p=0.02), while there was no significant time or interaction effects for MHC I or IIa expression. Results suggest that AA supplementation during resistance training may exert some potentially favorable alterations in an inflammatory marker, fasting hormonal, and gene expression patterns and that additional research is necessary to further examine this hypothesis.
SAFETY: Cancer #1
Cancer. 1999 Sep 15;86(6):1019-27.
Association of energy and fat intake with prostate carcinoma risk: results from The Netherlands Cohort Study.
Schuurman AG, van den Brandt PA, Dorant E, Brants HA, Goldbohm RA.
Department of Epidemiology, Maastricht University, Maastricht, The Netherlands.
BACKGROUND: The roles of energy and fat intake as risk factors for prostate carcinoma are still questionable. Therefore, these factors were evaluated in the Netherlands Cohort Study described in this article. METHODS: The cohort study consisted of 58,279 men ages 55-69 years at baseline in 1986. After 6.3 years of follow-up, 642 incident prostate carcinoma cases were available for analysis. Intake of energy, fat, and separate fatty acids were measured by means of a self-administered questionnaire; fat intake was adjusted for energy by regression analysis. The case-cohort method was used to calculate rate ratios (RRs). Analyses were conducted for all prostate carcinoma cases together as well as for case subgroups (latent vs. nonlatent and localized vs. advanced). RESULTS: No associations were found in multivariate analyses between prostate carcinoma and intake of energy, total fat, total saturated fatty acids, or total trans unsaturated fatty acids (RR highest vs. lowest quintile: 0.99, 1.10, 1.19, and 0.99, respectively). Oleic acid intake showed a nonsignificant positive association (RR = 1.38, 95% CI: 0.88-2.19). Positive associations were also observed for intake of oleic acid in subgroup analyses. Linoleic (RR = 0.78, 95% CI: 0. 56-1.09) and linolenic (RR = 0.76, 95% CI: 0.66-1.04) acid intake were associated with nonsignificantly decreased risks; only for linolenic acid did these associations persist in subgroup analyses. No associations were found for intake of arachidonic acid, eicosapentaenoic acid, or docosahexaenoic acid. CONCLUSIONS: These data suggest that certain fatty acids might be involved in prostate carcinoma occurrence, although the possibility that these were chance findings cannot be ruled out. Copyright 1999 American Cancer Society.
Am J Clin Nutr. 2004 Jul;80(1):204-16.
Dietary intake of n-3 and n-6 fatty acids and the risk of prostate cancer.
Leitzmann MF, Stampfer MJ, Michaud DS, Augustsson K, Colditz GC, Willett WC, Giovannucci EL.
Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA. email@example.com
BACKGROUND: Laboratory studies have shown that n-3 fatty acids inhibit and n-6 fatty acids stimulate prostate tumor growth, but whether the dietary intake of these fatty acids affects prostate cancer risk in humans remains unclear. OBJECTIVE: We prospectively evaluated the association between intakes of alpha-linolenic (ALA; 18:3n-3), eicosapentaenoic (EPA; 20:5n-3), docosahexaenoic (DHA; 22:6n-3), linoleic (LA; 18:2n-6), and arachidonic (AA; 20:4n-6) acids and prostate cancer risk. DESIGN: A cohort of 47866 US men aged 40-75 y with no cancer history in 1986 was followed for 14 y. RESULTS: During follow-up, 2965 new cases of total prostate cancer were ascertained, 448 of which were advanced prostate cancer. ALA intake was unrelated to the risk of total prostate cancer. In contrast, the multivariate relative risks (RRs) of advanced prostate cancer from comparisons of extreme quintiles of ALA from nonanimal sources and ALA from meat and dairy sources were 2.02 (95% CI: 1.35, 3.03) and 1.53 (0.88, 2.66), respectively. EPA and DHA intakes were related to lower prostate cancer risk. The multivariate RRs of total and advanced prostate cancer from comparisons of extreme quintiles of the combination of EPA and DHA were 0.89 (0.77, 1.04) and 0.74 (0.49, 1.08), respectively. LA and AA intakes were unrelated to the risk of prostate cancer. The multivariate RR of advanced prostate cancer from a comparison of extreme quintiles of the ratio of LA to ALA was 0.62 (0.45, 0.86). CONCLUSIONS: Increased dietary intakes of ALA may increase the risk of advanced prostate cancer. In contrast, EPA and DHA intakes may reduce the risk of total and advanced prostate cancer.
SAFETY: Cancer #2
Bull Cancer. 2005 Jul;92(7):670-84. Related Articles, Links
Dietary fatty acids and colorectal and prostate cancers: epidemiological studies
Astorg P. UMR Inserm 557/INRA/CNAM Epidemiologie nutritionnelle, Institut scientifique et technique de l'Alimentation, Conservatoire national des Arts et Metiers, 5 rue du Vertbois, 75003 Paris. firstname.lastname@example.org
OBJECTIVE: This study reviews epidemiological works having studied the associations of dietary fatty acids, especially of n-6 or n-3 polyunsaturated fatty acids (PUFA), with the risks of colorectal and prostate cancers. METHODS: The epidemiological studies reviewed were those having tested the association of colorectal and prostate cancer risk with the dietary intake or the blood or adipose tissue levels of fatty acids, especially of n-6 and n-3 PUFA, and with the dietary intake of fish and seafood. RESULTS: Most studies based on a dietary questionnaire did not find any association of the risk of colorectal cancer with the consumption of either total fatty acids or any particular fatty acid, after adjustment for total energy intake had been made. A few studies suggest that trans fatty acid consumption could increase colorectal cancer risk. Most studies based either on a dietary questionnaire or on biomarkers, did not find any association of total, saturated or monounsaturated fatty acid, as well as of linoleic or arachidonic acids, with prostate cancer risk, after adjustment for total energy intake. Most studies failed to find an association of prostate cancer risk with fish or long-chain n-3 PUFA intake, but recent cohort studies did find an inverse association of fish consumption with the risk of the latest stages of prostate cancer. In contrast, alpha-linolenic acid intake was associated with an increase of prostate cancer risk in a majority of epidemiological studies, but other studies did not find this association. This latter point might be of concern, and needs to be clarified by other results, especially those of ongoing prospective studies.
J Nutr. 2004 Dec;134(12 Suppl):3421S-3426S.
Dietary (n-6) PUFA and intestinal tumorigenesis. Whelan J, McEntee MF.
Cancer is the second leading cause of death in the United States, and mortality due to colorectal cancer is only surpassed by lung cancer. Epidemiological studies demonstrate that dietary polyunsaturated fats can have a profound effect on colorectal cancer risk. Experimental data indicate that modulation of cellular (n-6) PUFA metabolism can affect the progression of the disease. This paper discusses the role (n-6) PUFA play in promoting intestinal tumorigenesis and how dietary PUFA from different families interact to modify the neoplastic process. Dietary PUFA that attenuate arachidonic acid metabolism [such as (n-3) PUFA] have antineoplastic properties, whereas those that augment arachidonic acid metabolism, such as linoleic, gamma-linolenic, and arachidonic acids do not appear to enhance tumorigenesis when added to the Western diet but may diminish the beneficial effects of other dietary lipids. It is the relative contributions of the different dietary PUFA that may determine overall risk for and progression of the disease.