[loverius]

Eftersom ni skriver "efter påtryckningar från många kunder har Eiselt återintroducerat Xpress, en produkt som hjälper dig att bränna fett och öka muskelmassan. Många kunder varit väldigt nöjda med denna"

...så undrar jag Henrik, gjorde ni ett val innan detta, att inte tillverka Xpress längre, och i så fall varför?
Var det pga hälsofarligheten eller andra faktorer?

[Gymvaruhuset]

Det var främst för att den att den är dyr att tillverka och förtjänsten kontra lagervärdet och omsättningshastigheten är inte så jättemotiverande.

Verkade som att efterfrågan ökade när JW försvann och då bestämde vi oss för att köpa in igen.

[martenk]

Det är lustigt att något som ökar inflammationer i muskler och leder samt ökar muskelnedbrytningen är så populärt att folk är beredda att betala dyrt för det. Jag har för mig att det ökar risken för hjärt-/kärlsjukdomar också. Rätta mig gärna om jag är ute och cyklar

[loverius]

Och cancerframkallande. Men tydligen mår hjärnans neuroner bra av det.
Dosera lika stor del Omega 3, som AA...är väl det bästa.

[Jocke]

Ursprungligen postat av loverius

Och cancerframkallande. Men tydligen mår hjärnans neuroner bra av det.
Dosera lika stor del Omega 3, som AA...är väl det bästa.

var val "bara" dåligt om man hade cancer? Inte så att den framkallade det?

[Johan.S]

Ursprungligen postat av loverius

Dosera lika stor del Omega 3, som AA...är väl det bästa.

Om man läser runt lite på amerikanska brädor så verkar det vara helt ok att ta 2-3 kapslar omega3 om dagen samtidigt som man tar AA.

Så att ta lika delar är vad jag vet inte rekomenderat men jag kan ju ha missat nått

[Pepz]

det ni missar är att man vill skada muskeln så mycket som möjligt för att den ska växa

kanske så att fria radikaler skulle funka som kostillskott

[R2D2]

Ursprungligen postat av martenk

Det är lustigt att något som ökar inflammationer i muskler och leder samt ökar muskelnedbrytningen är så populärt att folk är beredda att betala dyrt för det. Jag har för mig att det ökar risken för hjärt-/kärlsjukdomar också. Rätta mig gärna om jag är ute och cyklar

AA förstärker muskelnedbrytningen i samband med träning ja, det bör leda till stimulerad muskeltillväxt. Några ökade inflammationer i negativ bemärkelse märkte inte jag på mina 1250 mg / dag.

Muscle growth
Arachidonic acid is necessary for the repair and growth of skeletal muscle tissue. One of the lead researchers of the Baylor study on arachidonic acid, Mike Roberts MS, CSCS, has authored an article published under the title Arachidonic Acid, The New Mass Builder explaining the role of this nutrient in muscle anabolism, and its potential for the enhancement of muscle size and strength.[9]

Roberts claims that for optimal muscle growth a training stimulus must elicit localized inflammation and soreness. He also shows that arachidonic acid (AA, 20:4n-6) is an essential Omega-6 (1-6) polyunsaturated fatty acid that is abundant in skeletal muscle membrane phospholipids (figure 2). It is also the body's principle building block for the production of prostaglandins, which are known to have various physiological roles including a close involvement in inflammation. Also, the prostaglandin isomer PGF2a has a potent ability to stimulate muscle growth. As such, Roberts says that arachidonic acid is a regulator of localized muscle inflammation, and he claims that it may be a central nutrient controlling the intensity of the anabolic/tissue-rebuilding response to weight training

Källa: Arachidonic acid - Wikipedia, the free encyclopedia

Men det är riktigt att det finns frågetecken och forskare som varnar för AA, ökad risk för Alzheimer, hjärt/kärl sjukdommar, kan snabba på en prostatacancer, men man vet inte om det kan utlösa själva cancern.
Jag har tagit upp detta i min recension av Xpress:
http://www.optimalbody.se/forum/141756-post18.html

[Dr Nick]

Ursprungligen postat av loverius

Och cancerframkallande. Men tydligen mår hjärnans neuroner bra av det.
Dosera lika stor del Omega 3, som AA...är väl det bästa.

Intressant(?) att du skriver att AA är direkt cancerframkallande när det mesta tyder på att så inte är fallet.

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.

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.

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. pierre.astorg@cnam.fr

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.

Am J Clin Nutr. 2004 Jul;80(1):204-16. Related Articles, Links
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. leitzmann@mail.nih.gov

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.

[Dr Nick]

En riktigt bra tråd om AA med en hel del källor.

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