Γιωργοςbioherbal
Active Member
Η DHA ειναι πολυ ποιο ισχυρος παρεμποδιστης της COX1 απο οτι η EPA.η ερευνα ειναι στα αγγλικα. με λίγα λόγια τα συμπληρώματα των φαρμακειών τα ομεγα-3 περιέχουν 2 ουσίες την EPA και την DHA. σύμφωνα με την ερευνα η ουσία EPA εμποδίζει την δημιουργια της PGD2 που είναι η αιτία της τριχόπτωσης.επειδή παίρνω 1,5 χρόνο ομεγα-3 απο την Healthaid αυτο που εχω παρατηρησει ειναι οτι ενω ειχα τριχοπτωση αυτη σταματησε. δεν είχα επανέκφυση αλλα η τριχόπτωση σταμάτησε πράγμα πολύ σημαντικό.
A cure for male baldness – Omega3 EPA may be the solution to male pattern baldness / hairloss in men
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Male baldness/ hairloss is a major issue for a lot of men hence the reason for them spending so much money treatment shampoo / hair loss prevention treatemnts . Research however may have identified what the actual cause is and also that the solution is to reduce or block levels of PGD2
Is TakeOmega3 the highest source of EPA per capsule the solution to male pattern baldness ?
Recent research has found that with regards male pattern baldness they found that an excessive amount of a protein called prostaglandin D2 or PGD2 was present in those areas of the scalp affected., according to a study. Earlier studies carried out in Japan found that Eicospentenoic Acid (EPA) effectively reduced / blocked the production of the protein PGD2.
EPA or Eicosapentenoic Acid one of the active ingredients in Omega3 – The highest concentration of EPA per capsule is found in a supplement called TakeOmega3 which is an 85% omega3 product with 750mg EPA per capsule. It is also uniquely manufactured in MHRA licensed facilities here in UK and entirely manufactured here in the UK .
The study concluded that men may be able to regrow all their hair if the inhibiting protein is removed, said George Cotsarelis, chairman of dermatology at The Perelman School of Medicine in Philadelphia.
We really do think if you remove the inhibition, you get longer hair, Cotsarelis, a study author, said in a telephone interview. We dont know if the follicles will return to their former lengths, he said.
The study was funded by grants from the US National Institute of Health the Pennsylvania Department of Health, and other medical groups.
The researchers looked at all the genes in the scalp samples from five men, comparing the bald parts to the haired parts. They found higher expressions of the gene that produces PGD2 in the bald samples, compared to the spots with hair. With that as a guide, they found in samples of 17 men with hair loss that PGD2 was three times higher in the bald spots than where hair was growing. The scientists then used mice to show that excessive PGD2 decreased follicles.
Previous work has shown that the stem cells that create hair are still intact in bald men, Cotsarelis said. The follicles are also there, though they look smaller and produce thinner, shorter hair. Over time, the hair is so short it no longer passes the surface of the skin.
The study concluded that men may be able to regrow all their hair if the inhibiting protein is removed, said George Cotsarelis, chairman of dermatology at The Perelman School of Medicine in Philadelphia.
We really do think if you remove the inhibition, you get longer hair, Cotsarelis, a study author, said in a telephone interview. We dont know if the follicles will return to their former lengths, he said.
The study was funded by grants from the US National Institute of Health the Pennsylvania Department of Health, and other medical groups.
Whilst there are drugs in development and existance that block the D2 pathway surely a natural alternative would be preferable ?
In an earlier study carried out in Japan it showed that Eicosapentaenoic acid (Omega 3 EPA ) inhibits prostaglandin D2 generation by inhibiting cyclo-oxygenase-2 in cultured human mast cells.-
Obata T, Nagakura T, Masaki T, Maekawa K, Yamashita K.
Source
Department of Molecular Cell Biology, Institute of DNA Medicine, Jikei University School of Medicine, Tokyo, Japan.
Abstract
BACKGROUND:
Eicosapentaenoic acid (EPA) is catalysed by cyclo-oxygenase (COX), as is arachidonic acid, and is a competitive inhibitor of arachidonate metabolism.
OBJECTIVES:
We examined the effect of EPA on prostaglandin (PG) D2 generation in the cultured human mast cells with IgE-anti-IgE challenge incubation.
METHODS:
Cultured human mast cells were incubated with EPA (1 micromol/L) for 20 h, then challenged with anti-IgE incubation after treatment with IgE. At the same time, COX inhibitors were tested to identify COX-1 and COX-2 activity. PGD2 synthetic activity was also assayed in a cell-free homogenate of cultured mast cells with COX inhibitors and EPA. Histamine in the culture medium and in cells was assayed with the HPLC-fluorescent method. PGD2 and PGD3 were assayed with gas chromatography-mass spectrometry and the stable isotope dilution method.
RESULTS:
Although EPA incubation did not affect histamine release by cultured human mast cells in response to IgE-anti-IgE challenge incubation, it did decrease PGD2 generation by inhibiting the COX-2 pathway. In contrast, in the cell-free homogenate of cultured human mast cells, EPA inhibited both COX-1 and COX-2 activities.
CONCLUSION:
Pre-incubation with EPA primarily affects the COX-2 pathway in cultured human mast cells and reduces PGD2 generation in response to IgE-anti-IgE challenge incubation. These findings suggest that COX-1 and COX-2 have different substrate flow systems in mast cells. They also suggest that endogenous EPA diet supplementation would reduce PGD2 production and could serve as an anti-inflammatory substrate in human mast cells.
Omega-3 fatty acids attenuate constitutive and insulin-induced CD36 expression through a suppression of PPAR α/γ activity in microvascular endothelial cells.
Madonna R, Salerni S, Schiavone D, Glatz JF, Geng YJ, De Caterina R.
Author information
Abstract
Microvascular dysfunction occurs in insulin resistance and/or hyperinsulinaemia.
Enhanced uptake of free fatty acids (FFA) and oxidised low-density lipoproteins (oxLDL) may lead to oxidative stress and microvascular dysfunction interacting with CD36, a PPARα/γ-regulated scavenger receptor and long-chain FFA transporter.
We investigated CD36 expression and CD36-mediated oxLDL uptake before and after insulin treatment in human dermal microvascular endothelial cells (HMVECs), ± different types of fatty acids (FA), including palmitic, oleic, linoleic, arachidonic, eicosapentaenoic (EPA), and docosahexaenoic (DHA) acids.
Insulin (10(-Cool and 10(-7) M) time-dependently increased DiI-oxLDL uptake and CD36 surface expression (by 30 ± 13%, p<0.05 vs. untreated control after 24 hours incubation), as assessed by ELISA and flow cytometry, an effect that was potentiated by the PI3-kinase inhibitor wortmannin and reverted by the ERK1/2 inhibitor PD98059 and the PPARα/γ antagonist GW9662.
A ≥ 24 hour exposure to 50 μM DHA or EPA, but not other FA, blunted both the constitutive (by 23 ± 3% and 29 ± 2%, respectively, p<0.05 for both) and insulin-induced CD36 expressions (by 45 ± 27 % and 12 ± 3 %, respectively, p<0.05 for both), along with insulin-induced uptake of DiI-oxLDL and the downregulation of phosphorylated endothelial nitric oxide synthase (P-eNOS).
At gel shift assays, DHA reverted insulin-induced basal and oxLDL-stimulated transactivation of PPRE and DNA binding of PPARα/γ and NF-κB.
In conclusion, omega-3 fatty acids blunt the increased CD36 expression and activity promoted by high concentrations of insulin. Such mechanisms may be the basis for the use of omega-3 fatty acids in diabetic microvasculopathy.
θελουμε και 500mg dha,by kapa :18m:
Επισης η DHA ειναι παρα πολυ σπουδαιο λιπαρο οξυ (βεβαια δεν μπορει να παραχθει απο τον οργανισμο, πρεπει να το βρει ετοιμο), και καταλαβαινουμε την ισχυρη ελλειψη του οταν σχηματιζονται οι λεγομενες "σακουλες" κατω απο τα ματια.
Βοηθαει παρα πολυ το δερμα (γιαυτο το κανουν κ κρεμα),
και ειναι δομικο στοιχειο που χρειαζεται ο εγκεφαλος.
Οσο για ενα πολυ καλο συμπηρωμα ειναι το
http://www.skroutz.gr/s/6692947/Natural-Vitamins-Omega-3-1000mg-700mg-EPA-DHA-60-tabs.html
