Archive for May, 2012

A cure for male baldness – Omega3 EPA may be the solution to male pattern baldness / hairloss in men

Thursday, May 31st, 2012

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-3s intake Linked to Lower Amyloid Levels and reduced risk of Alzheimers

Monday, May 7th, 2012

A study of diet and plasma beta-amyloid in cognitively normal individuals over 65 found that increased consumption of omega-3 fatty acids was significantly associated with lower plasma levels of beta-amyloid protein 42.
Note that none of the other nutrients were found to have a significant association with plasma beta-amyloid.

People who had a lot of omega-3 fatty acids in their diets tended to have lower plasma levels of beta-amyloid proteins, possibly reducing their risk of Alzheimer’s disease, researchers said.

In a cross-sectional study of more than 1,200 cognitively normal individuals older than 65, omega-3 fatty acid intake was significantly predictive of plasma levels of the 40- and 42-residue forms of beta-amyloid protein (AB40 and AB42, respectively), according to Nikolaos Scarmeas, MD, of Columbia University in New York City, and colleagues.

Adjusting for age, education level, and other factors pushed the relationship between AB40 and omega-3 intake into a strong but nonsignificant trend (beta statistic -10.13, P=0.13). But the association with AB42 remained significant, Scarmeas and colleagues reported online in Neurology (beta statistic -7.70, P=0.02).

The same group had previously published results indicating that a Mediterranean-type diet was associated with lower risk of cognitive impairment and Alzheimer’s disease.

Because one of the hallmarks of Alzheimer’s disease is beta-amyloid plaque deposits in the brain, Scarmeas and colleagues sought to determine if dietary factors were related to blood levels of AB40 and AB42.

Their study population was drawn from participants in the Washington Heights/Hamilton Heights Columbia Aging Project in New York City, first recruited in 1992 with a second group enrolled in 1999.

As part of this study, participants completed a detailed diet questionnaire and also provided blood samples. The latter were drawn a mean of 1.2 years after collection of dietary information.

The researchers excluded participants already showing dementia when the dietary questionnaire was administered, since their mental status could affect their self-reporting on diet.

A total of 1,219 participants out of the original 2,778 were included in the current analysis. In addition to 345 with prevalent dementia, another 1,025 could not be included because beta-amyloid levels in plasma weren’t measured.

In addition to omega-3 intake, Scarmeas and colleagues also estimated intake of nine other nutrients: folate, beta-carotene, monounsaturated fats, saturated fats, omega-6 fatty acids, and vitamins C, D, E, and B12.

Only omega-3 intake was significantly associated with plasma AB40 or AB42 levels in any analysis.

The raw data suggested a powerful link:

AB40: beta -24.74, P<0.001

AB42: beta -12.31, P<0.001

But analysis of participant characteristics revealed a number of covariates. Adjusting for age, race-ethnicity, education level, APOE genotype, total caloric intake, and recruitment wave attenuated the relationships noticeably. The beta value for AB40 shrank to -11.96 and the P value increased to 0.06.

The beta value for AB42 also declined, to -7.31, but it remained significant at P=0.02.

Adding adjustments for alcohol drinking and use of certain drugs and nutritional supplements changed the strength of the associations only slightly.

The researchers' conclusion: "The potential beneficial effects of omega-3 [fatty acid] intake on Alzheimer's disease and cognitive function in the literature might be at least partly explained by an AB-related mechanism," they wrote.

Scarmeas and colleagues noted several limitations to the study, including its cross-sectional design and its reliance on a single measurement of plasma AB40 and AB42 levels, which they characterized as "a moving target" during development of cognitive decline.

Also, the researchers relied on participants' self-reports on diet and examined only 10 of many nutrients contained in food.

Finally, Scarmeas and colleagues acknowledged that plasma beta-amyloid proteins do not necessarily reflect amyloid protein levels in the brain.

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