Doesnt revivogen kind of revolve around this idea of free form fatty acids much like this article mentions? I dont consider though a small study with 4 people conclusive evidence though, but I think free form fatty acids can help to some degree from we know so far. How much or anything specific who knows.
Treatment of male pattern baldness.... results from 1988!
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The Natural
Established Member
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I don't know of anyone who has had sustained success with borage oil and fish oil; and personally, will not take these two supplements ever again.
But I have been persuaded, for general health purposes, to include (again) EFAs into my regimen. They all will be from plant sources (primsrose oil and algae) this time around. Still, not convinced that changes to my hair will be anything other than cosmetic as a result of these additions.
Concentration: 1. Improving circulation 2. Reducing inflammation
Will update periodically.
But I have been persuaded, for general health purposes, to include (again) EFAs into my regimen. They all will be from plant sources (primsrose oil and algae) this time around. Still, not convinced that changes to my hair will be anything other than cosmetic as a result of these additions.
Concentration: 1. Improving circulation 2. Reducing inflammation
Will update periodically.
squeegee
Banned
- Reaction score
- 132
Animal and human studies have shown that greatly increasing the amounts of flaxseed oil [rich in the (n-3) polyunsaturated fatty acid (PUFA) alpha-linolenic acid (ALNA)] or fish oil [FO; rich in the long chain (n-3) PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] in the diet can decrease mitogen-stimulated lymphocyte proliferation. The objective of this study was to determine the effect of dietary supplementation with moderate levels of ALNA, gamma-linolenic acid (GLA), arachidonic acid (ARA), DHA or FO on the proliferation of mitogen-stimulated human peripheral blood mononuclear cells (PBMC) and on the production of cytokines by those cells. The study was randomized, placebo-controlled, double-blinded and parallel. Healthy subjects ages 55-75 y consumed nine capsules/d for 12 wk; the capsules contained placebo oil (an 80:20 mix of palm and sunflower seed oils) or blends of placebo oil with oils rich in ALNA, GLA, ARA or DHA or FO. Subjects in these groups consumed 2 g of ALNA or 770 mg of GLA or 680 mg of ARA or 720 mg of DHA or 1 g of EPA plus DHA (720 mg of EPA 280 mg of DHA) daily from the capsules. Total fat intake from the capsules was 4 g/d. The fatty acid composition of PBMC phospholipids was significantly changed in the GLA, ARA, DHA and FO groups. Lymphocyte proliferation was not significantly affected by the placebo, ALNA, ARA or DHA treatments. GLA and FO caused a significant decrease (up to 65%) in lymphocyte proliferation. This decrease was partly reversed by 4 wk after stopping the supplementation. None of the treatments affected the production of interleukin-2 or interferon-gamma by PBMC and none of the treatments affected the number or proportion of T or B lymphocytes, helper or cytotoxic T lymphocytes or memory helper T lymphocytes in the circulation. We conclude that a moderate level GLA or EPA but not of other (n-6) or (n-3) PUFA can decrease lymphocyte proliferation but not production of interleukin-2 or interferon-gamma.
PMID: 11435508
In the following only the EPA portion of fish oil caused a decrease in natural killer cell activity (harmful in healthy people).
Am J Clin Nutr 2001 Mar;73(3):539-48
Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n-3 or n-6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y.
Thies F, Nebe-von-Caron G, Powell JR, Yaqoob P, Newsholme EA, Calder PC.
Department of Biochemistry, University of Oxford, Oxford, United Kingdom.
BACKGROUND: Animal studies showed that dietary flaxseed oil [rich in the n-3 polyunsaturated fatty acid alpha-linolenic acid (ALA)], evening primrose oil [rich in the n-6 polyunsaturated fatty acid gamma-linolenic acid (GLA)], and fish oil [rich in the long-chain n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] can decrease natural killer (NK) cell activity. There have been no studies of the effect on NK cell activity of adding these oils to the diet of humans.
OBJECTIVE: Our objective was to determine the effect of dietary supplementation with oil blends rich in ALA, GLA, arachidonic acid (AA), DHA, or EPA plus DHA (fish oil) on the NK cell activity of human peripheral blood mononuclear cells.
DESIGN: A randomized, placebo-controlled, double-blind, parallel study was conducted. Healthy subjects aged 55-75 y consumed 9 capsules/d for 12 wk; the capsules contained placebo oil (an 80:20 mix of palm and sunflower seed oils) or blends of placebo oil and oils rich in ALA, GLA, AA, DHA, or EPA plus DHA. Subjects in these groups consumed 2 g ALA, 770 mg GLA, 680 mg AA, 720 mg DHA, or 1 g EPA plus DHA (720 mg EPA 280
mg DHA) daily, respectively. Total fat intake from the capsules was 4 g/d.
RESULTS: The fatty acid composition of plasma phospholipids changed significantly in the GLA, AA, DHA, and fish oil groups. NK cell activity was not significantly affected by the placebo, ALA, GLA, AA, or DHA treatment. Fish oil caused a significant reduction (mean decline: 48%) in NK cell activity that was fully reversed by 4 wk after supplementation had ceased.
CONCLUSION: A moderate amount of EPA but not of other n-6 or n-3 polyunsaturated fatty acids can decrease NK cell activity in healthy subjects.
Publication Types:
Clinical trial
Randomized controlled trial
PMID: 11237929
Here is a study which illustrates part of the feedback mechanisms which I explained above. This study shows that it is likely important to take EPA if you are also taking GLA.
J Nutr 2000 Aug;130(8):1925-31
Addition of eicosapentaenoic acid to gamma-linolenic acid-supplemented diets prevents serum arachidonic acid accumulation in humans.
Barham JB, Edens MB, Fonteh AN, Johnson MM, Easter L, Chilton FH.
Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Previous studies reveal that supplementation of human diets with gamma-linolenic acid (GLA) reduces the generation of lipid mediators of inflammation and attenuates clinical symptoms of chronic inflammatory disorders such as rheumatoid arthritis. However, we have shown that supplementation with this same fatty acid also causes a marked increase in serum arachidonate (AA) levels, a potentially harmful side effect. The objective of this study was to design a supplementation strategy that maintained the capacity of GLA to reduce lipid mediators without causing elevations in serum AA levels. Initial in vitro studies utilizing HEP-G2 liver cells revealed that addition of eicosapentaenoic acid (EPA) blocked Delta-5-desaturase activity, the terminal enzymatic step in AA synthesis. To test the in vivo effects of a GLA and EPA combination in humans, adult volunteers consuming controlled diets supplemented these diets with 3.0 g/d of GLA and EPA. This supplementation strategy significantly increased serum levels of EPA, but did not increase AA levels. EPA and the elongation product of GLA, dihomo-gamma-linolenic acid (DGLA) levels in neutrophil glycerolipids increased significantly during the 3-wk supplementation period. Neutrophils isolated from volunteers fed diets supplemented with GLA and EPA released similar quantities of AA, but synthesized significantly lower quantities of leukotrienes compared with their neutrophils before supplementation. This study revealed that a GLA and EPA supplement combination may be utilized to reduce the synthesis of proinflammatory AA metabolites, and importantly, not induce potentially harmful increases in serum AA levels.
PMID: 10917903
Finally, the following study shows that the feedback effects do not go the other way. Ie, GLA supplementation or AA accumulation will not upregulate the conversion of alpha linolenic acid to EPA. This is why it is so important to take EPA and DHA *directly* rather than to rely on conversion from ALNA.
Prostaglandins Leukot Essent Fatty Acids 1998 Nov;59(5):329-34
Gamma-linolenic acid does not augment long-chain polyunsaturated fatty acid omega-3 status.
Brouwer DA, Hettema Y, van Doormaal JJ, Muskiet FA.
Central Laboratory for Clinical Chemistry, University Hospital Groningen, The Netherlands. d.a.j.brouwer@lab.azg.nl
Augmentation of long chain polyunsaturated omega3 fatty acid (LCPUFA omega3) status can be reached by consumption of fish oil or by improvement of the conversion of alpha-linolenic acid (ALA) to LCPUFA omega3. Since gamma-linolenic acid (GLA) might activate the rate-limiting delta-6 desaturation, we investigated whether GLA augments LCPUFA omega3 status. Eight adults received 1.4 g GLA for 4 weeks and subsequently 2.2 g ALA 1.4 g GLA daily during another 4 weeks. Another seven adults received a daily oral dose of 2.2 g ALA for 4 weeks, and subsequently 2.2 g ALA 1.4 g GLA during another 4 weeks. ALA, or ALA GLA, did not significantly augment EPA and DHA contents. We conclude that the LCPUFA omega3 status can not be improved by supplementation of low dose GLA, neither by co-supplementation of ALA. Poor conversion of ALA to LCPUFA omega3 may be caused by preferential beta-oxidation of ALA, negative feedback of arachidonic acid from the omnivorous diet, or by the low dietary ALA/LA ratio.
Publication Types:
Clinical trial
PMID: 9888208::
PMID: 11435508
In the following only the EPA portion of fish oil caused a decrease in natural killer cell activity (harmful in healthy people).
Am J Clin Nutr 2001 Mar;73(3):539-48
Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n-3 or n-6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y.
Thies F, Nebe-von-Caron G, Powell JR, Yaqoob P, Newsholme EA, Calder PC.
Department of Biochemistry, University of Oxford, Oxford, United Kingdom.
BACKGROUND: Animal studies showed that dietary flaxseed oil [rich in the n-3 polyunsaturated fatty acid alpha-linolenic acid (ALA)], evening primrose oil [rich in the n-6 polyunsaturated fatty acid gamma-linolenic acid (GLA)], and fish oil [rich in the long-chain n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] can decrease natural killer (NK) cell activity. There have been no studies of the effect on NK cell activity of adding these oils to the diet of humans.
OBJECTIVE: Our objective was to determine the effect of dietary supplementation with oil blends rich in ALA, GLA, arachidonic acid (AA), DHA, or EPA plus DHA (fish oil) on the NK cell activity of human peripheral blood mononuclear cells.
DESIGN: A randomized, placebo-controlled, double-blind, parallel study was conducted. Healthy subjects aged 55-75 y consumed 9 capsules/d for 12 wk; the capsules contained placebo oil (an 80:20 mix of palm and sunflower seed oils) or blends of placebo oil and oils rich in ALA, GLA, AA, DHA, or EPA plus DHA. Subjects in these groups consumed 2 g ALA, 770 mg GLA, 680 mg AA, 720 mg DHA, or 1 g EPA plus DHA (720 mg EPA 280
mg DHA) daily, respectively. Total fat intake from the capsules was 4 g/d.
RESULTS: The fatty acid composition of plasma phospholipids changed significantly in the GLA, AA, DHA, and fish oil groups. NK cell activity was not significantly affected by the placebo, ALA, GLA, AA, or DHA treatment. Fish oil caused a significant reduction (mean decline: 48%) in NK cell activity that was fully reversed by 4 wk after supplementation had ceased.
CONCLUSION: A moderate amount of EPA but not of other n-6 or n-3 polyunsaturated fatty acids can decrease NK cell activity in healthy subjects.
Publication Types:
Clinical trial
Randomized controlled trial
PMID: 11237929
Here is a study which illustrates part of the feedback mechanisms which I explained above. This study shows that it is likely important to take EPA if you are also taking GLA.
J Nutr 2000 Aug;130(8):1925-31
Addition of eicosapentaenoic acid to gamma-linolenic acid-supplemented diets prevents serum arachidonic acid accumulation in humans.
Barham JB, Edens MB, Fonteh AN, Johnson MM, Easter L, Chilton FH.
Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Previous studies reveal that supplementation of human diets with gamma-linolenic acid (GLA) reduces the generation of lipid mediators of inflammation and attenuates clinical symptoms of chronic inflammatory disorders such as rheumatoid arthritis. However, we have shown that supplementation with this same fatty acid also causes a marked increase in serum arachidonate (AA) levels, a potentially harmful side effect. The objective of this study was to design a supplementation strategy that maintained the capacity of GLA to reduce lipid mediators without causing elevations in serum AA levels. Initial in vitro studies utilizing HEP-G2 liver cells revealed that addition of eicosapentaenoic acid (EPA) blocked Delta-5-desaturase activity, the terminal enzymatic step in AA synthesis. To test the in vivo effects of a GLA and EPA combination in humans, adult volunteers consuming controlled diets supplemented these diets with 3.0 g/d of GLA and EPA. This supplementation strategy significantly increased serum levels of EPA, but did not increase AA levels. EPA and the elongation product of GLA, dihomo-gamma-linolenic acid (DGLA) levels in neutrophil glycerolipids increased significantly during the 3-wk supplementation period. Neutrophils isolated from volunteers fed diets supplemented with GLA and EPA released similar quantities of AA, but synthesized significantly lower quantities of leukotrienes compared with their neutrophils before supplementation. This study revealed that a GLA and EPA supplement combination may be utilized to reduce the synthesis of proinflammatory AA metabolites, and importantly, not induce potentially harmful increases in serum AA levels.
PMID: 10917903
Finally, the following study shows that the feedback effects do not go the other way. Ie, GLA supplementation or AA accumulation will not upregulate the conversion of alpha linolenic acid to EPA. This is why it is so important to take EPA and DHA *directly* rather than to rely on conversion from ALNA.
Prostaglandins Leukot Essent Fatty Acids 1998 Nov;59(5):329-34
Gamma-linolenic acid does not augment long-chain polyunsaturated fatty acid omega-3 status.
Brouwer DA, Hettema Y, van Doormaal JJ, Muskiet FA.
Central Laboratory for Clinical Chemistry, University Hospital Groningen, The Netherlands. d.a.j.brouwer@lab.azg.nl
Augmentation of long chain polyunsaturated omega3 fatty acid (LCPUFA omega3) status can be reached by consumption of fish oil or by improvement of the conversion of alpha-linolenic acid (ALA) to LCPUFA omega3. Since gamma-linolenic acid (GLA) might activate the rate-limiting delta-6 desaturation, we investigated whether GLA augments LCPUFA omega3 status. Eight adults received 1.4 g GLA for 4 weeks and subsequently 2.2 g ALA 1.4 g GLA daily during another 4 weeks. Another seven adults received a daily oral dose of 2.2 g ALA for 4 weeks, and subsequently 2.2 g ALA 1.4 g GLA during another 4 weeks. ALA, or ALA GLA, did not significantly augment EPA and DHA contents. We conclude that the LCPUFA omega3 status can not be improved by supplementation of low dose GLA, neither by co-supplementation of ALA. Poor conversion of ALA to LCPUFA omega3 may be caused by preferential beta-oxidation of ALA, negative feedback of arachidonic acid from the omnivorous diet, or by the low dietary ALA/LA ratio.
Publication Types:
Clinical trial
PMID: 9888208::
- Reaction score
- 42
abcdefg said:
I don't know which of the numerous articles it is that you're talking about, but I guarantee you that the specific purpose of the fatty acids used in Revivogen is to act as 5a-reductase inhibitors. That's why they use only free form fatty acids in that product.
- Reaction score
- 42
CCS said:
The studies examining fatty acids as 5a-reductase inhibitors? No, I don't believe they ever specified whether the fatty acids work on type 1 or type 2. Or both. I hope I'm not forgetting one of them!
We know that GLA _does_ apparently work on the type 1 form of the enzyme, because those scientists were able to reduce sebum production by applying a small amount to the forehead of a human volunteer. But whether or not it also inhibits the type 2 enzyme, I don't know...
Jacob
Senior Member
- Reaction score
- 44
Bryan said:
It's amazing you can't remember even something like this. It wasn't even "years and years ago". "Mr. Stupid" :shakehead:
http://www.hairlosshelp.com/forums/...d=94982&STARTPAGE=2&FTVAR_FORUMVIEWTMP=Linear
http://www.hairlosstalk.com/interact/viewtopic.php?f=61&t=66889&st=0&sk=t&sd=a&start=10
http://www.hairlosshelp.com/forums/messageview.cfm?catid=10&threadid=95185&highlight_key=y
Some of the products mentioned..I'm sure there are plenty of others out there:
http://www.theraprohair.com/therapro/numinox_topical_treatment.htm
http://www.combat-hair-loss.co.uk/procerin_xt_foam.htm
http://www.orinova.org/nuhair_topical_serum.html#serum
http://www.hlcconline.com/001HLMGT02.html
Read the discussions in those links before wasting our time saying they're not in the "Free form" blah blah blah. But I'll be happy to just repost the responses here
Jacob
Senior Member
- Reaction score
- 44
And to make it simple for those not wanting to read it all..here is the list of ingredients for Revivogen, as found at Amazon.
BTW...wt_ is Azelaic acid doing in there? :woot:
And the (active) ingredients for the last product I linked to above:
Again..that is just one other product/example.
BTW...wt_ is Azelaic acid doing in there? :woot:
And the (active) ingredients for the last product I linked to above:
Again..that is just one other product/example.
- Reaction score
- 42
Jacob said:
I stand by everything I said in those old posts, stupid.
Jacob said:Some of the products mentioned..I'm sure there are plenty of others out there:
http://www.theraprohair.com/therapro/numinox_topical_treatment.htm
http://www.combat-hair-loss.co.uk/procerin_xt_foam.htm
http://www.orinova.org/nuhair_topical_serum.html#serum
http://www.hlcconline.com/001HLMGT02.html
Read the discussions in those links before wasting our time saying they're not in the "Free form" blah blah blah. But I'll be happy to just repost the responses here
As I've already told you, there is no indication just in the advertisements for those products that they really do contain "free-form" fatty acids.
Jacob
Senior Member
- Reaction score
- 44
Hey.."stupid"...is your memory coming back?
There is absolutely nothing unique about Revivogen- see the threads linked to above. Oh btw..each company told me their products also contain the FA's in "Free Form". Next they'll be talking about mysterious ingredients. What's not to believe? :shakehead:
There is absolutely nothing unique about Revivogen- see the threads linked to above. Oh btw..each company told me their products also contain the FA's in "Free Form". Next they'll be talking about mysterious ingredients. What's not to believe? :shakehead: