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Sagging Skin
Page 2 of 2 • 
1, 2
Re: Sagging Skin
jdp710 on Tue Jun 09, 2009 7:44 am
Passwater: Are there any side effects from taking oral HA supplements?
Sardi: Yes, there are, though they are not common. First, understand that oral HA causes water to gel up, like Jell-O in the refrigerator. Now if a person were to be dehydrated, or be taking extra doses of a diuretic, he or she might experience a whopping headache due to a rise in blood pressure. This actually happened to a woman who inadvertently doubled up on her water pills and had a hypertensive crisis while taking oral HA. Fortunately, the problem subsided. Patients with high blood pressure on diuretics should be aware and take lower doses of HA, let’s say no more than 150 mg per day, and they must remember to drink water. Many hypertensive patients take oral HA supplements and report no problems. One of the pieces of advice I offer in my book is to not to forget to drink water. HA plus H2O is the way it all works.
Then there are cancer patients who have lymphedema, a condition in which the lymph glands are filled with HA degraded by the tumor and the HA has blocked the drainage from the lymph glands. This results in swelling in the legs. Oral HA would be contraindicated in cancer patients with lymphedema.
Probably, oral HA should be avoided by patients with rheumatoid arthritis, which comprises less than 5% of the cases of arthritis. The classic symptoms of morning stiffness in a rheumatoid arthritis patient are caused by an autoimmune reaction degrading HA during sleep. Upon awakening, the rheumatoid patients find their joints are rigid because they are filled with excessive amounts of degraded HA. Once physical activity and the circulation gets moving, the stiffness disappears.
Passwater: What do we know about how well the various sources of HA work?
Sardi: All of the oral HA products work. I hesitate to say that one type is superior to another because it may create the false impression that one source is problematic or even undesirable. Manufacturers are often too eager to oversell their products, and in seeking to point out the weaknesses in their competitors’ products, they destroy any interest or demand for the product in general.
Therefore, I prefer to say that HA is good for the aging body, and you’d better get some. Period. Even higher molecular weight products seem to yield some benefits. To be accurate, HA is a long, thin molecule, which is how it gets its high molecular weight. In simplistic terms, it isn’t a wide molecule, it’s a long one. It is a disaccharide, that is, two sugar-like molecules strung together and repeated over and over. Some manufacturers appear a bit reluctant to reveal their molecular weight for fear it will be used against them. The lowest number is not necessarily superior. It just helps to have low molecular weight material. Someday there will be a study comparing the various sources.
Passwater: How does oral HA compare to glucosamine and chondroitin sulfate?
Sardi: HA is a double molecule, glucosamine that holds hands with glucuronic acid. Glucosamine (technically in the form of N-acetyl-glucosamine while a constituent of the complex molecule of HA) is only one half of the HA molecule, hence the reason why glucosamine only yields mild benefits for arthritis sufferers who usually have to take it in high doses (1,500 mg) for prolonged periods of time to experience any results. Just 150-300 mg of oral HA will work better and faster at restoring joint health.
Chondroitin sulfate raises the production of HA in the body. Dr. Lester Morrison, a cardiologist at Loma Linda University in the 1970s, used very high doses of chondroitin sulfate (5,000 mg tapered to 1,500 mg over three or four months) following a heart attack or bouts of angina to successfully rebuild and heal cardiac tissue. Some of these patients also experienced anti-aging benefits, such as renewed hair growth, cancellation of prostate surgery and disappearance of angina.
Passwater: I’ve put some basic information about the structure of HA in a box (Page XX) for readers wishing to know more about the biochemistry of HA. How much HA does the body lose each day?
Sardi: The body makes and degrades a few thousand mg of HA per day. With advancing age or disease, the degradation rate is not completely made for up by the rate of synthesis, resulting in what we know as the slow progressive signs of visible aging. Not all HA loss is systemic. HA wears out in localized tissues where there is repetitive use, the knees, the wrist (carpal tunnel), the shoulder, the temporomandibular joint (symptoms of TMJ), or where there is greater exposure to the sun (crow’s feet, shrinkage of the HA gel inside the eyes that leads to vitreous detachment and floaters).
Passwater: What dosage of oral HA do you recommend for various conditions—joints, skin, and so on?
Sardi: HA is appropriate for adults, age 40 or 50 and up, or anyone who has worn out HA in a particular area. I had a 32-year old piano mover write to me that he was ready to give up his job and undergo knee surgery. He took oral HA and within a month had no pain. The loss of HA can occur early, depending upon wear and tear. Imagine what oral HA supplements could do to extend the career of athletes. I expect Olympic athletes to be using oral HA soon. Oral dosage should be 150 mg per day, with possibly a loading dose for one month of 300 mg per day. More HA is not always better.
Passwater: Let’s get back to aging. You mentioned that the aging process results in a loss of hydration due to a loss of HA. How would oral HA help besides making skin look younger?
Sardi: I have predicted that oral HA supplements will result in people literally walking out of their wheelchairs. I would like to see actor Christopher Reeve try a course of oral HA. Recall that Reeve suffered paralysis following a horse riding accident. The healing of nerves simply can’t take place adequately without the cushioning provided by HA.
I also have observed other profound effects of oral HA. For example, as oral HA refills the eyes, it slightly lengthens the front-to-back length of the eye. This means the focus point of the eyes is altered. Therefore, farsighted people who take oral HA supplements may find their vision improving without glasses. Since all adults become a bit farsighted with advancing age, this has enormous possibilities to keep people out of reading glasses.
Also, the other half of the HA molecule, glucuronic acid, is similar to the food supplement calcium D-glucarate, which helps maintain hormone levels. Many women taking oral HA supplements have reported that their hot flashes and symptoms of menopause have abated with use. This is not surprising. Women have been advised that oral estrogen supplementation doesn’t prevent disease, and may in fact slightly increase the risk of disease. An alternative to estrogen would be oral HA. Why do women have beautiful skin? Because estrogen elevates HA levels in the skin and body. Once natural estrogen production has ceased (menopause), the natural alternative would be oral HA.
Passwater: What impact will oral HA make upon the natural products industry?
Sardi: There is so much hyperbole, so much pseudoscience, among all the natural products now available, it is difficult today to determine the good "waterholes" from the bad ones. Understand, the natural products industry often doesn’t fully understand what it is selling.
For example, take red yeast rice, which now has been removed from the market by the Food and Drug Administration (FDA) because it has been declared a drug. Patients sought red yeast rice because they wanted an alternative to the sometimes troublesome statin drugs. But red yeast rice contained statin molecules and posed the same risk for side effects. The industry simply wasn’t helping the public find a good non-toxic alternative when it began selling red yeast rice.
Similarly, there are a lot of collagen products being marketed for joint health, and they are cause for confusion. Even though Type II collagen accompanies some oral HA products, the collagen is a sideshow. It’s the HA that is doing all the healing. Collagen products promoted for joint health simply aren’t going to produce the results that HA does. Once the industry sorts all this out, there will be a stampede for these HA products. Go into a health food store today and ask about hyaluronic acid. They haven’t a clue what you are talking about.
There are so many natural products that lay claim to "anti-aging" benefits it is often confusing. There is no argument that the visible signs of aging—baldness, voice change, skin wrinkling and dryness, shrinkage in height, joint pain and dependency upon eyeglasses—all emanate from the loss of HA and not to direct shortages of any hormones like DHEA, or minerals like coral calcium, or any other widely promoted natural remedies.
Passwater: Thanks Bill for sharing this information about HA with us.
Sardi: It’s my pleasure. What I have shared with you here should have profound impact on anyone who reads this interview. It should have a profound impact upon medicine and in particular natural medicine. Understand, just like glucosamine, the demand for oral HA is being led by the public. It is not a doctor-driven revolution. This is probably the way it should be. For readers who want to learn more about HA’s age reversing properties, they might be interested in picking up a copy of my new book How to Live 100 Years Without Growing Old, available at www.hereandnowbooks.com. For further questions about HA, readers may wish to contact me at my website www.askbillsardi.com. WF
Note:
How and Why HA Promises Benefits
Hyaluronic acid (HA) is not a single compound, but a family of similar structures. Let’s start with a brief review of the compounds and nomenclature involved with HA. The monosaccharide glucose, the principal sugar of the body, is the most important carbohydrate in the body. This is true not only because it is the primary fuel for producing energy, but because it is used for building many complex compounds.
When an amino group is added to glucose, glucosamine is formed. The body uses glucosamine to form several other larger compounds, but when it uses glucosamine this way, an acetyl group is added. Thus, the form of glucosamine found in complex compounds is actually N-acetyl-glucosamine.
Glucuronic acid is formed from glucose when it is converted into an organic acid by essentially replacing the hydroxyl group on carbon #6 with a carboxylic acid group. Galactose is another monosaccharide. It has almost the same structure as glucose, except that the hydroxyl group on carbon #4 points in the opposite direction. Galactosamine is formed with the addition of an amino group. Likewise, in complex molecules, galactose is converted into N-acetyl-glactosamine.
Hyaluronic acid (HA) is a member of the glycosaminoglycan (GAG) family, which includes chondroitin sulfate, dermatin sulfate and heparin sulfate. Unlike other members of this family, HA is not bound covalently to proteins. HA is comprised of linear, unbranching, polyanionic disaccharide units consisting of glucuronic acid and N-acetyl-glucosamine joined alternately by beta 1-3 and beta glycosidic bonds.
Figure 1 (Page XX) shows the chemical structure of HA. The ring structure on the left is glucuronic acid and the ring structure on the right is N-acetyl-glucosamine. The brackets indicate that these two components are repeated " n" times. Thus, HA is not a single compound having a single formula. Technically, any compound where " n" is greater than 10 can be called HA. However, the final synthesis of HA normally produces compounds where " n" can range widely from a few thousand to several million.
Chondroitin sulfate is a closely related family member, but it doesn’t hold as much water. The structure is similar, but the difference is biochemically significant. In chondroitin sulfate, there is the same glucuronic acid ring, but the other ring is n-acetyl-galatosamine. Chitin is also very similar except that it is basically a polymer of N-acetyl-glucosamine.
Sardi: Yes, there are, though they are not common. First, understand that oral HA causes water to gel up, like Jell-O in the refrigerator. Now if a person were to be dehydrated, or be taking extra doses of a diuretic, he or she might experience a whopping headache due to a rise in blood pressure. This actually happened to a woman who inadvertently doubled up on her water pills and had a hypertensive crisis while taking oral HA. Fortunately, the problem subsided. Patients with high blood pressure on diuretics should be aware and take lower doses of HA, let’s say no more than 150 mg per day, and they must remember to drink water. Many hypertensive patients take oral HA supplements and report no problems. One of the pieces of advice I offer in my book is to not to forget to drink water. HA plus H2O is the way it all works.
Then there are cancer patients who have lymphedema, a condition in which the lymph glands are filled with HA degraded by the tumor and the HA has blocked the drainage from the lymph glands. This results in swelling in the legs. Oral HA would be contraindicated in cancer patients with lymphedema.
Probably, oral HA should be avoided by patients with rheumatoid arthritis, which comprises less than 5% of the cases of arthritis. The classic symptoms of morning stiffness in a rheumatoid arthritis patient are caused by an autoimmune reaction degrading HA during sleep. Upon awakening, the rheumatoid patients find their joints are rigid because they are filled with excessive amounts of degraded HA. Once physical activity and the circulation gets moving, the stiffness disappears.
Passwater: What do we know about how well the various sources of HA work?
Sardi: All of the oral HA products work. I hesitate to say that one type is superior to another because it may create the false impression that one source is problematic or even undesirable. Manufacturers are often too eager to oversell their products, and in seeking to point out the weaknesses in their competitors’ products, they destroy any interest or demand for the product in general.
Therefore, I prefer to say that HA is good for the aging body, and you’d better get some. Period. Even higher molecular weight products seem to yield some benefits. To be accurate, HA is a long, thin molecule, which is how it gets its high molecular weight. In simplistic terms, it isn’t a wide molecule, it’s a long one. It is a disaccharide, that is, two sugar-like molecules strung together and repeated over and over. Some manufacturers appear a bit reluctant to reveal their molecular weight for fear it will be used against them. The lowest number is not necessarily superior. It just helps to have low molecular weight material. Someday there will be a study comparing the various sources.
Passwater: How does oral HA compare to glucosamine and chondroitin sulfate?
Sardi: HA is a double molecule, glucosamine that holds hands with glucuronic acid. Glucosamine (technically in the form of N-acetyl-glucosamine while a constituent of the complex molecule of HA) is only one half of the HA molecule, hence the reason why glucosamine only yields mild benefits for arthritis sufferers who usually have to take it in high doses (1,500 mg) for prolonged periods of time to experience any results. Just 150-300 mg of oral HA will work better and faster at restoring joint health.
Chondroitin sulfate raises the production of HA in the body. Dr. Lester Morrison, a cardiologist at Loma Linda University in the 1970s, used very high doses of chondroitin sulfate (5,000 mg tapered to 1,500 mg over three or four months) following a heart attack or bouts of angina to successfully rebuild and heal cardiac tissue. Some of these patients also experienced anti-aging benefits, such as renewed hair growth, cancellation of prostate surgery and disappearance of angina.
Passwater: I’ve put some basic information about the structure of HA in a box (Page XX) for readers wishing to know more about the biochemistry of HA. How much HA does the body lose each day?
Sardi: The body makes and degrades a few thousand mg of HA per day. With advancing age or disease, the degradation rate is not completely made for up by the rate of synthesis, resulting in what we know as the slow progressive signs of visible aging. Not all HA loss is systemic. HA wears out in localized tissues where there is repetitive use, the knees, the wrist (carpal tunnel), the shoulder, the temporomandibular joint (symptoms of TMJ), or where there is greater exposure to the sun (crow’s feet, shrinkage of the HA gel inside the eyes that leads to vitreous detachment and floaters).
Passwater: What dosage of oral HA do you recommend for various conditions—joints, skin, and so on?
Sardi: HA is appropriate for adults, age 40 or 50 and up, or anyone who has worn out HA in a particular area. I had a 32-year old piano mover write to me that he was ready to give up his job and undergo knee surgery. He took oral HA and within a month had no pain. The loss of HA can occur early, depending upon wear and tear. Imagine what oral HA supplements could do to extend the career of athletes. I expect Olympic athletes to be using oral HA soon. Oral dosage should be 150 mg per day, with possibly a loading dose for one month of 300 mg per day. More HA is not always better.
Passwater: Let’s get back to aging. You mentioned that the aging process results in a loss of hydration due to a loss of HA. How would oral HA help besides making skin look younger?
Sardi: I have predicted that oral HA supplements will result in people literally walking out of their wheelchairs. I would like to see actor Christopher Reeve try a course of oral HA. Recall that Reeve suffered paralysis following a horse riding accident. The healing of nerves simply can’t take place adequately without the cushioning provided by HA.
I also have observed other profound effects of oral HA. For example, as oral HA refills the eyes, it slightly lengthens the front-to-back length of the eye. This means the focus point of the eyes is altered. Therefore, farsighted people who take oral HA supplements may find their vision improving without glasses. Since all adults become a bit farsighted with advancing age, this has enormous possibilities to keep people out of reading glasses.
Also, the other half of the HA molecule, glucuronic acid, is similar to the food supplement calcium D-glucarate, which helps maintain hormone levels. Many women taking oral HA supplements have reported that their hot flashes and symptoms of menopause have abated with use. This is not surprising. Women have been advised that oral estrogen supplementation doesn’t prevent disease, and may in fact slightly increase the risk of disease. An alternative to estrogen would be oral HA. Why do women have beautiful skin? Because estrogen elevates HA levels in the skin and body. Once natural estrogen production has ceased (menopause), the natural alternative would be oral HA.
Passwater: What impact will oral HA make upon the natural products industry?
Sardi: There is so much hyperbole, so much pseudoscience, among all the natural products now available, it is difficult today to determine the good "waterholes" from the bad ones. Understand, the natural products industry often doesn’t fully understand what it is selling.
For example, take red yeast rice, which now has been removed from the market by the Food and Drug Administration (FDA) because it has been declared a drug. Patients sought red yeast rice because they wanted an alternative to the sometimes troublesome statin drugs. But red yeast rice contained statin molecules and posed the same risk for side effects. The industry simply wasn’t helping the public find a good non-toxic alternative when it began selling red yeast rice.
Similarly, there are a lot of collagen products being marketed for joint health, and they are cause for confusion. Even though Type II collagen accompanies some oral HA products, the collagen is a sideshow. It’s the HA that is doing all the healing. Collagen products promoted for joint health simply aren’t going to produce the results that HA does. Once the industry sorts all this out, there will be a stampede for these HA products. Go into a health food store today and ask about hyaluronic acid. They haven’t a clue what you are talking about.
There are so many natural products that lay claim to "anti-aging" benefits it is often confusing. There is no argument that the visible signs of aging—baldness, voice change, skin wrinkling and dryness, shrinkage in height, joint pain and dependency upon eyeglasses—all emanate from the loss of HA and not to direct shortages of any hormones like DHEA, or minerals like coral calcium, or any other widely promoted natural remedies.
Passwater: Thanks Bill for sharing this information about HA with us.
Sardi: It’s my pleasure. What I have shared with you here should have profound impact on anyone who reads this interview. It should have a profound impact upon medicine and in particular natural medicine. Understand, just like glucosamine, the demand for oral HA is being led by the public. It is not a doctor-driven revolution. This is probably the way it should be. For readers who want to learn more about HA’s age reversing properties, they might be interested in picking up a copy of my new book How to Live 100 Years Without Growing Old, available at www.hereandnowbooks.com. For further questions about HA, readers may wish to contact me at my website www.askbillsardi.com. WF
Note:
How and Why HA Promises Benefits
Hyaluronic acid (HA) is not a single compound, but a family of similar structures. Let’s start with a brief review of the compounds and nomenclature involved with HA. The monosaccharide glucose, the principal sugar of the body, is the most important carbohydrate in the body. This is true not only because it is the primary fuel for producing energy, but because it is used for building many complex compounds.
When an amino group is added to glucose, glucosamine is formed. The body uses glucosamine to form several other larger compounds, but when it uses glucosamine this way, an acetyl group is added. Thus, the form of glucosamine found in complex compounds is actually N-acetyl-glucosamine.
Glucuronic acid is formed from glucose when it is converted into an organic acid by essentially replacing the hydroxyl group on carbon #6 with a carboxylic acid group. Galactose is another monosaccharide. It has almost the same structure as glucose, except that the hydroxyl group on carbon #4 points in the opposite direction. Galactosamine is formed with the addition of an amino group. Likewise, in complex molecules, galactose is converted into N-acetyl-glactosamine.
Hyaluronic acid (HA) is a member of the glycosaminoglycan (GAG) family, which includes chondroitin sulfate, dermatin sulfate and heparin sulfate. Unlike other members of this family, HA is not bound covalently to proteins. HA is comprised of linear, unbranching, polyanionic disaccharide units consisting of glucuronic acid and N-acetyl-glucosamine joined alternately by beta 1-3 and beta glycosidic bonds.
Figure 1 (Page XX) shows the chemical structure of HA. The ring structure on the left is glucuronic acid and the ring structure on the right is N-acetyl-glucosamine. The brackets indicate that these two components are repeated " n" times. Thus, HA is not a single compound having a single formula. Technically, any compound where " n" is greater than 10 can be called HA. However, the final synthesis of HA normally produces compounds where " n" can range widely from a few thousand to several million.
Chondroitin sulfate is a closely related family member, but it doesn’t hold as much water. The structure is similar, but the difference is biochemically significant. In chondroitin sulfate, there is the same glucuronic acid ring, but the other ring is n-acetyl-galatosamine. Chitin is also very similar except that it is basically a polymer of N-acetyl-glucosamine.
jdp710- Posts: 471
Join date: 2008-11-28 
Re: Sagging Skin
jdp710 on Tue Jun 09, 2009 9:27 am
CausticSymmetry,
BTW, I'm not sure if you've noticed but instead of taking the NOW hyaluronic acid pills like you've mentioned in the past, you can always experiment with this hyaluronic acid to save money
http://www.iherb.com/Neocell-Labs-ImmuCell-Collagen-Type-2-120-Capsules/8368?at=0
If I'm not mistaken, this brand appears to be the same but would cost more than taking the NOW hyaluronic acid ...
http://www.iherb.com/Doctor-s-Best-Best-Hyaluronic-Acid-with-Chondroitin-Sulfate-60-Capsules/4457?at=0
The reason why I posted the Doctors Best brand is it appears you get 100 mg of hyaluronic acid per 1000 mg from the "patented Biocell Collagen II." So I assume that would be the same for the Neocell brand as well. There is also another brand by Jarrow but would also be more expensive than the NOW hyaluronic acid http://www.iherb.com/Jarrow-Formulas-Type-II-Collagen-Complex-500-mg-Per-Capsule-60-Capsules/15926?at=0
But again, check out the Neocell brand. It appears this may save some money buying this over the NOW hyaluronic acid.
BTW, I'm not sure if you've noticed but instead of taking the NOW hyaluronic acid pills like you've mentioned in the past, you can always experiment with this hyaluronic acid to save money
http://www.iherb.com/Neocell-Labs-ImmuCell-Collagen-Type-2-120-Capsules/8368?at=0
If I'm not mistaken, this brand appears to be the same but would cost more than taking the NOW hyaluronic acid ...
http://www.iherb.com/Doctor-s-Best-Best-Hyaluronic-Acid-with-Chondroitin-Sulfate-60-Capsules/4457?at=0
The reason why I posted the Doctors Best brand is it appears you get 100 mg of hyaluronic acid per 1000 mg from the "patented Biocell Collagen II." So I assume that would be the same for the Neocell brand as well. There is also another brand by Jarrow but would also be more expensive than the NOW hyaluronic acid http://www.iherb.com/Jarrow-Formulas-Type-II-Collagen-Complex-500-mg-Per-Capsule-60-Capsules/15926?at=0
But again, check out the Neocell brand. It appears this may save some money buying this over the NOW hyaluronic acid.
jdp710- Posts: 471
Join date: 2008-11-28 -
Re: Sagging Skin
CausticSymmetry on Tue Jun 09, 2009 4:18 pm
dp710 - Thanks for the very informative article on HA. I thought I "knew" everything about this, but I didn't!
Assuming that collagen type II products yield a 10% supply of HA, that would mean that product you suggested might supply about 240 mg of HA.
I'll add that taking Ecklonia Cava helps preserve the body's HA supply.
Having tried the more expensive, lower molecular weight versions of HA, I can attest that regular HA is cheaper and works just as well but at more reasonable cost.
I've been taking 200 milligrams of HA for quite a while now (two of those double-strength from Now brand). I compared the value difference between Neocell Labs, ImmuCell, Collagen Type 2 and Now's double-strength HA.
Assuming Neocell Labs supplies 240 mg of HA per serving (4-capsules) and Now Brand-double strength (2-capsules) 200 milligrams. Based on using these products into a 30-day supply, It breaks down to Neocell Lab's at 9.27 cents per milligram and Now-DS at 9.4 cents per mg. Pretty close.
Thanks again for the article.
Assuming that collagen type II products yield a 10% supply of HA, that would mean that product you suggested might supply about 240 mg of HA.
I'll add that taking Ecklonia Cava helps preserve the body's HA supply.
Having tried the more expensive, lower molecular weight versions of HA, I can attest that regular HA is cheaper and works just as well but at more reasonable cost.
I've been taking 200 milligrams of HA for quite a while now (two of those double-strength from Now brand). I compared the value difference between Neocell Labs, ImmuCell, Collagen Type 2 and Now's double-strength HA.
Assuming Neocell Labs supplies 240 mg of HA per serving (4-capsules) and Now Brand-double strength (2-capsules) 200 milligrams. Based on using these products into a 30-day supply, It breaks down to Neocell Lab's at 9.27 cents per milligram and Now-DS at 9.4 cents per mg. Pretty close.
Thanks again for the article.
CausticSymmetry- Posts: 3802
Join date: 2008-07-09 -
Re: Sagging Skin
jdp710 on Wed Jun 10, 2009 9:28 am
Thanks for doing the math CS. It looks like my math skills at 3:00 in the morning aren't as good as they use to be, lol. I ordered some anyway as I was running low on the NOW hyaluronic acid and I know Neocell labs is really good stuff as I use their Type I and Type III collagen pills for skin as well. http://www.iherb.com/Neocell-Labs-Super-Collagen-Type-I-III-Powder-7-oz-198-g/6074?at=0
Oh, thanks for the info about the info about Ecklonia Cava preserving hyaluronic acid. I was hoping it would do this. I've just recently been taking this as there doesn't appear to be anything that it can't do, lol. I took grapeseed extract for over 10 years but I replaced it with something much more powerful ... Ecklonia Cava.
Here is an interesting quote about hyaluronic acid that I had stored on my computer
"As Hyaluronic Acid is present in every tissue of the body; hyaluronic acid’s importance cannot be underestimated. Retention of water is one of the most important biological functions of hyaluronic acid, 1 second only to providing nutrients and removing waste from cells that do not have a direct blood supply, such as cartilage cells. With a lower than adequate amount of hyaluronic acid, nutrients cannot be moved into these cells and waste cannot be eliminated from cells."
You're probably aware of all this but here is some good info on Ecklonia Cava,
----------------------------------------------------
http://www.springboard4health.com/notebook/nutrients_ecklonia.html
Ecklonia Cava Extract - Super Antioxidant & Beyond
Ecklonia Cava Extract: Polyphenol / Phlorotannin Derived from Brown Algae
Ecklonia Cava Extract (ECE) is a standardized natural complex of unique marine molecules that originate from a specific species of brown algae (Ecklonia cava). ECE represents a unique category of polyphenols often called phlorotannins. Their unique polyphenolic structure endows them with biological activities that are not found in land-based plants.
ECE naturally occurs as high-molecular weight tannin (Mw> 2,000 Dalton) and low-molecular weight tannin (Mw=400-1000 Dalton). ECE can be classified into four types depending on the ratio of high molecular weight and low molecular weight tannins. Various physiological activities of ECE have been evaluated in vitro, in vivo and clinically as individual compounds (ECE1-ECE14) and complex forms (ECE, Type I-IV).
Millions on Research
Dr. Haengwoo Lee and his team of M.D.’s and Ph.D.’s have spent over thirty million dollars on research, from in vitro to animal and human studies. Much of the work was done in Korea, and some at the University of Washington. ECE has been found to be an impressive therapeutic agent in a wide array of clinical applications.
SUPER ANTIOXIDANT
The power of an antioxidant is determined by its structure, which is made up of rings. These rings capture stray electrons from free radicals. Most flavonoids generally have three interconnected rings. ECE has up to eight interconnected rings, making its free-radical scavenging ability 10-100 times more powerful than other polyphenols. It is substantially more powerful than green tea catechins, which only have four rings.
Multiple Antioxidant Profiles of ECE
ECE’s antioxidant activities against various reactive oxygen species have been confirmed to be highly potent in physiologically relevant concentrations. The effective dose of ECE for free radical scavenging is in the 10-20 µg/mL range which belongs to most potent families of natural antioxidants. ECE itself and its individual compounds have demonstrated potent reducing power and radical scavenging activities against DPPH radical, oxidized LDL and peroxynitrite.*
Much Longer Half-Life
ECE is a unique polyphenol in that it has a very long half-life in the body. This is because ECE is a marine-based polyphenol which is 40% fat-soluble. Virtually all other polyphenols are derived from land-based plants and are water-soluble. The half-life of ECE is up to 12 hours, compared to 30 minutes for water-soluble, land-based polyphenols. ECE has the ability to cross the blood-brain barrier.
The Research of Martin Pall, Ph.D.
Peroxynitrite is the most notorious of the free radicals incriminated by Martin Pall, Ph.D.'s groundbreaking research on multiple chemical sensitivity, fibromyalgia, chronic fatigue syndrome, post traumatic stress disorder, Gulf War syndrome, and fourteen other conditions. Peroxynitrite plays a main role in Dr. Pall’s mechanism, along with NF-kappaB and other inflammatory mediators. ECE also reduces tissue specific NF-kappaB.
*Peroxynitrate is a central reactive oxidant, which appears to play a major role in many disease processes.
FIBROMYALGIA
ECE: Phase I Clinical Trial Results (Preliminary)
In an 8-week, double-blinded, placebo-controlled study of established fibromyalgia patients, ECE was used as an adjunct therapy to the patients’ current standard of physician care. The results established the general safety of ECE. ECE cut the time it took the participants to fall asleep by 47 minutes; it increased total nighttime sleep by 1.6 hours; it improved soundness of sleep by 80%; it boosted their energy levels by 71%; it gave them 2 1/4 more good days per week; it helped reduce their pain by 31%; and their general condition improved by 39%. Interestingly, these improvements were achieved at all doses. Patients given the placebo had no improvement during the study.
BRAIN FUNCTION: MEMORY, RELAXATION, ALERTNESS
Acetylcholine & Memory
Memory is dependent on the neurotransmitter acetylcholine (ACh). In an animal study, ECE increased rodent ACh by 140% in brain regions responsible for learning and memory in seven days. Memory enhancement increased by 100-200% at an oral dose as low as 0.2-1mg/kg.
With regard to mechanism, it is thought that the mild acetylcholinesterase inhibitory activity of two phlorotannin compounds found in ECE, dieckol (DE) and phlorofurofucoeckol (PFF), may be involved in the up-regulation of acetylcholine.
Increased Blood Flow
ECE crosses the blood-brain barrier and significantly improves blood flow, which is likely another way ECE improves memory. More specifically, Dr. Lee’s group found that ECE can increase the velocity of blood flow in the carotid artery from an average of 36.68 cm/sec. to 40.09 cm/sec., while the placebo showed no improvement.
Relaxation & Alpha-Waves
An EEG study on brain waves of healthy middle age volunteers found that ECE compounds increase alpha-waves. Alpha-waves are an indicator of relaxation.
Alertness
Yet another study found that ECE compounds prevented sleepiness in bus drivers and in high school students during daytime activities. This is likely due to increased blood flow and oxygen delivery.
Neuroprotective Effects
ECE demonstrated powerful neuroprotective effects owing to several features of its components. ECE compounds are both powerful antioxidants and anti-inflammatory agents capable of scavenging free radicals and suppressing excessive inflammatory reactions. Fucoidan in ECE has recently been found to protect neuronal cells from ischemia-induced inflammatory reactions which often occur in the aged and highly stressed brain. ECE compounds also neutralize the neurotoxic free-radical peroxynitrite.
Enhancement of Acetylcholine Levels in Mice
After 7 days oral administration of two ECE compounds (DE 10mg/kg and PFF 2mg/kg), mice under ethanol-induced cognitive impairment showed substantial enhancement of acetylcholine in three brain regions related to memory formation, as compared with non-treated mice. Especially, 140% enhancement was observed in the frontal cortex that is crucial in long-term memory and associative thinking.
Resistance of Stress-Induced Learning Deficit in Mice
In a 5-day study, ECE treated mice showed significant resistance to electric shock treatment-induced learning deficiency, as compared to non-treated mice whose learning process was significantly retarded during the test period.
Memory Enhancement in Mice
The beneficial effects of ECE compounds on memory enhancement were further demonstrated by measuring the latency time avoiding the previously experienced electric shock treatment in mice as passive-avoidance memory testing. After 7 days oral administration of two ECE compounds DE and PFF (as low as 1 and 0.2mg/kg), mice under ethanol-induced cognitive impairment showed 130-140% improvement, especially in the PFF group.
Beta-Amyloid Deposition Inhibition in Rats
Researchers at the National Institute of Health’s aging research labs in Baltimore studied ECE in rats, and found it to inhibit beta-amyloid deposition in the brain. Beta-amyloid is the same substance that accumulates in Alzheimer’s disease. The rats also learned maze challenges faster, which demonstrated improvement in short-term memory.
ARTHRITIS, INFLAMMATION, NEURALGIA
Dr. Lee and colleagues found ECE to naturally suppress inflammatory responses and neutralize inflammatory damage caused by reactive oxygen species. The optimal combination of ECE’s natural anti-inflammatory and tissue-protective properties appears to enable dramatic improvement in both arthritis and neuralgia. In a human trial, ECE significantly reduced pain in a group of knee arthritis patients compared with placebo.
Comparable to CelebrexÆ
ECE’s ability to treat arthritis was found to be comparable to CelebrexÆ, the prescription drug that reduces inflammatory cox enzymes.
The influence of ECE in lipopolysaccharide (LPS)-induced generation of prostaglandin E2 (PGE2) using RAW 246.7 cells was studied. While PGE2 was barely detectable in non-stimulated cells, more than one hundred times the amount of PGE2 was detected in the stimulated cells. ECE, celecoxib (CelebrexÆ) and aspirin all showed significant inhibition of PGE2 generation in the concentration range tested. ECE showed inhibition of 61%, 85%, 92% and 99% at concentrations of 10, 30, 60 and 100 µg/mL, showing similar activity to celecoxib which showed 65%, 79%, 85% and 96%.
Cartilage Protecting Activities
As demonstrated above, ECE compared almost identically to celecoxib in the ability to reduce PGE2 by slowing down the lipoxygenase (LOX) system. ECE compounds have more than double the ability of resveratrol to inhibit LOX. These results were demonstrated in a study on rabbit cartilage cells. Those cells treated with ECE had up to an 80% reduction in degeneration.
Rabbit Model
In an animal study, rabbit articular cartilage explant culture was treated with recombinant human interleukin 1 (rhIL-1) to induce proteoglycan degradation. The amount of glycosaminoglycan released into the medium was measured as an index of proteoglycan degradation. When the rabbit cartilage explants were treated with rhIL-1 for 60 hours, the amount of released glycosaminoglycan into the culture medium increased significantly compared to the vehicle group (1.44 ± 0.06µg/mg vs. 0.30 ± 0.01µg/mg). Diclofenac, which is known as a selective COX-2 inhibitor was used as a positive control at a dose of 10µM (3.2µg/mL). ECE significantly interfered with the rhIL-1-mediated degradation of proteoglycan in all concentrations tested (p <0.001). It showed 53%, 79%, 81% and 70% of inhibition at 1, 3, 10 and 30 µg/mL concentration.
Neuropathy: 4-Week Clinical Trial
Researchers recently studied ECE on 40 patients with neuropathy. ECE reduced nerve pain by 40% in four weeks. Overall, 80% of the patients responded favorably.
Speculation about Neuropathy Mechanism
The strong lipid and cholesterol reducing potential of ECE supports reduced vascular inflammation. Increasingly, the scientific literature supports the notion that many forms of nerve pain or neuropathy are caused by nerve pressure, as exerted by swollen, inflamed blood vessels adjacent to the nerves.
Oh, thanks for the info about the info about Ecklonia Cava preserving hyaluronic acid. I was hoping it would do this. I've just recently been taking this as there doesn't appear to be anything that it can't do, lol. I took grapeseed extract for over 10 years but I replaced it with something much more powerful ... Ecklonia Cava.
Here is an interesting quote about hyaluronic acid that I had stored on my computer
"As Hyaluronic Acid is present in every tissue of the body; hyaluronic acid’s importance cannot be underestimated. Retention of water is one of the most important biological functions of hyaluronic acid, 1 second only to providing nutrients and removing waste from cells that do not have a direct blood supply, such as cartilage cells. With a lower than adequate amount of hyaluronic acid, nutrients cannot be moved into these cells and waste cannot be eliminated from cells."
You're probably aware of all this but here is some good info on Ecklonia Cava,
----------------------------------------------------
http://www.springboard4health.com/notebook/nutrients_ecklonia.html
Ecklonia Cava Extract - Super Antioxidant & Beyond
Ecklonia Cava Extract: Polyphenol / Phlorotannin Derived from Brown Algae
Ecklonia Cava Extract (ECE) is a standardized natural complex of unique marine molecules that originate from a specific species of brown algae (Ecklonia cava). ECE represents a unique category of polyphenols often called phlorotannins. Their unique polyphenolic structure endows them with biological activities that are not found in land-based plants.
ECE naturally occurs as high-molecular weight tannin (Mw> 2,000 Dalton) and low-molecular weight tannin (Mw=400-1000 Dalton). ECE can be classified into four types depending on the ratio of high molecular weight and low molecular weight tannins. Various physiological activities of ECE have been evaluated in vitro, in vivo and clinically as individual compounds (ECE1-ECE14) and complex forms (ECE, Type I-IV).
Millions on Research
Dr. Haengwoo Lee and his team of M.D.’s and Ph.D.’s have spent over thirty million dollars on research, from in vitro to animal and human studies. Much of the work was done in Korea, and some at the University of Washington. ECE has been found to be an impressive therapeutic agent in a wide array of clinical applications.
SUPER ANTIOXIDANT
The power of an antioxidant is determined by its structure, which is made up of rings. These rings capture stray electrons from free radicals. Most flavonoids generally have three interconnected rings. ECE has up to eight interconnected rings, making its free-radical scavenging ability 10-100 times more powerful than other polyphenols. It is substantially more powerful than green tea catechins, which only have four rings.
Multiple Antioxidant Profiles of ECE
ECE’s antioxidant activities against various reactive oxygen species have been confirmed to be highly potent in physiologically relevant concentrations. The effective dose of ECE for free radical scavenging is in the 10-20 µg/mL range which belongs to most potent families of natural antioxidants. ECE itself and its individual compounds have demonstrated potent reducing power and radical scavenging activities against DPPH radical, oxidized LDL and peroxynitrite.*
Much Longer Half-Life
ECE is a unique polyphenol in that it has a very long half-life in the body. This is because ECE is a marine-based polyphenol which is 40% fat-soluble. Virtually all other polyphenols are derived from land-based plants and are water-soluble. The half-life of ECE is up to 12 hours, compared to 30 minutes for water-soluble, land-based polyphenols. ECE has the ability to cross the blood-brain barrier.
The Research of Martin Pall, Ph.D.
Peroxynitrite is the most notorious of the free radicals incriminated by Martin Pall, Ph.D.'s groundbreaking research on multiple chemical sensitivity, fibromyalgia, chronic fatigue syndrome, post traumatic stress disorder, Gulf War syndrome, and fourteen other conditions. Peroxynitrite plays a main role in Dr. Pall’s mechanism, along with NF-kappaB and other inflammatory mediators. ECE also reduces tissue specific NF-kappaB.
*Peroxynitrate is a central reactive oxidant, which appears to play a major role in many disease processes.
FIBROMYALGIA
ECE: Phase I Clinical Trial Results (Preliminary)
In an 8-week, double-blinded, placebo-controlled study of established fibromyalgia patients, ECE was used as an adjunct therapy to the patients’ current standard of physician care. The results established the general safety of ECE. ECE cut the time it took the participants to fall asleep by 47 minutes; it increased total nighttime sleep by 1.6 hours; it improved soundness of sleep by 80%; it boosted their energy levels by 71%; it gave them 2 1/4 more good days per week; it helped reduce their pain by 31%; and their general condition improved by 39%. Interestingly, these improvements were achieved at all doses. Patients given the placebo had no improvement during the study.
BRAIN FUNCTION: MEMORY, RELAXATION, ALERTNESS
Acetylcholine & Memory
Memory is dependent on the neurotransmitter acetylcholine (ACh). In an animal study, ECE increased rodent ACh by 140% in brain regions responsible for learning and memory in seven days. Memory enhancement increased by 100-200% at an oral dose as low as 0.2-1mg/kg.
With regard to mechanism, it is thought that the mild acetylcholinesterase inhibitory activity of two phlorotannin compounds found in ECE, dieckol (DE) and phlorofurofucoeckol (PFF), may be involved in the up-regulation of acetylcholine.
Increased Blood Flow
ECE crosses the blood-brain barrier and significantly improves blood flow, which is likely another way ECE improves memory. More specifically, Dr. Lee’s group found that ECE can increase the velocity of blood flow in the carotid artery from an average of 36.68 cm/sec. to 40.09 cm/sec., while the placebo showed no improvement.
Relaxation & Alpha-Waves
An EEG study on brain waves of healthy middle age volunteers found that ECE compounds increase alpha-waves. Alpha-waves are an indicator of relaxation.
Alertness
Yet another study found that ECE compounds prevented sleepiness in bus drivers and in high school students during daytime activities. This is likely due to increased blood flow and oxygen delivery.
Neuroprotective Effects
ECE demonstrated powerful neuroprotective effects owing to several features of its components. ECE compounds are both powerful antioxidants and anti-inflammatory agents capable of scavenging free radicals and suppressing excessive inflammatory reactions. Fucoidan in ECE has recently been found to protect neuronal cells from ischemia-induced inflammatory reactions which often occur in the aged and highly stressed brain. ECE compounds also neutralize the neurotoxic free-radical peroxynitrite.
Enhancement of Acetylcholine Levels in Mice
After 7 days oral administration of two ECE compounds (DE 10mg/kg and PFF 2mg/kg), mice under ethanol-induced cognitive impairment showed substantial enhancement of acetylcholine in three brain regions related to memory formation, as compared with non-treated mice. Especially, 140% enhancement was observed in the frontal cortex that is crucial in long-term memory and associative thinking.
Resistance of Stress-Induced Learning Deficit in Mice
In a 5-day study, ECE treated mice showed significant resistance to electric shock treatment-induced learning deficiency, as compared to non-treated mice whose learning process was significantly retarded during the test period.
Memory Enhancement in Mice
The beneficial effects of ECE compounds on memory enhancement were further demonstrated by measuring the latency time avoiding the previously experienced electric shock treatment in mice as passive-avoidance memory testing. After 7 days oral administration of two ECE compounds DE and PFF (as low as 1 and 0.2mg/kg), mice under ethanol-induced cognitive impairment showed 130-140% improvement, especially in the PFF group.
Beta-Amyloid Deposition Inhibition in Rats
Researchers at the National Institute of Health’s aging research labs in Baltimore studied ECE in rats, and found it to inhibit beta-amyloid deposition in the brain. Beta-amyloid is the same substance that accumulates in Alzheimer’s disease. The rats also learned maze challenges faster, which demonstrated improvement in short-term memory.
ARTHRITIS, INFLAMMATION, NEURALGIA
Dr. Lee and colleagues found ECE to naturally suppress inflammatory responses and neutralize inflammatory damage caused by reactive oxygen species. The optimal combination of ECE’s natural anti-inflammatory and tissue-protective properties appears to enable dramatic improvement in both arthritis and neuralgia. In a human trial, ECE significantly reduced pain in a group of knee arthritis patients compared with placebo.
Comparable to CelebrexÆ
ECE’s ability to treat arthritis was found to be comparable to CelebrexÆ, the prescription drug that reduces inflammatory cox enzymes.
The influence of ECE in lipopolysaccharide (LPS)-induced generation of prostaglandin E2 (PGE2) using RAW 246.7 cells was studied. While PGE2 was barely detectable in non-stimulated cells, more than one hundred times the amount of PGE2 was detected in the stimulated cells. ECE, celecoxib (CelebrexÆ) and aspirin all showed significant inhibition of PGE2 generation in the concentration range tested. ECE showed inhibition of 61%, 85%, 92% and 99% at concentrations of 10, 30, 60 and 100 µg/mL, showing similar activity to celecoxib which showed 65%, 79%, 85% and 96%.
Cartilage Protecting Activities
As demonstrated above, ECE compared almost identically to celecoxib in the ability to reduce PGE2 by slowing down the lipoxygenase (LOX) system. ECE compounds have more than double the ability of resveratrol to inhibit LOX. These results were demonstrated in a study on rabbit cartilage cells. Those cells treated with ECE had up to an 80% reduction in degeneration.
Rabbit Model
In an animal study, rabbit articular cartilage explant culture was treated with recombinant human interleukin 1 (rhIL-1) to induce proteoglycan degradation. The amount of glycosaminoglycan released into the medium was measured as an index of proteoglycan degradation. When the rabbit cartilage explants were treated with rhIL-1 for 60 hours, the amount of released glycosaminoglycan into the culture medium increased significantly compared to the vehicle group (1.44 ± 0.06µg/mg vs. 0.30 ± 0.01µg/mg). Diclofenac, which is known as a selective COX-2 inhibitor was used as a positive control at a dose of 10µM (3.2µg/mL). ECE significantly interfered with the rhIL-1-mediated degradation of proteoglycan in all concentrations tested (p <0.001). It showed 53%, 79%, 81% and 70% of inhibition at 1, 3, 10 and 30 µg/mL concentration.
Neuropathy: 4-Week Clinical Trial
Researchers recently studied ECE on 40 patients with neuropathy. ECE reduced nerve pain by 40% in four weeks. Overall, 80% of the patients responded favorably.
Speculation about Neuropathy Mechanism
The strong lipid and cholesterol reducing potential of ECE supports reduced vascular inflammation. Increasingly, the scientific literature supports the notion that many forms of nerve pain or neuropathy are caused by nerve pressure, as exerted by swollen, inflamed blood vessels adjacent to the nerves.
jdp710- Posts: 471
Join date: 2008-11-28 -
Re: Sagging Skin
jdp710 on Wed Jun 10, 2009 9:29 am
ALLERGIES / ASTHMA
Overall, ECE appears to significantly relieve allergic reactions without drowsiness, dizziness and other side effects of anti-histamine drugs.
Allergic Inflammation: Mouse Model
Dr. Lee and his team found that ECE significantly reduced allergic inflammation in mice. Specifically, ECE reduced the migration of eosinophils to the lungs by 75%. Inflammatory white blood cells (CD4+4 T Cells, resultant cytokines Il-4, 5, 13) were reduced by 50%. Mucus plugs in the airways were reduced by 75%. Airway epithelial hyperplasia reduced by 75%. Collagen-causing fibrosis in lung interstitium (fibrosis, airway remodeling) and smooth muscle cell thickness was reduced by 20% and 32%. These latter findings suggest that ECE compounds can prevent or reverse the progression of chronic lung disease such as asthma and Chronic Obstructive Pulmonary Disease (COPD).
5-Lipoxygenase (5-LOX)
5-Lipoxygenase (5-LOX) catalyzes the first step in the oxygenation of arachidonic acid, thus leading to the production of biologically active compounds such as leukotrienes and 5-hydroxyeicosatetraenoic acid. The peptidoleukotrienes (leukotriene C4, leukotriene D4 and leukotriene E4) are powerful spasmogens, which have been implicated in inflammatory and allergic responses. Therefore, inhibition of 5-LOX is a medicinal target for the treatment of inflammatory diseases. One of the ECE compounds (8,8-BE) significantly inhibits 5-LOX compared with other well-known natural medicinal compounds such as resveratrol and EGCG.
University of Washington Asthma Mouse Model
The efficacy of ECE for asthma was demonstrated in an allergen-induced murine asthma mouse model by Dr. Emil Chi, Chairman, Department of Histopathology, University of Washington.
The researchers tested an ECE product (KLS) in a mouse model of allergen-induced chronic lung inflammation and fibrosis. BALB/c mice, after intraperitoneal antigen sensitization on day 0 and day 14, were given weekly intranasal inhalations of antigen from day 14-60. The antigen-treated and challenged mice developed an extensive eosinophil and mononuclear cell inflammatory response, mucus cell hyperplasia and mucus occlusion of the airway.
KLS was found to be effective in reducing allergic reaction in inflammation. By feeding at a concentration of 5.4 mg/ml in the drinking water for 12 days, KLS reduced the airway mucus plugging, and sub-epithelial fibrosis in the antigen-sensitized / challenged mice. The reduced BAL fluid eosinophil indicated that KLS is effective in improving the asthmatic lung structures. No pathological alterations in the liver, kidney, spleen, or small intestine were found.
CARDIOVASCULAR BENEFITS
Coronary Artery Disease
ECE has been shown to improve coronary artery disease (CAD). Researchers found that ECE is even more potent at inhibiting the oxidation of LDL cholesterol than green tea catechins, and appears to scrub the plaque off the endothelial lining. ECE also reduces vascular inflammation by preventing oxidation, which also directly effects inflammatory mediators such as inflammatory prostaglandins, etc.
Coronary Artery Disease: 6-Week Clinical Trial
A clinical trial using ECE was conducted confirming its capacity to regenerate vascular endothelium and recover plasticity of blood vessels after 6 weeks of treatment by measuring flow-mediated dilation (FMD) & nitroglycerin-mediated dilation (NMD) of normal and CAD patients with narrowed coronary arteries by 50+%. FMD indicates nitric oxide (NO) releasing ability of endothelial cells to expand blood vessels by detecting shear stress caused by incoming blood flow (low FMD value can indicate endothelium damage).
After 6 weeks of treatment with ECE, clinical data showed that FMD, the endothelium-dependent dilation, was greatly enhanced in the CAD group, indicating its remarkable activity of inducing recovery of endothelial cells. NMD, the endothelium-independent dilation, which represents the vascular plasticity, also showed remarkable improvement in the CAD group, again supporting ECE’s ability to support restoration of vascular integrity by reversing atherosclerosis.
Cholesterol: 6-Week ClinicalTrial
Researchers gave 39 adults (average age 55.6) low dose (100 mg) ECE compounds for six weeks. Their average cholesterol dropped from 228 to 224. LDL dropped from 141 to 135. HDL rose from 46.5 to 50.7 (highly significant). Triglycerides fell from 215 to 195, and the atherogenic index dropped 12.5%.
Some of the parameters from the above study show very mild changes, which in themselves, may not be statistically significant. However, all parameters went in a health-positive direction, so taken together, the changes in LDL, HDL, triglycerides, blood pressure, and antioxidant protection are very significant. Also, endothelial cells were protected against oxidative damage, and were able to produce significantly more NO, which dilates blood vessels. Dramatic increases in blood flow were also found at this low dose.
Hypertension: 4-Week Animal Study
The remarkable effect of ECE on vasodilation was clearly demonstrated in renovascular clipping induced hypertensive rats. Renovascular clipping surgery is known to increase ACE activity via the renin-angiotensin-aldosterone system, which increased systolic blood pressure (SBP) from 140 to over 200 mm Hg after 4 weeks. Upon oral administration of phlorotannin (99.4%, 50 mg/kg) or enalapril (commercial hypotensive drug, 10 mg/kg) SBP dropped to as low as 160 and 140 mm Hg. Upon cessation of treatment, SBP increased again in both cases. Although ECE showed a similar pattern to the drugs, it also showed a slower rebounding of blood pressure during the no treatment period, which indicates its potential as a vascular protector with prolonged oral administration.
ACE Inhibition
Angiotensin-converting enzyme (ACE), is responsible for conversion of angiotensin I to angiotensin II and degradation of bradykinin, and is a key component in the renin-angiotensin-aldosterone system. Angiotensin II regulates cellular proliferation, inflammation, and endothelial function, and is therefore important in the pathogenesis of atherosclerosis and its complications. Aging or various vascular risk factors tend to increase ACE levels resulting in excessive vasoconstriction and hypertension. Current hypotensive drugs block the action of ACE or its by-product angiotensin II.
ECE tannins have been found to be potent natural ACE inhibitors, demonstrating more than 15 times the power to inhibit ACE as the most powerful land-based polyphenols, including the natural hypotensive substance catechin found in green tea. One of the compounds found in ECE, THP-BE is comparable to the physiological vasodilative hormone bradykinin.
Antiplasmin Inhibition
Plasmin (a fibrinolytic enzyme that breaks down blood clots) is rapidly blocked by a protein called antiplasmin. ECE compounds are natural potent inhibitors of anti-plasmin, capable of efficient promotion of plasmin that performs fibrinolysis. ECE compounds have shown remarkable activity which is 40-200 times greater than synthetic compounds Flufenamate and Chloramine T. One study on ECE compounds found a small but significant rise in prothrombin time and a fall in fibrinogen levels.
ERECTILE FUNCTION - ECE V. VIAGRAÆ
Nitric Oxide
ECE can regenerate the vascular endothelium, the cells critical to the inner lining of the blood vessels. They generate the chemical nitric oxide (NO), which keeps the arterial walls relaxed and dilated. After a six-week study of ECE, flow mediated dilation and NO mediated dilation increased by 60% and 50%. In another study, coronary artery disease patients were given ECE for six weeks. Blood flow controlled by NO increased 50-60%. These results confirm that ECE can rejuvenate damaged endothelial cells to produce NO. This effect was further confirmed in a study on erectile dysfunction (see below). Interestingly, ViagraÆ works by increasing NO in the penile artery.
ECE v.ViagraÆ: 8-Week Clinical Trial
Scientists studied 31 men with erectile dysfunction (ED) for over six months. They compared eight weeks of ECE use to ViagraÆ. They looked at orgasmic function (OF), intercourse satisfaction (IS), overall satisfaction (OS), and erectile function (EF). Over those eight weeks, ECE scored 87%, 74%, 62%, and 66%. ViagraÆ scored 27%, 44%, 39%, and 66%. No side effects were reported with ECE:
Population with 25+% Improvement in IIEF (International Index of Erectile Function) score was as high as 81%. Total IIEF score significantly increased from 29.1 ± 13.1 to 47.0 ± 14.5 with 62% of improvement. When the IIEF scores were grouped into five separate domains, mean IIEF scores at the 8th week were significantly greater than those at week 0 for all domains (all p<0.01). The degree of improvement was significant in the following order: OF (87%), IS (74%), EF (66%), and OS (62%). Scores on key questions (asking frequency of penetration and asking frequency of maintaining an erection after penetration), which directly indicate the ability to achieve and maintain an erection sufficient for sexual activity, were improved up to 74% and 77%, respectively (p<0.01).
It is very important to note that despite the marginal improvement in sexual desire (20%) that is of psychological nature, great improvements were reported in the domains directly related with erection that is of physical nature and dependent on normal vascular function of the penile artery.
Also noteworthy, was a significant increase in the orgasmic function score (87%), intercourse satisfaction (74%) and overall satisfaction (62%) as well as erectile function (66%) in comparison with the results for sildenafil reported by Marks, et al. (Marks, et al., 1999) (27%, 44%, 39% and 66%, respectively), which indicates that ECE significantly contributed to the normalization of the general vascular conditions around the sexual organ.
These results strongly indicate that the long-term administration of ECE significantly contributes to the neutralization of oxidative risk factors, thereby improving peripheral blood circulation around muscles and nerves involved in sexual function as well as the penile artery. No side effects were reported.
Vasodilation & Erectile Function
It has been reported that vasculogenic ED patients have elevated levels of angiotensin II for the duration of the erection process. The demonstrated action of ECE on ACE and resulting vasodilation is thought to play an important role in inducing successful erectile function.
Long-Term Improvement Via Vascular Protection
As discussed, ECE phlorotanins have potent antioxidant and anti-inflammatory effects. Together with ECE's ACE inhibitory activity, which is also beneficial to vascular homeostasis, these activities, upon long-term oral administration, may all contribute to supporting a healthy vascular system, including the penile artery.
WEIGHT LOSS
DGAT Inhibition
Diacylglycerol acetyl transferase (DGAT) is the enzyme involved in the final step of triglyceride synthesis. Triglycerides are circulating fat bodies that ultimately wind up in the fat cells, and are almost always elevated in diabetes. They also have emerged as a major risk factor in vascular disease.
Dr. Lee found that ECE compounds inhibited DGAT more than 50%. In genetically caused obese laboratory rats, ECE reduced body fat and increased physical activity. In another study, ECE caused leanness and fat-resistance in animals given a high fat diet.
ECE Beverage: 2-Week Clinical Trial
In a human study, 141 young adults were given a beverage containing ECE at 200 mg daily. In two weeks their average weight dropped nearly 2.5 pounds, muscle mass increased by nearly 2.5 pounds, and body fat dropped by 4 pounds, or 7.48%. ECE stimulates the body to burn fat by increasing muscle mass.
OBESITY
Obesity & Cardiovascular Disease
As discussed, ECE contains an optimal combination of natural compounds capable of suppressing triglyceride synthesis, while promoting cholesterol removal and cardiovascular protection. ECE provides additional cardiovascular protection for obese patients prone to CVD and CHD through lowering LDL cholesterol and scavenging free radicals.
DGAT Inhibition & Obesity
DGAT inhibition has recently been recognized as a novel and safe target for the treatment of obesity. DGAT is involved in intestinal fat absorption, lipoprotein assembly, regulation of plasma TG concentration, fat storage in adipocytes, and energy metabolism in muscle. DGAT knockout mice have been shown to have obesity resistance with a high-fat diet, the mechanism of which was confirmed to be through energy expenditure.
DIABETES
Aldose Reductase Inhibition
When blood sugar levels become elevated, aldose reductase is the enzyme that converts excess glucose into the sugar alcohol sorbitol. Sorbitol can build up in critical cells and cause damage. Recent research found that animals deficient in aldose reductase were protected from the retinal complications of diabetes. ECE compounds have been found to be potent aldose reductase inhibitors, which may be of benefit for patients with metabolic syndrome, syndrome X, or diabetes.
Reduced Fat in Liver & Pancreas
A mouse study showed that ECE reversed fat deposition in liver and pancreas cells. Furthermore, this same study showed that ECE served to markedly inhibit NF-kappaB inflammation in the pancreas. A recent Harvard (Joslin School of Diabetes) mouse study directly implicates excessive fat deposition in the mouse pancreas as turning on the NF-kappaB inflammation pathway, resulting in full-blown type II diabetes and insulin insensitivity in the mice.
Overall, ECE appears to significantly relieve allergic reactions without drowsiness, dizziness and other side effects of anti-histamine drugs.
Allergic Inflammation: Mouse Model
Dr. Lee and his team found that ECE significantly reduced allergic inflammation in mice. Specifically, ECE reduced the migration of eosinophils to the lungs by 75%. Inflammatory white blood cells (CD4+4 T Cells, resultant cytokines Il-4, 5, 13) were reduced by 50%. Mucus plugs in the airways were reduced by 75%. Airway epithelial hyperplasia reduced by 75%. Collagen-causing fibrosis in lung interstitium (fibrosis, airway remodeling) and smooth muscle cell thickness was reduced by 20% and 32%. These latter findings suggest that ECE compounds can prevent or reverse the progression of chronic lung disease such as asthma and Chronic Obstructive Pulmonary Disease (COPD).
5-Lipoxygenase (5-LOX)
5-Lipoxygenase (5-LOX) catalyzes the first step in the oxygenation of arachidonic acid, thus leading to the production of biologically active compounds such as leukotrienes and 5-hydroxyeicosatetraenoic acid. The peptidoleukotrienes (leukotriene C4, leukotriene D4 and leukotriene E4) are powerful spasmogens, which have been implicated in inflammatory and allergic responses. Therefore, inhibition of 5-LOX is a medicinal target for the treatment of inflammatory diseases. One of the ECE compounds (8,8-BE) significantly inhibits 5-LOX compared with other well-known natural medicinal compounds such as resveratrol and EGCG.
University of Washington Asthma Mouse Model
The efficacy of ECE for asthma was demonstrated in an allergen-induced murine asthma mouse model by Dr. Emil Chi, Chairman, Department of Histopathology, University of Washington.
The researchers tested an ECE product (KLS) in a mouse model of allergen-induced chronic lung inflammation and fibrosis. BALB/c mice, after intraperitoneal antigen sensitization on day 0 and day 14, were given weekly intranasal inhalations of antigen from day 14-60. The antigen-treated and challenged mice developed an extensive eosinophil and mononuclear cell inflammatory response, mucus cell hyperplasia and mucus occlusion of the airway.
KLS was found to be effective in reducing allergic reaction in inflammation. By feeding at a concentration of 5.4 mg/ml in the drinking water for 12 days, KLS reduced the airway mucus plugging, and sub-epithelial fibrosis in the antigen-sensitized / challenged mice. The reduced BAL fluid eosinophil indicated that KLS is effective in improving the asthmatic lung structures. No pathological alterations in the liver, kidney, spleen, or small intestine were found.
CARDIOVASCULAR BENEFITS
Coronary Artery Disease
ECE has been shown to improve coronary artery disease (CAD). Researchers found that ECE is even more potent at inhibiting the oxidation of LDL cholesterol than green tea catechins, and appears to scrub the plaque off the endothelial lining. ECE also reduces vascular inflammation by preventing oxidation, which also directly effects inflammatory mediators such as inflammatory prostaglandins, etc.
Coronary Artery Disease: 6-Week Clinical Trial
A clinical trial using ECE was conducted confirming its capacity to regenerate vascular endothelium and recover plasticity of blood vessels after 6 weeks of treatment by measuring flow-mediated dilation (FMD) & nitroglycerin-mediated dilation (NMD) of normal and CAD patients with narrowed coronary arteries by 50+%. FMD indicates nitric oxide (NO) releasing ability of endothelial cells to expand blood vessels by detecting shear stress caused by incoming blood flow (low FMD value can indicate endothelium damage).
After 6 weeks of treatment with ECE, clinical data showed that FMD, the endothelium-dependent dilation, was greatly enhanced in the CAD group, indicating its remarkable activity of inducing recovery of endothelial cells. NMD, the endothelium-independent dilation, which represents the vascular plasticity, also showed remarkable improvement in the CAD group, again supporting ECE’s ability to support restoration of vascular integrity by reversing atherosclerosis.
Cholesterol: 6-Week ClinicalTrial
Researchers gave 39 adults (average age 55.6) low dose (100 mg) ECE compounds for six weeks. Their average cholesterol dropped from 228 to 224. LDL dropped from 141 to 135. HDL rose from 46.5 to 50.7 (highly significant). Triglycerides fell from 215 to 195, and the atherogenic index dropped 12.5%.
Some of the parameters from the above study show very mild changes, which in themselves, may not be statistically significant. However, all parameters went in a health-positive direction, so taken together, the changes in LDL, HDL, triglycerides, blood pressure, and antioxidant protection are very significant. Also, endothelial cells were protected against oxidative damage, and were able to produce significantly more NO, which dilates blood vessels. Dramatic increases in blood flow were also found at this low dose.
Hypertension: 4-Week Animal Study
The remarkable effect of ECE on vasodilation was clearly demonstrated in renovascular clipping induced hypertensive rats. Renovascular clipping surgery is known to increase ACE activity via the renin-angiotensin-aldosterone system, which increased systolic blood pressure (SBP) from 140 to over 200 mm Hg after 4 weeks. Upon oral administration of phlorotannin (99.4%, 50 mg/kg) or enalapril (commercial hypotensive drug, 10 mg/kg) SBP dropped to as low as 160 and 140 mm Hg. Upon cessation of treatment, SBP increased again in both cases. Although ECE showed a similar pattern to the drugs, it also showed a slower rebounding of blood pressure during the no treatment period, which indicates its potential as a vascular protector with prolonged oral administration.
ACE Inhibition
Angiotensin-converting enzyme (ACE), is responsible for conversion of angiotensin I to angiotensin II and degradation of bradykinin, and is a key component in the renin-angiotensin-aldosterone system. Angiotensin II regulates cellular proliferation, inflammation, and endothelial function, and is therefore important in the pathogenesis of atherosclerosis and its complications. Aging or various vascular risk factors tend to increase ACE levels resulting in excessive vasoconstriction and hypertension. Current hypotensive drugs block the action of ACE or its by-product angiotensin II.
ECE tannins have been found to be potent natural ACE inhibitors, demonstrating more than 15 times the power to inhibit ACE as the most powerful land-based polyphenols, including the natural hypotensive substance catechin found in green tea. One of the compounds found in ECE, THP-BE is comparable to the physiological vasodilative hormone bradykinin.
Antiplasmin Inhibition
Plasmin (a fibrinolytic enzyme that breaks down blood clots) is rapidly blocked by a protein called antiplasmin. ECE compounds are natural potent inhibitors of anti-plasmin, capable of efficient promotion of plasmin that performs fibrinolysis. ECE compounds have shown remarkable activity which is 40-200 times greater than synthetic compounds Flufenamate and Chloramine T. One study on ECE compounds found a small but significant rise in prothrombin time and a fall in fibrinogen levels.
ERECTILE FUNCTION - ECE V. VIAGRAÆ
Nitric Oxide
ECE can regenerate the vascular endothelium, the cells critical to the inner lining of the blood vessels. They generate the chemical nitric oxide (NO), which keeps the arterial walls relaxed and dilated. After a six-week study of ECE, flow mediated dilation and NO mediated dilation increased by 60% and 50%. In another study, coronary artery disease patients were given ECE for six weeks. Blood flow controlled by NO increased 50-60%. These results confirm that ECE can rejuvenate damaged endothelial cells to produce NO. This effect was further confirmed in a study on erectile dysfunction (see below). Interestingly, ViagraÆ works by increasing NO in the penile artery.
ECE v.ViagraÆ: 8-Week Clinical Trial
Scientists studied 31 men with erectile dysfunction (ED) for over six months. They compared eight weeks of ECE use to ViagraÆ. They looked at orgasmic function (OF), intercourse satisfaction (IS), overall satisfaction (OS), and erectile function (EF). Over those eight weeks, ECE scored 87%, 74%, 62%, and 66%. ViagraÆ scored 27%, 44%, 39%, and 66%. No side effects were reported with ECE:
Population with 25+% Improvement in IIEF (International Index of Erectile Function) score was as high as 81%. Total IIEF score significantly increased from 29.1 ± 13.1 to 47.0 ± 14.5 with 62% of improvement. When the IIEF scores were grouped into five separate domains, mean IIEF scores at the 8th week were significantly greater than those at week 0 for all domains (all p<0.01). The degree of improvement was significant in the following order: OF (87%), IS (74%), EF (66%), and OS (62%). Scores on key questions (asking frequency of penetration and asking frequency of maintaining an erection after penetration), which directly indicate the ability to achieve and maintain an erection sufficient for sexual activity, were improved up to 74% and 77%, respectively (p<0.01).
It is very important to note that despite the marginal improvement in sexual desire (20%) that is of psychological nature, great improvements were reported in the domains directly related with erection that is of physical nature and dependent on normal vascular function of the penile artery.
Also noteworthy, was a significant increase in the orgasmic function score (87%), intercourse satisfaction (74%) and overall satisfaction (62%) as well as erectile function (66%) in comparison with the results for sildenafil reported by Marks, et al. (Marks, et al., 1999) (27%, 44%, 39% and 66%, respectively), which indicates that ECE significantly contributed to the normalization of the general vascular conditions around the sexual organ.
These results strongly indicate that the long-term administration of ECE significantly contributes to the neutralization of oxidative risk factors, thereby improving peripheral blood circulation around muscles and nerves involved in sexual function as well as the penile artery. No side effects were reported.
Vasodilation & Erectile Function
It has been reported that vasculogenic ED patients have elevated levels of angiotensin II for the duration of the erection process. The demonstrated action of ECE on ACE and resulting vasodilation is thought to play an important role in inducing successful erectile function.
Long-Term Improvement Via Vascular Protection
As discussed, ECE phlorotanins have potent antioxidant and anti-inflammatory effects. Together with ECE's ACE inhibitory activity, which is also beneficial to vascular homeostasis, these activities, upon long-term oral administration, may all contribute to supporting a healthy vascular system, including the penile artery.
WEIGHT LOSS
DGAT Inhibition
Diacylglycerol acetyl transferase (DGAT) is the enzyme involved in the final step of triglyceride synthesis. Triglycerides are circulating fat bodies that ultimately wind up in the fat cells, and are almost always elevated in diabetes. They also have emerged as a major risk factor in vascular disease.
Dr. Lee found that ECE compounds inhibited DGAT more than 50%. In genetically caused obese laboratory rats, ECE reduced body fat and increased physical activity. In another study, ECE caused leanness and fat-resistance in animals given a high fat diet.
ECE Beverage: 2-Week Clinical Trial
In a human study, 141 young adults were given a beverage containing ECE at 200 mg daily. In two weeks their average weight dropped nearly 2.5 pounds, muscle mass increased by nearly 2.5 pounds, and body fat dropped by 4 pounds, or 7.48%. ECE stimulates the body to burn fat by increasing muscle mass.
OBESITY
Obesity & Cardiovascular Disease
As discussed, ECE contains an optimal combination of natural compounds capable of suppressing triglyceride synthesis, while promoting cholesterol removal and cardiovascular protection. ECE provides additional cardiovascular protection for obese patients prone to CVD and CHD through lowering LDL cholesterol and scavenging free radicals.
DGAT Inhibition & Obesity
DGAT inhibition has recently been recognized as a novel and safe target for the treatment of obesity. DGAT is involved in intestinal fat absorption, lipoprotein assembly, regulation of plasma TG concentration, fat storage in adipocytes, and energy metabolism in muscle. DGAT knockout mice have been shown to have obesity resistance with a high-fat diet, the mechanism of which was confirmed to be through energy expenditure.
DIABETES
Aldose Reductase Inhibition
When blood sugar levels become elevated, aldose reductase is the enzyme that converts excess glucose into the sugar alcohol sorbitol. Sorbitol can build up in critical cells and cause damage. Recent research found that animals deficient in aldose reductase were protected from the retinal complications of diabetes. ECE compounds have been found to be potent aldose reductase inhibitors, which may be of benefit for patients with metabolic syndrome, syndrome X, or diabetes.
Reduced Fat in Liver & Pancreas
A mouse study showed that ECE reversed fat deposition in liver and pancreas cells. Furthermore, this same study showed that ECE served to markedly inhibit NF-kappaB inflammation in the pancreas. A recent Harvard (Joslin School of Diabetes) mouse study directly implicates excessive fat deposition in the mouse pancreas as turning on the NF-kappaB inflammation pathway, resulting in full-blown type II diabetes and insulin insensitivity in the mice.
jdp710- Posts: 471
Join date: 2008-11-28 -
Re: Sagging Skin
jdp710 on Wed Jun 10, 2009 9:41 am
BTW, I'm not sure if you've heard this role for hyaluronic acid but check out the sentence in bold ...
"Potentiating Agents
Hyaluronic acid is a major carbohydrate component of the extracellular matrix and can be found in the skin, joints, eyes and most other organs and tissues. It has a simple, repeated disaccharide linear copolymer structure that is completely conserved throughout a large span of the evolutionary tree, indicating a fundamental biological importance. Through its complex interactions with matrix components and cells, hyaluronic acid has multifaceted roles in biology utilizing both its physicochemical and biological properties. These biological roles range from a purely structural function in the extracellular matrix to developmental regulation through effects of cellular behavior via control of the tissue macro- and microenvironments, as well as through direct receptor mediated effects on gene expression.73 Hyaluronic acid is utilized in many chemotherapy protocols as a potentiating agent.74 Hyaluronic acid is also being utilized for many novel applications in medicine.75 76 Personal experience has shown that the addition of 2 ml with the DMPS tends to improve the excretion of mercury by two-fold. There is virtually no toxicity with this agent.
http://www.klinghardtneurobiology.org/MercuryToxicityandDetoxification.pdf
"Potentiating Agents
Hyaluronic acid is a major carbohydrate component of the extracellular matrix and can be found in the skin, joints, eyes and most other organs and tissues. It has a simple, repeated disaccharide linear copolymer structure that is completely conserved throughout a large span of the evolutionary tree, indicating a fundamental biological importance. Through its complex interactions with matrix components and cells, hyaluronic acid has multifaceted roles in biology utilizing both its physicochemical and biological properties. These biological roles range from a purely structural function in the extracellular matrix to developmental regulation through effects of cellular behavior via control of the tissue macro- and microenvironments, as well as through direct receptor mediated effects on gene expression.73 Hyaluronic acid is utilized in many chemotherapy protocols as a potentiating agent.74 Hyaluronic acid is also being utilized for many novel applications in medicine.75 76 Personal experience has shown that the addition of 2 ml with the DMPS tends to improve the excretion of mercury by two-fold. There is virtually no toxicity with this agent.
http://www.klinghardtneurobiology.org/MercuryToxicityandDetoxification.pdf
jdp710- Posts: 471
Join date: 2008-11-28 -
Re: Sagging Skin
europe on Wed Jun 10, 2009 1:32 pm
itiches - if you hagerty's scalp exercice, it 's very important to put some oil on your forehead, and more generally your face. to prevent wrinkles, and perhaps sagging skin...
i hope you do it....and i hope you do the scalp exercice WELL.
i hope you do it....and i hope you do the scalp exercice WELL.
europe- Posts: 280
Join date: 2008-10-16 -
Re: Sagging Skin
halfempty on Thu Jun 11, 2009 1:01 pm
Do any of you guys know if Tom Hagerty has received a face lift? It looks like it to me.
halfempty- Posts: 138
Join date: 2008-07-09 -
Re: Sagging Skin
europe on Fri Jun 12, 2009 8:10 am
nope.
but it takes a lot of work to achieve his results. Every day. exercices.
But you know, it's better to go and make a lift.
I assume this is why people prefer have transplants instead of searching to combat hairloss with natural supps....
As always, results always make people jalous. what is his secret ??!!???
Good news : He tell us.
Fell free to believe him or not. I know the guy, and i can assure you he's an honnest one.
But that's my word.
but it takes a lot of work to achieve his results. Every day. exercices.
But you know, it's better to go and make a lift.
I assume this is why people prefer have transplants instead of searching to combat hairloss with natural supps....
As always, results always make people jalous. what is his secret ??!!???
Good news : He tell us.
Fell free to believe him or not. I know the guy, and i can assure you he's an honnest one.
But that's my word.
europe- Posts: 280
Join date: 2008-10-16 -
Re: Sagging Skin
europe on Fri Jun 12, 2009 8:22 am
oh, by the way halfempty, I only do the fifth exercice, also know as the "scalp exercice".
I do not do the 1,2,3 and 4 ones. Funny, i deciced 2 days ago to make them a go, i see lots of benefits in there, and especially for me that cannot blink my eyes individually ! ;-)
But what i can tell you is that only with the scalp exercice ( apart the hair benefit that i cannot attribute : what would be my hairs without the scalp ??) , my face is very toned up, i look more youngfull, forehead etc.... i get used to it now, but at the first, that's my relatives that told me that. That says it all.
And apparence speaking, because hair is all about apparence at the end, i can assure you that a firm and youngfull face make ALSO the difference in term of apparence.
But for doing this for a long time ( MARCH 2003 ) , i just can say that it really a pain in the as to do that. Not every day a pain in the ass, sometimes a pleasure, an habit. But, it's always difficult to do it on busy days, or days with people. MAke it in toilets , reading the news paper...but it sometimes difficult for the concentration to do many things together. sort of workout of your brain, and i'm sure brian is gonna love it that way, aren't you brian ? ;-)
;-) ;-) ;;;;;-)
;-) yeahh !!! i can do that now !! blink my eeeeeeyes ! thank you so much CausticS !!!!
;-)
I do not do the 1,2,3 and 4 ones. Funny, i deciced 2 days ago to make them a go, i see lots of benefits in there, and especially for me that cannot blink my eyes individually ! ;-)
But what i can tell you is that only with the scalp exercice ( apart the hair benefit that i cannot attribute : what would be my hairs without the scalp ??) , my face is very toned up, i look more youngfull, forehead etc.... i get used to it now, but at the first, that's my relatives that told me that. That says it all.
And apparence speaking, because hair is all about apparence at the end, i can assure you that a firm and youngfull face make ALSO the difference in term of apparence.
But for doing this for a long time ( MARCH 2003 ) , i just can say that it really a pain in the as to do that. Not every day a pain in the ass, sometimes a pleasure, an habit. But, it's always difficult to do it on busy days, or days with people. MAke it in toilets , reading the news paper...but it sometimes difficult for the concentration to do many things together. sort of workout of your brain, and i'm sure brian is gonna love it that way, aren't you brian ? ;-)
;-) ;-) ;;;;;-)
;-) yeahh !!! i can do that now !! blink my eeeeeeyes ! thank you so much CausticS !!!!
;-)
europe- Posts: 280
Join date: 2008-10-16 -
Re: Sagging Skin
jdp710 on Sat Jun 13, 2009 6:55 am
I thought this was an interesting quote
"The half-life of hyaluronic acid in the cartilage is 2-3 weeks. But the half-life of hyaluronic acid in the skin is less than 1 day! Hyaluronic acid is present in both the dermis and the epidermis. 50% of the body’s naturally produced hyaluronic acid that is found in the epidermis is metabolized and excreted in less than 24 hours."
http://www.qfhaitao.com/cgi/search-en.cgi?f=product_en1+product_en_1_+company_en_1_+contact_en&id=591928&t=product_en_1_
"The half-life of hyaluronic acid in the cartilage is 2-3 weeks. But the half-life of hyaluronic acid in the skin is less than 1 day! Hyaluronic acid is present in both the dermis and the epidermis. 50% of the body’s naturally produced hyaluronic acid that is found in the epidermis is metabolized and excreted in less than 24 hours."
http://www.qfhaitao.com/cgi/search-en.cgi?f=product_en1+product_en_1_+company_en_1_+contact_en&id=591928&t=product_en_1_
jdp710- Posts: 471
Join date: 2008-11-28 -
Re: Sagging Skin
Socceroo on Sun Jun 14, 2009 5:01 am
I would also consider using emu oil as an internal supplement, and also rub some emu oil into the affected areas of the skin. I use emu oil for burns, cuts and scratches and it helps heal the skin in no time at all. May prove beneficial for wrinkles or sagging skin.
Socceroo- Posts: 55
Join date: 2008-07-13 -
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