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I've started another post regarding B5 Megadosing which has always been my primary successful way of controlling my oily skin. In an effort to reduce my reliance on B5 megadosing owing to the side effects and the unknown long term affects I've been trying to find an alternative solution that I can use to keep my oily skin under control.
One such attempt has been Green Tea and Soy products after reading one of the informative threads on this board. I also found other details indicating that high Green Tea consumption could help promote bacteria capable of metabolising the Soy Isoflavone Daidzein into Equol.
I've tried taking both these in extract and in high amounts using food forms to see if they could offer me a way out of using B5 for the rest of my life. I've also tried using a mixture of both whole foods and supplements.
I'd just finished on B5 and as the effects started to wear off as my oily skin was returning. I started drinking green tea heavily throughout the day and used supplements during times when I wasn't necessarily able to drink green tea for a period of time.
The idea behind green tea was it could act as an androgen receptor blocker, help control my blood sugar levels, act as a 5ar Type 1 blocker and also raise SHBG levels.
In addition to the Green Tea I also started eating soy products and using Soy milk. Again where it wasn't always possible to consume these products, e.g. if I was out or stopping away, I'd use a supplement to provide me with Soy Isoflavones.
The theory behind the Soy was if I was one of the lucky ones to metabolise Daidzein into Equol it would block DHT in my body which would help with my B5 accelerated MPB and also if my acne was caused by DHT. I was hopeful, especially after reading Green Tea may help with this metabolism.
I'd also read that Soy, being a plant estrogen could help raise SHBG levels to bind more Free Testosterone so overall a win win situation.
Initially my bodies reaction from Green Tea and Soy seemed quite promising. My skin stayed fairly dry and I was feeling positive and healthier than when I was megadosing with B5, but all of a sudden the oiliness returned and my Oily Skin / Acne / Baldness fighting combination seemed to lose it's effectiveness.
Now I'm not sure whether this was B5 finally wearing off from before or whether something genuinely did reduce the effectiveness of my Green Tea / Soy combo. Assuming it wasn't the B5 wearing off causing my Acne to return the only theory I could come up with with was that it has been suggested that both Green Tea and Soy can be responsible for inducing Hypothyroidism which would negatively have impacted my SHBG levels resulting in higher levels of Free Testosterone.
The confusing thing really is whether it's DHT or Testosterone that is responsible for Oily Skin. At the moment I'd have to say it's Free Testosterone rather than DHT but that's just an educated guess.
I've ordered some Thyroid supplements (NOW Thyroid Energy Capsules) containing Iodine to try and help prevent Green Tea and Soy from having a negative impact on my Thyroid. I'm hoping that by ensuring my Thyroid is working as expected using the Thyroid supplements, that the Green Tea and Soy combination will then help raise my SHBG levels which in turn will reduce my oily skin and acne and as an added bonus if I manager to product any Equol then it will help me stop losing my hair!
Until they arrive though I've resorted to megadosing with B5 again as it's the only thing that's ever worked for me.
Cheers
Craig
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Green Tea & Soy
Started by Craigy, Jun 03 2006 11:55 AM
6 replies to this topic
#1
Craigy
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Posted 03 June 2006 - 11:55 AM
#2
Legend
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Posted 03 June 2006 - 12:27 PM
Well soy is estrogenic...which is exactly why I stay away from it. Testosterone gives you low body fat%, energy, more muscles, etc.
See what FDA scientists think about it.
http://www.t-nation.com/readTopic.do?id=461709&pageNo=0
Scientists' Letter
DEPARTMENT OF HEALTH and HUMAN SERVICES Public Health Service Food and Drug Administration National Center For Toxicological Research Jefferson, Ark. 72079-9502 Daniel M. Sheehan, Ph.D. Director, Estrogen Base Program Division of Genetic and Reproductive Toxicology and Daniel R. Doerge, Ph.D. Division of Biochemical Toxicology February 18, 1999 Dockets Management Branch (HFA-305) Food and Drug Administration Rockville, MD 20852
To whom it may concern,
We are writing in reference to Docket # 98P-0683; "Food Labeling: Health Claims; Soy Protein and Coronary Heart Disease." We oppose this health claim because there is abundant evidence that some of the isoflavones found in soy, including genistein and equol, a metabolize of daidzen, demonstrate toxicity in estrogen sensitive tissues and in the thyroid. This is true for a number of species, including humans.
Additionally, the adverse effects in humans occur in several tissues and, apparently, by several distinct mechanisms. Genistein is clearly estrogenic; it possesses the chemical structural features necessary for estrogenic activity (; Sheehan and Medlock, 1995; Tong, et al, 1997; Miksicek, 1998) and induces estrogenic responses in developing and adult animals and in adult humans.
In rodents, equol is estrogenic and acts as an estrogenic endocrine disruptor during development (Medlock, et al, 1995a,b). Faber and Hughes (1993) showed alterations in LH regulation following this developmental treatment with genistein. Thus, during pregnancy in humans, isoflavones per se could be a risk factor for abnormal brain and reproductive tract development.
Furthermore, pregnant Rhesus monkeys fed genistein had serum estradiol levels 50- 100 percent higher than the controls in three different areas of the maternal circulation (Harrison, et al, 1998). Given that the Rhesus monkey is the best experimental model for humans, and that a women's own estrogens are a very significant risk factor for breast cancer, it is unreasonable to approve the health claim until complete safety studies of soy protein are conducted.
Of equally grave concern is the finding that the fetuses of genistein fed monkeys had a 70 percent higher serum estradiol level than did the controls (Harrison, et al, 1998). Development is recognized as the most sensitive life stage for estrogen toxicity because of the indisputable evidence of a very wide variety of frank malformations and serious functional deficits in experimental animals and humans.
In the human population, DES exposure stands as a prime example of adverse estrogenic effects during development. About 50 percent of the female offspring and a smaller fraction of male offspring displayed one or more malformations in the reproductive tract, as well as a lower prevalence (about 1 in a thousand) of malignancies.
In adults, genistein could be a risk factor for a number of estrogen-associated diseases. Even without the evidence of elevated serum estradiol levels in Rhesus fetuses, potency and dose differences between DES and the soy isoflavones do not provide any assurance that the soy protein isoflavones per se will be without adverse effects.
First, calculations, based on the literature, show that doses of soy protein isoflavones used in clinical trials which demonstrated estrogenic effects were as potent as low but active doses of DES in Rhesus monkeys (Sheehan, unpublished data). Second, we have recently shown that estradiol shows no threshold in an extremely large dose-response experiment (Sheehan, et al, 1999), and we subsequently have found 31 dose-response curves for hormone-mimicking chemicals that also fail to show a threshold (Sheehan, 1998a).
Our conclusions are that no dose is without risk; the extent of risk is simply a function of dose. These two features support and extend the conclusion that it is inappropriate to allow health claims for soy protein isolate. Additionally, isoflavones are inhibitors of the thyroid peroxidase which makes T3 and T4. Inhibition can be expected to generate thyroid abnormalities, including goiter and autoimmune thyroiditis. There exists a significant body of animal data that demonstrates goitrogenic and even carcinogenic effects of soy products (cf., Kimura et al., 1976). Moreover, there are significant reports of goitrogenic effects from soy consumption in human infants (cf., Van Wyk et al., 1959; Hydovitz, 1960; Shepard et al., 1960; Pinchers et al., 1965; Chorazy et al., 1995) and adults (McCarrison, 1933; Ishizuki, et al., 1991).
Recently, we have identified genistein and daidzein as the goitrogenic isoflavonoid components of soy and defined the mechanisms for inhibition of thyroid peroxidase (TPO)- catalyzed thyroid hormone synthesis in vitro (Divi et al., 1997; Divi et al., 1996). The observed suicide inactivation of TPO by isoflavones, through covalent binding to TPO, raises the possibility of neoantigen formation and because anti-TPO is the principal autoantibody present in auto immune thyroid disease. This hypothetical mechanism is consistent with the reports of Fort et al. (1986, 1990) of a doubling of risk for autoimmune thyroiditis in children who had received soy formulas as infants compared to infants receiving other forms of milk.
The serum levels of isoflavones in infants receiving soy formula that are about five times higher than in women receiving soy supplements who show menstrual cycle disturbances, including an increased estradiol level in the follicular phase (Setchell, et al, 1997). Assuming a dose-dependent risk, it is unreasonable to assert that the infant findings are irrelevant to adults who may consume smaller amounts of isoflavones.
Additionally, while there is an unambiguous biological effect on menstrual cycle length (Cassidy, et al, 1994), it is unclear whether the soy effects are beneficial or adverse. Furthermore, we need to be concerned about transplacental passage of isoflavones as the DES case has shown us that estrogens can pass the placenta. No such studies have been conducted with genistein in humans or primates. As all estrogens which have been studied carefully in human populations are two-edged swords in humans (Sheehan and Medlock, 1995; Sheehan, 1997), with both beneficial and adverse effects resulting from the administration of the same estrogen, it is likely that the same characteristic is shared by the isoflavones. The animal data is also consistent with adverse effects in humans.
Finally, initial data fi-om a robust (7,000 men) long-term (30+ years) prospective epidemiological study in Hawaii showed that Alzheimer's disease prevalence in Hawaiian men was similar to European-ancestry Americans and to Japanese (White, et al, 1996a). In contrast, vascular dementia prevalence is similar in Hawaii and Japan and both are higher than in European-ancestry Americans.
This suggests that common ancestry or environmental factors in Japan and Hawaii are responsible for the higher prevalence of vascular dementia in these locations. Subsequently, this same group showed a significant dose-dependent risk (up to 2.4 fold) for development of vascular dementia and brain atrophy from consumption of tofu, a soy product rich in isoflavones (White, et al, 1996b).
This finding is consistent with the environmental causation suggested from the earlier analysis, and provides evidence that soy (tofu) phytoestrogens causes vascular dementia. Given that estrogens are important for maintenance of brain function in women; that the male brain contains aromatase, the enzyme that converts testosterone to estradiol; and that isoflavones inhibit this enzymatic activity (Irvine, 1998), there is a mechanistic basis for the human findings. Given the great difficulty in discerning the relationship between exposures and long latency adverse effects in the human population (Sheehan, 1998b), and the potential mechanistic explanation for the epidemiological findings, this is an important study.
It is one of the more robust, well-designed prospective epidemiological studies generally available. We rarely have such power in human studies, as well as a potential mechanism, and thus the results should be interpreted in this context. Does the Asian experience provide us with reassurance that the isoflavones are safe? A review of several examples lead to the conclusion, รข€” "Given the parallels with herbal medicines with respect to attitudes, monitoring deficiencies, and the general difficulty of detecting toxicities with long Iatencies, I am unconvinced that the long history of apparent safe use of soy products can provide confidence that they are indeed without risk." (Sheehan, 1998b).
It should also be noted that the claim on p. 62978 that soy protein foods are GRAS is in conflict with the recent return by CFSAN to Archer Daniels Midland of a petition for GRAS status for soy protein because of deficiencies in reporting adverse effects in the petition. Thus GRAS status has not been granted. Linda Kahl can provide you with details. It would seem appropriate for FDA to speak with a single voice regarding soy protein isolate. Taken together, the findings presented here are self-consistent and demonstrate that genistein and other isoflavones can have adverse effects in a variety of species, including humans. Animal studies are the front line in evaluating toxicity, as they predict, with good accuracy, adverse effects in humans.
For the isoflavones, we additionally have evidence of two types of adverse effects in humans, despite the very few studies that have addressed this subject. While isoflavones may have beneficial effects at some ages or circumstances, this cannot be assumed to be true at all ages. Isoflavones are like other estrogens in that they are two-edged swords, conferring both benefits and risk (Sheehan and Medlock, 1995; Sheehan, 1997).
The health labeling of soy protein isolate for foods needs to considered just as would the addition of any estrogen or goitrogen to foods, which are bad ideas. Estrogenic and goitrogenic drugs are regulated by FDA, and are taken under a physician's care. Patients are informed of risks, and are monitored by their physicians for evidence of toxicity. There are no similar safeguards in place for foods, so the public will be put at potential risk from soy isoflavones in soy protein isolate without adequate warning and information.
Finally, NCTR is currently conducting a long-term multigeneration study of genistein administered in feed to rats. The analysis of the dose range-finding studies are nearly complete now. As preliminary data, which is still confidential, may be relevant to your decision, I suggest you contact Dr. Barry Delclos at the address on the letterhead, or email him.
Sincerely,
Daniel M. Sheehan
Daniel R. Doerge
Not good for women either.
http://www.t-nation.com/findArticle.do?article=302poison2
See what FDA scientists think about it.
http://www.t-nation.com/readTopic.do?id=461709&pageNo=0
QUOTE
Scientists' Letter
DEPARTMENT OF HEALTH and HUMAN SERVICES Public Health Service Food and Drug Administration National Center For Toxicological Research Jefferson, Ark. 72079-9502 Daniel M. Sheehan, Ph.D. Director, Estrogen Base Program Division of Genetic and Reproductive Toxicology and Daniel R. Doerge, Ph.D. Division of Biochemical Toxicology February 18, 1999 Dockets Management Branch (HFA-305) Food and Drug Administration Rockville, MD 20852
To whom it may concern,
We are writing in reference to Docket # 98P-0683; "Food Labeling: Health Claims; Soy Protein and Coronary Heart Disease." We oppose this health claim because there is abundant evidence that some of the isoflavones found in soy, including genistein and equol, a metabolize of daidzen, demonstrate toxicity in estrogen sensitive tissues and in the thyroid. This is true for a number of species, including humans.
Additionally, the adverse effects in humans occur in several tissues and, apparently, by several distinct mechanisms. Genistein is clearly estrogenic; it possesses the chemical structural features necessary for estrogenic activity (; Sheehan and Medlock, 1995; Tong, et al, 1997; Miksicek, 1998) and induces estrogenic responses in developing and adult animals and in adult humans.
In rodents, equol is estrogenic and acts as an estrogenic endocrine disruptor during development (Medlock, et al, 1995a,b). Faber and Hughes (1993) showed alterations in LH regulation following this developmental treatment with genistein. Thus, during pregnancy in humans, isoflavones per se could be a risk factor for abnormal brain and reproductive tract development.
Furthermore, pregnant Rhesus monkeys fed genistein had serum estradiol levels 50- 100 percent higher than the controls in three different areas of the maternal circulation (Harrison, et al, 1998). Given that the Rhesus monkey is the best experimental model for humans, and that a women's own estrogens are a very significant risk factor for breast cancer, it is unreasonable to approve the health claim until complete safety studies of soy protein are conducted.
Of equally grave concern is the finding that the fetuses of genistein fed monkeys had a 70 percent higher serum estradiol level than did the controls (Harrison, et al, 1998). Development is recognized as the most sensitive life stage for estrogen toxicity because of the indisputable evidence of a very wide variety of frank malformations and serious functional deficits in experimental animals and humans.
In the human population, DES exposure stands as a prime example of adverse estrogenic effects during development. About 50 percent of the female offspring and a smaller fraction of male offspring displayed one or more malformations in the reproductive tract, as well as a lower prevalence (about 1 in a thousand) of malignancies.
In adults, genistein could be a risk factor for a number of estrogen-associated diseases. Even without the evidence of elevated serum estradiol levels in Rhesus fetuses, potency and dose differences between DES and the soy isoflavones do not provide any assurance that the soy protein isoflavones per se will be without adverse effects.
First, calculations, based on the literature, show that doses of soy protein isoflavones used in clinical trials which demonstrated estrogenic effects were as potent as low but active doses of DES in Rhesus monkeys (Sheehan, unpublished data). Second, we have recently shown that estradiol shows no threshold in an extremely large dose-response experiment (Sheehan, et al, 1999), and we subsequently have found 31 dose-response curves for hormone-mimicking chemicals that also fail to show a threshold (Sheehan, 1998a).
Our conclusions are that no dose is without risk; the extent of risk is simply a function of dose. These two features support and extend the conclusion that it is inappropriate to allow health claims for soy protein isolate. Additionally, isoflavones are inhibitors of the thyroid peroxidase which makes T3 and T4. Inhibition can be expected to generate thyroid abnormalities, including goiter and autoimmune thyroiditis. There exists a significant body of animal data that demonstrates goitrogenic and even carcinogenic effects of soy products (cf., Kimura et al., 1976). Moreover, there are significant reports of goitrogenic effects from soy consumption in human infants (cf., Van Wyk et al., 1959; Hydovitz, 1960; Shepard et al., 1960; Pinchers et al., 1965; Chorazy et al., 1995) and adults (McCarrison, 1933; Ishizuki, et al., 1991).
Recently, we have identified genistein and daidzein as the goitrogenic isoflavonoid components of soy and defined the mechanisms for inhibition of thyroid peroxidase (TPO)- catalyzed thyroid hormone synthesis in vitro (Divi et al., 1997; Divi et al., 1996). The observed suicide inactivation of TPO by isoflavones, through covalent binding to TPO, raises the possibility of neoantigen formation and because anti-TPO is the principal autoantibody present in auto immune thyroid disease. This hypothetical mechanism is consistent with the reports of Fort et al. (1986, 1990) of a doubling of risk for autoimmune thyroiditis in children who had received soy formulas as infants compared to infants receiving other forms of milk.
The serum levels of isoflavones in infants receiving soy formula that are about five times higher than in women receiving soy supplements who show menstrual cycle disturbances, including an increased estradiol level in the follicular phase (Setchell, et al, 1997). Assuming a dose-dependent risk, it is unreasonable to assert that the infant findings are irrelevant to adults who may consume smaller amounts of isoflavones.
Additionally, while there is an unambiguous biological effect on menstrual cycle length (Cassidy, et al, 1994), it is unclear whether the soy effects are beneficial or adverse. Furthermore, we need to be concerned about transplacental passage of isoflavones as the DES case has shown us that estrogens can pass the placenta. No such studies have been conducted with genistein in humans or primates. As all estrogens which have been studied carefully in human populations are two-edged swords in humans (Sheehan and Medlock, 1995; Sheehan, 1997), with both beneficial and adverse effects resulting from the administration of the same estrogen, it is likely that the same characteristic is shared by the isoflavones. The animal data is also consistent with adverse effects in humans.
Finally, initial data fi-om a robust (7,000 men) long-term (30+ years) prospective epidemiological study in Hawaii showed that Alzheimer's disease prevalence in Hawaiian men was similar to European-ancestry Americans and to Japanese (White, et al, 1996a). In contrast, vascular dementia prevalence is similar in Hawaii and Japan and both are higher than in European-ancestry Americans.
This suggests that common ancestry or environmental factors in Japan and Hawaii are responsible for the higher prevalence of vascular dementia in these locations. Subsequently, this same group showed a significant dose-dependent risk (up to 2.4 fold) for development of vascular dementia and brain atrophy from consumption of tofu, a soy product rich in isoflavones (White, et al, 1996b).
This finding is consistent with the environmental causation suggested from the earlier analysis, and provides evidence that soy (tofu) phytoestrogens causes vascular dementia. Given that estrogens are important for maintenance of brain function in women; that the male brain contains aromatase, the enzyme that converts testosterone to estradiol; and that isoflavones inhibit this enzymatic activity (Irvine, 1998), there is a mechanistic basis for the human findings. Given the great difficulty in discerning the relationship between exposures and long latency adverse effects in the human population (Sheehan, 1998b), and the potential mechanistic explanation for the epidemiological findings, this is an important study.
It is one of the more robust, well-designed prospective epidemiological studies generally available. We rarely have such power in human studies, as well as a potential mechanism, and thus the results should be interpreted in this context. Does the Asian experience provide us with reassurance that the isoflavones are safe? A review of several examples lead to the conclusion, รข€” "Given the parallels with herbal medicines with respect to attitudes, monitoring deficiencies, and the general difficulty of detecting toxicities with long Iatencies, I am unconvinced that the long history of apparent safe use of soy products can provide confidence that they are indeed without risk." (Sheehan, 1998b).
It should also be noted that the claim on p. 62978 that soy protein foods are GRAS is in conflict with the recent return by CFSAN to Archer Daniels Midland of a petition for GRAS status for soy protein because of deficiencies in reporting adverse effects in the petition. Thus GRAS status has not been granted. Linda Kahl can provide you with details. It would seem appropriate for FDA to speak with a single voice regarding soy protein isolate. Taken together, the findings presented here are self-consistent and demonstrate that genistein and other isoflavones can have adverse effects in a variety of species, including humans. Animal studies are the front line in evaluating toxicity, as they predict, with good accuracy, adverse effects in humans.
For the isoflavones, we additionally have evidence of two types of adverse effects in humans, despite the very few studies that have addressed this subject. While isoflavones may have beneficial effects at some ages or circumstances, this cannot be assumed to be true at all ages. Isoflavones are like other estrogens in that they are two-edged swords, conferring both benefits and risk (Sheehan and Medlock, 1995; Sheehan, 1997).
The health labeling of soy protein isolate for foods needs to considered just as would the addition of any estrogen or goitrogen to foods, which are bad ideas. Estrogenic and goitrogenic drugs are regulated by FDA, and are taken under a physician's care. Patients are informed of risks, and are monitored by their physicians for evidence of toxicity. There are no similar safeguards in place for foods, so the public will be put at potential risk from soy isoflavones in soy protein isolate without adequate warning and information.
Finally, NCTR is currently conducting a long-term multigeneration study of genistein administered in feed to rats. The analysis of the dose range-finding studies are nearly complete now. As preliminary data, which is still confidential, may be relevant to your decision, I suggest you contact Dr. Barry Delclos at the address on the letterhead, or email him.
Sincerely,
Daniel M. Sheehan
Daniel R. Doerge
Not good for women either.
http://www.t-nation.com/findArticle.do?article=302poison2
QUOTE
Women who eat a lot of soy are also more likely to have reproductive system problems — heavier menstrual flow, increased cramping, infertility, as well as the loss of sex drive mentioned earlier. There are increasing reports of a painful urinary tract condition known as interstitial cystitis and a painful condition called vulvodynia or vulvardynia. This last refers to pain of the external female genitals — excruciating pain that's often so severe that sex is impossible.
Finally, we’re getting more and more reports of vegan mothers giving birth to sons with hypospadias.
Finally, we’re getting more and more reports of vegan mothers giving birth to sons with hypospadias.
#3
Craigy
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Posted 04 June 2006 - 04:09 AM
QUOTE(Legend @ Jun 3 2006, 07:27 PM) 
Well soy is estrogenic...which is exactly why I stay away from it. Testosterone gives you low body fat%, energy, more muscles, etc.
Testosterone is also responsible, either directly or indirectly, for causing Acne, Oily Skin and Male Pattern Baldness. The idea behind taking Soy was based upon the fact that it's estrogenic as it should cause the body to raise SHBG levels which would bind more Free Testosterone leaving less available to cause Acne and be converted into DHT to cause hair loss.
The green tea and soy seem to increase my skins oiliness if anything, not reduce it so I'm somewhat confused.
Cheers
Craig
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Posted 04 June 2006 - 04:30 AM
i drink lots of green tea each day
3-4 cups
its anti-oxident properties are meant to flush out some of the unwanted toxins inyour body!
3-4 cups
its anti-oxident properties are meant to flush out some of the unwanted toxins inyour body!
#5
Craigy
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Posted 06 June 2006 - 11:49 AM
I feel an overall health benefit when i drink Green Tea, although that might just be the caffeine giving me a bit of an energy boost!
The one thing I don't really see is any change in skin oiliness, and when I add Soy to my diet the oiliness either gets worse or doesn't change.
I find it very difficult to understand what's going on. I'm taking two things that have been said to raise SHBG, yet noticing an increase in Oily Skin and acne, especially when the Soy is added.
I've theorised that it's down to the negative impact on my Thyroid gland which is actually reducing my SHBG levels, but I'm nervous about adding Iodine into my diet to counteract that as that's been known to cause Acne too so I could be making things worse.
To top it off my doctor won't give me a Thyroid blood test (or any other hormonal blood test) as I keep getting pointed in the direction of topicals.
Cheers
Craig
The one thing I don't really see is any change in skin oiliness, and when I add Soy to my diet the oiliness either gets worse or doesn't change.
I find it very difficult to understand what's going on. I'm taking two things that have been said to raise SHBG, yet noticing an increase in Oily Skin and acne, especially when the Soy is added.
I've theorised that it's down to the negative impact on my Thyroid gland which is actually reducing my SHBG levels, but I'm nervous about adding Iodine into my diet to counteract that as that's been known to cause Acne too so I could be making things worse.
To top it off my doctor won't give me a Thyroid blood test (or any other hormonal blood test) as I keep getting pointed in the direction of topicals.
Cheers
Craig
#6
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Posted 06 June 2006 - 08:23 PM
lol I find myself having atleast 6 cups of tea a day.
Is herbal tea, like chamomile just as good as green tea, or is it.... NOT AS GOOD?!?!??!?!?!??!?!!!!!!!!!!!??????????????!!!!!!!!!!!!?!?!?!??!?!??!?!?!!!!!!!!!!!
Is herbal tea, like chamomile just as good as green tea, or is it.... NOT AS GOOD?!?!??!?!?!??!?!!!!!!!!!!!??????????????!!!!!!!!!!!!?!?!?!??!?!??!?!?!!!!!!!!!!!
#7
Craigy
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Posted 14 June 2006 - 12:33 AM
Due to the negative response on the B5 thread I started I thought I'd give Green Tea and Soy another go but am still having no luck, infact I'm sure they make my skin worse and even more oily. I've tried Green Tea and Soy together, and also both on their own for a while.
Green Tea is contains EGCG which is an androgen receptor blocker, it is also a Type I 5ar inhibitor which should mean no DHT in the skin. It also can help with sugar metabolism which has been linked to oily skin in the past. My oily skin seems to get no better, but sometimes can get worse when I drink and/or supplement with Green Tea which I find confusing considering it's suggested benefits.
Soy is another strange one, as a Phytoestrogen it mimics estrogen. This in theory should increase the levels of SHBG in the blood stream, which will bind to Free Testosterone. This should mean reduced oily skin directly caused by Free Testosterone and indirectly by any DHT that is produced. Also if you're own of the lucky ones then you can produce Equol when Soy isoflavones are metabolised which directly binds to DHT. Again though despite this, it seems to make my skin no better and can sometimes make it even more oily!
Anyone got any theories as to why this is the case?
Cheers
Craig
Green Tea is contains EGCG which is an androgen receptor blocker, it is also a Type I 5ar inhibitor which should mean no DHT in the skin. It also can help with sugar metabolism which has been linked to oily skin in the past. My oily skin seems to get no better, but sometimes can get worse when I drink and/or supplement with Green Tea which I find confusing considering it's suggested benefits.
Soy is another strange one, as a Phytoestrogen it mimics estrogen. This in theory should increase the levels of SHBG in the blood stream, which will bind to Free Testosterone. This should mean reduced oily skin directly caused by Free Testosterone and indirectly by any DHT that is produced. Also if you're own of the lucky ones then you can produce Equol when Soy isoflavones are metabolised which directly binds to DHT. Again though despite this, it seems to make my skin no better and can sometimes make it even more oily!
Anyone got any theories as to why this is the case?
Cheers
Craig
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