OverMachoGrande
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IGF-1/Milk/Estrogen
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OverMachoGrande
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Insulin controls energy metabolism and increases the activity of IGF-1by increasing its synthesis and by decreasing binding proteins, such as IGFBP-1. Both Insulin and IGF-1 stimulated anabolic processes based on the availability of energy and basic substrates, such as amino acids. Insulin and IGF-1 promote cancer by inhibiting apoptosis and by stimulating cell proliferation (Kaaks and Lukanova, 2001; Parr, 1999). In addition, insulin and IGF-1 promote the synthesis of sex hormones and inhibit the synthesis of Sex Hormone Binding Globulin (S.H.B.G.), which regulates the bio-availability of circulating sex hormones to tissues (Kaaks and Lukanova, 2001; Cordain et al 2003). Elevated levels of insulin and IGF-1 are thus ties to increased cancer experienced in the developed world (Giovannucci et al, 2004). Bartke et al (2003) and Parr (1999) have suggested that low levels of insulin may be an effective way of increasing longevity. Their conclusions are based on calorie restricted animals which have much reduced insulin and IGF-1 concentrations compared to normally fed shorter lived animals.
McCarty (2000) suggested that simultaneous intake of animal protein and high-glycemic foods cause sharp raises in insulin that subsequently lead to Syndrome X, which is also associated with insulin resistance which leads to increased hyperinsulinmia, decreased IGFBP-1 and S.H.B.G. production and increased free serum IGF-1 (Hursting et al, 2003).
It should be noted that although protein and high-glycemic foods are often identified as drivers of insulin and IGF-1 levels, Cordain et al (2002) reported that hunter-gather diets were very high in meat intake, but low in high glycemic carbohydrates. Possible explanations for this paradox are the consumption of low-fat animals, high intake of plants and vegetables, and relatively low total calorie intake in comparison to a high-energy expenditure. In addition high levels of monounsaturated and polyunsaturated fat and a higher omega-3/omega-6 ratio, antioxidants, fiber, vitamins and phytochemicals with low salt intake was favorable for cardio vascular disease.
S.H.B.G. is an important regulator of plasma sex hormones and a sensitive marker of insulin resistance (gates et al, 1996). Low S.H.B.G. levels are tied to increased risk of type 2 diabetes, cancer, cardio vascular disease and mortality (Gates et al, 1996). Higher insulin levels reduce serum levels of S.H.B.G. (Lonning et al, 1995; Gates et al, 1996; Chen et al, 1990; Cordain et al, 2003), which as mentioned before are related to protein and high-glycemic carbs. Food types affect levels of S.H.B.G.; e.g., wheat lowers S.H.B.G. while vegetables appear to raise it. However, total food intake is negatively related to S.H.B.G. when it increases weight and B.M.I. because weight and B.M.I. are independently and negatively correlated with S.H.B.G.
The level of IGFBP-1 controls the bioavailability of IGF-1. Wolk et al (2004) found low levels of IGFBP-1 correlate with increased insulin resistance, obesity and cardio vascular disease. They also found that the only significant positive association between IGFBP-1 and diet was attained when carb intake was increased. They also reported that a study of women vegans had 20-40% higher IGFBP-1 and IGFBP-2 levels compared to women on both vegetarian and meat diets.
Another Study (Giovannucci et al, 2004), found insulin secretion positively correlated with greater intakes of meat, dairy, refind carbs, saturated and trans fat and lower intakes of whole grain products and fiber. Since IGFBP-1 and insulin are inversely related, their findings indicate that reducing the consumption of animals; dairy, and sugar can increase IGFBP-1.
McCarty (2000) suggested that simultaneous intake of animal protein and high-glycemic foods cause sharp raises in insulin that subsequently lead to Syndrome X, which is also associated with insulin resistance which leads to increased hyperinsulinmia, decreased IGFBP-1 and S.H.B.G. production and increased free serum IGF-1 (Hursting et al, 2003).
It should be noted that although protein and high-glycemic foods are often identified as drivers of insulin and IGF-1 levels, Cordain et al (2002) reported that hunter-gather diets were very high in meat intake, but low in high glycemic carbohydrates. Possible explanations for this paradox are the consumption of low-fat animals, high intake of plants and vegetables, and relatively low total calorie intake in comparison to a high-energy expenditure. In addition high levels of monounsaturated and polyunsaturated fat and a higher omega-3/omega-6 ratio, antioxidants, fiber, vitamins and phytochemicals with low salt intake was favorable for cardio vascular disease.
S.H.B.G. is an important regulator of plasma sex hormones and a sensitive marker of insulin resistance (gates et al, 1996). Low S.H.B.G. levels are tied to increased risk of type 2 diabetes, cancer, cardio vascular disease and mortality (Gates et al, 1996). Higher insulin levels reduce serum levels of S.H.B.G. (Lonning et al, 1995; Gates et al, 1996; Chen et al, 1990; Cordain et al, 2003), which as mentioned before are related to protein and high-glycemic carbs. Food types affect levels of S.H.B.G.; e.g., wheat lowers S.H.B.G. while vegetables appear to raise it. However, total food intake is negatively related to S.H.B.G. when it increases weight and B.M.I. because weight and B.M.I. are independently and negatively correlated with S.H.B.G.
The level of IGFBP-1 controls the bioavailability of IGF-1. Wolk et al (2004) found low levels of IGFBP-1 correlate with increased insulin resistance, obesity and cardio vascular disease. They also found that the only significant positive association between IGFBP-1 and diet was attained when carb intake was increased. They also reported that a study of women vegans had 20-40% higher IGFBP-1 and IGFBP-2 levels compared to women on both vegetarian and meat diets.
Another Study (Giovannucci et al, 2004), found insulin secretion positively correlated with greater intakes of meat, dairy, refind carbs, saturated and trans fat and lower intakes of whole grain products and fiber. Since IGFBP-1 and insulin are inversely related, their findings indicate that reducing the consumption of animals; dairy, and sugar can increase IGFBP-1.
Hairlossdep
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mykal_P said:
This is a great question and I'm interested in misterE's reply to that. Males who go female take big amounts of estrogen and yet their hair usually improves!
HairDont
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This is not always true mykel_P
This was taken from a Transsexual forum:
i'll just ignore your first question since i think it's pretty obvious. estrogen injections are usually prescribed to women to combat menopausal symptoms (hot flashes, etc.) because of low estrogen levels.
when estrogen levels are already low and estrogen is injected, these symptoms can occur:
* breast pain or tenderness
* upset stomach
* vomiting
* weight gain or loss
* dizziness
* nervousness
* depression
* irritability
* changes in sexual desire
* hair loss
* unwanted hair growth
* spotty darkening of the skin on the face
* difficulty wearing contact lenses
* leg cramps
* swelling, redness, burning, itching, or irritation of the vagina
* vaginal discharge
if there is too much estrogen in a woman's system (or anyone's system, i suppose) these more serious symptoms can occur:
* bulging eyes
* pain, swelling, or tenderness in the stomach
* loss of appetite
* weakness
* yellowing of the skin or eyes
* joint pain
* movements that are difficult to control
* rash or blisters
* hives
* itching
* swelling of the eyes, face, tongue, throat, hands, arms, feet, ankles, or lower legs
* hoarseness
* difficulty breathing or swallowing
Estrogen may increase your risk of developing cancer of the ovaries or gallbladder disease that may need to be treated with surgery.
bottom line: don't mess around with estrogen. talk to your doctor before using it, even if you only want it for aesthetic reasons (as in transgendered individuals).
Source(s):
http://www.nlm.nih.gov/medlineplus/drugi…
*****************************************************
So you see mykel_P, Incresed estrogen is a factor in hair loss.
This was taken from a Transsexual forum:
i'll just ignore your first question since i think it's pretty obvious. estrogen injections are usually prescribed to women to combat menopausal symptoms (hot flashes, etc.) because of low estrogen levels.
when estrogen levels are already low and estrogen is injected, these symptoms can occur:
* breast pain or tenderness
* upset stomach
* vomiting
* weight gain or loss
* dizziness
* nervousness
* depression
* irritability
* changes in sexual desire
* hair loss
* unwanted hair growth
* spotty darkening of the skin on the face
* difficulty wearing contact lenses
* leg cramps
* swelling, redness, burning, itching, or irritation of the vagina
* vaginal discharge
if there is too much estrogen in a woman's system (or anyone's system, i suppose) these more serious symptoms can occur:
* bulging eyes
* pain, swelling, or tenderness in the stomach
* loss of appetite
* weakness
* yellowing of the skin or eyes
* joint pain
* movements that are difficult to control
* rash or blisters
* hives
* itching
* swelling of the eyes, face, tongue, throat, hands, arms, feet, ankles, or lower legs
* hoarseness
* difficulty breathing or swallowing
Estrogen may increase your risk of developing cancer of the ovaries or gallbladder disease that may need to be treated with surgery.
bottom line: don't mess around with estrogen. talk to your doctor before using it, even if you only want it for aesthetic reasons (as in transgendered individuals).
Source(s):
http://www.nlm.nih.gov/medlineplus/drugi…
*****************************************************
So you see mykel_P, Incresed estrogen is a factor in hair loss.
OverMachoGrande
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Hairlossdep said:
I will explain it the best I can...here is what I make of it. The more estrogenic activity in your body makes you metabolize estrogen into 16-hydroxyestrogen/estrone, instead of the good protective estrogen metabolite called 2-hydroxyestrogen or 2-hydroxyestrone. 2-hydroxyestrogen is known to increase IGFBP-3 (Insulin-like Growth Factor Binding Protein 3). When IGF-1 is not bound to IGFBP-1 or IGFBP-3 it floats free in the blood. IGF-1 that is free is known to inhibit the synthesis of S.H.B.G. The consumption of sugar and red meat makes your body produce large amounts of IGF-1, and like I said...IGF-1 inhibits the production of S.H.B.G. (Sex Hormone Binding Globulin) (Kaaks and Lukanova, 2001; Cordain et al 2003).
I've stressed it before... Dairy increases IGF-1 the most (Giovannucci et al, 2004),! Milk is what you call the "big offender" cheese; butter, ice cream and yogurt directly increase IGF-1 levels the most!!!!!!!!!!!!!!!!!!!!!!
Sugary food like: soda, candy, cakes, deserts, table sugar, and refind grains will make you produce more insulin. McCarty (2000) suggested that simultaneous intake of animal protein and high-glycemic foods cause sharp raises in insulin that subsequently lead to Syndrome X, which is also associated with insulin resistance which leads to increased hyperinsulinmia, decreased IGFBP-1 and S.H.B.G. production and increased free serum IGF-1 (Hursting et al, 2003).... not only does insulin inhibit S.H.B.G. it also increases the synthesis IGF-1 which increases the synthesis of sex hormones and inhibits S.HB.G. (Kaaks and Lukanova, 2001; Parr, 1999)!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Milk's purpose is to promote growth, maturity, and aging. Milk is known to increase IGF-1 levels within the body (and when you think about it, that's milk's purpose...to increase growth!). On top of that, ever since 1993, most cows have been given hormones like rBGH that make them produce more milk and the milk they do produce has higher concentration of IGF-1 levels... Research rBGH!
And like I've stressed before... IGF-1 inhibits S.H.B.G. (Sex Hormone Binding Globulin) production. (Kaaks and Lukanova, 2001; Cordain et al 2003). Understand?
With low levels of Sex Hormone Binding Globulin testosterone is left "free" to be either convert to estradiol, or convert to D.H.T.!
So attack the top of the "chain of command"...IGF-1 and insulin has a direct effect on S.H.B.G., which has a direct effect on the activity of sex hormones like testosterone, D.H.T. and estradiol, and as a “back-up†or a “plan-b†inhibit both aromatase and alpha-5-reductase enzymes with beta-sitosterol!
Hairlossdep
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misterE can you point to any studies where beta sitosterol lowers estrogen ?
OverMachoGrande
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abcdv12 said:
Yes, 375mg is my daily dosage. I take it before my only meal of the day; Supper. I've ben taking beta sitosterol, since febuary of 2009. I have had good side effects off beta sitosterol; increased sex-drive and perfromance and also began developing lean muscle mass.
OverMachoGrande
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...
OverMachoGrande
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Hairlossdep said:
Autors: Young H. Ju, Laura M. Clausen, Kimberly F. Allred, Anthony L. Almada and William G. Helferich
Research Institute: Department of Food Science and Human Nutrition and Department of Animal Sciences, University of Illinois at Urbana-Champaign, Urbana (USA), Department of Physiology, University of Kentucky, Lexington (USA) and IMAGINutrition and MetaResponse Science, Laguna Niguel (USA)
Publication: Journal of Nutrition, 2004, 134:1145-1151
There are many plant sterols but the best known are beta-sitosterol, stigmasterol and campesterol. Plant sterols have many claimed health benefits. Studies show that plant sterols have a weak estrogenic effect and that they act as weak agonist for estrogen receptors. Plant sterols have a structure similar to that of cholesterol. Plant sterols can modulate the immune system and can replace cholesterol in the intestinal micelles, thereby reducing cholesterol absorption. Epidemiological studies also show that consumption of plant sterols reduces the risk of cancer of colon, prostate, ovary, stomach and breast.
The aim of this study was to investigate the estrogenic effects of the plant sterols beta-sitosterol, beta-sitosterol glucoside and Moducare (mixture of beta-sitosterol, beta-sitosterol glucoside). The test was carried out on estrogen dependent (this means that estrogen stimulates cancer growth) human breast cancer cells in vitro and in vivo.
First the effect of the plant sterols was determined in vitro on cancer cells. Only beta-sitosterol and Moducare increased cell growth. In the second test, the cancer cells were implanted in ovariectomized athymic mice and the estrogenic and anti-estrogenic effects of the plant sterols were determined. Dietary beta-sitosterol, beta-sitosterol glucoside and Moducare did not influence tumor growth, but they markedly reduced estradiol induced tumor growth and also reduced serum estradiol levels. The expression of the antiapoptotic marker B-cell lymphoma/leukaemia in tumours was downregulated.
The researchers concluded that beta-sitosterol and Moducare stimulated cancer cells in vitro and that dietary beta-sitosterol and Moducare protected against estrogen stimulated tumor growth. These findings suggest that beta-sitosterol could have potential benefits for women with a risk for estrogen-dependent breast cancer. However more studies are required to investigate the short and long term effects of plant sterols, their interactions with other drugs and their possible use as dietary supplements.
OverMachoGrande
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legion00 said:
I practice calorie restriction (one of the best ways to reduce IGF-1). I let my body detoxify and burn fat during the day, and eat at night while I drink red wine to clean out my veins.
Thickandthin
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misterE said:
WHAT!!!
And you believe that to be healthy?
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Despite the hysterical rantings of certain indivduals who are convinced that IGF-1 is bad for hair, here's a study by a well-known hairloss researcher who says that IGF-1 is an important hormone for hair growth (see the excerpt from this study, which I include below after the abstract):
Eur J Dermatol. 2001 Jul-Aug;11(4):315-20. "Do androgens influence hair growth by altering the paracrine factors secreted by dermal papilla cells?"
Randall VA, Hibberts NA, Thornton MJ, Merrick AE, Hamada K, Kato S, Jenner TJ, de Oliveira I, Messenger AG.
Department of Biomedical Sciences, University of Bradford, Bradford, BD7 1DP, UK.
"Androgens regulate many aspects of human hair growth in both sexes. After puberty they transform tiny vellus follicles in many areas, e.g. the face, to terminal ones producing long, thick, pigmented hairs. In genetically predisposed individuals, androgens also cause the reverse transformation of terminal scalp follicles into vellus ones, causing balding. In the current hypothesis for androgen action, androgens control most follicular cells indirectly acting via the mesenchyme-derived dermal papilla which regulates many aspects of follicular activity. In this model androgens binding to androgen receptors in dermal papilla cells alter their production of regulatory molecules which influence other follicular components; these molecules may be soluble paracrine factors and/or extracellular matrix proteins. This hypothesis is supported by immunohistochemical localisation of androgen receptors in dermal papilla cell nuclei and the demonstrations that androgen receptor content and testosterone metabolism patterns of cultured dermal papilla cells from various body sites reflect hair growth in androgen-insensitivity syndromes. The next question is whether androgens alter the paracrine factors secreted by dermal papilla cells. Cultured dermal papilla cells do release soluble, proteinaceous factors into their media which stimulate the growth of keratinocytes and other dermal papilla cells. This mitogenic potential can cross species from humans to rodents. Importantly, testosterone in vitro stimulates the mitogenic potential of beard cells, but in contrast inhibits production by balding scalp cells reflecting their in vivo androgenic responses. Since androgens in vitro do alter the secretion of paracrine factors the current focus lies in identifying specific factors produced, e.g. IGF-I and stem cell factor (SCF), using ELISA and RT-PCR, and comparing their expression in cells from follicles with varying responses to androgens in vivo or under androgen stimulation in vitro. This should lead to greater understanding of androgen action and enable the development of better treatment for androgen-potentiated disorders."
The following excerpt is from page 318 of this study: "A range of growth factors and cytokines have been implicated in hair growth....One of the most studied of these is insulin like growth factor-1, IGF-1, a potent mitogen which plays an important role in maintaining angen in cultured human scalp follicles in vitro and which causes abnormal patterns of growth and differentiation of hair follicles when its effects are blocked in the IGF-1 receptor deficient knockout mouse. Itami and colleagues have identified the expression of mRNA for IGF-1 in beard dermal papilla cells and confirmed its importance by blocking the mitogenic effect of dermal papilla cells on co-cultured outer root sheath cells with an antibody to IGF-1."
Eur J Dermatol. 2001 Jul-Aug;11(4):315-20. "Do androgens influence hair growth by altering the paracrine factors secreted by dermal papilla cells?"
Randall VA, Hibberts NA, Thornton MJ, Merrick AE, Hamada K, Kato S, Jenner TJ, de Oliveira I, Messenger AG.
Department of Biomedical Sciences, University of Bradford, Bradford, BD7 1DP, UK.
"Androgens regulate many aspects of human hair growth in both sexes. After puberty they transform tiny vellus follicles in many areas, e.g. the face, to terminal ones producing long, thick, pigmented hairs. In genetically predisposed individuals, androgens also cause the reverse transformation of terminal scalp follicles into vellus ones, causing balding. In the current hypothesis for androgen action, androgens control most follicular cells indirectly acting via the mesenchyme-derived dermal papilla which regulates many aspects of follicular activity. In this model androgens binding to androgen receptors in dermal papilla cells alter their production of regulatory molecules which influence other follicular components; these molecules may be soluble paracrine factors and/or extracellular matrix proteins. This hypothesis is supported by immunohistochemical localisation of androgen receptors in dermal papilla cell nuclei and the demonstrations that androgen receptor content and testosterone metabolism patterns of cultured dermal papilla cells from various body sites reflect hair growth in androgen-insensitivity syndromes. The next question is whether androgens alter the paracrine factors secreted by dermal papilla cells. Cultured dermal papilla cells do release soluble, proteinaceous factors into their media which stimulate the growth of keratinocytes and other dermal papilla cells. This mitogenic potential can cross species from humans to rodents. Importantly, testosterone in vitro stimulates the mitogenic potential of beard cells, but in contrast inhibits production by balding scalp cells reflecting their in vivo androgenic responses. Since androgens in vitro do alter the secretion of paracrine factors the current focus lies in identifying specific factors produced, e.g. IGF-I and stem cell factor (SCF), using ELISA and RT-PCR, and comparing their expression in cells from follicles with varying responses to androgens in vivo or under androgen stimulation in vitro. This should lead to greater understanding of androgen action and enable the development of better treatment for androgen-potentiated disorders."
The following excerpt is from page 318 of this study: "A range of growth factors and cytokines have been implicated in hair growth....One of the most studied of these is insulin like growth factor-1, IGF-1, a potent mitogen which plays an important role in maintaining angen in cultured human scalp follicles in vitro and which causes abnormal patterns of growth and differentiation of hair follicles when its effects are blocked in the IGF-1 receptor deficient knockout mouse. Itami and colleagues have identified the expression of mRNA for IGF-1 in beard dermal papilla cells and confirmed its importance by blocking the mitogenic effect of dermal papilla cells on co-cultured outer root sheath cells with an antibody to IGF-1."
OverMachoGrande
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Diet, Exercise & Prostate Cancer.
Authors: Barnard, R. James and Aronson, William J. (University of California, Los Angeles)
Abstract:
It has been suggested that a large part of the international variation in prostate cancer mortality might be explained by diet and exercise. Countries with a very low mortality generally consume a low-fat diet and are physically active compared to countries with a high prostate cancer mortality. When men from countries with a high prostate cancer mortality are placed on a low-fat diet and/or exercise program serum levels of insulin, free testosterone, estradiol and IGF-1 are reduced while SHBG and IGFBP-1 are elevated. These in vivo serum changes directly impact on androgen-dependent prostate cancer cell lines in vitro to reduce cell growth and induce apoptosis. The reduction in serum IGF-1 and increase in IGFBP-1 with diet and exercise appear to be the most significant as they lead to an increase in tumor cell p53 protein and its down-stream effector p21 which are responsible for the reduction in cell growth and induced apoptosis. Preliminary results from a clinical study with men on “Watchful Waiting†indicate that the observed in vitro effects of diet and exercise on prostate cancer cell growth also occur in vivo.
Authors: Barnard, R. James and Aronson, William J. (University of California, Los Angeles)
Abstract:
It has been suggested that a large part of the international variation in prostate cancer mortality might be explained by diet and exercise. Countries with a very low mortality generally consume a low-fat diet and are physically active compared to countries with a high prostate cancer mortality. When men from countries with a high prostate cancer mortality are placed on a low-fat diet and/or exercise program serum levels of insulin, free testosterone, estradiol and IGF-1 are reduced while SHBG and IGFBP-1 are elevated. These in vivo serum changes directly impact on androgen-dependent prostate cancer cell lines in vitro to reduce cell growth and induce apoptosis. The reduction in serum IGF-1 and increase in IGFBP-1 with diet and exercise appear to be the most significant as they lead to an increase in tumor cell p53 protein and its down-stream effector p21 which are responsible for the reduction in cell growth and induced apoptosis. Preliminary results from a clinical study with men on “Watchful Waiting†indicate that the observed in vitro effects of diet and exercise on prostate cancer cell growth also occur in vivo.