Watch Your Sugar if you Have Gyno

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  1. Watch Your Sugar if you Have Gyno


    Looks like a definite interaction between IGF-1 levels and breast growth and development. Probably best to take an AI and a SERM with your carbs!

    Biochim Biophys Acta. 2013 Dec;1836(2):345-53. doi: 10.1016/j.bbcan.2013.10.005. Epub 2013 Nov 2.
    Insulin-like growth factor - oestradiol crosstalk and mammary gland tumourigenesis.

    Hawsawi Y1, El-Gendy R, Twelves C, Speirs V, Beattie J.
    Author information
    Abstract
    Development and differentiation of the mammary gland are dependent on the appropriate temporal expression of both systemically acting hormones and locally produced growth factors. A large body of evidence suggests that molecular crosstalk between these hormonal and growth factor axes is crucial for appropriate cell and tissue function. Two of the most important trophic factors involved in this process are the oestrogen (E) and insulin-like growth factor (IGF) molecular axes. The reciprocal crosstalk that exists between these pathways occurs at transcriptional/post-transcriptional and translational/post-translational levels regulate the expression and activity of genes involved in this process. In a clinical context an important consequence of such crosstalk in the mammary gland is the role which it may play in the aetiology, maintenance and development of breast tumours. Although oestradiol (E2) acting through oestrogen receptors α and β (ERα/β) is important for normal mammary gland function it can also provide a mitogenic drive to ER+ breast tumours. Therefore over several years anti-oestrogen therapeutic regimens in the form of selective oestrogen receptor modulators (SERMs - e.g. tamoxifen), aromatase inhibitors (AI e.g. anastrozole) or selective oestrogen receptor down regulators (SERDs - e.g. fulvestrant) have been used in an adjuvant setting to control tumour growth. Although initial response is usually encouraging, large cohorts of patients eventually develop resistance to these treatments leading to tumour recurrence and poor prognosis. There are potentially many routes by which breast cancer (BC) cells could escape anti-oestrogen based therapeutic strategies and one of the most studied is the possible growth factor mediated activation of ER(s). Because of this, growth factor modulation of ER activity has been an intensively studied route of molecular crosstalk in the mammary gland. The insulin-like growth factors (IGF-1 and -2) are amongst the most potent mitogens for mammary epithelial cells and there is accumulating evidence that they interact with the E2 axis to regulate mitogenesis, apoptosis, adhesion, migration and differentiation of mammary epithelial cells. Such interactions are bi-directional and E2 has been shown to regulate the expression and activity of IGF axis genes with the general effect of sensitising breast epithelial cells to the actions of IGFs and insulin. In this short review we discuss the evidence for the involvement of crosstalk between the insulin-like growth factor (IGF) and oestrogen axes in the mammary gland and comment on the relevance of such studies in the aetiology and treatment of BC.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
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  2. Quote Originally Posted by Eric Mar View Post
    Probably best to take an AI and a SERM with your carbs!
    *...awaits multiple threads cropping up asking what doses of exemestane and Clomid to take with refeeds and carb loads*

    Also inb4 sketchy supplement maker sees this and starts including aforementioned drugs in their GDA product.
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  3. Natural AI and SERM lol
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
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  4. Lol. Are you fukking serious?
    Training log:

    http://anabolicminds.com/forum/workout-logs/267913-jswains-training-log.html

  5. Please for the love of god tell me this is a joke...

    In before black tea is the ultimate gyno redux tool
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  6. Don't take ais with prohormones or serms with pct... Take them both with your carbohydrates lol
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  7. Quote Originally Posted by Godstrength View Post
    Don't take ais with prohormones or serms with pct... Take them both with your carbohydrates lol
    Yes, I am serious. Looks like there is interaction between IGF-1 and ERa. lol If you have been following my logic here I am big on nutrient timing. Timing of carbs and estrogen blockers (detoxifiers like I3C would be great too) should help reduce the chance of gyno.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
    http://mindandmuscle.net/articles/pr...nd-and-muscle/

  8. Name:  3d17c901dfcae519454ff30c10ff5fee1cf8ec2e2cccedec5be12d2b7f4ae68e.jpg
Views: 163
Size:  20.0 KB


    ...after high carb meals

  9. Lol
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  10. Watch Your Sugar if you Have Gyno


    Quote Originally Posted by Eric Mar View Post
    Yes, I am serious. Looks like there is interaction between IGF-1 and ERa. lol If you have been following my logic here I am big on nutrient timing. Timing of carbs and estrogen blockers (detoxifiers like I3C would be great too) should help reduce the chance of gyno.
    From what ive seen, you're big on being completely full of sht...lol. Hahaha omg im sorry but the ignorance is unfathomable.
    Training log:

    http://anabolicminds.com/forum/workout-logs/267913-jswains-training-log.html

  11. Quote Originally Posted by ZachH View Post
    Name:  3d17c901dfcae519454ff30c10ff5fee1cf8ec2e2cccedec5be12d2b7f4ae68e.jpg
Views: 163
Size:  20.0 KB


    ...after high carb meals
    Haha, right?! Like every dude that ever ate carbs without being on a serm or AI has gyno....LOL
    Training log:

    http://anabolicminds.com/forum/workout-logs/267913-jswains-training-log.html

  12. Quote Originally Posted by jswain34 View Post
    From what ive seen, you're big on being completely full of sht...lol. Hahaha omg im sorry but the ignorance is unfathomable.
    Yes, researching studies on nutrient timing is ignorant. The body is a very complex organism and it has many interactions that we need to explore. I posted a study showing ERa cross talk with IGF-1. What about that did you find ignorant? Many people don't have gyno issues, but for the men who have it, it can be devastating.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
    http://mindandmuscle.net/articles/pr...nd-and-muscle/

  13. Eur J Endocrinol. 2017 Aug;177(2):137-143. doi: 10.1530/EJE-17-0151. Epub 2017 May 12.
    Tamoxifen reduces hepatic VLDL production and GH secretion in women: a possible mechanism for steatosis development.

    Birzniece V1,2,3, Barrett PHR4, Ho KKY5,6.
    Author information
    Abstract
    CONTEXT:
    Growth hormone (GH) stimulates hepatic synthesis of very-low-density lipoproteins (VLDL), whereas hepatic steatosis develops as a result of GH deficiency. Steatosis is also a complication of tamoxifen treatment, the cause of which is not known. As tamoxifen inhibits the secretion and action of GH, we hypothesize that it induces steatosis by inhibiting hepatic VLDL export.
    AIM:
    To investigate whether tamoxifen reduces hepatic VLDL secretion.
    DESIGN:
    Eight healthy, normolipidemic women (age: 64.4  2.1 years) were studied in random sequence at baseline, after 2 weeks of tamoxifen (20 mg/day) and after 2 weeks of estradiol valerate (EV; 2 mg/day) treatments, separated by a 4-week washout period. The kinetics of apolipoprotein B (apoB), the structural protein of VLDL particles, were measured using a stable isotope 2H3-leucine turnover technique. VLDL-apoB fractional catabolic rate (FCR) was determined using a multicompartment model. VLDL-apoB secretion was estimated as the product of FCR and VLDL-apoB concentration. GH response to arginine stimulation, circulating levels of IGF-1, FFA, and TG, along with TG content in VLDL were measured.
    RESULTS:
    Tamoxifen significantly (P < 0.05) reduced VLDL-apoB concentration and secretion by 27.3  7.8% and 29.8  10.2%, respectively. In contrast, EV did not significantly change VLDL-apoB concentration or secretion. Tamoxifen but not EV significantly reduced (P < 0.05) GH response to arginine stimulation. Both treatments significantly lowered (P < 0.05) circulating IGF-1.
    CONCLUSION:
    Inhibition of VLDL secretion may contribute to the development of fatty liver during tamoxifen therapy. As GH stimulates VLDL secretion, the development of steatosis may arise secondarily from GH insufficiency induced by tamoxifen.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
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  14. It appears that insulin resistance and lowered IGF-1 levels impacts muscle development. it appears that the right concentration of estrogen (estradiol) is what we need. Too much is bad and too little is bad. Makes sense!

    It is my contention that the more we can reduce the dependency on IGF-1 and Insulin, the better our effects. Appears that high circulating IGF-1 is not healthy, but it is required for growth via glycogen loading EXCEPT when we carb backload. That's why it seems like the most interesting choice is to use IGF-1 in a fasted state (which is how the body releases it) and enjoy our carbs when the Skeletal GLUT-4 is most active!

    Sheer ignorance...lol


    J Musculoskelet Neuronal Interact. 2016 Dec 14;16(4):302-309.
    Lower insulin sensitivity is related to lower relative muscle cross-sectional area, lower muscle density and lower handgrip force in young and middle aged non-diabetic men.

    Gysel T1, Tonoli C, Pardaens S, Cambier D, Kaufman JM, Zmierczak HG, Goemaere S, Lapauw B, Calders P.
    Author information
    Abstract
    OBJECTIVES:
    This study investigated whether an association between insulin resistance (IR) and muscle parameters is appreciable in young healthy men, independent of obesity. Furthermore, markers of muscle metabolism and hormones/possible determinants, were explored.
    METHODS:
    358 healthy young men were divided into a less and more insulin sensitive (LIS [age=33.25.4, BMI=23.42.3] and MIS [age=35.55.3, BMI=28.13.7]) group based on upper and lower quartile of HOMA-IR. Muscle cross-sectional area (CSA), -density, handgrip force, serum testosterone, estradiol, SHBG, Vitamin 25(OH)D, creatinine, IGF-1, IGFBP-3 and leptin levels were compared between these groups, correcting for differences in age, physical activity and fat mass. Correlations between HOMA-IR and these parameters, and between muscle measures and biochemical parameters, were calculated.
    RESULTS:
    LIS is related to lower relative muscle CSA, muscle density, muscle/fat CSA ratio, relative handgrip force and level of physical activity. Furthermore, lower levels in SHBG, testosterone, Vitamin 25(OH)D and higher leptin, IGF-1 and IGFBP-3 levels were observed in LIS. Bio available T, FT, TE2, FE2, bioavailable E2, serum and urinary creatinine levels did not differ between groups.
    CONCLUSION:
    Differences in muscle performance are already present in healthy men with lower insulin sensitivity and could be possibly modifiable risk factors for the development of type 2 diabetes.

    Aging Male. 2016;19(1):40-5. doi: 10.3109/13685538.2015.1100600. Epub 2015 Nov 2.
    Complex relationship between sex hormones, insulin resistance and leptin in men with and without prostatic disease.

    Grosman H1, Fabre B1, Lopez M2, Scorticati C2, Lopez Silva M2, Mesch V1, Mazza O2, Berg G1.
    Author information
    Abstract
    OBJECTIVES:
    To assess sex hormones, leptin and insulin-resistance in men with prostate cancer (PCa) and benign prostatic hyperplasia (BPH) and to study associations between androgens and histologic score of prostate tissue in PCa.
    SUBJECTS AND METHODS:
    Two hundred ten men older than 45 years selected from 2906 participants of a population screening for PCa were studied: 70 with PCa, 70 with BPH and 70 controls (CG), matched by body mass index and age. Insulin, IGF-1, PSA, leptin, total, free (fT) and bioavailable testosterone (bT) and estradiol were measured. Each group was subdivided into two subgroups considering the presence of metabolic syndrome (MS); androgens and leptin levels were analyzed in the subgroups.
    RESULTS:
    Prostate cancer and BPH patients presented higher total, fT and bT levels than CG. IGF-1, insulin and HOMA index were higher in BPH than in the other two groups. PCa presented higher leptin [median (range) 6.5 (1.3-28.0) versus 4.8 (1.1-12.3) ng/ml; p < 0.01] and estradiol [median (range) 37.0 (20-90) versus 29.0 (20-118) pg/ml; p = 0.025] levels than CG. After dividing men considering the presence of MS, leptin was higher and total testosterone was lower in MS patients in all the groups.
    CONCLUSIONS:
    It was observed a coexistence of an altered hormone profile with increased sex hormones and leptin in PCa patients, in accordance with the new perspective of PCa pathogenesis.

    Breast Cancer Res. 2011 May 19;13(3):R52. doi: 10.1186/bcr2883.
    Elevated insulin-like growth factor 1 receptor signaling induces antiestrogen resistance through the MAPK/ERK and PI3K/Akt signaling routes.

    Zhang Y1, Moerkens M, Ramaiahgari S, de Bont H, Price L, Meerman J, van de Water B.
    Author information
    Abstract
    INTRODUCTION:
    Insulin-like growth factor 1 (IGF-1) receptor (IGF-1R) is phosphorylated in all breast cancer subtypes. Past findings have shown that IGF-1R mediates antiestrogen resistance through cross-talk with estrogen receptor (ER) signaling and via its action upstream of the epidermal growth factor receptor and human epidermal growth factor receptor 2. Yet, the direct role of IGF-1R signaling itself in antiestrogen resistance remains obscure. In the present study, we sought to elucidate whether antiestrogen resistance is induced directly by IGF-1R signaling in response to its ligand IGF-1 stimulation.
    METHODS:
    A breast cancer cell line ectopically expressing human wild-type IGF-1R, MCF7/IGF-1R, was established by retroviral transduction and colony selection. Cellular antiestrogen sensitivity was evaluated under estrogen-depleted two-dimensional (2D) and 3D culture conditions. Functional activities of the key IGF-1R signaling components in antiestrogen resistance were assessed by specific kinase inhibitor compounds and small interfering RNA.
    RESULTS:
    Ectopic expression of IGF-1R in ER-positive MCF7 human breast cancer cells enhanced IGF-1R tyrosine kinase signaling in response to IGF-1 ligand stimulation. The elevated IGF-1R signaling rendered MCF7/IGF-1R cells highly resistant to the antiestrogens tamoxifen and fulvestrant. This antiestrogen-resistant phenotype involved mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) and phosphatidylinositol 3-kinase/protein kinase B pathways downstream of the IGF-1R signaling hub and was independent of ER signaling. Intriguingly, a MAPK/ERK-dependent agonistic behavior of tamoxifen at low doses was triggered in the presence of IGF-1, showing a mild promitogenic effect and increasing ER transcriptional activity.
    CONCLUSIONS:
    Our data provide evidence that the IGF-1/IGF-1R signaling axis may play a causal role in antiestrogen resistance of breast cancer cells, despite continuous suppression of ER transcriptional function by antiestrogens.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
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  15. What I suggest is that Insulin and IGF-1 are active in other tissues besides the intended targets. The best thing is to increase sensitivity because it seems that insensitivity allows more insulin to circulate (along with IGF-1) and causes damage.

    To me it would make more sense that insulin sensitivity would INCREASE fat storage but in fact that's the exact opposite of what we find. You'd think that a higher rate of insulin activity would increase fat storage but it doesn't it reduces it in study after study.

    Diabetes. 1995 May;44(5):555-60.
    Skeletal muscle GLUT4 protein concentration and aging in humans.

    Houmard JA1, Weidner MD, Dolan PL, Leggett-Frazier N, Gavigan KE, Hickey MS, Tyndall GL, Zheng D, Alshami A, Dohm GL.
    Author information
    Abstract
    The insulin resistance of aging has been attributed to a postreceptor defect in skeletal muscle. The present study examined whether a reduction in the concentration of the insulin-stimulated glucose transporter (GLUT4) in skeletal muscle was associated with advancing age in men (n = 55) and women (n = 29). Insulin sensitivity (minimal model) was negatively associated (P < 0.001) with age (range, 18-80 years) in men (r = -0.44) and women (r = -0.58). GLUT4 protein concentration in the vastus lateralis was also negatively associated (P < 0.05) with age (men, r = -0.28; women, r = -0.51). There was no relation (P > 0.15) between GLUT4 content in the gastrocnemius and age. GLUT4 concentration in the vastus lateralis was positively associated (P < 0.01) with insulin sensitivity in both sexes (r = 0.42); this relationship persisted in the men after adjusting for overall adiposity, regional adiposity, and cardiorespiratory fitness. These findings suggest that a decrement in GLUT4 protein concentration in skeletal muscle may at least partially contribute to the insulin resistance of aging in humans.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
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  16. Just to be clear, the first text is talking about IGF 1, not insulin.

    This text is not discussing, at all, carbohydrates role in growing breast tissue.
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  17. Watch Your Sugar if you Have Gyno


    Quote Originally Posted by Eric Mar View Post
    Yes, researching studies on nutrient timing is ignorant. The body is a very complex organism and it has many interactions that we need to explore. I posted a study showing ERa cross talk with IGF-1. What about that did you find ignorant? Many people don't have gyno issues, but for the men who have it, it can be devastating.
    This is what I found ignorant:

    Quote Originally Posted by Eric Mar View Post
    Looks like a definite interaction between IGF-1 levels and breast growth and development. Probably best to take an AI and a SERM with your carbs! .
    That is just a completely asinine statement. And ignorant, ludicrous, etc. You're making statements recommending pharmaceutical drugs, think before you type and post.
    Training log:

    http://anabolicminds.com/forum/workout-logs/267913-jswains-training-log.html

  18. Quote Originally Posted by jswain34 View Post
    This is what I found ignorant:



    That is just a completely asinine statement. And ignorant, ludicrous, etc. You're making statements recommending pharmaceutical drugs, think before you type and post.
    I never said that the SERM and AI need to be drugs! There are plenty of natural options. Benzoflavone, ATDHEA, Resveratrol plus detoxifiers like I3C and DIM are great too!

    I am suggesting that it's odd that better blood sugar would result in a reduction in obesity. It would appear that as a fall back mechanism the body cuts GLUT-4 activity to the fat cells absolutely last which makes total sense. The best method to achieving weight loss it appears is to keep healthy GLUT-4 sensitivity in the muscles which is done through exercise and sensitizing agents like ALA etc...
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
    http://mindandmuscle.net/articles/pr...nd-and-muscle/

  19. Quote Originally Posted by Eric Mar View Post
    I never said that the SERM and AI need to be drugs! There are plenty of natural options. Benzoflavone, ATDHEA, Resveratrol plus detoxifiers like I3C and DIM are great too!
    You've completely missed the point of the text though and are just randomly making up conclusions lol. The first text is talking about breast tumour growth, not breast growth, and certainly is not discussing carbohydrate and breast development.
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  20. I am not missing the point. There isn't much research on gynocomastia since it is a relatively rare condition to treat. I am going to further look into the IGF-1 and Insulin relationship as a means of storing fat and promoting adiposity. There seems to be something here worth exploring and it appears that IGF-1 may potentiate fat growth around the breast.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
    http://mindandmuscle.net/articles/pr...nd-and-muscle/

  21. Quote Originally Posted by Eric Mar View Post
    Yes, researching studies on nutrient timing is ignorant. The body is a very complex organism and it has many interactions that we need to explore. I posted a study showing ERa cross talk with IGF-1. What about that did you find ignorant? Many people don't have gyno issues, but for the men who have it, it can be devastating.
    But, but... nothing in the article text you posted has anything to do with gyno and it doesn't support the conclusions you've made, as Jiigzz pointed out. The article you posted is about tumourigenesis in breast cancer...

  22. Quote Originally Posted by Eric Mar View Post
    There seems to be something here worth exploring and it appears that IGF-1 may potentiate fat growth around the breast.
    I'm sure you know that adipose tissue around the breast area isn't the same thing as gynecomastia...

    Quote Originally Posted by Eric Mar View Post
    There isn't much research on gynocomastia since it is a relatively rare condition to treat.
    True, but the pathophysiology of gynecomastia is fairly well understood.

  23. https://articles.a1supplements.com/n...muscle-growth/

    This is a good starter article on the subject! It does appear that Insulin/IGF-1 signalling may cause more estrogen activity and fat storage which we want to avoid.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
    http://mindandmuscle.net/articles/pr...nd-and-muscle/

  24. Quote Originally Posted by TheNietzsche View Post
    I'm sure you know that adipose tissue around the breast area isn't the same thing as gynecomastia...



    True, but the pathophysiology of gynecomastia is fairly well understood.
    I contend that there isn't much true gynocomastia. Most laymen call pseudogynocomastia "gyno". I should have clarified but the term "pseudogynocomastia" isn't well known by most people. I think most men suffer more from pseudogynocomastia and I believe that may be impacted by IGF-1.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
    http://mindandmuscle.net/articles/pr...nd-and-muscle/

  25. Looks like with IGF-1 it would be advisable to keep estrogen activity low to blunt fat storage and to take it in a fasted state. It's a pretty complex topic.

    "However a number of studies demonstrated that IGF, as well as other growth factors, directly increased the transcriptional activity of ER and that activation was specifically inhibited by antiestrogens"

    Thus it would seem like a good idea to limit carbohydrate and estrogen levels while boosting IGF-1.
    Nothing I say is medical advice and supplements only enhance and optimize your diet and exercise check with a medical professional before starting any program.
    Try Rise and Swell, the most advanced testosterone booster on the market!
    http://mindandmuscle.net/articles/pr...nd-and-muscle/
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