The liver can store about 5% of its weight (~50-75 gram) of sugar as glycogen in w/c any more it'll convert the sugar to fat. WHEN it starts to convert the sugar into fat, it stops making SEX HORMONE BINDING GLOBULIN (SHBG) hence SHBG in the blood decreases. SHBG protein plays a key role in controlling the amount of testosterone and estrogen that’s available throughout the body. If there’s less SHBG protein, then more testosterone and estrogen will be released throughout the body, which is associated with an increased risk of acne.
Observational evidence suggests that dietary glycemic load may be one environmental factor contributing to the variation in acne prevalence worldwide. To investigate the effect of a low glycemic load (LGL) diet on endocrine aspects of acne vulgaris, 12 male acne sufferers (17.0 +/- 0.4 years) completed a parallel, controlled feeding trial involving a 7-day admission to a housing facility. Subjects consumed either an LGL diet (n = 7; 25% energy from protein and 45% from carbohydrates) or a high glycemic load (HGL) diet (n = 5; 15% energy from protein, 55% energy from carbohydrate). Study outcomes included changes in the homeostasis model assessment of insulin resistance (HOMA-IR), sex hormone binding globulin (SHBG), free androgen index (FAI), insulin-like growth factor-I (IGF-I), and its binding proteins (IGFBP-I and IGFBP-3). Changes in HOMA-IR were significantly different between groups at day 7 (-0.57 for LGL vs. 0.14 for HGL, p = 0.03). SHBG levels decreased significantly from baseline in the HGL group (p = 0.03), while IGFBP-I and IGFBP-3 significantly increased (p = 0.03 and 0.03, respectively) in the LGL group. These results suggest that increases in dietary glycemic load may augment the biological activity of sex hormones and IGF-I, suggesting that these diets may aggravate potential factors involved in acne development.
PMID: 18496812 [PubMed - indexed for MEDLINE]
Higher free testosterone levels in women are a function of lower levels of sex hormone-binding globulins (SHBG), higher levels of total testosterone, or both. When free testosterone levels are decreased, sebum production, a pathogenic feature of acne vulgaris, is also decreased. Oral contraceptives (OCs) decrease free testosterone levels by reducing testosterone production by the ovaries and adrenal glands, increasing SHBG, and inhibiting conversion of free testosterone to dihydrotestosterone. Studies have shown that the progestin component of OCs lowers androgen levels, which are directly associated with the development of acne lesions. Currently, 3 OCs have received approval for acne from the US Food and Drug Administration. For patients with acne who are already benefiting from OC treatment, there is no need to change the OC; however, when an OC proves insufficient against sebum production, switching to a formulation that is approved for acne is recommended.
PMID: 18338652 [PubMed - indexed for MEDLINE]
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The liver can store about 5% of its weight (~50-75 gram) of sugar as glycogen in w/c any more it'll convert the sugar to fat. WHEN it starts to convert the sugar into fat, it stops making SEX HORMONE BINDING GLOBULIN (SHBG) hence SHBG in the blood decreases. SHBG protein plays a key role in controlling the amount of testosterone and estrogen that’s available throughout the body. If there’s less SHBG protein, then more testosterone and estrogen will be released throughout the body, which is associated with an increased risk of acne.
ReplyDeleteSmith R, Mann N, Mäkeläinen H, Roper J, Braue A, Varigos G.
ReplyDeleteSchool of Applied Sciences, RMIT University, Melbourne, Australia. robyn.smith@rmit.edu.au
Observational evidence suggests that dietary glycemic load may be one environmental factor contributing to the variation in acne prevalence worldwide. To investigate the effect of a low glycemic load (LGL) diet on endocrine aspects of acne vulgaris, 12 male acne sufferers (17.0 +/- 0.4 years) completed a parallel, controlled feeding trial involving a 7-day admission to a housing facility. Subjects consumed either an LGL diet (n = 7; 25% energy from protein and 45% from carbohydrates) or a high glycemic load (HGL) diet (n = 5; 15% energy from protein, 55% energy from carbohydrate). Study outcomes included changes in the homeostasis model assessment of insulin resistance (HOMA-IR), sex hormone binding globulin (SHBG), free androgen index (FAI), insulin-like growth factor-I (IGF-I), and its binding proteins (IGFBP-I and IGFBP-3). Changes in HOMA-IR were significantly different between groups at day 7 (-0.57 for LGL vs. 0.14 for HGL, p = 0.03). SHBG levels decreased significantly from baseline in the HGL group (p = 0.03), while IGFBP-I and IGFBP-3 significantly increased (p = 0.03 and 0.03, respectively) in the LGL group. These results suggest that increases in dietary glycemic load may augment the biological activity of sex hormones and IGF-I, suggesting that these diets may aggravate potential factors involved in acne development.
PMID: 18496812 [PubMed - indexed for MEDLINE]
O'Connell K, Westhoff C.
ReplyDeleteColumbia University College of Physicians and Surgeons, New York, New York, USA.
Higher free testosterone levels in women are a function of lower levels of sex hormone-binding globulins (SHBG), higher levels of total testosterone, or both. When free testosterone levels are decreased, sebum production, a pathogenic feature of acne vulgaris, is also decreased. Oral contraceptives (OCs) decrease free testosterone levels by reducing testosterone production by the ovaries and adrenal glands, increasing SHBG, and inhibiting conversion of free testosterone to dihydrotestosterone. Studies have shown that the progestin component of OCs lowers androgen levels, which are directly associated with the development of acne lesions. Currently, 3 OCs have received approval for acne from the US Food and Drug Administration. For patients with acne who are already benefiting from OC treatment, there is no need to change the OC; however, when an OC proves insufficient against sebum production, switching to a formulation that is approved for acne is recommended.
PMID: 18338652 [PubMed - indexed for MEDLINE]