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#1 Pika

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Posted 22 February 2005 - 04:06 PM

can someone give me a link of a study or something that says when you eat sugar your insulin levels spike and mess with your hormones please..
thx

#2 SweetJade1980

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Posted 22 February 2005 - 05:08 PM

QUOTE(Pika @ Feb 22 2005, 03:06 PM)
can someone give me a link of a study or something that says when you eat sugar your insulin levels spike and mess with your hormones please..
thx

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Glady, but that doesn't appear to readily change people's minds. That comes when they are ready for it.


FYI
(to clear up some misconceptions):

**Insulin Resistance = Decreased Insulin Sensitivity

** Insulin Resistance = Hyperinsulinism, Hypoglycemia, Metabolic Syndrome, Syndrome X

**Puberty (& Pregnancy) = A Temporary State of Insulin Resistance


About "DIET"
** Whatever you eat will spike your insulin levels, but some foods, especially simple carbohydrates and certain other carbohydrates do it BETTER than others

** "Sugar" = Carbohydrates

** High Calorie diets, High Fat Diets (especially Trans Fats & too much animal fat), and Fructose Sweeteners (Fructose, Fruit Juice, Corn Syrup, HFCS), will all increase your Insulin Resistance.


QUOTE
Insulin sensitivity decreased with pubertal development and its index reversely correlated with Tanner stage and serum level of leptin (r=-0.27 and -0.36, respectively, P<0.01). CONCLUSION: Obesity (BMI), serum level of leptin and pubertal development were independent risk factors for insulin resistance in children aged 7 to 17 years. http://www.ncbi.nlm....t_uids=15312580



QUOTE
Type 2 diabetes mellitus, once considered a disease only of adults, is now being diagnosed at an increasingly alarming rate in children. It is still unclear whether the presentation, risk factors, course, and treatment of the disease are the same in children as they are in adults. Pediatric-specific prevalence is being linked to obesity and inactivity, and risk factors include being overweight, family history of the disease, and conditions of insulin resistance such as pubertyhttp://www.ncbi.nlm....t_uids=15303451



QUOTE
Type A insulin resistance: In addition to glucose intolerance, patients with type A insulin resistance (absent or dysfunctional insulin receptor) may have certain clinical features such as (1) acanthosis nigricans, which is hyperpigmentation and skin thickening of flexural areas, or (2) features of hyperandrogenism, of which some variants may be characterized by thin or muscular body habitus or acral enlargement (pseudoacromegaly). http://www.emedicine...ed/topic897.htm 


QUOTE
J Clin Endocrinol Metab. 2004 Jun;89(6):2526-39. Related Articles, Links 

 
Insulin resistance syndrome in children.

Ten S, Maclaren N.

Pediatric Endocrinology Department, Maimonides Medical Center, Brooklyn, New York 11219, USA.

The insulin resistance syndrome (syndrome X, metabolic syndrome) has become the major health problem of our times. Associated obesity, dyslipidemia, atherosclerosis, hypertension, and type 2 diabetes conspire to shorten life spans, while hyperandrogenism with polycystic ovarian syndrome affect the quality of life and fertility of increasing numbers of women. Whereas a growing number of single genetic diseases affecting satiety or energy metabolism have been found to produce the clinical phenotype, strong familial occurrences, especially in racially prone groups such as those from the Indian subcontinent, or individuals of African, Hispanic, and American Indian descents, together with emerging genetic findings, are revealing the polygenetic nature of the syndrome. However, the strong lifestyle factors of excessive carbohydrate and fat consumption and lack of exercise are important keys to the phenotypic expression of the syndrome. The natural history includes small for gestational age birth weight, excessive weight gains during childhood, premature pubarche, an allergic diathesis, acanthosis nigricans, striae compounded by gynecomastia, hypertriglyceridemia, hepatic steatosis, premature atherosclerosis, hypertension, polycystic ovarian syndrome, and focal glomerulonephritis appearing increasingly through adolescence into adulthood. Type 2 diabetes, which develops because of an inherent and/or an acquired failure of an insulin compensatory response, is increasingly seen from early puberty onward, as is atheromatous disease leading to coronary heart disease and stroke. A predisposition to certain cancers and Alzheimer's disease is also now recognized. The looming tragedy from growing numbers of individuals affected by obesity/insulin resistance syndrome requires urgent public health approaches directed at their early identification and intervention during childhood. Such measures include educating the public on the topic, limiting the consumption of sucrose-containing drinks and foods with high carbohydrate and fat contents, and promoting exercise programs in our nation's homes and schools.
http://www.ncbi.nlm....t_uids=15181020


#3 SweetJade1980

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Posted 22 February 2005 - 05:09 PM

QUOTE
Insulin and IGFs are important regulators of ovarian function. Insulin resistance and hyperinsulinemia are thought to be responsible for the hyperandrogenism that is characteristic of polycystic ovary disease (PCOD). Other distinct manifestations of the IRS or related conditions involve various organs, as well as the skin.

....

Mortality and morbidity related to some other conditions associated with insulin resistance include the following:


PCOD - Infertility, menstrual irregularity, androgen excess


Rare conditions - Lipodystrophic states (fatty liver [Liver cirrhosis is a major cause of morbidity and mortality.])

Leprechaunism - Growth retardation, abnormal glucose homeostasis (especially occurrence of hypoglycemia), early death


Race: IRS is found in all races. The degree of clustering of the risk variables of syndrome X generally is considered to be higher among whites. However, prevalence rates of the various components of syndrome X tend to be higher among nonwhite populations.

Acanthosis nigricans, a common physical sign of IRS, occurs in all ethnic groups, but the prevalence is higher in Hispanics and blacks than in whites.

.....

Women with PCOD usually present in their mid twenties.

Many rare disorders of insulin resistance present in early life (eg, leprechaunism [first year of life], lipodystrophic states [ages 6-9 y until early puberty]).

Type A insulin resistance typically occurs in the younger patients, while type B insulin resistance occurs more often in older women.

....


Type A syndrome
Patients usually are tall and have features of hirsutism and abnormalities of the female reproductive tract that are related to hyperandrogenism (eg, PCOD).

The patient may have either thin or muscular body build.

Acral enlargement, a form of pseudoacromegaly, is not uncommon.


Acanthosis nigricans

Very common in type A patients - Patchy, velvety brown hyperpigmentation plaques usually found in flexural areas, especially axillae and nuchal region

The lesion may be due to the effect of high circulating levels of insulin on IGF receptors in the skin.

Found in a wide variety of clinical conditions that are associated with insulin resistance

Has been reported in nearly one tenth of women being evaluated for PCOD

Sometimes is a marker of malignant neoplasm
PCOD: Patients may have masculine habitus—coarse or greasy skin and acne, frontal alopecia, breast atrophy, hypertrophy of clitoris, and obesity—that is, varying degrees of hirsutism or virilization exist. These manifestations are due to hyperandrogenism.
http://www.emedicine...d/topic1173.htm


QUOTE
There is a transient drop in the level of adiponectin during male puberty, correlated with the increase in testosterone level in boys. Plasma adiponectin levels were inversely correlated with obesity and insulin resistance in boys and girls during the pubertal period.  http://www.ncbi.nlm....t_uids=14747205



QUOTE
Polycystic ovary syndrome (PCOS) appears to be a lifelong disorder. The stigmata of insulin resistance, including obesity and premature adrenarche, may be early forms of its presentation. Girls with premature pubarche, characterized by elevated dehydroepiandrosterone levels and hyperinsulinemia, are at high risk for developing the full PCOS phenotype, including ovarian hyperandrogenism and chronic anovulation. http://www.ncbi.nlm....t_uids=12510993



QUOTE
Decreased insulin sensitivity was suggested by decreased composite insulin sensitivity index. A trend toward greater triglycerides was observed in the boys with PA, compared with the controls. Prepubertal boys with PA show differences in the IGF system and decreased insulin sensitivity, independent of obesity, as observed in girls with PA. These findings suggest that both boys and girls with PA should be monitored for the development of insulin resistance and associated complications, including diabetes mellitus and cardiovascular disease. http://www.ncbi.nlm....t_uids=12466359


PA = Premature Adrenarche , early introduction adrenal androgen (DHEA or DHEA-S)

QUOTE
Although premature adrenarche has been thought to be a benign, normal variant of puberty, our findings indicate that, for certain girls, premature adrenarche represents an early clinical feature of syndrome X (obesity, hypertension, dyslipidemia, insulin resistance). Perhaps the early identification of these patients will permit early therapy, such as lifestyle changes, including dietary and activity level intervention. As insulin resistance is an underlying feature of premature adrenarche, it seems rational to assess the efficacy and safety of using insulin-sensitizing agents to treat these individuals. In the absence of controlled longitudinal studies, the cross-sectional data available from our studies suggest that premature pubarche driven by premature adrenarche and hyperinsulinemia may precede the development of ovarian hyperandrogenism, and this sequence may have an early origin with low birth weight serving as a marker. Premature adrenarche may thus be a forerunner of syndrome X in some girls. http://www.ncbi.nlm....t_uids=11716159


#4 SweetJade1980

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Posted 22 February 2005 - 05:36 PM

QUOTE
As growth hormone (GH), insulin-like growth factor I (IGF-I) and insulin levels normally peak during puberty, we examined the influence of insulin on IGF-I regulation by measuring basal GH, total and free IGF-I, and IGF binding protein (IGFBP) levels in lean adolescents and young adults. During the clamp studies, the adolescents exhibited low levels of IGFBP-1 and -2 as well as a reduced insulin-induced suppression of IGFBP-1, compared with lean adults. Thus, we postulate that the insulin resistance of puberty induces compensatory hyperinsulinaemia, which in turn suppresses circulating levels of IGFBP-1, which in turn leads to increased levels of free IGF-1.  http://www.ncbi.nlm....t_uids=10626552


IGF-1 is what retinoids like Accutane, suppress by increasing IGFBP-3 to bind it. IGF-1 also induces an increase in Inflammatory Products as well as overstimulating the sebaceous gland, thus increased growth & sebum production as well as skin cell hyperproliferation.


QUOTE
Diabetes. 1999 Oct;48(10):2039-44. Related Articles, Links 

 
Insulin resistance during puberty: results from clamp studies in 357 children.


Moran A, Jacobs DR Jr, Steinberger J, Hong CP, Prineas R, Luepker R, Sinaiko AR.

Department of Pediatrics, University of Minnesota, Minneapolis 55455, USA. moran001@tc.umn.edu

Insulin resistance may be an important cause of a constellation of cardiovascular risk factors in adults, and onset of this syndrome may occur in childhood. However, children normally experience transient insulin resistance at puberty. There were 357 normal children (159 girls, 198 boys) age 10-14 years who underwent euglycemic clamp studies to assess the effects of Tanner stage (T), sex, ethnicity, and BMI on insulin resistance. Insulin resistance increased immediately at the onset of puberty (T2), but returned to near prepubertal levels by the end of puberty (T5). Its peak occurred at T3 in both sexes, and girls were more insulin resistant than boys at all T stages. White boys appeared to be more insulin resistant than black boys; no difference was seen between white and black girls. Insulin resistance was strongly related to BMI, triceps skinfold thickness, and waist circumference, and this relationship was independent of Tanner stage or sex. Differences in BMI and adiposity did not, however, entirely explain the insulin resistance of puberty. These results demonstrate that 1) significant differences in insulin resistance are present between boys and girls; 2) insulin resistance increases significantly at T2, T3, and T4, but decreases to near prepubertal levels at T5; and 3) while insulin resistance is related to BMI and anthropometric measures of fatness, these factors do not completely explain the insulin resistance that occurs during the Tanner stages of puberty.  http://www.ncbi.nlm....t_uids=10512371


QUOTE
The syndrome of hyperandrogenism, insulin resistance, and acanthosis nigricans (HAIR-AN) is a subphenotype of the polycystic ovary syndrome. It is one of the most common causes of menstrual problems, hyperandrogenic symptoms, and insulin resistance among young women. http://www.ncbi.nlm....t_uids=15258677




QUOTE
Am J Med Sci. 1994 May;307(5):342-5. Related Articles, Links 


Case report: defective beta and alpha cell regulation in patients with hyperinsulinemia and acanthosis nigricans.

Schuster D, O'Dorisio TM, Osei K.

Division of Endocrinology & Metabolism, Ohio State University Hospitals, Columbus.

Beta cell hypersecretion is associated with the syndrome of hyperandrogenism, insulin resistance, and acanthosis nigricans. It is unknown whether concomitant alpha cell secretory dysfunction occurs in patients with this syndrome. The authors evaluated the gastroenteropancreatic hormones in four family members with varying degrees of the hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome. Gastroenteropancreatic hormones were measured during oral glucose tolerance test with and without subcutaneous octreotide injection. The study revealed that the administration of subcutaneous octreotide resulted in suppression of beta cell function (insulin and c-peptide) but had no effect or a delayed effect on alpha cell secretion (glucagon). Furthermore, the severity of glucagon abnormalities paralleled that of beta cell hypersecretion and the clinical and phenotypic manifestations of acanthosis nigricans in our four patients. We speculate that this alpha cell aberration could potentially be involved in the altered glucose homeostasis and perhaps the skin manifestations of this syndrome. Therefore, glucagon levels should be evaluated in the hormonal studies in patients with hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome.


In this case, Beta Cells are located on the pancreas and secrete insulin (decreases sugar levels), while the alpha cells secrete glucagon (increases sugar levels).

QUOTE
Ann Pediatr (Paris). 1990 Mar;37(3):143-9. Related Articles, Links 


[Hyperinsulinism syndromes caused by insulin resistance]

[Article in French]

Robert JJ.

Unite d'Endocrinologie et Diabetologie de l'Enfant, Hopital Necker, Paris.

Resistance to insulin consists in a decrease in insulin's biologic action and is manifested mainly by hyperinsulinism. Clinical investigation of insulin resistance states relies on specialized tests, performed both in vitro and in vivo. The hyperinsulinemic-euglycemic clamp is the reference method for quantifying insulin resistance and can differentiate decreased insulin sensitivity and decreased maximal capacity for glucose uptake. Glucose flux measurements, using glucose labelled with stable isotopes, distinguish hepatic and peripheral factors involved in insulin resistance. In vitro studies include investigations for antibodies against insulin and insulin receptors, studies of insulin receptors and their tyrosine kinase activity, and studies of postreceptor cell metabolism. These investigations are especially useful in genetic syndromes of extreme insulin resistance, whose pathophysiology is largely unelucidated, including: insulin resistance syndromes with acanthosis nigricans, obesity-acanthosis nigricans-hyperandrogenism syndrome, lipoatrophic diabetes, leprechaunism, and other syndromes. But insulin resistance also plays a major role in non-insulin-dependent diabetes mellitus, insulin-dependent diabetes mellitus, and various pathological or even physiological endocrine alterations. http://www.ncbi.nlm....st_uids=2190520



QUOTE
Proc Soc Exp Biol Med. 1991 Mar;196(3):351-8. Related Articles, Links 


Growth factor-mediated regulation of aromatase activity in human skin fibroblasts.

Emoto N, Ling N, Baird A.

Department of Molecular and Cellular Growth Biology, Whittier Institute for Diabetes and Endocrinology, La Jolla, California 92037.

We investigated the effects of various hormones and growth factors on aromatase activity in cultured human skin fibroblasts. Several potential trophic factors were tested for their ability to modify basal aromatase activity or the response to dibutyryladenosine 3',5'-cyclic monophosphate and dexamethasone because (i) no endogenous ligand has been identified that is responsible for stimulating aromatase activity in the periphery, and (ii) dexamethasone and cAMP analogs can increase this enzyme's activity in fibroblasts. The effect of insulin and insulin-like growth factors were examined in closer detail because of the clinical association between insulin and hyperandrogenism. Pituitary hormones and hypothalamic releasing factors, such as human ACTH (10 nM), beta-endorphin (10 nM), beta-lipotropin (10 nM), alpha-MSH (10 nM), gamma 3-MSH (10 nM), ovine luteinizing hormone (10 ng/ml), ovine follicle-stimulating hormone (10 ng/ml), ovine thyroid-stimulating hormone (10 ng/ml), rat growth hormone (10 ng/ml), rat prolactin (10 ng/ml), rat corticotropin-releasing factor (10 nM), luteinizing hormone-releasing factor (10 nM), thyrotropin-releasing factor (10 nM), human growth hormone-releasing factor (10 nM), and somatostatin (10 nM), have no significant effects on aromatase activity. Porcine inhibin A (10 ng/ml) and porcine activin AB (10 ng/ml), two ovarian hormones with structural transforming homology to transforming growth factor-beta, also have no effect on aromatase activity. Although basic fibroblast growth factor (1-100 ng/ml), acidic fibroblast growth factor (1 ng/ml), epidermal growth factor (1 ng/ml), platelet-derived growth factor (1 ng/ml), tumor necrosis factor (1 ng/ml), and transforming growth factor-beta 1 (1 ng/ml) have no effect on basal aromatase activity in human skin fibroblasts, all of these growth factors inhibited the ability of dibutyryladenosine 3',5'-cyclic monophosphate to stimulate aromatase activity. In contrast, both insulin (100 pg/ml-10 ng/ml) and insulin-like growth factor-1 (1-100 ng/ml) had no effect on cAMP-stimulated aromatase but potentiated the action of dexamethasone (100 nM). Thus, there is a clear distinction between the effects of dexamethasone and cAMP on peripheral aromatase. On the basis of the results presented here, it is interesting to speculate that the hyperandrogenism that is often associated with insulin resistance may be due to a combination of growth factor-mediated inhibition of aromatase activity and the failure of peripheral tissues to respond to insulin and metabolize androgens to estrogens.  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1671798


Females tend to show (more) signs of hyperandrogenism & insulin resistance much more often than males because in the order of things, Androgens are produced BEFORE Estrogens. Therefore our bodies rely on an enzyme known as aromatse to convert Androgens into Estrogen, but if your system is imbalanced in some way that alters the production of aromatase (Insulin Resitance can do this), then hyperandrogenism can result.

QUOTE
Breast Cancer Res Treat. 1998 Jun;49(3):187-93. Related Articles, Links 

 
Western diet, early puberty, and breast cancer risk.

Stoll BA.

Oncology Department, St. Thomas' Hospital, London, UK.

The typical high fat, low fibre diet of the industrialised West, particularly when associated with inadequate exercise, is likely to advance the onset of puberty. This will manifest in girls as an earlier menarche, earlier onset of breast development, and an earlier growth spurt. Both earlier menarche and adult tallness are markers of increased risk to breast cancer. Earlier menarche in the West is usually associated with earlier onset of hyperinsulinaemia, and multiple case-control studies report that hyperinsulinaemia too is a marker of increased breast cancer risk. Although the Western diet is linked both to earlier menarche and also to earlier hyperinsulinaemia, the mechanism involved is not necessarily the same. While menarche is likely to be triggered by a threshold level of fatness, manifestation of insulin resistance is genetically-determined and strongly influenced by the fatty acid profile of the diet. The putative mechanisms by which they influence mammary carcinogenesis also differ. Early menarche is reported to be associated with a raised oestradiol level persisting into early adult life. On the other hand, hyperinsulinaemia is commonly associated with abnormal aromatase activity in the ovaries. In addition, the concomitant increase in bioactive levels of insulin-like growth factor-I may synergise with oestrogen in stimulating proliferative activity in mammary epithelium. Dietary modification and exercise regimens are proposed in families at high risk to breast cancer. The measures have been shown to reduce insulin levels in both children and adults, and serial monitoring of insulin and sex steroid levels could be used to detect a metabolic-endocrine effect. http://www.ncbi.nlm....st_uids=9776502


#5 SweetJade1980

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Posted 22 February 2005 - 06:17 PM

QUOTE
Comp Biochem Physiol A Mol Integr Physiol. 2003 Sep;136(1):95-112. Related Articles, Links 

 
Hyperinsulinemic diseases of civilization: more than just Syndrome X.

Cordain L, Eades MR, Eades MD.

Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523, USA. cordain@cahs.colostate.edu

Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor alpha, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body's endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X.  http://www.ncbi.nlm....t_uids=14527633


This is key as SHBG binds Free Testosterone & IGFPBs bind IGFs, yet increased insulin decreases these binding proteins. If you have an excess of Free Testosterone, or any, it is free to convert into DHT. Now recently there are studies stating that DHT is not a factor in acne, yet just the presence of Free Testosterone, especially in those of us susceptible, is enough to bring about an increase in IGF-1, PPAR-beta/deltas, and Proinflammatory Products (cytokines, prostaglinds, leukotrienes) that all work to create acne.

QUOTE
J Clin Endocrinol Metab. 1995 Jul;80(7):2057-62. Related Articles, Links 


Effects of diet and metformin administration on sex hormone-binding globulin, androgens, and insulin in hirsute and obese women.

Crave JC, Fimbel S, Lejeune H, Cugnardey N, Dechaud H, Pugeat M.

Hospices Civils de Lyon, Laboratoire de la Clinique Endocrinologique, Hopital de l'Antiquaille, France.

Evidence suggests that hyperinsulinemic insulin resistance may increase serum levels of ovarian androgens and reduce sex hormone-binding globulin (SHBG) levels in humans. The present study was conducted to assess the effect of administration of the biguanide metformin, a drug commonly used in the treatment of diabetes mellitus, on androgen and insulin levels in 24 hirsute patients. The patients selected for the study were obese, with a body mass index higher than 25 kg/m2 and high fasting insulin (> 90 pmol/L) and low SHBG levels (< 30 nmol/L). All patients were given a low calorie diet (1500 Cal/day) and randomized for either metformin administration at a dose of 850 mg or a placebo, twice daily for 4 months, in a double blind study. In the placebo group, diet resulted in a significant decrease in body mass index (30.8 +/- 1.0 vs. 32.7 +/- 1.5 kg/m2; P < 0.0001), fasting insulin (127 +/- 11 vs. 156 +/- 14 pmol/L; P < 0.01), non-SHBG-bound testosterone (0.19 +/- 0.02 vs. 0.28 +/- 0.03 nmol/L; P < 0.02), androstenedione (5.8 +/- 0.5 vs. 9.0 +/- 1.1 nmol/L; P < 0.03), and 3 alpha-diolglucuronide (8.6 +/- 1.1 vs. 11.7 +/- 1.9; P < 0.005) plasma concentrations and a significant increase in the glucose/insulin ratio (0.047 +/- 0.005 vs. 0.035 +/- 0.003; P < 0.001) and plasma concentrations of SHBG (26.0 +/- 3.3 vs. 19.1 +/- 1.9 nmol/L; P < 0.001) and dehydroepiandrosterone sulfate (8.7 +/- 1.5 vs. 8.4 +/- 1.3; P < 0.05). Beneficial effects of diet were not significantly different in the patients who were given metformin instead of placebo. These results confirm that weight loss induced by a low calorie diet is effective in improving hyperinsulinemia and hyperandrogenism in obese and hirsute women. With our study design, metformin administration had no additional benefit over the effect of diet. http://www.ncbi.nlm....st_uids=7608255


QUOTE
Br J Nutr. 2000 Oct;84(4):557-63. Related Articles, Links 


Effects of replacing meat with soyabean in the diet on sex hormone concentrations in healthy adult males.

Habito RC, Montalto J, Leslie E, Ball MJ.

School of Biological and Chemical Sciences, Deakin University, Melbourne, Australia.

A randomised crossover dietary intervention study was performed to evaluate the effects of replacing meat protein in the diet with a soyabean product, tofu, on blood concentrations of testosterone, dihydrotestosterone, androstanediol glucuronide, oestradiol, sex hormone-binding globulin (SHBG), and the free androgen index (total testosterone concentration/SHBG concentration x 100; FAI). Forty-two healthy adult males aged 35-62 years were studied. Diets were isoenergetic, with either 150 g lean meat or 290 g tofu daily providing an equivalent amount of macronutrients, with only the source of protein differing between the two diets. Each diet lasted for 4 weeks, with a 2-week interval between interventions. Fasting blood samples were taken between 07.00 and 09.30 hours. Urinary excretion of genistein and daidzein was significantly higher after the tofu diet (P < 0.001). Blood concentrations of sex hormones did not differ after the two diets, but the mean testosterone:oestradiol value was 10% higher (P = 0.06) after the meat diet. SHBG was 3% higher (P = 0.07), whereas the FAI was 7% lower (P = 0.06), after the tofu diet compared with the meat diet. There was a significant correlation between the difference in SHBG and testosterone:oestradiol and weight change. Adjusting for weight change revealed SHBG to be 8.8% higher on the tofu diet (mean difference 3 (95% CI 0.7, 5.2) nmol/l; P = 0.01) and testosterone:oestradiol to be significantly lower, P = 0.049). Thus, replacement of meat protein with soyabean protein, as tofu, may have a minor effect on biologically-active sex hormones, which could influence prostate cancer risk. However, other factors or mechanisms may also be responsible for the different incidence rates in men on different diets. http://www.ncbi.nlm....t_uids=11103227


I hesistate to post studies using soy because it can backfire on some acne sufferers and actually make ones' acne worse due to activating hypothyroidism in them. This is probably due to them already having an off gene for hypothyroidism that was then activated, from consuming too much soy, or (too much) processed soy. Hypothyroidism means lacking of T3/Thyroxine hormone that also happens to be responsible for the amount of SHBG produced in the body.

QUOTE
Metabolism. 2001 May;50(5):505-11. Related Articles, Links 

 
Postprandial changes in sex hormones after meals of different composition.

Habito RC, Ball MJ.

School of Biomedical Sciences, University of Tasmania, Launcastor, Australia.

The postprandial effects of different meals on serum testosterone, serum sex hormone-binding globulin (SHBG), and free androgen index were sequentially evaluated in 15 healthy men. The isocaloric meals contained different proteins and different quantities and type of fat as a mixed meal. Four test meals were given to subjects in random order: a lean meat meal, a tofu meal (both containing approximately 20% energy from fat), and meat meals with added animal fat or safflower oil (both 54% energy from fat). Blood samples were obtained at baseline and at 2, 3, and 6 hours after each meal. There was a significant decrease in testosterone and free androgen index after both tofu and lean meat meals. The 2-hour serum testosterone and the decremental area under the curve were significantly more negative after the lean meat meal than the meat meal with added animal fat. The testosterone area under the curve was least for the high animal fat meal indicating little change from baseline. As men are postprandial for a significant proportion of the day, the lower sex hormone values after a low animal fat meal may provide long-term benefits in reducing the risk of diseases, such as prostate cancer, which appear to be sex hormone-dependent. Copyright 2001 by W.B. Saunders Company  http://www.ncbi.nlm....t_uids=11319710


#6 BlackBetty

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Posted 22 February 2005 - 07:39 PM

why all that? It is pretty simple when you eat sugar insulin is triggered and it takes sugar out of the blood and stores in the liver as glycogen. When you have low glucose levels the glycogen is released.

#7 Pika

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Posted 22 February 2005 - 07:59 PM

holy crap thank you SJ

#8 SweetJade1980

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Posted 22 February 2005 - 08:15 PM

QUOTE(BlackBetty @ Feb 22 2005, 06:39 PM)
why all that? It is pretty simple when you eat sugar insulin is triggered and it takes sugar out of the blood and stores in the liver as glycogen.  When you have low glucose levels the glycogen is released.

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I know that you get this, but most members of this board do not seem to understand that Insulin controls a variety of factors (steriod hormones, growth factors, pro-inflammatory cytokines, pro-inflammatory prostaglandins, LDL, etc) that have an increased prevalence in acne sufferers. Thus, they do not understand how "diet' can affect the development of acne.

Of course, this is just one version of how diet can affect acne, but it is one that people seem quite happy to ignore or are quick to mislabel as a simple food intolerane or allergy, which it is not and thus, it couldn't possibly affect their hormonal disorder or "genetic" acne. Sigh...how incredibly misinformed they are =(

#9 SweetJade1980

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Posted 22 February 2005 - 08:27 PM

QUOTE(Pika @ Feb 22 2005, 06:59 PM)
holy crap thank you SJ

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LOL, sorry. I just kinda wanted to lay it all on the table for ya. While there's plenty more, those should be relevant enough for you. ;-)

#10 blackbirdbeatle

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Posted 23 February 2005 - 01:53 AM

It's obviously not that simple as a lot of the glucose/insulin isn't stored in the liver. Ask any bodybuilder what's the most important thing to fast muscle gains and they'll tell you manipulating insulin.