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James Michael Howard
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 Posted: Thu Oct 16, 2003 3:08 am Post subject: the obesity epidemic and overeating, overweight kids |
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Testosterone reduces leptin. Leptin reduces appetite. Therefore, children of
higher testosterone have less appetite suppression. It is my hypothesis that
the percentage of individuals of higher testosterone is increasing. Therefore,
overeating is increasing. This accounts for the obesity "epidemic" in the U.S.
James Michael Howard
www.anthropogeny.com |
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Rich
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| Posted: Thu Oct 16, 2003 9:59 pm Post subject: Re: the obesity epidemic and overeating, overweight kids |
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James Michael Howard replied:
[quote]Testosterone reduces leptin. Leptin reduces appetite. Therefore, children of
higher testosterone have less appetite suppression. It is my hypothesis that
the percentage of individuals of higher testosterone is increasing. Therefore,
overeating is increasing. This accounts for the obesity "epidemic" in the U.S.
[/quote]
Really? How do your model account for fat women?
Rich
[quote]James Michael Howard
www.anthropogeny.com[/quote] |
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James Michael Howard
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| Posted: Fri Oct 17, 2003 12:05 am Post subject: Re: the obesity epidemic and overeating, overweight kids |
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On Thu, 16 Oct 2003 09:59:55 -0700, Rich <someone@someplace.com> wrote:
[quote]
James Michael Howard replied:
Testosterone reduces leptin. Leptin reduces appetite. Therefore, children of
higher testosterone have less appetite suppression. It is my hypothesis that
the percentage of individuals of higher testosterone is increasing. Therefore,
overeating is increasing. This accounts for the obesity "epidemic" in the U.S.
Really? How do your model account for fat women?
Rich
"Serum levels of estradiol, non-sex hormone binding globulin bound estradiol,[/quote]
estrone, estrone sulfate, and testosterone increased significantly with
increasing body mass index (BMI), whereas sex hormone binding globulin levels
decreased. After adjusting for BMI, nulliparous women tended to have higher
testosterone levels compared with parous women (P = 0.05), ..." Cancer Epidemiol
Biomarkers Prev. 2003 Apr;12(4):380-3 |
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James Michael Howard
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| Posted: Fri Oct 17, 2003 2:45 am Post subject: Re: the obesity epidemic and overeating, overweight kids |
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I forgot these two:
Nutr Cancer. 2001;41(1-2):47-56
Sex hormone levels in premenopausal African-American women with upper and lower body fat phenotypes.
Barnett JB, Woods MN, Rosner B, McCormack C, Longcope C, Houser RF Jr, Gorbach SL.
Nutrition Unit, Department of Family Medicine and Community Health, Tufts University School of Medicine, Boston, MA 02111, USA.
Body fat distribution may be a better marker of a hormonal pattern associated with increased breast cancer risk than obesity. This cross-sectional study of 106 healthy premenopausal African-American (AA) women compared the midfollicular phase sex hormone and sex hormone-binding globulin levels in upper body fat (UBF) and lower body fat (LBF) phenotype and obese and nonobese women. Multivariate regression analyses were used to control for various confounders, including dietary factors. UBF phenotype women had 37% (P = 0.02), 50% (P = 0.01), 52% (P = 0.007), and 50% (P = 0.009) higher levels of estradiol (E2), free E2, testosterone (T), and free T, respectively, than LBF phenotype women. Only %free T was higher in obese than in nonobese women (P = 0.02). The levels of E2, free E2, %free E2, T, and free T were higher [by 42% (P = 0.01), 68% (P = 0.001), 18% (P = 0.04), 36% (P = 0.04), and 61% (P = 0.01), respectively] and the level of sex hormone-binding globulin was lower [by 28% (P = 0.04)] in obese UBF than in nonobese LBF phenotype women. These findings support the hypothesis that body fat distribution may be a better marker of a hormonal pattern associated with increased breast cancer risk than obesity. Obese UBF phenotype AA women, in particular, have a high-risk hormonal profile. Future breast cancer studies might consider controlling for measures of obesity and body fat distribution to minimize confounding.
and:
Wien Klin Wochenschr. 2002 May 15;114(8-9):321-6. Related Articles, Links
Insulin resistance and androgens in healthy women with different body fat distributions.
Ivandic A, Prpic-Krizevac I, Bozic D, Barbir A, Peljhan V, Balog Z, Glasnovic M.
Department of Internal Medicine, Osijek University Hospital, Osijek, Croatia
OBJECTIVE: To compare androgens and sex hormone-binding globulin (SHBG) levels, and indices of insulin sensitivity (the response of plasma insulin and C-peptide in OGTT, insulin resistance and beta-cell activity estimated with the homeostasis assessment model (HOMA model) in healthy obese premenopausal women with different body fat distributions. PATIENTS AND METHODS: Free testosterone, androstenedione, SHBG levels and responses of plasma glucose, insulin and C-peptide in OGTT were examined in 74 healthy premenopausal women (19 with lower-body obesity (WHR < 0.80), 20 with pure abdominal obesity (WHR > 0.85), 19 with predominant abdominal obesity (WHR 0.81-0.85) and 18 normal-weight women). Insulin resistance and beta-cell function were estimated with the HOMA model. RESULTS: Both fasting and glucose-induced insulin levels were higher in women with pure abdominal obesity than in the controls (p < 0.001) and in those with lower-body obesity (P < 0.01). Insulin resistance was also higher in women with pure abdominal obesity than in the controls (p < 0.01) and those with lower-body obesity (p < 0.05). Free testosterone (p < 0.01) was higher and SHBG (p < 0.001) was lower in women with abdominal obesity than in the control group and those with lower-body obesity. Insulin significantly correlated with SHBG, and this correlation was independent of androgens, obesity and obesity type. Beta-cell function positively correlated with free testosterone, whereas insulin resistance negatively correlated with SHBG, and was independent of obesity and obesity type. CONCLUSIONS: In healthy premenopausal women, increased BMI and more pronounced abdominal fat accumulation was associated with increased androgenic activity (higher free testosterone and lower SHBG levels) and with insulin resistance estimated using the HOMA model, as well as with increasing basal and glucose-induced insulin levels. SHBG levels correlated with insulin and insulin resistance independently of the degree of obesity, obesity type and androgens, whereas beta-cell function correlated only with free testosterone.
"James Michael Howard" <jmhoward@arkansas.net> wrote in message news:ctqtovoqfsp3urdqfam6q030sujou5atll@4ax.com...
[quote]On Thu, 16 Oct 2003 09:59:55 -0700, Rich <someone@someplace.com> wrote:
James Michael Howard replied:
Testosterone reduces leptin. Leptin reduces appetite. Therefore, children of
higher testosterone have less appetite suppression. It is my hypothesis that
the percentage of individuals of higher testosterone is increasing. Therefore,
overeating is increasing. This accounts for the obesity "epidemic" in the U.S.
Really? How do your model account for fat women?
Rich
"Serum levels of estradiol, non-sex hormone binding globulin bound estradiol,
estrone, estrone sulfate, and testosterone increased significantly with
increasing body mass index (BMI), whereas sex hormone binding globulin levels
decreased. After adjusting for BMI, nulliparous women tended to have higher
testosterone levels compared with parous women (P = 0.05), ..." Cancer Epidemiol
Biomarkers Prev. 2003 Apr;12(4):380-3[/quote] |
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James Michael Howard
Guest
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| Posted: Fri Oct 17, 2003 2:55 am Post subject: Re: the obesity epidemic and overeating, overweight kids (RE |
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I forgot these two:
Nutr Cancer. 2001;41(1-2):47-56
Sex hormone levels in premenopausal African-American women with upper and lower
body fat phenotypes.
Barnett JB, Woods MN, Rosner B, McCormack C, Longcope C, Houser RF Jr, Gorbach
SL.
Nutrition Unit, Department of Family Medicine and Community Health, Tufts
University School of Medicine, Boston, MA 02111, USA.
Body fat distribution may be a better marker of a hormonal pattern associated
with increased breast cancer risk than obesity. This cross-sectional study of
106 healthy premenopausal African-American (AA) women compared the midfollicular
phase sex hormone and sex hormone-binding globulin levels in upper body fat
(UBF) and lower body fat (LBF) phenotype and obese and nonobese women.
Multivariate regression analyses were used to control for various confounders,
including dietary factors. UBF phenotype women had 37% (P = 0.02), 50% (P =
0.01), 52% (P = 0.007), and 50% (P = 0.009) higher levels of estradiol (E2),
free E2, testosterone (T), and free T, respectively, than LBF phenotype women.
*************Only %free T was higher in obese than in nonobese women (P =
0.02).*********** The levels of E2, free E2, %free E2, T, and free T were higher
[by 42% (P = 0.01), 68% (P = 0.001), 18% (P = 0.04), 36% (P = 0.04), and 61% (P
= 0.01), respectively] and the level of sex hormone-binding globulin was lower
[by 28% (P = 0.04)] in obese UBF than in nonobese LBF phenotype women. These
findings support the hypothesis that body fat distribution may be a better
marker of a hormonal pattern associated with increased breast cancer risk than
obesity. Obese UBF phenotype AA women, in particular, have a high-risk hormonal
profile. Future breast cancer studies might consider controlling for measures of
obesity and body fat distribution to minimize confounding.
and:
Wien Klin Wochenschr. 2002 May 15;114(8-9):321-6. Related Articles, Links
Insulin resistance and androgens in healthy women with different body fat
distributions.
Ivandic A, Prpic-Krizevac I, Bozic D, Barbir A, Peljhan V, Balog Z, Glasnovic M.
Department of Internal Medicine, Osijek University Hospital, Osijek, Croatia
OBJECTIVE: To compare androgens and sex hormone-binding globulin (SHBG) levels,
and indices of insulin sensitivity (the response of plasma insulin and C-peptide
in OGTT, insulin resistance and beta-cell activity estimated with the
homeostasis assessment model (HOMA model) in healthy obese premenopausal women
with different body fat distributions. PATIENTS AND METHODS: Free testosterone,
androstenedione, SHBG levels and responses of plasma glucose, insulin and
C-peptide in OGTT were examined in 74 healthy premenopausal women (19 with
lower-body obesity (WHR < 0.80), 20 with pure abdominal obesity (WHR > 0.85), 19
with predominant abdominal obesity (WHR 0.81-0.85) and 18 normal-weight women).
Insulin resistance and beta-cell function were estimated with the HOMA model.
RESULTS: Both fasting and glucose-induced insulin levels were higher in women
with pure abdominal obesity than in the controls (p < 0.001) and in those with
lower-body obesity (P < 0.01). Insulin resistance was also higher in women with
pure abdominal obesity than in the controls (p < 0.01) and those with lower-body
obesity (p < 0.05). Free testosterone (p < 0.01) was higher and SHBG (p < 0.001)
was lower in women with abdominal obesity than in the control group and those
with lower-body obesity. Insulin significantly correlated with SHBG, and this
correlation was independent of androgens, obesity and obesity type. Beta-cell
function positively correlated with free testosterone, whereas insulin
resistance negatively correlated with SHBG, and was independent of obesity and
obesity type. CONCLUSIONS: *******In healthy premenopausal women, increased BMI
and more pronounced abdominal fat accumulation was associated with increased
androgenic activity (higher free testosterone and lower SHBG levels)*********
and with insulin resistance estimated using the HOMA model, as well as with
increasing basal and glucose-induced insulin levels. SHBG levels correlated with
insulin and insulin resistance independently of the degree of obesity, obesity
type and androgens, whereas beta-cell function correlated only with free
testosterone.
"James Michael Howard" <jmhoward@arkansas.net> wrote in message
news:ctqtovoqfsp3urdqfam6q030sujou5atll@4ax.com...
[quote]On Thu, 16 Oct 2003 09:59:55 -0700, Rich <someone@someplace.com> wrote:
James Michael Howard replied:
Testosterone reduces leptin. Leptin reduces appetite. Therefore, children of
higher testosterone have less appetite suppression. It is my hypothesis that
the percentage of individuals of higher testosterone is increasing. Therefore,
overeating is increasing. This accounts for the obesity "epidemic" in the U.S.
Really? How do your model account for fat women?
Rich
"Serum levels of estradiol, non-sex hormone binding globulin bound estradiol,
estrone, estrone sulfate, and testosterone increased significantly with
increasing body mass index (BMI), whereas sex hormone binding globulin levels
decreased. After adjusting for BMI, nulliparous women tended to have higher
testosterone levels compared with parous women (P = 0.05), ..." Cancer Epidemiol
Biomarkers Prev. 2003 Apr;12(4):380-3[/quote] |
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