Thanks, guys! Have you been trying it? In the Braggs book, it describes it in this way: each hair follicle has its own oil can. The oil can gets clogged by this stuff called bottle bacilli which makes the hair stop growing. The acv kills the bottle bacilli and stimulates the oil can for greater activity. They even suggest adding a pinch of cayenne powder with it. (Page 26) I might give that a go, too.
Apple Cider Vinegar... part II
- Thread starter squeegee
- Start date
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Apple Cider Vinegar Attenuates Lipid Profile in Normal and Diabetic Rats
Research Article
Apple Cider Vinegar Attenuates Lipid Profile in Normal and Diabetic Rats
F. Shishehbor, A. Mansoori, A.R. Sarkaki, M.T. Jalali and S.M. Latifi
ABSTRACT
In this study, the effect of apple cider vinegar on Fasting Blood Glucose (FBG), glycated haemoglobin (HbA1c) and lipid profile in normal and diabetic rats was investigated. Diabetes was induced in male Wistar rats (300±30 g) by the intraperitoneal injection of streptozotocin (60 mg kg-1 of body weight). Both normal and diabetic animals were fed with standard animal food containing apple cider vinegar (6% w/w) for 4 weeks. Fasting blood glucose did not change, while HbA1c significantly decreased by apple cider vinegar in diabetic group (p<0.05). In normal rats fed with vinegar, significant reduction of low density lipoprotein-cholesterol (LDL-c) (p<0.005) and significant increase of high density lipoprotein-cholesterol (HDL-c) levels (p<0.005) were observed. Apple cider vinegar also reduced serum triglyceride (TG) levels (p<0.005) and increased HDL-c (p<0.005) in diabetic animals. These results indicate that apple cider vinegar improved the serum lipid profile in normal and diabetic rats by decreasing serum TG, LDL-c and increasing serum HDL-c and may be of great value in managing the diabetic complications.
Research Article
Apple Cider Vinegar Attenuates Lipid Profile in Normal and Diabetic Rats
F. Shishehbor, A. Mansoori, A.R. Sarkaki, M.T. Jalali and S.M. Latifi
ABSTRACT
In this study, the effect of apple cider vinegar on Fasting Blood Glucose (FBG), glycated haemoglobin (HbA1c) and lipid profile in normal and diabetic rats was investigated. Diabetes was induced in male Wistar rats (300±30 g) by the intraperitoneal injection of streptozotocin (60 mg kg-1 of body weight). Both normal and diabetic animals were fed with standard animal food containing apple cider vinegar (6% w/w) for 4 weeks. Fasting blood glucose did not change, while HbA1c significantly decreased by apple cider vinegar in diabetic group (p<0.05). In normal rats fed with vinegar, significant reduction of low density lipoprotein-cholesterol (LDL-c) (p<0.005) and significant increase of high density lipoprotein-cholesterol (HDL-c) levels (p<0.005) were observed. Apple cider vinegar also reduced serum triglyceride (TG) levels (p<0.005) and increased HDL-c (p<0.005) in diabetic animals. These results indicate that apple cider vinegar improved the serum lipid profile in normal and diabetic rats by decreasing serum TG, LDL-c and increasing serum HDL-c and may be of great value in managing the diabetic complications.
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djarr said:Just wanted to upload acvfan's progress pictures directly to the thread.
Progress looks legit, might start putting this stuff on my temples.
All I can say is Holly f***!!!!!!!!!!!!!!!!
unk: unk: a lot more hair. thicker and stronger,, everything seems healthier! Good job ACV fan! I am going to IV that sh*t!!!
squeegee
Banned
- Reaction score
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God.. is it because ACV improves insuline sensitivity? or others effects on Cholesterol??
OBJECTIVE: To investigate the influence of sodium acetate and acetic acid from vinegar on blood glucose and acetate response to a mixed meal in healthy subjects. DESIGN: Five healthy subjects consumed in random order six test meals consisting of 100 g of sliced lettuce dressed with olive oil (Blank), olive oil plus 1 g acetic acid in the form of vinegar (AcOH), or olive oil plus sodium acetate in the form of vinegar neutralized to pH 6.0 with sodium bicarbonate (AcNa). On three occasions test meals were followed by a challenge consisting of 50 g carbohydrate portions of white bread (Bread). Glucose and acetate concentrations were measured in arterialized capillary blood before and until 95 min after the meals. Ultrasonography was performed in four other subjects to measure gastric emptying times after AcOH + Bread and AcNa + Bread. RESULTS: Blood acetate response over 95 min was markedly reduced after AcOH and AcOH+Bread meals compared to AcNa and AcNa + Bread. Similarly, the glucose response was depressed by 31.4% (P = 0.0228) after AcOH+Bread with respect to AcNa + Bread and Blank + Bread. No difference was observed between gastric emptying times after AcOH + Bread and AcNa + Bread. CONCLUSIONS: The results suggest that oral acetic acid and acetate might have a different effect on acetataemia and that a limited dose of vinegar, in the form of salad dressing, is sufficient to influence significantly the glycaemic response to a mixed meal in normal subjects by a mechanism related to acidity but not to gastric emptying.
Blood Glucose Control
The antiglycemic effect of vinegar was first reported by Ebihara and Nakajima[47] in 1988. In rats, the blood glucose response to a 10% corn starch load was significantly reduced when coadministered with a 2% acetic acid solution.[45] In healthy human subjects, although the glucose response curve was not significantly altered, the area under the insulin response curve following the ingestion of 50 g sucrose was reduced 20% when coadministered with 60 mL strawberry vinegar.[47] Several years later, Brighenti and colleagues[48] demonstrated in normoglycemic subjects that 20 mL white vinegar (5% acetic acid) as a salad dressing ingredient reduced the glycemic response to a mixed meal (lettuce salad and white bread containing 50 g carbohydrate) by over 30% (P < .05). Salad dressings made from neutralized vinegar, formulated by adding 1.5 g sodium bicarbonate to 20 mL white vinegar, or a salt solution (1.5 g sodium chloride in 20 mL water) did not significantly affect the glycemic response to the mixed meal.[48] Separate placebo-controlled trials have corroborated the meal-time, antiglycemic effects of 20 g vinegar in healthy adults.[49?51]
While compiling a glycemic index (GI) table for 32 common Japanese foods, Sugiyama and colleagues[52] documented that the addition of vinegar or pickled foods to rice (eg, sushi) decreased the GI of rice by 20% to 35%. In these trials, healthy fasted subjects ingested the reference and test foods, each containing 50 g carbohydrate, on random days, and the food GI was calculated using the areas under the 2-hour blood glucose response curves. In the vinegar-containing foods, the amount of acetic acid was estimated to be 0.3-2.3 g, an amount similar to that found in 20 g vinegar (approximately 1 g). Ostman and colleagues[53] reported that substitution of a pickled cucumber (1.6 g acetic acid) for a fresh cucumber (0 g acetic acid) in a test meal (bread, butter, and yogurt) reduced meal GI by over 30%[53] in healthy subjects.
Recently, the antiglycemic property of vinegar was demonstrated to extend to individuals with marked insulin resistance or type 2 diabetes.[54] In this crossover trial, individuals with insulin resistance (n = 11, fasting insulin concentrations greater than 20 mU/mL) or with diagnosed type 2 diabetes (n = 10) consumed a vinegar test drink (20 g vinegar, 40 g water, 1 tsp saccharine) or placebo immediately before the consumption of a mixed meal (87 g total carbohydrate). In the insulin-resistant subjects, vinegar ingestion reduced postprandial glycemia 64% as compared with placebo values (P = .014) and improved postprandial insulin sensitivity by 34% (P= .01). In individuals with type 2 diabetes, vinegar ingestion was less effective at reducing mealtime glycemia (?17%, P = .149); however, vinegar ingestion was associated with a slight improvement in postprandial insulin sensitivity in these subjects (+19%, P = .07).[54] The lack of a significant effect of vinegar on mealtime glycemia in the type 2 diabetics may be related to the use of venous blood sampling in this trial. Greater within-subject variation in glucose concentrations are noted for venous blood as compared with capillary blood; moreover, the concentration of glucose in venous blood is lower than that in capillary blood. Thus, capillary blood sampling is preferred for determining the glycemic response to food.[55]
The marked antiglycemic effect of vinegar in insulin-resistant subjects is noteworthy and may have important implications. Multicenter trials have demonstrated that treatment with antiglycemic pharmaceuticals (metformin or acarbose) slowed the progression to diabetes in high-risk individuals[56,57]; moreover, because these drugs improved insulin sensitivity, the probability that individuals with impaired glucose tolerance would revert to a normal, glucose-tolerant state over time was increased.[57]
In healthy subjects, Ostman and colleagues[58] demonstrated that acetic acid had a dose-response effect on postprandial glycemia and insulinemia. Subjects consumed white bread (50 g carbohydrate) alone or with 3 portions of vinegar containing 1.1, 1.4, or 1.7 g acetic acid. At 30 minutes post-meal, blood glucose concentrations were significantly reduced by all concentrations of acetic acid as compared with the control value, and a negative linear relationship was calculated between blood glucose concentrations and the acetic acid content of the meal (r = ?0.47, P = .001). Subjects were also asked to rate feelings of hunger/satiety on a scale ranging from extreme hunger (?10) to extreme satiety (+10) before meal consumption and at 15-minute intervals after the meal. Bread consumption alone scored the lowest rating of satiety (calculated as area under the curve from time 0-120 minutes). Feelings of satiety increased when vinegar was ingested with the bread, and a linear relationship was observed between satiety and the acetic acid content of the test meals (r = 0.41, P = .004).[58]
In a separate trial, healthy adult women consumed fewer total calories on days that vinegar was ingested at the morning meal.[50] In this trial, which used a blinded, randomized, placebo-controlled, crossover design, fasting participants consumed a test drink (placebo or vinegar) followed by the test meal composed of a buttered bagel and orange juice (87 g carbohydrate). Blood samples were collected for 1 hour after the meal. At the end of testing, participants were allowed to follow their normal activities and eating patterns the remainder of the day, but they were instructed to record food and beverage consumption until bedtime. Vinegar ingestion, as compared with placebo, reduced the 60-minute glucose response to the test meal (?54%, P < .05) and weakly affected later energy consumption (?200 kilocalories, P = .111). Regression analyses indicated that 60-minute glucose responses to test meals explained 11% to 16% of the variance in later energy consumption (P < .05).[50] Thus, vinegar may affect satiety by reducing the meal-time glycemic load. Of 20 studies published between 1977 and 1999, 16 demonstrated that low-glycemic index foods promoted postmeal satiety and/or reduced subsequent hunger.[59]
It is not known how vinegar alters meal-induced glycemia, but several mechanisms have been proposed. Ogawa and colleagues examined the effects of acetic acid and other organic acids on disaccharidase activity in Caco-2 cells.[60] Acetic acid (5 mmol/L) suppressed sucrase, lactase, and maltase activities in concentration- and time-dependent manners as compared with control values, but the other organic acids (eg, citric, succinic, L-maric, and L-lactic acids) did not suppress enzyme activities. Because acetic acid treatment did not affect the de-novo synthesis of the sucrase-isomaltase complex at either the transcriptional or translational levels, the investigators concluded that the suppressive effect of acetic acid likely occurs during the posttranslational processing of the enzyme complex.[60] Of note, the lay literature has long proclaimed that vinegar interferes with starch digestion and should be avoided at meal times.[61]
Several investigations examined whether delayed gastric emptying contributed to the antiglycemic effect of vinegar. Using noninvasive ultrasonography, Brighenti and colleagues[50] did not observe a difference in gastric emptying rates in healthy subjects consuming bread (50 g carbohydrate) in association with acetic acid (ie, vinegar) vs sodium acetate (ie, vinegar neutralized by the addition of sodium bicarbonate); however, a significant difference in post-meal glycemia was noted between treatments with the acetic acid treatment lowering glycemia by 31.4%. In a later study, Liljeberg and Bjorck[62] added paracetamol to the bread test meal to permit indirect measurement of the gastric emptying rate. Compared with reference values, postmeal serum glucose and paracetamol concentrations were reduced significantly when the test meal was consumed with vinegar. The results of this study should be carefully considered, however, because paracetamol levels in blood may be affected by food factors and other gastrointestinal events. In rats fed experimental diets containing the indigestible marker polyethylenglycol and varying concentrations of acetic acid (0, 4, 8, 16 g acetic acid/100 g diet), dietary acetic acid did not alter gastric emptying, the rate of food intake, or glucose absorption.[63]
OBJECTIVE: To investigate the influence of sodium acetate and acetic acid from vinegar on blood glucose and acetate response to a mixed meal in healthy subjects. DESIGN: Five healthy subjects consumed in random order six test meals consisting of 100 g of sliced lettuce dressed with olive oil (Blank), olive oil plus 1 g acetic acid in the form of vinegar (AcOH), or olive oil plus sodium acetate in the form of vinegar neutralized to pH 6.0 with sodium bicarbonate (AcNa). On three occasions test meals were followed by a challenge consisting of 50 g carbohydrate portions of white bread (Bread). Glucose and acetate concentrations were measured in arterialized capillary blood before and until 95 min after the meals. Ultrasonography was performed in four other subjects to measure gastric emptying times after AcOH + Bread and AcNa + Bread. RESULTS: Blood acetate response over 95 min was markedly reduced after AcOH and AcOH+Bread meals compared to AcNa and AcNa + Bread. Similarly, the glucose response was depressed by 31.4% (P = 0.0228) after AcOH+Bread with respect to AcNa + Bread and Blank + Bread. No difference was observed between gastric emptying times after AcOH + Bread and AcNa + Bread. CONCLUSIONS: The results suggest that oral acetic acid and acetate might have a different effect on acetataemia and that a limited dose of vinegar, in the form of salad dressing, is sufficient to influence significantly the glycaemic response to a mixed meal in normal subjects by a mechanism related to acidity but not to gastric emptying.
Blood Glucose Control
The antiglycemic effect of vinegar was first reported by Ebihara and Nakajima[47] in 1988. In rats, the blood glucose response to a 10% corn starch load was significantly reduced when coadministered with a 2% acetic acid solution.[45] In healthy human subjects, although the glucose response curve was not significantly altered, the area under the insulin response curve following the ingestion of 50 g sucrose was reduced 20% when coadministered with 60 mL strawberry vinegar.[47] Several years later, Brighenti and colleagues[48] demonstrated in normoglycemic subjects that 20 mL white vinegar (5% acetic acid) as a salad dressing ingredient reduced the glycemic response to a mixed meal (lettuce salad and white bread containing 50 g carbohydrate) by over 30% (P < .05). Salad dressings made from neutralized vinegar, formulated by adding 1.5 g sodium bicarbonate to 20 mL white vinegar, or a salt solution (1.5 g sodium chloride in 20 mL water) did not significantly affect the glycemic response to the mixed meal.[48] Separate placebo-controlled trials have corroborated the meal-time, antiglycemic effects of 20 g vinegar in healthy adults.[49?51]
While compiling a glycemic index (GI) table for 32 common Japanese foods, Sugiyama and colleagues[52] documented that the addition of vinegar or pickled foods to rice (eg, sushi) decreased the GI of rice by 20% to 35%. In these trials, healthy fasted subjects ingested the reference and test foods, each containing 50 g carbohydrate, on random days, and the food GI was calculated using the areas under the 2-hour blood glucose response curves. In the vinegar-containing foods, the amount of acetic acid was estimated to be 0.3-2.3 g, an amount similar to that found in 20 g vinegar (approximately 1 g). Ostman and colleagues[53] reported that substitution of a pickled cucumber (1.6 g acetic acid) for a fresh cucumber (0 g acetic acid) in a test meal (bread, butter, and yogurt) reduced meal GI by over 30%[53] in healthy subjects.
Recently, the antiglycemic property of vinegar was demonstrated to extend to individuals with marked insulin resistance or type 2 diabetes.[54] In this crossover trial, individuals with insulin resistance (n = 11, fasting insulin concentrations greater than 20 mU/mL) or with diagnosed type 2 diabetes (n = 10) consumed a vinegar test drink (20 g vinegar, 40 g water, 1 tsp saccharine) or placebo immediately before the consumption of a mixed meal (87 g total carbohydrate). In the insulin-resistant subjects, vinegar ingestion reduced postprandial glycemia 64% as compared with placebo values (P = .014) and improved postprandial insulin sensitivity by 34% (P= .01). In individuals with type 2 diabetes, vinegar ingestion was less effective at reducing mealtime glycemia (?17%, P = .149); however, vinegar ingestion was associated with a slight improvement in postprandial insulin sensitivity in these subjects (+19%, P = .07).[54] The lack of a significant effect of vinegar on mealtime glycemia in the type 2 diabetics may be related to the use of venous blood sampling in this trial. Greater within-subject variation in glucose concentrations are noted for venous blood as compared with capillary blood; moreover, the concentration of glucose in venous blood is lower than that in capillary blood. Thus, capillary blood sampling is preferred for determining the glycemic response to food.[55]
The marked antiglycemic effect of vinegar in insulin-resistant subjects is noteworthy and may have important implications. Multicenter trials have demonstrated that treatment with antiglycemic pharmaceuticals (metformin or acarbose) slowed the progression to diabetes in high-risk individuals[56,57]; moreover, because these drugs improved insulin sensitivity, the probability that individuals with impaired glucose tolerance would revert to a normal, glucose-tolerant state over time was increased.[57]
In healthy subjects, Ostman and colleagues[58] demonstrated that acetic acid had a dose-response effect on postprandial glycemia and insulinemia. Subjects consumed white bread (50 g carbohydrate) alone or with 3 portions of vinegar containing 1.1, 1.4, or 1.7 g acetic acid. At 30 minutes post-meal, blood glucose concentrations were significantly reduced by all concentrations of acetic acid as compared with the control value, and a negative linear relationship was calculated between blood glucose concentrations and the acetic acid content of the meal (r = ?0.47, P = .001). Subjects were also asked to rate feelings of hunger/satiety on a scale ranging from extreme hunger (?10) to extreme satiety (+10) before meal consumption and at 15-minute intervals after the meal. Bread consumption alone scored the lowest rating of satiety (calculated as area under the curve from time 0-120 minutes). Feelings of satiety increased when vinegar was ingested with the bread, and a linear relationship was observed between satiety and the acetic acid content of the test meals (r = 0.41, P = .004).[58]
In a separate trial, healthy adult women consumed fewer total calories on days that vinegar was ingested at the morning meal.[50] In this trial, which used a blinded, randomized, placebo-controlled, crossover design, fasting participants consumed a test drink (placebo or vinegar) followed by the test meal composed of a buttered bagel and orange juice (87 g carbohydrate). Blood samples were collected for 1 hour after the meal. At the end of testing, participants were allowed to follow their normal activities and eating patterns the remainder of the day, but they were instructed to record food and beverage consumption until bedtime. Vinegar ingestion, as compared with placebo, reduced the 60-minute glucose response to the test meal (?54%, P < .05) and weakly affected later energy consumption (?200 kilocalories, P = .111). Regression analyses indicated that 60-minute glucose responses to test meals explained 11% to 16% of the variance in later energy consumption (P < .05).[50] Thus, vinegar may affect satiety by reducing the meal-time glycemic load. Of 20 studies published between 1977 and 1999, 16 demonstrated that low-glycemic index foods promoted postmeal satiety and/or reduced subsequent hunger.[59]
It is not known how vinegar alters meal-induced glycemia, but several mechanisms have been proposed. Ogawa and colleagues examined the effects of acetic acid and other organic acids on disaccharidase activity in Caco-2 cells.[60] Acetic acid (5 mmol/L) suppressed sucrase, lactase, and maltase activities in concentration- and time-dependent manners as compared with control values, but the other organic acids (eg, citric, succinic, L-maric, and L-lactic acids) did not suppress enzyme activities. Because acetic acid treatment did not affect the de-novo synthesis of the sucrase-isomaltase complex at either the transcriptional or translational levels, the investigators concluded that the suppressive effect of acetic acid likely occurs during the posttranslational processing of the enzyme complex.[60] Of note, the lay literature has long proclaimed that vinegar interferes with starch digestion and should be avoided at meal times.[61]
Several investigations examined whether delayed gastric emptying contributed to the antiglycemic effect of vinegar. Using noninvasive ultrasonography, Brighenti and colleagues[50] did not observe a difference in gastric emptying rates in healthy subjects consuming bread (50 g carbohydrate) in association with acetic acid (ie, vinegar) vs sodium acetate (ie, vinegar neutralized by the addition of sodium bicarbonate); however, a significant difference in post-meal glycemia was noted between treatments with the acetic acid treatment lowering glycemia by 31.4%. In a later study, Liljeberg and Bjorck[62] added paracetamol to the bread test meal to permit indirect measurement of the gastric emptying rate. Compared with reference values, postmeal serum glucose and paracetamol concentrations were reduced significantly when the test meal was consumed with vinegar. The results of this study should be carefully considered, however, because paracetamol levels in blood may be affected by food factors and other gastrointestinal events. In rats fed experimental diets containing the indigestible marker polyethylenglycol and varying concentrations of acetic acid (0, 4, 8, 16 g acetic acid/100 g diet), dietary acetic acid did not alter gastric emptying, the rate of food intake, or glucose absorption.[63]
squeegee
Banned
- Reaction score
- 132
What is the enzymes that break down sugars???? Amylase?
Apple Cider Vinegar - and all other acidic drinks (e.g., orange juice and lemon juice) - deactivate an enzyme, amylase, in the saliva. Amylase in the mouth splits food starches into glucose molecules, which can enter the blood stream immediately. (Amylase is also released by the pancreas and enters the small intestine later when the food finally arrives there.) The deactivation of amylase in the mouth might account for the lowering of blood sugar in individuals who drink ACV BEFORE a high-carb meal.
Vinegar Delight
Research suggests that a little bit of vinegar could have a beneficial effect on blood sugar levels.
In a study, ingesting a couple tablespoons of apple cider vinegar before a high-carbohydrate meal was found to help dampen expected spikes in blood sugar levels from the meal.
For a bit of vinegar's benefit, try starting off your next pasta meal with a salad splashed with red wine vinegar and olive oil.
Vinegar is no substitute for healthy eating habits or for proven methods of blood sugar control. The beneficial effects of vinegar on blood sugar levels may not apply to healthy individuals, and more research is needed to confirm its potential benefits for other populations.
In a recent study, ingesting 20 grams (approximately 2 tablespoons) of apple cider vinegar before eating a high-carbohydrate meal improved insulin resistance.
Study participants who experienced the blood sugar control benefits from vinegar were either diabetic or had insulin resistance syndrome. They followed the 20 grams of apple cider vinegar with a high-carbohydrate meal consisting of a white bagel, butter, and orange juice.
After the high-carbohydrate meal, the acetic acid from the earlier serving of vinegar appeared to reduce blood sugar levels by 19 percent in people with diabetes and by 34 percent in people with insulin resistance.
Acetic acid may help lower blood sugar levels by suppressing enzymes required to break down sugars, resulting in slower absorption.
Apple Cider Vinegar - and all other acidic drinks (e.g., orange juice and lemon juice) - deactivate an enzyme, amylase, in the saliva. Amylase in the mouth splits food starches into glucose molecules, which can enter the blood stream immediately. (Amylase is also released by the pancreas and enters the small intestine later when the food finally arrives there.) The deactivation of amylase in the mouth might account for the lowering of blood sugar in individuals who drink ACV BEFORE a high-carb meal.
Vinegar Delight
Research suggests that a little bit of vinegar could have a beneficial effect on blood sugar levels.
In a study, ingesting a couple tablespoons of apple cider vinegar before a high-carbohydrate meal was found to help dampen expected spikes in blood sugar levels from the meal.
For a bit of vinegar's benefit, try starting off your next pasta meal with a salad splashed with red wine vinegar and olive oil.
Vinegar is no substitute for healthy eating habits or for proven methods of blood sugar control. The beneficial effects of vinegar on blood sugar levels may not apply to healthy individuals, and more research is needed to confirm its potential benefits for other populations.
In a recent study, ingesting 20 grams (approximately 2 tablespoons) of apple cider vinegar before eating a high-carbohydrate meal improved insulin resistance.
Study participants who experienced the blood sugar control benefits from vinegar were either diabetic or had insulin resistance syndrome. They followed the 20 grams of apple cider vinegar with a high-carbohydrate meal consisting of a white bagel, butter, and orange juice.
After the high-carbohydrate meal, the acetic acid from the earlier serving of vinegar appeared to reduce blood sugar levels by 19 percent in people with diabetes and by 34 percent in people with insulin resistance.
Acetic acid may help lower blood sugar levels by suppressing enzymes required to break down sugars, resulting in slower absorption.
squeegee
Banned
- Reaction score
- 132
Premature androgenic alopecia and insulin resistance. Male equivalent of polycystic ovary syndrome?
Starka L, Duskova M, Cermakova I, Vrbiková J, Hill M.
Institute of Endocrinology, Narodni 8, CZ 116 94 Prague 1, Czech Republic. lstarka@endo.cz
Abstract
BACKGROUND: Polycystic ovary syndrome (PCOS), the most frequent endocrinopathy in women with estimated prevalence of 5-10 %, is characterised by a hormonal and metabolic imbalance of polygene autosomal trait. The complexity of symptoms and genetic base started up the hypothesis on the existence of male equivalent of PCOS. Precocious loss of hair before 30 years of age was suggested as one of the male symptoms of this syndrome.
OBJECTIVES: The aim was to confirm the association of lower levels of follicle stimulating hormone (FSH) and sexual hormone binding globulin (SHBG) or higher free androgen index (FAI) in premature balding men with a reduced insulin sensitivity.
PATIENTS/METHODS: The study included 30 men with premature hair loss (defined as grade 3 vertex or more on the alopecia classification scale by Hamilton with Norwood modification) starting before 30 years of age. The hormonal values of the investigated group were compared with those regarded as normal reference values obtained in a group of 256 males in the age of 20-40 years during the Czech population study of iodine deficiency. In all men with premature baldness besides hormonal level determinations insulin tolerance test was carried out.
RESULTS: The observed group was divided into two subgroups. The first one showed similar hormonal changes as women with PCOS, namely subnormal SHBG, FSH or increased FAI. The other had either no anomalies in steroid spectrum or only lower SHBG. The groups did not differ either in BMI or in age. The group with hormonal profile resembling that of women with PCOS, showed significantly higher insulin resistance than the group without these changes.
CONCLUSIONS: The findings are consistent with the hypothesis that at least a part of the men with premature androgenic alopecia could be considered as a male equivalent of the polycystic ovary syndrome of the women. These premature balding men represent a risk group for the development of impaired glucose tolerance or diabetes mellitus type 2.
Androgenetic alopecia and insulin resistance in young men.
González-González JG, Mancillas-Adame LG, Fernández-Reyes M, Gómez-Flores M, Lavalle-González FJ, Ocampo-Candiani J, Villarreal-Pérez JZ.
Servicio de Endocrinologia, Dr Jose Eleuterio Gonzalez University Hospital, Facultad de Medicina, Universidad Autonoma de Nuevo Leon, Ave. Madero y Gonzalitos S/N, Monterrey, Mexico. jgonzalezg@fm.uanl.mx
Abstract
BACKGROUND: Epidemiological studies have associated androgenetic alopecia (Androgenetic Alopecia) with severe young-age coronary artery disease and hypertension, and linked it to insulin resistance. We carried out a case-control study in age- and weight-matched young males to study the link between Androgenetic Alopecia and insulin resistance using the homeostasis model assessment of insulin resistance (HOMA-IR) index or metabolic syndrome clinical manifestations.
METHODS: Eighty young males, 18-35 years old, with Androgenetic Alopecia > or = stage III in the Hamilton-Norwood classification, and 80 weight- and age-matched controls were included. Alopecia, glucose, serum insulin, HOMA-IR index, lipid profile and androgen levels, as well as metabolic syndrome criteria, were evaluated.
RESULTS: The HOMA-IR index was significantly higher in cases than controls. Nonobese cases had a higher mean diastolic blood pressure and a more frequent family history of Androgenetic Alopecia than nonobese controls. A borderline difference in the HOMA-IR index was found in obese Androgenetic Alopecia cases vs. obese controls [P = 0.055, 95% confidence interval (CI) 2.36-4.20 vs. 1.75-2.73]. Free testosterone values were significantly higher in controls than cases, regardless of body mass index (BMI). A statistically significant additive effect for obesity plus alopecia was found, with significant trends for insulin, the HOMA-IR index, lipids and free testosterone when BMI and alopecia status were used to classify the participants.
CONCLUSIONS: Our results support the recommendation for assessing insulin resistance and cardiovascular-related features and disorders in all young males with stage III or higher Androgenetic Alopecia, according to the Hamilton-Norwood classification.
Starka L, Duskova M, Cermakova I, Vrbiková J, Hill M.
Institute of Endocrinology, Narodni 8, CZ 116 94 Prague 1, Czech Republic. lstarka@endo.cz
Abstract
BACKGROUND: Polycystic ovary syndrome (PCOS), the most frequent endocrinopathy in women with estimated prevalence of 5-10 %, is characterised by a hormonal and metabolic imbalance of polygene autosomal trait. The complexity of symptoms and genetic base started up the hypothesis on the existence of male equivalent of PCOS. Precocious loss of hair before 30 years of age was suggested as one of the male symptoms of this syndrome.
OBJECTIVES: The aim was to confirm the association of lower levels of follicle stimulating hormone (FSH) and sexual hormone binding globulin (SHBG) or higher free androgen index (FAI) in premature balding men with a reduced insulin sensitivity.
PATIENTS/METHODS: The study included 30 men with premature hair loss (defined as grade 3 vertex or more on the alopecia classification scale by Hamilton with Norwood modification) starting before 30 years of age. The hormonal values of the investigated group were compared with those regarded as normal reference values obtained in a group of 256 males in the age of 20-40 years during the Czech population study of iodine deficiency. In all men with premature baldness besides hormonal level determinations insulin tolerance test was carried out.
RESULTS: The observed group was divided into two subgroups. The first one showed similar hormonal changes as women with PCOS, namely subnormal SHBG, FSH or increased FAI. The other had either no anomalies in steroid spectrum or only lower SHBG. The groups did not differ either in BMI or in age. The group with hormonal profile resembling that of women with PCOS, showed significantly higher insulin resistance than the group without these changes.
CONCLUSIONS: The findings are consistent with the hypothesis that at least a part of the men with premature androgenic alopecia could be considered as a male equivalent of the polycystic ovary syndrome of the women. These premature balding men represent a risk group for the development of impaired glucose tolerance or diabetes mellitus type 2.
Androgenetic alopecia and insulin resistance in young men.
González-González JG, Mancillas-Adame LG, Fernández-Reyes M, Gómez-Flores M, Lavalle-González FJ, Ocampo-Candiani J, Villarreal-Pérez JZ.
Servicio de Endocrinologia, Dr Jose Eleuterio Gonzalez University Hospital, Facultad de Medicina, Universidad Autonoma de Nuevo Leon, Ave. Madero y Gonzalitos S/N, Monterrey, Mexico. jgonzalezg@fm.uanl.mx
Abstract
BACKGROUND: Epidemiological studies have associated androgenetic alopecia (Androgenetic Alopecia) with severe young-age coronary artery disease and hypertension, and linked it to insulin resistance. We carried out a case-control study in age- and weight-matched young males to study the link between Androgenetic Alopecia and insulin resistance using the homeostasis model assessment of insulin resistance (HOMA-IR) index or metabolic syndrome clinical manifestations.
METHODS: Eighty young males, 18-35 years old, with Androgenetic Alopecia > or = stage III in the Hamilton-Norwood classification, and 80 weight- and age-matched controls were included. Alopecia, glucose, serum insulin, HOMA-IR index, lipid profile and androgen levels, as well as metabolic syndrome criteria, were evaluated.
RESULTS: The HOMA-IR index was significantly higher in cases than controls. Nonobese cases had a higher mean diastolic blood pressure and a more frequent family history of Androgenetic Alopecia than nonobese controls. A borderline difference in the HOMA-IR index was found in obese Androgenetic Alopecia cases vs. obese controls [P = 0.055, 95% confidence interval (CI) 2.36-4.20 vs. 1.75-2.73]. Free testosterone values were significantly higher in controls than cases, regardless of body mass index (BMI). A statistically significant additive effect for obesity plus alopecia was found, with significant trends for insulin, the HOMA-IR index, lipids and free testosterone when BMI and alopecia status were used to classify the participants.
CONCLUSIONS: Our results support the recommendation for assessing insulin resistance and cardiovascular-related features and disorders in all young males with stage III or higher Androgenetic Alopecia, according to the Hamilton-Norwood classification.
Hoppi
Senior Member
- Reaction score
- 61
Sorry to be a broken record but I believe insulin is only a factor in male pattern baldness because like cortisol it burdens the liver. It does also reduce SHBG (also released by the liver) but it's unclear which source of hormonal imbalance is the strongest
Thanks again Squeegee for helping with the photos. Is there a place on this forum that explains how to upload? I only hope that tons of other guys start having the same results as me - PLEASE document what is happening to you and share it. I don't want to be alone! Yes, it's doing great on the front- for some reason I've never lost any hair on the sides. As I apply the acv I take the cotton ball and basically smear it over the entire top of my head, including where there is still hair. It takes about three saturations of the cotton (I only use one cotton ball at a time). I rub it pretty vigorously on the very bald areas- like it was an astringent. It tingles for about 5 minutes after it's on. When I take photos again in March, I'll include include the front. (Yes, I'm still drinking it about 2 - 3 times a day - first Christmas in 20 years I haven't been sick with a cold.)
squeegee
Banned
- Reaction score
- 132
Hi!
Sorry for the questions here, but the whole thread is just to long for me to read, so hopefully someone can answer my questions concerning Apple cider vinegar. What is the "cure" that you are using? Is it any point for me to take a couple of glasses per day with this? I dont want to put any more on my head (using rogain), but have been thinking about trying this. Does it help the frontals?
In advance, many thanks!
Btw... Anyone else having problems uploading pictures? It seems that when I try to upload it only stays in the "upload mode", but never finishes. Any good advice?
Sorry for the questions here, but the whole thread is just to long for me to read, so hopefully someone can answer my questions concerning Apple cider vinegar. What is the "cure" that you are using? Is it any point for me to take a couple of glasses per day with this? I dont want to put any more on my head (using rogain), but have been thinking about trying this. Does it help the frontals?
In advance, many thanks!
Btw... Anyone else having problems uploading pictures? It seems that when I try to upload it only stays in the "upload mode", but never finishes. Any good advice?
Brasileirao
Experienced Member
- Reaction score
- 9
acvfan said:
I thought you were only drinking the stuff? I'm doing 1 tablespoon in the a.m. and one in the p.m. (before bed) Do you apply it after showering? Once a day to the scalp?
Man, your pics look great!
squeegee
Banned
- Reaction score
- 132
monty1978 said:I just saw the photos. Holy sh*t, that is quite unbelievable.
How old is/was your bald patch ACVfan?
You aren't playing some kind of cruel joke are you, I have to ask!
Assuming you aren't. I looked through my fluridil online order history and found that my first order was in March this year and I remember around May ish being over the moon at the result I was getting on my hair line. It all went to sh*t when I started adding other topicals. Anyway I do remember being more consistent using acv on my scalp around April/May and I also drank the odd capfull too as I had heard a rumour and thought it couldn't hurt.
Well I'm sold basically, I am gonna start having a cap full daily and commit to rinsing my scalp with it twice a week.
AWESOME photos
He just added the topical rinse regimen later ..impressive results! We had a guy on here ( a year or 2 ago) that had pretty much the same results with topical Aloe Vera.. ! Yes you can have results without the poison..
squeegee
Banned
- Reaction score
- 132
I bet Malic Acid is the magic ingredient in it..
Malic acid is a natural constituent of many fruits and vegetables that are preserved by fermentation. This acid may be broken down during fermentation by certain bacteria into lactic acid and carbon dioxide. This reaction is desired to reduce the acidity in certain types of wines, and is undesired in the fermentation of cucumbers because of gaseous spoilage from carbon dioxide accumulation inside the fruit.
Many traditional fresh and fermented ready-to-eat foods are dependent on their acidity as the primary means for controlling the presence of disease- causing bacteria. In such foods, how quickly pathogenic microorganisms are inactivated is dependent on both the level of acidity (pH) and the identity and amount of the specific acid associated with the food. Recent concern about the survival of acid resistant pathogens in apple cider produced a need for better information on how malic acid, the principal acid in apples, affects bacteria. The current study helps address that need by providing information on how malic acid and pH interact to inactivate the foodborne pathogen, Listeria monocytogenes. These results demonstrate that malic acid is one of the gentler food acids.
Malic acid is both derived from food sources and synthesized in the body through the citric acid cycle. Its importance to the production of energy in the body during both aerobic and anaerobic conditions is well established. Under aerobic conditions, the oxidation of malate to oxaloacetate provides reducing equivalents to the mitochondria through the malate-aspartate redox shuttle. During anaerobic conditions, where a buildup of excess of reducing equivalents inhibits glycolysis, malic acid's simultaneous reduction to succinate and oxidation to oxaloacetate is capable of removing the accumulating reducing equivalents. This allows malic acid to reverse hypoxia's inhibition of glycolysis and energy production. This may allow malic acid to improve energy production in Primary fibromyalgia (FM), reversing the negative effect of the relative hypoxia that has been found in these patients.
Because of its obvious relationship to energy depletion during exercise, malic acid may be of benefit to healthy individuals interested in maximizing their energy production, as well as those with FM. In the rat it has been found that only tissue malate is depleted following exhaustive physical activity. Other key metabolites from the citric acid cycle needed for energy production were found to be unchanged. Because of this, a deficiency of malic acid has been hypothesized to be a major cause of physical exhaustion. The administration of malic acid to rats has been shown to elevate mitochondrial malate and increase mitochondrial respiration and energy production. Surprisingly, relatively small amounts of exogenous malic acid were required to increase mitochondrial energy production and ATP formation. Under hypoxic conditions there is an increased demand and utilization of malic acid, and this demand is normally met by increasing the synthesis of malic acid through gluconeogenesis and muscle protein breakdown. This ultimately results in muscle breakdown and damage.
In a study on the effect of the oral administration of malic acid to rats, a significant increase in anaerobic endurance was found. Interestingly, the improvement in endurance was not accompanied by an increase in carbohydrate and oxygen utilization, suggesting that malic acid has carbohydrate and oxygen-sparing effects. In addition, malic acid is the only metabolite of the citric acid cycle positively correlated with physical activity. It has also been demonstrated that exercise-induced mitochondrial respiration is associated with an accumulation of malic acid. In humans, endurance training is associated with a significant increase in the enzymes involved with malic acid metabolism.
Because of the compelling evidence that malic acid plays a central role in energy production, especially during hypoxic conditions, malic acid supplements have been examined for their effects on FM. Subjective improvement in pain was observed within 48 hours of supplementation with 1200 - 2400 milligrams of malic acid, and this improvement was lost following the discontinuation of malic acid for 48 hours. While these studies also used magnesium supplements, due to the fact that magnesium is often low in FM patients, the rapid improvement following malic acid, as well as the rapid deterioration after discontinuation, suggests that malic acid is the most important component. This interesting theory of localized hypoxia in FM, and the ability of malic acid to overcome the block in energy production that this causes, should provide hope for those afflicted with FM. The potential for malic acid supplements, however, reaches much farther than FM. In light of malic acid's ability to improve animal exercise performance, its potential for human athletes is particularly exciting.
Additionally, many hypoxia related conditions, such as respiratory and circulatory insufficiency, are associated with deficient energy production. Therefore, malic acid supplements may be of benefit in these conditions. Chronic Fatigue Syndrome has also been found to be associated with FM, and malic acid supplementation may be of use in improving energy production in this condition as well.. Lastly, malic acid may be of use as a general supplement aimed at ensuring an optimal level of malic acid within the cells, and thus, maintaining an optimal level of energy production.
Hypoxia, or hypoxiation, is a pathological condition in which the body as a whole (generalized hypoxia) or a region of the body (tissue hypoxia) is deprived of adequate oxygen supply
Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle.
Goldman BE, Fisher DM, Ringler SL.
Department of Plastic Surgery, Butterworth Hospital, Grand Rapids, Mich., USA.
Our study was designed to measure the transcutaneous PO2 of the scalp to determine if there was a relative microvascular insufficiency and associated tissue hypoxia in areas of hair loss in male pattern baldness. A controlled prospective study was performed at Butterworth Hospital, Grand Rapids, Michigan. Eighteen nonsmoking male volunteers aged 18 years and older were studied. Nine men had male pattern baldness (Juri degree II or III), and nine were controls (no male pattern baldness). Scalp temperature and transcutaneous PO2 were obtained at frontal and temporal sites in each subject. Peripheral circulation was assessed from postocclusive transcutaneous PO2 recovery time by means of maximum initial slope measurements. Statistical significance was assessed at p < 0.05. There was no significant difference in scalp temperature between male pattern baldness subjects and controls. Temporal scalp blood flow was significantly higher than frontal scalp blood flow in male pattern baldness subjects; however, there was no significant difference in controls. Transcutaneous PO2 was significantly lower in bald frontal scalp (32.2 +/- 2.0 mmHg) than in hair-bearing temporal scalp (51.8 +/- 4.4 mmHg) in men with male pattern baldness. In controls, there was no significant difference in transcutaneous PO2 of frontal scalp (53.9 +/- 3.5 mmHg) and temporal scalp (61.4 +/- 2.7 mmHg). Transcutaneous PO2 also was significantly lower in the frontal scalp of male pattern baldness subjects (32.2 +/- 2.0 mmHg) than in either frontal or temporal scalp of controls (53.9 +/- 3.5 mmHg and 61.4 +/- 2.7 mmHg, respectively). There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. We have identified a previously unreported tissue hypoxia in bald scalp compared with hair-bearing scalp.
Malic acid is a natural constituent of many fruits and vegetables that are preserved by fermentation. This acid may be broken down during fermentation by certain bacteria into lactic acid and carbon dioxide. This reaction is desired to reduce the acidity in certain types of wines, and is undesired in the fermentation of cucumbers because of gaseous spoilage from carbon dioxide accumulation inside the fruit.
Many traditional fresh and fermented ready-to-eat foods are dependent on their acidity as the primary means for controlling the presence of disease- causing bacteria. In such foods, how quickly pathogenic microorganisms are inactivated is dependent on both the level of acidity (pH) and the identity and amount of the specific acid associated with the food. Recent concern about the survival of acid resistant pathogens in apple cider produced a need for better information on how malic acid, the principal acid in apples, affects bacteria. The current study helps address that need by providing information on how malic acid and pH interact to inactivate the foodborne pathogen, Listeria monocytogenes. These results demonstrate that malic acid is one of the gentler food acids.
Malic acid is both derived from food sources and synthesized in the body through the citric acid cycle. Its importance to the production of energy in the body during both aerobic and anaerobic conditions is well established. Under aerobic conditions, the oxidation of malate to oxaloacetate provides reducing equivalents to the mitochondria through the malate-aspartate redox shuttle. During anaerobic conditions, where a buildup of excess of reducing equivalents inhibits glycolysis, malic acid's simultaneous reduction to succinate and oxidation to oxaloacetate is capable of removing the accumulating reducing equivalents. This allows malic acid to reverse hypoxia's inhibition of glycolysis and energy production. This may allow malic acid to improve energy production in Primary fibromyalgia (FM), reversing the negative effect of the relative hypoxia that has been found in these patients.
Because of its obvious relationship to energy depletion during exercise, malic acid may be of benefit to healthy individuals interested in maximizing their energy production, as well as those with FM. In the rat it has been found that only tissue malate is depleted following exhaustive physical activity. Other key metabolites from the citric acid cycle needed for energy production were found to be unchanged. Because of this, a deficiency of malic acid has been hypothesized to be a major cause of physical exhaustion. The administration of malic acid to rats has been shown to elevate mitochondrial malate and increase mitochondrial respiration and energy production. Surprisingly, relatively small amounts of exogenous malic acid were required to increase mitochondrial energy production and ATP formation. Under hypoxic conditions there is an increased demand and utilization of malic acid, and this demand is normally met by increasing the synthesis of malic acid through gluconeogenesis and muscle protein breakdown. This ultimately results in muscle breakdown and damage.
In a study on the effect of the oral administration of malic acid to rats, a significant increase in anaerobic endurance was found. Interestingly, the improvement in endurance was not accompanied by an increase in carbohydrate and oxygen utilization, suggesting that malic acid has carbohydrate and oxygen-sparing effects. In addition, malic acid is the only metabolite of the citric acid cycle positively correlated with physical activity. It has also been demonstrated that exercise-induced mitochondrial respiration is associated with an accumulation of malic acid. In humans, endurance training is associated with a significant increase in the enzymes involved with malic acid metabolism.
Because of the compelling evidence that malic acid plays a central role in energy production, especially during hypoxic conditions, malic acid supplements have been examined for their effects on FM. Subjective improvement in pain was observed within 48 hours of supplementation with 1200 - 2400 milligrams of malic acid, and this improvement was lost following the discontinuation of malic acid for 48 hours. While these studies also used magnesium supplements, due to the fact that magnesium is often low in FM patients, the rapid improvement following malic acid, as well as the rapid deterioration after discontinuation, suggests that malic acid is the most important component. This interesting theory of localized hypoxia in FM, and the ability of malic acid to overcome the block in energy production that this causes, should provide hope for those afflicted with FM. The potential for malic acid supplements, however, reaches much farther than FM. In light of malic acid's ability to improve animal exercise performance, its potential for human athletes is particularly exciting.
Additionally, many hypoxia related conditions, such as respiratory and circulatory insufficiency, are associated with deficient energy production. Therefore, malic acid supplements may be of benefit in these conditions. Chronic Fatigue Syndrome has also been found to be associated with FM, and malic acid supplementation may be of use in improving energy production in this condition as well.. Lastly, malic acid may be of use as a general supplement aimed at ensuring an optimal level of malic acid within the cells, and thus, maintaining an optimal level of energy production.
Hypoxia, or hypoxiation, is a pathological condition in which the body as a whole (generalized hypoxia) or a region of the body (tissue hypoxia) is deprived of adequate oxygen supply
Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle.
Goldman BE, Fisher DM, Ringler SL.
Department of Plastic Surgery, Butterworth Hospital, Grand Rapids, Mich., USA.
Our study was designed to measure the transcutaneous PO2 of the scalp to determine if there was a relative microvascular insufficiency and associated tissue hypoxia in areas of hair loss in male pattern baldness. A controlled prospective study was performed at Butterworth Hospital, Grand Rapids, Michigan. Eighteen nonsmoking male volunteers aged 18 years and older were studied. Nine men had male pattern baldness (Juri degree II or III), and nine were controls (no male pattern baldness). Scalp temperature and transcutaneous PO2 were obtained at frontal and temporal sites in each subject. Peripheral circulation was assessed from postocclusive transcutaneous PO2 recovery time by means of maximum initial slope measurements. Statistical significance was assessed at p < 0.05. There was no significant difference in scalp temperature between male pattern baldness subjects and controls. Temporal scalp blood flow was significantly higher than frontal scalp blood flow in male pattern baldness subjects; however, there was no significant difference in controls. Transcutaneous PO2 was significantly lower in bald frontal scalp (32.2 +/- 2.0 mmHg) than in hair-bearing temporal scalp (51.8 +/- 4.4 mmHg) in men with male pattern baldness. In controls, there was no significant difference in transcutaneous PO2 of frontal scalp (53.9 +/- 3.5 mmHg) and temporal scalp (61.4 +/- 2.7 mmHg). Transcutaneous PO2 also was significantly lower in the frontal scalp of male pattern baldness subjects (32.2 +/- 2.0 mmHg) than in either frontal or temporal scalp of controls (53.9 +/- 3.5 mmHg and 61.4 +/- 2.7 mmHg, respectively). There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. We have identified a previously unreported tissue hypoxia in bald scalp compared with hair-bearing scalp.
squeegee
Banned
- Reaction score
- 132
Also if you guys want to look at acvfan pictures at the beginning of the treatment with ACV:
viewtopic.php?f=23&t=61988&hilit=+apple+cider
We are creatures of habits, we need to start thinking outside of the box...
viewtopic.php?f=23&t=61988&hilit=+apple+cider
We are creatures of habits, we need to start thinking outside of the box...
