squeegee
Banned
- Reaction score
- 132
Dihydrotestosterone stimulates aldosterone secretion by H295R human adrenocortical cells.
Yanes LL, Romero DG.
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA. lyanes@physiology.umsmed.edu
Abstract
Men exhibit a higher incidence of cardiovascular diseases than do women. The cardiovascular actions of sex steroids have been suggested as primary factors in mediating this sex difference. The mechanisms by which sex steroids, androgens and estrogens, mediate cardiovascular actions remain unclear. Excess aldosterone secretion has been associated with cardiovascular diseases. The hypothesis tested in this study was that at physiological concentrations, androgens stimulate and estradiol inhibits aldosterone secretion by human adrenal cells. In contrast to our hypothesis, physiological concentrations of sex steroids did not modify aldosterone secretion by H295R human adrenocortical cells. However, supraphysiological concentrations (300-1000 nM) of dihydrotestosterone (DHT) significantly stimulated basal and Angiotensin II-mediated aldosterone secretion. The stimulatory effect of DHT on aldosterone secretion was not blocked by the classical androgen receptor blocker flutamide. The stimulatory effect of DHT on aldosterone secretion was also independent of the intra-adrenal renin-angiotensin system since it was neither modified by treatment with the Angiotensin II receptor type 1 blocker losartan or the angiotensin converting enzyme inhibitor captopril. Inhibitors of the calmodulin/calmodulin-dependent protein kinase (CaMK) and protein kinase C intracellular signaling pathways abolished the DHT stimulatory effect on aldosterone secretion by H295R cells. In conclusion, physiological concentrations of sex steroids did not modify aldosterone secretion by human adrenal cells. However, supraphysiological concentrations of DHT-stimulated aldosterone secretion by human adrenal cells by the calmodulin/CaMK and protein kinase C intracellular signaling pathways but independently of the classical androgen receptor. Supraphysiological doses of androgen may promote cardiovascular diseases via stimulation of aldosterone secretion.
Br J Dermatol. 2009 Jun 9.
Elevated aldosterone levels in patients with androgenetic alopecia
Arias-Santiago S, Gutiérrez-Salmerón MT, Castellote-Caballero L, Naranjo-Sintes R.
Dermatology Unit, San Cecilio University Hospital, Av Dr Oloriz 16, Granada 18012, Spain.
Summary Background There is reported to be an elevated prevalence of hypertension among patients with androgenetic alopecia (Androgenetic Alopecia), and it has been proposed that both phenomena may be explained by the presence of hyperaldosteronism. However, no data on aldosterone levels in patients with Androgenetic Alopecia have been published to date. Objectives The objective of this pilot study was to evaluate aldosterone levels and the presence of hypertension in patients with Androgenetic Alopecia and in healthy controls. Methods This case-control study included 40 patients with Androgenetic Alopecia and 40 healthy controls from the Dermatology Department of San Cecilio Hospital, Granada, Spain. Results Patients with Androgenetic Alopecia showed significantly higher systolic blood pressure values (136.23 vs. 124.10 mmHg, P = 0.01) and aldosterone levels (197.35 vs. 133.71 pg mL(-1), P = 0.007) vs. controls. Conclusion The elevated aldosterone values in these patients may contribute, together with other mechanisms, to the development of Androgenetic Alopecia and may also explain the higher prevalence of hypertension. Blood pressure screening of patients with Androgenetic Alopecia will permit earlier diagnosis of an unknown hypertension and initiation of appropriate treatment.
PMID: 19519833
In this article, I will discuss two disorders of the adrenal gland which involve the hormone aldosterone. These two disorders are hyperaldosteronism and hypoaldosteronism. They refer to increased secretion of the aldosterone hormone and its decreased secretion by the adrenal gland respectively. These two disorders will be mentioned here one after the other after giving a review about the hormone aldosterone.
Aldosterone is a steroid hormone that is secreted by the adrenal gland from its cortical area. It is synthesized and secreted to the blood circulation by a specialized type of cells in the adrenal cortex that are different that those that synthesize and secret the hormone cortisol. Cortisol is also secreted by cells of the adrenal cortex.
The difference between these two hormones although they are both steroid hormones lies in the fact that cortisol is under the regulation from the pituitary gland by the hormone adrenocorticotropic hormone. This type of feedback is negative in nature in which increased level of cortisol in the blood decreases the secretion of the adrenocorticotropic hormone by the pituirary gland and vice versa.
Aldosterone on the other hand is not under the control of a hormone from the pituitary gland. Instead it is under a different type of feedback regulation which has its source in the kidney cells. The kidney usually secretes to the blood circulation a hormone which is known as renin in response to low blood volume or due to decreased blood perfusion to the kidney as occurs in renal artery stenosis or in shock states.
Under these conditions in which renin begins to be secreted there is stimulation of the adrenal cortex by renin to secrete to the blod circulation the hormone aldosterone which has specialized function in the body which eventually leads to restoration of homeostasis by increasing the blood pressure in the blood aretries.
Aldosterone has a direct effect on sodium and potassium ions in the body through its action on the important Na+/K+ ion pump. Aldosterone exerts its effect on the kidney tubules to conserve sodium ions in excessive amount in exchange for potassium which is excreted in the urine.
Aldosterone exerts its effect probably by modifying the action of the Na+/K+ ionp pump causing retention of sodium ions in exchange for potassium ions which are pumped in the other direction into the urine. The excessive amount of sodium that is conserved
in the kidney tubules exerts an osmotic effect in which it withdraws more and more water in the same direction by a diffusional process into the blood. This function is especially important in the case of excessive secretion of this hormone in hyperaldosteronism.
The first disorder which involves aldosterone and which is discussed here is oversecretion of this hormone to the blood circulation or hyperaldosteronism. This disorder is sometimes called Conn's syndrome. In this condition of excessive secretion of aldosterone there is usually hyperplasia of the adrenal cortex cells which causes excessive activity of the adrenal gland. Thus causing excessive secretion this hormone.
Disorders of the adrenal cortex can sometimes involve bothe cells that secrete aldosterone and cortisol. The net result is increased amount of sodium ioms and water that are retained by the kidney tubules by the action of of the hormone aldosterone. This type of oversecretion of aldosterone is not dependent in this case on the level of the hormone renin in the blood but is largely dependent on the hyperplasia of the cells of the adrenal cortex. Also carcinoma of the adrenal cortex can give similar manifestsations of increased aldosterone secretion.
The clinical result is that of high blood pressure or hypertension and accompanying hypokalemia which results from due to excessive secretion of potassium ions in the urine in exchange for sodium which is retained in the body.
Hypoaldosteronism can occur mostly due to an autoimmune reaction of the body against the adrenal cortex cells. It can often occur as part of the clinical picture of addison's disease. The net result of this syndrome is the development of hyperkalemia which can be confused with hyperkalemia due to other medical conditions such as due to renal failure. Also there is wasting of sodium and water in the urine which can be excessive.
Vinegar Improves Insulin Sensitivity to a High-Carbohydrate Meal in Subjects With Insulin Resistance or Type 2 Diabetes
Carol S. Johnston, PHD, Cindy M. Kim, MS and Amanda J. Buller, MS
From the Department of Nutrition, Arizona State University, Mesa, Arizona
Address correspondence to Carol S. Johnston, Department of Nutrition, Arizona State University, East Campus, 7001 E. Williams Field Rd, Mesa, AZ 85212. E-mail: carol.johnston@asu.edu
The number of Americans with type 2 diabetes is expected to increase by 50% in the next 25 years; hence, the prevention of type 2 diabetes is an important objective. Recent large-scale trials (the Diabetes Prevention Program and STOP-NIDDM) have demonstrated that therapeutic agents used to improve insulin sensitivity in diabetes, metformin and acarbose, may also delay or prevent the onset of type 2 diabetes in high-risk populations. Interestingly, an early report showed that vinegar attenuated the glucose and insulin responses to a sucrose or starch load (1). In the present report, we assessed the effectiveness of vinegar in reducing postprandial glycemia and insulinemia in subjects with varying degrees of insulin sensitivity. These data indicate that vinegar can significantly improve postprandial insulin sensitivity in insulin-resistant subjects. Acetic acid has been shown to suppress disaccharidase activity (3) and to raise glucose-6-phosphate concentrations in skeletal muscle (4); thus, vinegar may possess physiological effects similar to acarbose or metformin. Further investigations to examine the efficacy of vinegar as an antidiabetic therapy are warranted.
********************************************************************************
*************************************************
Vinegar: Medicinal Uses and Antiglycemic Effect
Carol S. Johnston, PhD, RD and Cindy A. Gaas, BS
Carol S. Johnston, Department of Nutrition, Arizona State University, Mesa, Arizona.
All author affiliations.
Disclosure: Carol S. Johnston, PhD, RD, has disclosed no relevant financial relationships.
Disclosure: Cindy A. Gaas, BS, has disclosed no relevant financial relationships.
[...]
Cardiovascular Effects
Kondo and colleagues[30] reported a significant reduction in systolic blood pressure (approximately 20 mm Hg) in spontaneously hypertensive (SHR) rats fed a standard laboratory diet mixed with either vinegar or an acetic acid solution (approximately 0.86 mmol acetic acid/day for 6 weeks) as compared with SHR rats fed the same diet mixed with deionized water. These observed reductions in systolic blood pressure were associated with reductions in both plasma renin activity and plasma aldosterone concentrations (35% to 40% and 15% to 25% reductions in renin activity and aldosterone concentrations, respectively, in the experimental vs control SHR rats). Others have reported that vinegar administration (approximately 0.57 mmol acetic acid, orally) inhibited the renin-angiotensin system in nonhypertensive Sprague-Dawley rats.[31]
[...]
Antitumor Activity
In vitro, sugar cane vinegar (Kibizu) induced apoptosis in human leukemia cells,[36] and a traditional Japanese rice vinegar (Kurosu) inhibited the proliferation of human cancer cells in a dose-dependent manner.[37] An ethyl acetate extract of Kurosu added to drinking water (0.05% to 0.1% w/v) significantly inhibited the incidence (?60%) and multiplicity (?50%) of azoxymethane-induced colon carcinogenesis in male F344 rats when compared with the same markers in control animals.[38] In a separate trial, mice fed a rice-shochu vinegar-fortified feed (0.3% to 1.5% w/w) or control diet were inoculated with sarcoma 180 (group 1) or colon 38 (group 2) tumor cells (2 × 106 cells subcutaneously).[39] At 40 days post-inoculation, vinegar-fed mice in both experimental groups had significantly smaller tumor volumes when compared with their control counterparts. A prolonged life span due to tumor regression was also noted in the mice ingesting rice-shochu vinegar as compared with controls, and in vitro, the rice-shochu vinegar stimulated natural killer cell cytotoxic activity.[39]
The antitumor factors in vinegar have not been identified. In the human colonic adenocarcinoma cell line Caco-2, acetate treatment, as well as treatment with the other short-chain fatty acids (SCFA) n-butyrate and propionate, significantly prolonged cell doubling time, promoted cell differentiation, and inhibited cell motility.[40] Because bacterial fermentation of dietary fiber in the colon yields the SCFA, the investigators concluded that the antineoplastic effects of dietary fiber may relate in part to the formation of SCFA. Others have also documented the antineoplastic effects of the SCFA in the colon, particularly n-butyrate.[41] Thus, because acetic acid in vinegar deprotonates in the stomach to form acetate ions, it may possess antitumor effects.
Vinegars are also a dietary source of polyphenols,[6] compounds synthesized by plants to defend against oxidative stress. Ingestion of polyphenols in humans enhances in vivo antioxidant protection and reduces cancer risk.[42] Kurosu vinegar is particularly rich in phenolic compounds, and the in-vitro antioxidant activity of an ethyl acetate extract of Kurosu vinegar was similar to the antioxidant activity of alpha-tocopherol (vitamin E) and significantly greater than the antioxidant activities of other vinegar extracts, including wine and apple vinegars.[43] Kurosu vinegar extracts also suppressed lipid peroxidation in mice treated topically with H2O2-generating chemicals.[43] Currently, much interest surrounds the role of dietary polyphenols, particularly from fruits, vegetables, wine, coffee, and chocolate, in the prevention of cancers as well as other conditions including cardiovascular disease[44]; perhaps vinegar can be added to this list of foods and its consumption evaluated for disease risk.
Epidemiologic data, however, is scarce and unequivocal. A case-control study conducted in Linzhou, China, demonstrated that vinegar ingestion was associated with a decreased risk for esophageal cancer (OR: 0.37).[45] However, vinegar ingestion was associated with a 4.4-fold greater risk for bladder cancer in a case-control investigation in Serbia.[46]
Blood Glucose Control
[...]
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]
Yanes LL, Romero DG.
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA. lyanes@physiology.umsmed.edu
Abstract
Men exhibit a higher incidence of cardiovascular diseases than do women. The cardiovascular actions of sex steroids have been suggested as primary factors in mediating this sex difference. The mechanisms by which sex steroids, androgens and estrogens, mediate cardiovascular actions remain unclear. Excess aldosterone secretion has been associated with cardiovascular diseases. The hypothesis tested in this study was that at physiological concentrations, androgens stimulate and estradiol inhibits aldosterone secretion by human adrenal cells. In contrast to our hypothesis, physiological concentrations of sex steroids did not modify aldosterone secretion by H295R human adrenocortical cells. However, supraphysiological concentrations (300-1000 nM) of dihydrotestosterone (DHT) significantly stimulated basal and Angiotensin II-mediated aldosterone secretion. The stimulatory effect of DHT on aldosterone secretion was not blocked by the classical androgen receptor blocker flutamide. The stimulatory effect of DHT on aldosterone secretion was also independent of the intra-adrenal renin-angiotensin system since it was neither modified by treatment with the Angiotensin II receptor type 1 blocker losartan or the angiotensin converting enzyme inhibitor captopril. Inhibitors of the calmodulin/calmodulin-dependent protein kinase (CaMK) and protein kinase C intracellular signaling pathways abolished the DHT stimulatory effect on aldosterone secretion by H295R cells. In conclusion, physiological concentrations of sex steroids did not modify aldosterone secretion by human adrenal cells. However, supraphysiological concentrations of DHT-stimulated aldosterone secretion by human adrenal cells by the calmodulin/CaMK and protein kinase C intracellular signaling pathways but independently of the classical androgen receptor. Supraphysiological doses of androgen may promote cardiovascular diseases via stimulation of aldosterone secretion.
Br J Dermatol. 2009 Jun 9.
Elevated aldosterone levels in patients with androgenetic alopecia
Arias-Santiago S, Gutiérrez-Salmerón MT, Castellote-Caballero L, Naranjo-Sintes R.
Dermatology Unit, San Cecilio University Hospital, Av Dr Oloriz 16, Granada 18012, Spain.
Summary Background There is reported to be an elevated prevalence of hypertension among patients with androgenetic alopecia (Androgenetic Alopecia), and it has been proposed that both phenomena may be explained by the presence of hyperaldosteronism. However, no data on aldosterone levels in patients with Androgenetic Alopecia have been published to date. Objectives The objective of this pilot study was to evaluate aldosterone levels and the presence of hypertension in patients with Androgenetic Alopecia and in healthy controls. Methods This case-control study included 40 patients with Androgenetic Alopecia and 40 healthy controls from the Dermatology Department of San Cecilio Hospital, Granada, Spain. Results Patients with Androgenetic Alopecia showed significantly higher systolic blood pressure values (136.23 vs. 124.10 mmHg, P = 0.01) and aldosterone levels (197.35 vs. 133.71 pg mL(-1), P = 0.007) vs. controls. Conclusion The elevated aldosterone values in these patients may contribute, together with other mechanisms, to the development of Androgenetic Alopecia and may also explain the higher prevalence of hypertension. Blood pressure screening of patients with Androgenetic Alopecia will permit earlier diagnosis of an unknown hypertension and initiation of appropriate treatment.
PMID: 19519833
In this article, I will discuss two disorders of the adrenal gland which involve the hormone aldosterone. These two disorders are hyperaldosteronism and hypoaldosteronism. They refer to increased secretion of the aldosterone hormone and its decreased secretion by the adrenal gland respectively. These two disorders will be mentioned here one after the other after giving a review about the hormone aldosterone.
Aldosterone is a steroid hormone that is secreted by the adrenal gland from its cortical area. It is synthesized and secreted to the blood circulation by a specialized type of cells in the adrenal cortex that are different that those that synthesize and secret the hormone cortisol. Cortisol is also secreted by cells of the adrenal cortex.
The difference between these two hormones although they are both steroid hormones lies in the fact that cortisol is under the regulation from the pituitary gland by the hormone adrenocorticotropic hormone. This type of feedback is negative in nature in which increased level of cortisol in the blood decreases the secretion of the adrenocorticotropic hormone by the pituirary gland and vice versa.
Aldosterone on the other hand is not under the control of a hormone from the pituitary gland. Instead it is under a different type of feedback regulation which has its source in the kidney cells. The kidney usually secretes to the blood circulation a hormone which is known as renin in response to low blood volume or due to decreased blood perfusion to the kidney as occurs in renal artery stenosis or in shock states.
Under these conditions in which renin begins to be secreted there is stimulation of the adrenal cortex by renin to secrete to the blod circulation the hormone aldosterone which has specialized function in the body which eventually leads to restoration of homeostasis by increasing the blood pressure in the blood aretries.
Aldosterone has a direct effect on sodium and potassium ions in the body through its action on the important Na+/K+ ion pump. Aldosterone exerts its effect on the kidney tubules to conserve sodium ions in excessive amount in exchange for potassium which is excreted in the urine.
Aldosterone exerts its effect probably by modifying the action of the Na+/K+ ionp pump causing retention of sodium ions in exchange for potassium ions which are pumped in the other direction into the urine. The excessive amount of sodium that is conserved
in the kidney tubules exerts an osmotic effect in which it withdraws more and more water in the same direction by a diffusional process into the blood. This function is especially important in the case of excessive secretion of this hormone in hyperaldosteronism.
The first disorder which involves aldosterone and which is discussed here is oversecretion of this hormone to the blood circulation or hyperaldosteronism. This disorder is sometimes called Conn's syndrome. In this condition of excessive secretion of aldosterone there is usually hyperplasia of the adrenal cortex cells which causes excessive activity of the adrenal gland. Thus causing excessive secretion this hormone.
Disorders of the adrenal cortex can sometimes involve bothe cells that secrete aldosterone and cortisol. The net result is increased amount of sodium ioms and water that are retained by the kidney tubules by the action of of the hormone aldosterone. This type of oversecretion of aldosterone is not dependent in this case on the level of the hormone renin in the blood but is largely dependent on the hyperplasia of the cells of the adrenal cortex. Also carcinoma of the adrenal cortex can give similar manifestsations of increased aldosterone secretion.
The clinical result is that of high blood pressure or hypertension and accompanying hypokalemia which results from due to excessive secretion of potassium ions in the urine in exchange for sodium which is retained in the body.
Hypoaldosteronism can occur mostly due to an autoimmune reaction of the body against the adrenal cortex cells. It can often occur as part of the clinical picture of addison's disease. The net result of this syndrome is the development of hyperkalemia which can be confused with hyperkalemia due to other medical conditions such as due to renal failure. Also there is wasting of sodium and water in the urine which can be excessive.
Vinegar Improves Insulin Sensitivity to a High-Carbohydrate Meal in Subjects With Insulin Resistance or Type 2 Diabetes
Carol S. Johnston, PHD, Cindy M. Kim, MS and Amanda J. Buller, MS
From the Department of Nutrition, Arizona State University, Mesa, Arizona
Address correspondence to Carol S. Johnston, Department of Nutrition, Arizona State University, East Campus, 7001 E. Williams Field Rd, Mesa, AZ 85212. E-mail: carol.johnston@asu.edu
The number of Americans with type 2 diabetes is expected to increase by 50% in the next 25 years; hence, the prevention of type 2 diabetes is an important objective. Recent large-scale trials (the Diabetes Prevention Program and STOP-NIDDM) have demonstrated that therapeutic agents used to improve insulin sensitivity in diabetes, metformin and acarbose, may also delay or prevent the onset of type 2 diabetes in high-risk populations. Interestingly, an early report showed that vinegar attenuated the glucose and insulin responses to a sucrose or starch load (1). In the present report, we assessed the effectiveness of vinegar in reducing postprandial glycemia and insulinemia in subjects with varying degrees of insulin sensitivity. These data indicate that vinegar can significantly improve postprandial insulin sensitivity in insulin-resistant subjects. Acetic acid has been shown to suppress disaccharidase activity (3) and to raise glucose-6-phosphate concentrations in skeletal muscle (4); thus, vinegar may possess physiological effects similar to acarbose or metformin. Further investigations to examine the efficacy of vinegar as an antidiabetic therapy are warranted.
********************************************************************************
*************************************************
Vinegar: Medicinal Uses and Antiglycemic Effect
Carol S. Johnston, PhD, RD and Cindy A. Gaas, BS
Carol S. Johnston, Department of Nutrition, Arizona State University, Mesa, Arizona.
All author affiliations.
Disclosure: Carol S. Johnston, PhD, RD, has disclosed no relevant financial relationships.
Disclosure: Cindy A. Gaas, BS, has disclosed no relevant financial relationships.
[...]
Cardiovascular Effects
Kondo and colleagues[30] reported a significant reduction in systolic blood pressure (approximately 20 mm Hg) in spontaneously hypertensive (SHR) rats fed a standard laboratory diet mixed with either vinegar or an acetic acid solution (approximately 0.86 mmol acetic acid/day for 6 weeks) as compared with SHR rats fed the same diet mixed with deionized water. These observed reductions in systolic blood pressure were associated with reductions in both plasma renin activity and plasma aldosterone concentrations (35% to 40% and 15% to 25% reductions in renin activity and aldosterone concentrations, respectively, in the experimental vs control SHR rats). Others have reported that vinegar administration (approximately 0.57 mmol acetic acid, orally) inhibited the renin-angiotensin system in nonhypertensive Sprague-Dawley rats.[31]
[...]
Antitumor Activity
In vitro, sugar cane vinegar (Kibizu) induced apoptosis in human leukemia cells,[36] and a traditional Japanese rice vinegar (Kurosu) inhibited the proliferation of human cancer cells in a dose-dependent manner.[37] An ethyl acetate extract of Kurosu added to drinking water (0.05% to 0.1% w/v) significantly inhibited the incidence (?60%) and multiplicity (?50%) of azoxymethane-induced colon carcinogenesis in male F344 rats when compared with the same markers in control animals.[38] In a separate trial, mice fed a rice-shochu vinegar-fortified feed (0.3% to 1.5% w/w) or control diet were inoculated with sarcoma 180 (group 1) or colon 38 (group 2) tumor cells (2 × 106 cells subcutaneously).[39] At 40 days post-inoculation, vinegar-fed mice in both experimental groups had significantly smaller tumor volumes when compared with their control counterparts. A prolonged life span due to tumor regression was also noted in the mice ingesting rice-shochu vinegar as compared with controls, and in vitro, the rice-shochu vinegar stimulated natural killer cell cytotoxic activity.[39]
The antitumor factors in vinegar have not been identified. In the human colonic adenocarcinoma cell line Caco-2, acetate treatment, as well as treatment with the other short-chain fatty acids (SCFA) n-butyrate and propionate, significantly prolonged cell doubling time, promoted cell differentiation, and inhibited cell motility.[40] Because bacterial fermentation of dietary fiber in the colon yields the SCFA, the investigators concluded that the antineoplastic effects of dietary fiber may relate in part to the formation of SCFA. Others have also documented the antineoplastic effects of the SCFA in the colon, particularly n-butyrate.[41] Thus, because acetic acid in vinegar deprotonates in the stomach to form acetate ions, it may possess antitumor effects.
Vinegars are also a dietary source of polyphenols,[6] compounds synthesized by plants to defend against oxidative stress. Ingestion of polyphenols in humans enhances in vivo antioxidant protection and reduces cancer risk.[42] Kurosu vinegar is particularly rich in phenolic compounds, and the in-vitro antioxidant activity of an ethyl acetate extract of Kurosu vinegar was similar to the antioxidant activity of alpha-tocopherol (vitamin E) and significantly greater than the antioxidant activities of other vinegar extracts, including wine and apple vinegars.[43] Kurosu vinegar extracts also suppressed lipid peroxidation in mice treated topically with H2O2-generating chemicals.[43] Currently, much interest surrounds the role of dietary polyphenols, particularly from fruits, vegetables, wine, coffee, and chocolate, in the prevention of cancers as well as other conditions including cardiovascular disease[44]; perhaps vinegar can be added to this list of foods and its consumption evaluated for disease risk.
Epidemiologic data, however, is scarce and unequivocal. A case-control study conducted in Linzhou, China, demonstrated that vinegar ingestion was associated with a decreased risk for esophageal cancer (OR: 0.37).[45] However, vinegar ingestion was associated with a 4.4-fold greater risk for bladder cancer in a case-control investigation in Serbia.[46]
Blood Glucose Control
[...]
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]
