AI Glycobol vs LG Slin

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    AI Glycobol vs LG Slin


    Can anyone compare and contrast these popular products?

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    never used the first one, but have used slin and ap and luved them both.
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    isnt slin just VS and chromium?

    glycobol has a more active bio available form of VS with a longer halflife called BMOV

    plus glycobol has other glucose disposal agents and works through the glucose 4 transporter.
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    Quote Originally Posted by crazyfool405 View Post
    isnt slin just VS and chromium?....
    No.
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    Wats in it then?
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    Quote Originally Posted by crazyfool405 View Post
    Wats in it then?
    Amount Per Serving
    Alpha-Lipoic Acid 125 mg

    Insulin Potentiator Complex 630 mg
    Momordica Charantia (Bitter Melon)
    Cinnamon Extract
    Vanadyl Sulfate
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    Ok I knew vs was in it

    I don't know the mechanism of bitter melon. I've used it before tho. Decent
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    Glycobol has a lot of reviews on it. I do not know a lot about the LG Slin.
    Ask me for samples of the new RecoverPRO and Maniac. 3Z is coming July 1st Facebook for more info and maybe a great deal on it coming.
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    Well if someone wants their review my refeed is friday and I could use some lol
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    Quote Originally Posted by pembroke3355 View Post
    Glycobol has a lot of reviews on it. I do not know a lot about the LG Slin.
    Ive heard one or two reviews on LG Slin . . all positive, but not so much 'official' reviews.

    . . . but hey let's not turn this into a rep p1ssing contest.

    I'm just after those who have tried both products and can draw comparisons between the two

    One thing I have noted is the cost. Despite the popularity of the product, Glycobol is pricy. But so is Anabolic Pump. Slin on the other hand is not . . .
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    Quote Originally Posted by jakellpet View Post
    Ive heard one or two reviews on LG Slin . . all positive, but not so much 'official' reviews.

    . . . but hey let's not turn this into a rep p1ssing contest.

    I'm just after those who have tried both products and can draw comparisons between the two

    One thing I have noted is the cost. Despite the popularity of the product, Glycobol is pricy. But so is Anabolic Pump. Slin on the other hand is not . . .
    No pissing contest was intended. I simply do not know much about Slin and that is what I stated. Nothing bad was said about Slin. You bring up price and Glycobol is more money butit is a full months supply. Slin says 2-4 caps before meals so if you go the low end and take 2 caps and eat 4 times a day you only have a 15 day supply so I think it more than equals out. Slin is probally a very good product.
    Ask me for samples of the new RecoverPRO and Maniac. 3Z is coming July 1st Facebook for more info and maybe a great deal on it coming.
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    i reallly like bitter melon and ALA

    however i have used all ingredients of LGs SLIN seperately i can imagine them working very well.

    i wish i knew more on the mechanism of the bitter melon.

    maybe ill buy some and use it alone for a few days and then stack it with all the other GDAs i use lol

    \try it out i like LGs line, i loved their Transform and their IGH1 is awesome
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    Antidiabetic and Adaptogenic Properties of Momordica charantia Extract: An Experimental and Clinical Evaluation
    Author: Y. Srivastava, H. Venkatakrishna-Bhatt, Y. Verma, K. Venkaiah
    Type of Publication: Pre-clinical
    Date of Publication: 1993
    Publication: Phytotherapy Research, Vol. 7, pp 285-289, 1993
    Organization: B.J. Medical College and National Institute of Occupational Health
    Abstract: The hypoglycaemic properties of Momordica charantia (bitter gourd) water extract was tested on alloxan diabetic rats experimentally. A fall of blood sugar after 3 week’s treatment with aqueous extract of fruits of the herb was found to be significant (p<0.01). The aqueous extract of fruit was more effective in diabetes (fall of blood sugar 54% after 3 week’s therapy) than the powder of the dried fruit (fall 25% nonsignificant). Hypoglycaemic effects in diabetic patients were found to be highly significant (p>0.01) at the end of the trial but were cumulative and gradual, unlike that produced bu insulin. Adaptogenic properties are indicated by the delay in the appearance of cataracts, the secondary complications of diabetes and relief in neurological and other common symptoms even before the hypoglycaemia occurred



    INTRODUCTION
    The commonly practiced treatment of diabetes includes oral antidiabetics and/or insulin injections. Insulin can maintain blood glucose within a normal range but cannot simulate the pancreas of a healthy individual. Hence, diabetics within 15 to 20 years of diagnosis begin to develop complications (Engerman et al., 1977). Diabetes is the leading cause of noncongenital blindness among adults aged 20 to 70 years, the leading cause of kidney failure, it doubles the risk of heart disease, gangrene of the extremities and there is a clinical recognition of cataract as a diabetic complication. The range of these complications is directly related to the hour-to-hour fluctuations in blood sugar that persist even when insulin is taken once or twice a day (Job et al., 1975; Piters et al., 1975). Certain Indian plants have antidiabetic properties as reported by various authors (Srivastava et al., 1983, 1985) such as hypoglycaemic agents (Srivastava et al., 1986; 1988) and retardation of retinopathy (Srivastava et al., 1987a, b). A number of reports have appeared concerning the hypoglycaemic properties of the fruit and seed of the bitter gourd (Bildwa et al., 1977; Yaqub, 1980; Padminikadar and Chakrabarthi, 1982; Khanna, 1985; Ng et al., 1986; Welihinda et al., 1986). The bitter fruit variety is reported to be more effective in diabetes (Satyavati et al., 1987). The fruit and seed showed the presence of the polypeptide (P) (Khanna, 1985). The present work concerns an experimental and clinical study to determine whether bitter gourd has any adaptogenic effect as reflected in the checking or delaying of the appearance of cataract, a secondary complications of diabetes.

    MATERIALS AND METHODS
    Pharmacological studies. The experimental part of this study was carried out with Charles Foster rats, of both sexes weighing 150-200 g reared on standard laboratory, diet containing 70% cracked wheat, 20% cracked bengal gram, 5% shark liver oil n the form of dry mash and water adaptogenic libitum. A freshly prepared solution of alloxan in normal saline was injected subcutaneously (120 mg/ kg body wt.) to overnight fasted rats. Blood samples were drawn from the caudal vein by the pinch clip method. Blood sugar was estimated using a dextrometer before fasting and after 36 hr of allxan treatment. Rats with a blood sugar of 150 mg% or more were included in the diabetic group. Two such rats were maintained in each cage, under uniform husbandry conditions. Rats died during the experiment were excluded. A dose response curve was produced. From studies, 4 g of bitter gourd fruit was found to yield optimum results, the period of treatment being 3 weeks. An aqueous extract of 4 g of fruit was given per rat in 2 mL volumes by oral intubation. Diabetic rats included in the control group were administered 2 mL of placebo. Blood sugar, fundus, lenticular opacity and apparent signs and symptoms were examined periodically in diabetic rats for development of cataract (Srivastava et al., 1987a, b).
    Clinical study. The clinical part of this study was carried out on diabetic patients after confirmation by oral glucose tolerance test of postprandial blood sugar (PPBS) according to the criteria of the World Health Organization. The subjects were maintained on a diabetic diet until the blood sugar was stabilized. Pre and post liver function test, kidney function test, haemogram and urine examination were done to determine any side effects of the herbal treatment.
    Preparation of the extract. Bitter gourd (Momordica charantia Linn family: Cucurbitaceae) fruit was obtained fresh locally. An aqueous extract was made by chopping 100 g of fruit and boiling 200 mL of water until the volume was reduced to 100 mL. The chips were then smashed and the decoction was filtered with muslin cloth. The aqueous extract thus prepared was given as a standard single dose in the morning. The other set of diabetic patients were given powder of dried fruit, 15 g (equivalent to 100 g wet weight) thrice a day in equal doses of 5 g each. Glycosylated haemoglobin was estimated (Fischer et al., 1980). Besides these parameters, symptoms such as polyurea, poly****ia, burning in the hands and feet, pain in calf muscles and generalized weakness were observed before and after the trial.

    RESULTS AND DISCUSSION
    The results of the present investigations are summarized in Tables 1-7. The aqueous extract of Momordica charantia was tested on laboratory animals for the preliminary confirmation of its hypoglycaemic potential. The diabetic group of animals administered 2 mL of aqueous extract for a period of 3 weeks showed a reduction of the initial blood sugar from 220 mg% to 105 mg% which is significant (p<0.01). The control group of diabetic rats treated with placebo recorded no such fall. The results (Table 1) demonstrate the hypoglycaemic effect of the herb in rats. A number of reports have been published claimng a marked hypoglycaemic effect of M. charantia extract in laboratory animals, in normal as well diabetic animals (Sharma et al., 1960). The ether extract of the residue of the alcohol extract from leaves of M. charantia was reported to have hypoglycaemic activity comparable to tolbutamide. Powdered seeds tested against streptozotocin diabetic rabbits (1-30 g/day) produced hypoglycaemia comparable to tolbutamide (Venkanna-Babu et al., 1988). Normal as well as diabetic rabbits when treated with the fruit of M. charantia recorded a fall in blood sugar (Yakub, 1980). Momordica charantia extract showed the highest hypoglycaemic effect when tried on diabetes recovered rabbits (Venkanna-Babu et al., 1988). Charantin isolated from M. charantia fruit is a hypoglycaemic in normal and fasting rabbits. It was found to be more potent hypoglycaemic than tolbutamide given in equivalent doses. The result suggested a pancreatic as well as an extrapancreatic action of charantia (Ng et al., 1986; Welihinda, et al., 1986; Welihinda and Karunanayake, 1986).
    Our confirmatory study in laboratory animals was followed by a clinical trial. The group of diabetic patients was given powder of sun-dried fruit of M. charantia three times a day (5 g each time, and 15 g in total). The second group was given aqueous extract of 100 g of the fruit in a 100 mL volume in a single standard dose in the morning. A variation in the preparation was tried to determine differences in the hypoglycaemic effect of these preparations.
    Table 2 shows the results of the clinical trial with patients administered powder of M. charantia dried fruit concluded within 21 days. The fall in blood sugarwas 25% of the initial level, however, statistically it is insignificant. Table 3 shows the result of the aqueous extract trial. The subjects included were severe (433 mg %) to mild (260% diabetics, aged 42 to 70 years, all males. Blood sugar was estimated after 2, 3, 4 and 7 weeks of treatmen. The fall in blood sugar was highly significant at the termination of treatment. The response was overwhelming when compared with hypoglycaemia caused by the powder of M. charantia (Table 5) after an initial period of 3 weeks of therapy. The fall in blood sugar in aqueous extract treated diabetics was 54.0% (p<0.01) as against 25% observed in the powder treated group. Further the aqueous extract treated diabetics showed a time-related gradual hypoglycaemic response as revealed in blood sugar and urine sugar data obtained at 2, 3, 4 and 7 weeks. This feature of the herbal treatment of diabetes is unlike conventional treatment. In almost all cases the blood sugar level was restored within the normal limits.
    The pure protein known as P-insulin or polypeptide-P extracted from M. charantia fruit in crystalline form was tested in controlled clinical trials for its efficacy as an hypoglycaemic agent. When administered s.c. it produced a mean fall in blood sugar of 45.8  13.6 mg% in juvenile and maturity onset diabetics as well as in chemical diabetes. No hypersensitivity reaction was noticed (Baldwa et al., 1987). It was found effective through the oral route (Khanna, 1985). Pollypeptide-P obtained from the fruit seed and cultured M. charantia cells produced hypoglycaemia in maturity onset as well as juvenile diabetics. Now fruits of M. charantia are reported to have hypoglycaemic effects in clinical trials with mildly diabetic patients. Blood glucose reduction by seeds was comparable to glybenclamide. Its extrapancreatic (Welihinda and Karunanayake, 1986) as well as pancreatic activity has been reported in rats and cats respectively (Lolitkar and Rajaram-Rao, 1962; 1966). Three non-steroidal hypoglycaemic principles have been isolated, from unripened fruits of bitter gourd, different from the earlier reported principles, and named as kakra 1b, kakra 111a and kakra 111b but their chemistry is unknown as yet. Kakra 1b has been reported to act by suppressing free fatty acid levels. Hypoglycaemic effects were evident in the glucose tolerance test. Our findings are in agreement with the earlier reports regarding hypoglycaemia caused by M. charantia. So far most workers have tried to isolate active principles of the fruit, administered orally or by injection (as is the case for insulin or oral hypoglycaemics) compared in terms of reduction of blood sugar after a given number of hours. From the animal experiments we found the response to aqueous extract of M. charantia fruit increased over a number of days of treatment indicating a time-related cumulative response. Hence in the clinical trial, the blood sugar level was monitored after 2, 3, 4 and 7 weeks until the level stabilized or returned to normal limits. In almost all cases it returned to normal limits. None of the earlier published reports on M. charantia followed our criteria or an exactly similar plan of work.
    Simultaneously with blood sugar, a qualitative urine sugar level examination was carried out. Other trials with aqueous extract also showed an absence of sugar in urine when blood sugar registered within normal limits. Urine sugar estimation was done just before and after a gap in the treatment of these subjects. The results expressed in Table 7 show that the sugar appears in urine in the absence of treatment but to a much lesser extent compared with the initial urine sugar levels. This indicates that the reversal of the control of diabetes is not total and immediate, unlike other conventional treatments practised.
    Table 4 shows the levels of glycosylated haemoglobin in patients before and after the clinical trial. The rate of glycosylation is proportional to the concentration of blood glucose (Cerami et al., 1979; Monnier and Cerami, 1982). Blood sugar at the peak of the glucose tolerance curve correlates with glycosylation (Koeing et al, 1976) and with the improvement glycaemic control, glycosylation of haemoglobin also decreases. Hence, estimation of glycosylated haemoglobin is a well-accepted parameter useful in the management and prognosis of the disease (Bunn et al., 1978; Stevans et al., 1977; Koeing et al., 1977; Chang nad Noble, 1979). The initial level of haemoglobin glycosylation in diabetic subjects in the present study was 8.37 0.4. The value was reduced to 6.1 after the control of glycaemia. This finding is in agreement with earlier reports.
    Under normal physiological conditions glucose can react nonenzymatically with proteins to form covalent adducts which form brown fluorescent pigments. In diabetes, this takes place at an accelerated rate causing structural and functional changes in physiologically active proteins leading to pathogenesis and diabetic complications, viz., neuropathy (Cerami et al., 1979) and neuropathic changes (Vlassora et al., 1981). In in vivo and in vitro studies of the crystalline lens, it was observed that glycosylated lens proteins cross-link by disulphide bonds to form high molecular weight forming aggregates which display opalescence in solution similar to that observed in diabetic cataract (Monnier and Cerami, 1982; Srivastava et al., 1987a, b). There is clinical recognition of cataract as a diabetic complication. Its incidence and severity increases with the advancement of diabetes. Of the groups of alloxan diabetic rats one was used as control and other was treated with the aqueous extract of bitter gourd fruit for 2 months. The average period of appearance of apparent sugar cataract in the control group was 3 months, while in the treated group it was 5 months. The delay in the cataract formation was significant (p<0.01). The results are presented in Table 6. It gives some indications of the adaptogenic properties of the herb, since herbs are know to have many principlec anatagonistic and synergistic to each other but their combined result produces the desired effect.
    The aqueous extract of M. charantia seems to induce a better adaptation against diabetes with control of glycaemia as reflected by a delay in the appearance of cataract. An inability to totally reverse glycosuria is evidenced by the gap in the treatment and the relief in symptoms such as poly****ia, polydipsia, burnng in hands and feet, pain in calf muscle and generalized weakness at a stage of treatment before the control of hyperglycaemia. A hypothesis regarding the mode of action needs further study since the hypoglycaemic properties of this herb cannot be attributed to a single principle.
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    Antidiabetic and Adaptogenic Properties of Momordica charantia Extract: An Experimental and Clinical Evaluation
    Author: Y. Srivastava, H. Venkatakrishna-Bhatt, Y. Verma, K. Venkaiah
    Type of Publication: Pre-clinical
    Date of Publication: 1993
    Publication: Phytotherapy Research, Vol. 7, pp 285-289, 1993
    Organization: B.J. Medical College and National Institute of Occupational Health
    Abstract: The hypoglycaemic properties of Momordica charantia (bitter gourd) water extract was tested on alloxan diabetic rats experimentally. A fall of blood sugar after 3 week’s treatment with aqueous extract of fruits of the herb was found to be significant (p<0.01). The aqueous extract of fruit was more effective in diabetes (fall of blood sugar 54% after 3 week’s therapy) than the powder of the dried fruit (fall 25% nonsignificant). Hypoglycaemic effects in diabetic patients were found to be highly significant (p>0.01) at the end of the trial but were cumulative and gradual, unlike that produced bu insulin. Adaptogenic properties are indicated by the delay in the appearance of cataracts, the secondary complications of diabetes and relief in neurological and other common symptoms even before the hypoglycaemia occurred



    INTRODUCTION
    The commonly practiced treatment of diabetes includes oral antidiabetics and/or insulin injections. Insulin can maintain blood glucose within a normal range but cannot simulate the pancreas of a healthy individual. Hence, diabetics within 15 to 20 years of diagnosis begin to develop complications (Engerman et al., 1977). Diabetes is the leading cause of noncongenital blindness among adults aged 20 to 70 years, the leading cause of kidney failure, it doubles the risk of heart disease, gangrene of the extremities and there is a clinical recognition of cataract as a diabetic complication. The range of these complications is directly related to the hour-to-hour fluctuations in blood sugar that persist even when insulin is taken once or twice a day (Job et al., 1975; Piters et al., 1975). Certain Indian plants have antidiabetic properties as reported by various authors (Srivastava et al., 1983, 1985) such as hypoglycaemic agents (Srivastava et al., 1986; 1988) and retardation of retinopathy (Srivastava et al., 1987a, b). A number of reports have appeared concerning the hypoglycaemic properties of the fruit and seed of the bitter gourd (Bildwa et al., 1977; Yaqub, 1980; Padminikadar and Chakrabarthi, 1982; Khanna, 1985; Ng et al., 1986; Welihinda et al., 1986). The bitter fruit variety is reported to be more effective in diabetes (Satyavati et al., 1987). The fruit and seed showed the presence of the polypeptide (P) (Khanna, 1985). The present work concerns an experimental and clinical study to determine whether bitter gourd has any adaptogenic effect as reflected in the checking or delaying of the appearance of cataract, a secondary complications of diabetes.

    MATERIALS AND METHODS
    Pharmacological studies. The experimental part of this study was carried out with Charles Foster rats, of both sexes weighing 150-200 g reared on standard laboratory, diet containing 70% cracked wheat, 20% cracked bengal gram, 5% shark liver oil n the form of dry mash and water adaptogenic libitum. A freshly prepared solution of alloxan in normal saline was injected subcutaneously (120 mg/ kg body wt.) to overnight fasted rats. Blood samples were drawn from the caudal vein by the pinch clip method. Blood sugar was estimated using a dextrometer before fasting and after 36 hr of allxan treatment. Rats with a blood sugar of 150 mg% or more were included in the diabetic group. Two such rats were maintained in each cage, under uniform husbandry conditions. Rats died during the experiment were excluded. A dose response curve was produced. From studies, 4 g of bitter gourd fruit was found to yield optimum results, the period of treatment being 3 weeks. An aqueous extract of 4 g of fruit was given per rat in 2 mL volumes by oral intubation. Diabetic rats included in the control group were administered 2 mL of placebo. Blood sugar, fundus, lenticular opacity and apparent signs and symptoms were examined periodically in diabetic rats for development of cataract (Srivastava et al., 1987a, b).
    Clinical study. The clinical part of this study was carried out on diabetic patients after confirmation by oral glucose tolerance test of postprandial blood sugar (PPBS) according to the criteria of the World Health Organization. The subjects were maintained on a diabetic diet until the blood sugar was stabilized. Pre and post liver function test, kidney function test, haemogram and urine examination were done to determine any side effects of the herbal treatment.
    Preparation of the extract. Bitter gourd (Momordica charantia Linn family: Cucurbitaceae) fruit was obtained fresh locally. An aqueous extract was made by chopping 100 g of fruit and boiling 200 mL of water until the volume was reduced to 100 mL. The chips were then smashed and the decoction was filtered with muslin cloth. The aqueous extract thus prepared was given as a standard single dose in the morning. The other set of diabetic patients were given powder of dried fruit, 15 g (equivalent to 100 g wet weight) thrice a day in equal doses of 5 g each. Glycosylated haemoglobin was estimated (Fischer et al., 1980). Besides these parameters, symptoms such as polyurea, poly****ia, burning in the hands and feet, pain in calf muscles and generalized weakness were observed before and after the trial.

    RESULTS AND DISCUSSION
    The results of the present investigations are summarized in Tables 1-7. The aqueous extract of Momordica charantia was tested on laboratory animals for the preliminary confirmation of its hypoglycaemic potential. The diabetic group of animals administered 2 mL of aqueous extract for a period of 3 weeks showed a reduction of the initial blood sugar from 220 mg% to 105 mg% which is significant (p<0.01). The control group of diabetic rats treated with placebo recorded no such fall. The results (Table 1) demonstrate the hypoglycaemic effect of the herb in rats. A number of reports have been published claimng a marked hypoglycaemic effect of M. charantia extract in laboratory animals, in normal as well diabetic animals (Sharma et al., 1960). The ether extract of the residue of the alcohol extract from leaves of M. charantia was reported to have hypoglycaemic activity comparable to tolbutamide. Powdered seeds tested against streptozotocin diabetic rabbits (1-30 g/day) produced hypoglycaemia comparable to tolbutamide (Venkanna-Babu et al., 1988). Normal as well as diabetic rabbits when treated with the fruit of M. charantia recorded a fall in blood sugar (Yakub, 1980). Momordica charantia extract showed the highest hypoglycaemic effect when tried on diabetes recovered rabbits (Venkanna-Babu et al., 1988). Charantin isolated from M. charantia fruit is a hypoglycaemic in normal and fasting rabbits. It was found to be more potent hypoglycaemic than tolbutamide given in equivalent doses. The result suggested a pancreatic as well as an extrapancreatic action of charantia (Ng et al., 1986; Welihinda, et al., 1986; Welihinda and Karunanayake, 1986).
    Our confirmatory study in laboratory animals was followed by a clinical trial. The group of diabetic patients was given powder of sun-dried fruit of M. charantia three times a day (5 g each time, and 15 g in total). The second group was given aqueous extract of 100 g of the fruit in a 100 mL volume in a single standard dose in the morning. A variation in the preparation was tried to determine differences in the hypoglycaemic effect of these preparations.
    Table 2 shows the results of the clinical trial with patients administered powder of M. charantia dried fruit concluded within 21 days. The fall in blood sugarwas 25% of the initial level, however, statistically it is insignificant. Table 3 shows the result of the aqueous extract trial. The subjects included were severe (433 mg %) to mild (260% diabetics, aged 42 to 70 years, all males. Blood sugar was estimated after 2, 3, 4 and 7 weeks of treatmen. The fall in blood sugar was highly significant at the termination of treatment. The response was overwhelming when compared with hypoglycaemia caused by the powder of M. charantia (Table 5) after an initial period of 3 weeks of therapy. The fall in blood sugar in aqueous extract treated diabetics was 54.0% (p<0.01) as against 25% observed in the powder treated group. Further the aqueous extract treated diabetics showed a time-related gradual hypoglycaemic response as revealed in blood sugar and urine sugar data obtained at 2, 3, 4 and 7 weeks. This feature of the herbal treatment of diabetes is unlike conventional treatment. In almost all cases the blood sugar level was restored within the normal limits.
    The pure protein known as P-insulin or polypeptide-P extracted from M. charantia fruit in crystalline form was tested in controlled clinical trials for its efficacy as an hypoglycaemic agent. When administered s.c. it produced a mean fall in blood sugar of 45.8  13.6 mg% in juvenile and maturity onset diabetics as well as in chemical diabetes. No hypersensitivity reaction was noticed (Baldwa et al., 1987). It was found effective through the oral route (Khanna, 1985). Pollypeptide-P obtained from the fruit seed and cultured M. charantia cells produced hypoglycaemia in maturity onset as well as juvenile diabetics. Now fruits of M. charantia are reported to have hypoglycaemic effects in clinical trials with mildly diabetic patients. Blood glucose reduction by seeds was comparable to glybenclamide. Its extrapancreatic (Welihinda and Karunanayake, 1986) as well as pancreatic activity has been reported in rats and cats respectively (Lolitkar and Rajaram-Rao, 1962; 1966). Three non-steroidal hypoglycaemic principles have been isolated, from unripened fruits of bitter gourd, different from the earlier reported principles, and named as kakra 1b, kakra 111a and kakra 111b but their chemistry is unknown as yet. Kakra 1b has been reported to act by suppressing free fatty acid levels. Hypoglycaemic effects were evident in the glucose tolerance test. Our findings are in agreement with the earlier reports regarding hypoglycaemia caused by M. charantia. So far most workers have tried to isolate active principles of the fruit, administered orally or by injection (as is the case for insulin or oral hypoglycaemics) compared in terms of reduction of blood sugar after a given number of hours. From the animal experiments we found the response to aqueous extract of M. charantia fruit increased over a number of days of treatment indicating a time-related cumulative response. Hence in the clinical trial, the blood sugar level was monitored after 2, 3, 4 and 7 weeks until the level stabilized or returned to normal limits. In almost all cases it returned to normal limits. None of the earlier published reports on M. charantia followed our criteria or an exactly similar plan of work.
    Simultaneously with blood sugar, a qualitative urine sugar level examination was carried out. Other trials with aqueous extract also showed an absence of sugar in urine when blood sugar registered within normal limits. Urine sugar estimation was done just before and after a gap in the treatment of these subjects. The results expressed in Table 7 show that the sugar appears in urine in the absence of treatment but to a much lesser extent compared with the initial urine sugar levels. This indicates that the reversal of the control of diabetes is not total and immediate, unlike other conventional treatments practised.
    Table 4 shows the levels of glycosylated haemoglobin in patients before and after the clinical trial. The rate of glycosylation is proportional to the concentration of blood glucose (Cerami et al., 1979; Monnier and Cerami, 1982). Blood sugar at the peak of the glucose tolerance curve correlates with glycosylation (Koeing et al, 1976) and with the improvement glycaemic control, glycosylation of haemoglobin also decreases. Hence, estimation of glycosylated haemoglobin is a well-accepted parameter useful in the management and prognosis of the disease (Bunn et al., 1978; Stevans et al., 1977; Koeing et al., 1977; Chang nad Noble, 1979). The initial level of haemoglobin glycosylation in diabetic subjects in the present study was 8.37 0.4. The value was reduced to 6.1 after the control of glycaemia. This finding is in agreement with earlier reports.
    Under normal physiological conditions glucose can react nonenzymatically with proteins to form covalent adducts which form brown fluorescent pigments. In diabetes, this takes place at an accelerated rate causing structural and functional changes in physiologically active proteins leading to pathogenesis and diabetic complications, viz., neuropathy (Cerami et al., 1979) and neuropathic changes (Vlassora et al., 1981). In in vivo and in vitro studies of the crystalline lens, it was observed that glycosylated lens proteins cross-link by disulphide bonds to form high molecular weight forming aggregates which display opalescence in solution similar to that observed in diabetic cataract (Monnier and Cerami, 1982; Srivastava et al., 1987a, b). There is clinical recognition of cataract as a diabetic complication. Its incidence and severity increases with the advancement of diabetes. Of the groups of alloxan diabetic rats one was used as control and other was treated with the aqueous extract of bitter gourd fruit for 2 months. The average period of appearance of apparent sugar cataract in the control group was 3 months, while in the treated group it was 5 months. The delay in the cataract formation was significant (p<0.01). The results are presented in Table 6. It gives some indications of the adaptogenic properties of the herb, since herbs are know to have many principlec anatagonistic and synergistic to each other but their combined result produces the desired effect.
    The aqueous extract of M. charantia seems to induce a better adaptation against diabetes with control of glycaemia as reflected by a delay in the appearance of cataract. An inability to totally reverse glycosuria is evidenced by the gap in the treatment and the relief in symptoms such as poly****ia, polydipsia, burnng in hands and feet, pain in calf muscle and generalized weakness at a stage of treatment before the control of hyperglycaemia. A hypothesis regarding the mode of action needs further study since the hypoglycaemic properties of this herb cannot be attributed to a single principle.
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    REFERENCES
    Baldwa, V.S., Bahndari, C.M., Pangria, A. and Goyal, R.K. (1977). Clinical trial in patients of diabetes mellitus with insulin like compound obtained from plant sources. Ups. J. Med. Sci. 82, 39-41.
    Bunn, H.F., Gabby, K.H. and Callop, P.M. (1978). The glycosylation of Hb: Relevance of diabetes mellitus. Science 200, 21-23.
    Cerami, A., Stevans, V.J., and Monnier, V.M. (1979). Role of non-enzymatic glycosylation in development of the sequelae of diabetes mellitus. Metabolism 28, (suppl.), 431-435.
    Chang, A.T., and Noble, J. (1979). Estimation of HbAlc like glycosylated proteins in kidneys of streptozotocin diabetes and controlled rats. Diabetes 28, 408-415.
    Chopra, R.N., Chopra, I.C., Handa, K.L., and Kapur, L.D. (1958). Indigenous Drugs of India, p. 597. U. N. Dhur & Sons Calcutta.
    Engerman, R., Bloodworth, J. M. B., and Nelson Jr., S. (1977). Relationship of microvascular disease in diabetes mellitus to metabolic control. Diabetes 26, 760-767.
    Fischer, R. W., De Jong, C., Voigt, E., Berger, W., and Winterhalter, K. H. (1980). Colorimetric determinaton of Hblc in normal and diabetic subjects. Clinical . Laboratory. Haemat. 2, 129-138.
    Gupta, S. S., and Seth, C. B. (1978). Effect of Momordica charantia Linn. (karera) on glucose in albino rats. J. Med. Assn. 39, 581-590.
    Job, D., Eschwege, E., Gyet, G., and Tobobrontsky, J. (1975). Effect of multiple insulin daily injection on the course of retinopathy, Diabetes, DIAEAZ, 24 (suppl. 2), 393.
    Khanna, P. (1985). Insulin from bitter gourd-herbal drug. Eastern Pharmacist, pp.101-103.
    Koeing, R. J., Blobstein, S. B., and Cerami, A. (1977). Structure of carbohudrates of HBAIc. Diabetes 25, 230-238.
    Koeing, R. J., Peterson, C. M. and Kilo, C. (1976). Hblc as indicator of the degree of glucose intolerance in diabetes. Diabetes 25, 230-240.
    Lolitkar, M. M., and Rajaram-Rao, M. R. (1962). Note on hyperglycemia principle isolated from fruits of Momordica charantia Linn. J. Univ. Bombay, (India) 29, 223-235.
    Lolitkar, M. M., and Rajaram-Rao, M. R (1966). Pharmacology of hypoglycemic principle isolated from the fruits of Momordica charantia Linn. Indian J. Pharmac. 28, 129-137.
    Monnier, V. K., and Cerami, A. (1982). Non-enzymatic glycosylation and browning in diabetes and aging. Diabetes 31 (suppl.3), 57-66.
    Ng, T. B., Wong, C. M., Li, W. W., and Yeng, H. W. (1986). Insulin like molecules in Momordica charantia. J, Ethnopharmacol. 15, 107-108.
    Padmini-kedar, and Chakrabharathi, C. H. (1982). Effect of bitter gourd(Momordica charantia) seed and glibenclamide in streptozotocin induced diabetes mellitus. Indian J. Experimental. Biol. 20, 181-184.
    Piters, K., Goodman, J., and Bossman, A. (1975). Treatment of diabetic ketoacidosis dose intravenous insulin diabetes. DIEAZ (suppl.2) 24, 393.
    Satyavati, G. V., Gupta, A. K., and Tandan, N. (1987). Medicinal Plants of India, Vol. 2, pp. 261. Indian Council of Medical Research, New Delhi.
    Srivastava, Y., Nigam, S. K., Verma, Y., and Prem, A. S. (1987a). Experimental diabetic cataract in rats. J. Diabetes. Assoc. India 27, 25.
    Srivastava, Y., Rawal, B. H., and verma, Y. (9188a). Arogya Gymnema sylvestra in diabetes mellitus. J. Hlth. Sci. 24, 61.
    Srivastava, Y., Venkatakrishna-Bhatt, H., Gupta, O. P., and Gupta, P. S. (1983). Hypoglycemia induced by Syzigium cumini (Jambu) seeds in diabetes mellitus. Asian Med. J. 26, 289-291.
    Srivastava, Y., Venkatakrishna-Bhatt, Jhala, C. L., Nigam, S. K., Ashok Kumar, and Verma, Y. (1985). Hypoglycemia and life prolong properties og Gymnema sylvestre leaf extract in rats. Israel J. Med. Sci. 21, 540-542.
    Srivastava, Y., Venkatakrishna-Bhatt, Jhala, C. L., Nigam, S. K., Ashok Kumar, and Verma, Y. (1986). Oral Gymnema sylvestre R. Br., leaf extracts inducing protracted longevity and hypoglycemia in alloxan diabetic rats: review and experimental study. Int. Crude Drug Res. 24, 371-376.
    Srivastava, Y., Venkatakrishna-Bhatt, H., Verma, Y., and Prem, A. S. (1987b). Retardation of retinopathy by Momordica charantia L. (bitter gourd) fruit extract in alloxan diabetic rats. Indian J. Experimental. Biol. 25, 571-572.
    Srivastava, Y., Venkatakrishna-Bhatt, H., Verma, Y., and Prem, A. S. (1986b). Effect of Momordica charantia Linn. pomous aqueous extract on cataractogenesis in murin alloxan diabetics. Pharmacol. Res. Commun. 20. 201-209.
    Sharma, V. N., Sogani, R. K., and Arora, R. B. (1960). Some observations on hypoglycemic activityu of Momordica charantia . Indian J. Med. Res. 48, 47-56.
    Stevans, V. J., Vlassora, H., Abarti, A., and Cerami, A. (1977). Non-enzymatic glycosylation of Hb. J. Biol. Chem. 252, 2998.
    Venkanna-Babu, P., Radhamoorthi, B., Pugazhanthi, S., Prabhu, K. M., and Suryanarayana, P. 91988). Alloxan recovered rabbits as animal model for screening of hypoglycemic activity of compounds. Indian J. Biochem. Biophys. 25, 714-718.
    Vlassora, R., Brownlee, N., and Cerami, A. (1981). Non-enzymatic glycosylation of peripheral nerve proteins in diabetes mellitus. Proc. Natl. Acad. Sci. (USA) 78, 5190-5192.
    Welihinda, J., and Karunanayake. (1986). Extra-pancreatic effects of Momordica charantia in rats. J. Ethnopahrmacol. 17, 247-255.
    Welihinda, J., Karunanayake, E. H., Sheriff, M. R., and Jayasinghe, K. S. A. (1986). Effect of Momordica charantia on glucose tolerance in maturity onset diabetes j. Ethnopharmacol. 17, 277-282.
    Yaqub, N. (1980). Hypoglycemic activity of Momordica charantia in normal male albino rabbits. J. Pakistan Med. Assoc. 19, 181-184.
  16. Elite Member
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    Nice questions Jakellpet Have you tried the slin yet?
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    Quote Originally Posted by Craigmatthew View Post
    Nice questions Jakellpet Have you tried the slin yet?
    I have dosed it a few times - only two caps post WO and it's strong stuff. After about 15mins you have this urgency to eat . . . and it lets you know when you've had enough - it's a lot different to other nutrient partioners I have used.

    . . I'n a few weeks Im going to run a few different dosing regimes. Then report back.

    I know there are a lot of nutrient partioner fans out there - I'm surprised no-one has tried both of these great products!
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    I'm making something on custom capsule a mix btw pslin and this. At ridiculous high doses so I can dose a serving thruout the day

    When the funds come ill order it and use it in conjunction with other things on high carb days
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    Quote Originally Posted by jakellpet View Post
    I have dosed it a few times - only two caps post WO and it's strong stuff. After about 15mins you have this urgency to eat . . . and it lets you know when you've had enough - it's a lot different to other nutrient partioners I have used.

    . . I'n a few weeks Im going to run a few different dosing regimes. Then report back.

    I know there are a lot of nutrient partioner fans out there - I'm surprised no-one has tried both of these great products!
    These both appear to be fine products.
    Ask me for samples of the new RecoverPRO and Maniac. 3Z is coming July 1st Facebook for more info and maybe a great deal on it coming.
    http://twitter.com/#!/TeamAISports
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    Bulk pslin from Nutra is a very solid product as well. Especially when used in the USP Labs MassMonster shake. It's become a staple of mine.
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    Quote Originally Posted by crewchief182 View Post
    Bulk pslin from Nutra is a very solid product as well. Especially when used in the USP Labs MassMonster shake. It's become a staple of mine.
    Oh for sure. The bulk version is very cost effective.
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    the bulk banaba is MUCH more effective IMO then bulk Pslin
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    I'm always looking for good products, can you explain why you prefer the banaba?
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    More powerful at the extract np has which means less can handle more carbs
    And there are otherthings that increase insulin sensitvity
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    Quote Originally Posted by crazyfool405 View Post
    the bulk banaba is MUCH more effective IMO then bulk Pslin
    Quote Originally Posted by crewchief182 View Post
    I'm always looking for good products, can you explain why you prefer the banaba?
    CF - you're running some cool natty compounds. Give us a rundown on the what, when & why.
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    I have used AP, Pslin, Glycobol and soon i will be trying Slin.
    In order of which i liked the most.
    Glycobol
    AP(Anabolic Pump)
    PSlin

    I never was much a fan of LG but as the past few years have shown me alot of them like it and they seem to be coming out with more.
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    I've never tried Glycobol. It looks like a great product, and I hear it gives you an empty pit of a stomach which is nice when bulking.

    SLIN is real strong. I take 3 caps top or else I go real hypo. Once I took 3 caps before a fasted workout...never again! Hahaha. - I love SLIN and I get insane food pumps on it. I'm on a CKD right now, but once I go back to TKD I'll be using SLIN post-workout for my brown rice flour+Perfect Carb+Lipotropic shakes.
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    I'm going to try bitter melon on its own. I have all the slin ingredients seperate ill try next carb up day. Ill give yall my review
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    I should add i tried neovar also. I would put it 2nd - 3rd prolly. Irish reminded me cause i remember taking 3 1hr 30min preWO, 30min later i ate some oats with a scoop or protein, took my preWO booster(n.o. product but forgot which at time) and i had made it through 3 set and then i got cold, sweaty, light headed until i slowed down. My girlfriend said i looked a bit pale...so i was pretty sure i came close to some bad issues...
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    Oh how many grams of carbs can slin handle?

    For example what's optimum carb intake for 1 cap 2 cap and 3caps?

    IC. How many g of carb doid u take with 3 pills to make u go hypo?
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    From neovar? Really?

    I can take like 6-10 of those a day and not go hypo even on keto
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    Quote Originally Posted by crazyfool405 View Post

    IC. How many g of carb doid u take with 3 pills to make u go hypo?
    Are you talking about when I took it pre-wo? 0g. I used it to aid in lipolysis. - I don't go hypo if I eat within 15mins of taking 2-3 caps. If I take 4 caps, I go hypo regardless of how much I eat. 4 is too strong for me.
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    Looks like ill have to try thate with 2 glycobol 1 pslin 1 ginseng 300mg extra ala and 400mg bnanaba
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    I'm trying to figure out how many g carbs a cap can hjandle soo I can dose around it wirth my other supps. Gbol can handle 70 pslin bout 60 ala approx 30 same with ginseng. And the 400mg bamaba can handle bout 70ish as well from what I used
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    Ive used both and while neither are miracle supps, both are effective. I didnt notice any drastic difference between the two, and the Slin is much cheaper.

    On paper, the glycobol looks superior, but IMO it didnt live up to its price tag (though i got it from a trade, so i didnt mind the price )

    I am also very fond of Anabolic Pump, havent tried their p-slin though
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    Quote Originally Posted by crazyfool405 View Post
    From neovar? Really?

    I can take like 6-10 of those a day and not go hypo even on keto
    yeah Neovar is not that strong. I used to drop 4 before bedtime (w/o CHO) to lean me out
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    I just love the hypo feeling the cold sweats. Makes me know I'm in a good state to do so low intensity cardio and I'm burning some fats
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    Quote Originally Posted by jakellpet View Post
    CF - you're running some cool natty compounds. Give us a rundown on the what, when & why.
    oh man here it goes.....

    on carb up days.

    i take 300mg ALA with i thinnk its 585mg panax ginseng with 30g carbs (Cream of wheat or quinoa flakes) depletion workout

    then 1 glycobol 15 min before i have a serving of dark matter with extra BCAAs

    immediatly following that i take

    1 pslin, 1 glycobol 1 panax ginseng 300mg ALA i wait about 40 minute and eat 200-300g carbs as i start that meal i have another glycobol and i have 400mg bulk banaba 20% that i sip thruout the meal.

    the panax ginseng takes about 1hr to work and lower blood sugar as shown in some literature i read.

    consistent dosing of ALA shows to lower insulin output by pancrease and increase glut1/4 pathway when dosed continuously throughout the day (up to 2700mg)

    pslin we all know what that does i dont really need to give the run down, same with glycobol.

    i take the glycobol mid meal because i end up eating for quite some time lol and sip the banaba thruout to keep blood sugar low so i dont get that distended stomach

    the chromium i take with my meal because i chew it and it helps insulin do its job.

    blah there done lol
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    i did the neovar empty stomach and it did it. Maybe its just me or whatever, everyones different especially when it comes to this stuff.
    I wanted to be hooked when Anabolic Pump was out but i never got enough results from any of them to stick with them.
  

  
 

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