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The Only SANE Way To Burn Fat
- Thread starter Nelson Montana
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Goldprospector
New member
the cardio issue is about as personal as hat sizes. If I don't do a minimal amount of cardio...I get fat as hell. Even with a job where I sweat constantly for 8 hours a day and even with a decent diet.
But I do think too much cardio is a bad thing. I only hit the treadmill for 10 to 15 minutes prior to my weight training, that way, I have a high intensity lift that keeps my heartrate into the target HR zone.
But I do think too much cardio is a bad thing. I only hit the treadmill for 10 to 15 minutes prior to my weight training, that way, I have a high intensity lift that keeps my heartrate into the target HR zone.
By the way, ZIP! is $29.95 That's practically a wholsale price and the reason I agreed to work with PF. Their prices are right -- especially considering many less effective thermogenics can cost twice that much.
DeepZenPill
New member
Nelson Montana said:
Maybe a little off topic, but raising estrogen usually makes me break out more, so I doubt the acne clearing effect is from a surge in estrogen.
This is different than Armour Thyroid, right? And what exactly are the active elements of this extract?
IHateCrunches
New member
Nelson Montana said:
Nelson Montana said:
So your pushing "ZIP" whihc is a formula that has been made recently? And it increases thyroid function? What if we wanted to try the 7 Keto DHEA. Whats the differences between ZIP and this? Differences being i energy levelsand thyroid function.
BTW in your opinion are you for or against low carb diets, because you gave two different views.
macrophage69alpha
New member
Nelson Montana said:
green tea extract does not contain flouride.
and just as a note- most water in the united states is flouridated
btw- guggulsterones have not been shown to raise estrogen, though their thyroid raising abilities may be in dispute as with most supps that purport to do so.
macrophage69alpha
New member
btw-
T-rex= THERMOREXIN
T-rex= THERMOREXIN
Dr. M
New member
Nelson -
aspartame shutting down thyroid function permanently? I want a citation for that. You can't just throw out a statement like that without citing the study; that's the way rumours get started.
===
Physiol Behav. 2002 Feb 1-15;75(1-2):41-7.
Effects of long-term ingestion of aspartame on hypothalamic neuropeptide Y, plasma leptin and body weight gain and composition.
Beck B, Burlet A, Max JP, Stricker-Krongrad A.
Centre de Recherches UHP/EA 3453, IFR no. 111, Systemes Neuromodulateurs des Comportements Ingestifs; 38, rue Lionnois, 54000 Nancy, France. [email protected]
The aim of this study was to determine the effects of the chronic ingestion of aspartame (ASP) on brain neuropeptide Y (NPY) concentrations, plasma hormones, food intake and body fat. Two groups of male Long-Evans rats, fed on a control (C) well-balanced diet, had to drink either a 0.1% ASP solution or water for a period of 14 weeks starting at weaning. Food intake and body weight were weekly recorded. At the end of the experiment, fat pads were sampled, leptin and insulin were measured in the plasma and NPY in several microdissected brain areas. Substituting ASP for water led to lower body weight (-8%; P<.004) and lower fat depot weight (-20%; P<.01) with no differences in energy intake or plasma insulin concentrations. Plasma leptin was significantly reduced by 34% (P<.05). Leptin concentrations were well-correlated with final body weight (r=.47; P<.025) and fat pad mass (r=.53; P<.01). NPY concentrations were 23% lower (P<.03) in the arcuate nucleus of ASP rats with no differences in other brain areas. The beneficial effects on body composition could be related to the decreased effects of NPY on lipid and energy metabolism, independently of insulin. The reasons for the NPY decrease (regulatory or toxicological) are not obvious. The constitutive amino acids of the ASP molecule might participate in the NPY regulation.
===
Physiol Behav. 2003 Apr;78(4-5):557-62.
Physiological mechanisms mediating aspartame-induced satiety.
Hall WL, Millward DJ, Rogers PJ, Morgan LM.
Centre for Nutrition and Food Safety, School of Biomedical and Life Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK. [email protected]
Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect. The effects of the constituents of aspartame, phenylalanine and aspartic acid, were also examined. Six subjects consumed an encapsulated preload consisting of either 400 mg aspartame, 176 mg aspartic acid+224 mg phenylalanine, or 400 mg corn flour (control), with 1.5 g paracetamol dissolved in 450 ml water to measure gastric emptying. A 1983-kJ liquid meal was consumed 60 min later. Plasma CCK, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, and insulin were measured over 0-120 min. Gastric emptying was measured from 0 to 60 min. Plasma GLP-1 concentrations decreased following the liquid meal (60-120 min) after both the aspartame and amino acids preloads (control, 2096.9 pmol/l min; aspartame, 536.6 pmol/l min; amino acids, 861.8 pmol/l min; incremental area under the curve [AUC] 60-120 min, P<.05). Desire to eat was reduced from 60 to 120 min following the amino acids preload (control, -337.1 mm min; aspartame, -505.4 mm min; amino acids, -1497.1 mm min; incremental AUC 60-120 min, P<.05). However, gastric emptying rates, plasma CCK, GIP, insulin, and glucose concentrations were unaffected. There was a correlation between the increase in plasma phenylalanine and decrease in desire to eat after the liquid meal following the constituent amino acids (r=-.9774, P=.004). In conclusion, it is unlikely that aspartame increases satiety via CCK- or GLP-1-mediated mechanisms, but small changes in circulating phenylalanine concentrations may influence appetite.
===
Now, if THIS is the paper to which you're referring:
J Pharmacol Sci. 2003 Jan;91(1):83-6.
Formaldehyde-induced shrinkage of rat thymocytes.
Nakao H, Umebayashi C, Nakata M, Nishizaki Y, Noda K, Okano Y, Oyama Y.
Laboratory of Cell Signaling, Faculty of Integrated Arts and Sciences, The University of Tokushima, Tokushima, Japan.
To test the possibility that micromolar formaldehyde, a metabolite of methanol derived from aspartame, exerts cytotoxicity, its effect on rat thymocytes was examined under the in vitro condition using a flow cytometer. Incubation of thymocytes with formaldehyde at 100 micro M or more for 24 h significantly increased the populations of shrunken cells and cells with hypodiploid DNA. The peak blood concentration of methanol in human subjects administered abuse doses of aspartame has been reported to exceed 2 mg/dL (625 micro M). It would increase the population of thymocytes undergoing apoptosis if formaldehyde at 100 micro M or more appears in the blood after administration of aspartame.
===
Then Nelson, you've been led astray. The amount of aspartame needed to generate a 100uM concentration of methanol in the human bloodstream is MASSIVE. When they talk of studies with 'abuse doses' of aspartame, they're talking about the equivalent of approximately 16 CASES of diet coke (or whatever your aspartame vehicle is; many aspartame-sweetened products contain generally the same amount of aspartame for the same sweetness) administered in a SINGLE dose. That's right - one dose. Furthermore, the formaldehyde (when they talk of formaldehyde, this is because methanol is metabolized to formaldehyde in the human body) was administered ARTIFICIALLY, in vitro! It was a one-shot, kick 'em in the ass deal, unlike normal metabolism which would have tapered the dosage of methanol (formaldehyde) up and down, allowing the cells to react in a graduated fashion, because of its time of action on the aspartame.
Now, if any of you sit down and chug 16 cases of diet coke (with or without lemon) after you workout, then MAYBE you'll approach the doses they're talking about. The fact is, the normal dietary intake of methanol is much higher than that produced by one's normal consumption of aspartame - these studies that quote 'abuse doses', or direct administration of 100uM methanol in vitro instead of in vivo are NOT relevant to normal consumption of the substance in question.
It's like saying that if one were to hold 100,000,000 coffe cups worth of heat at once, one's hand would MELT! AAAAAAAAAAHHHHH! STOP HOLDING YOUR COFFEE EVERYONE! Oh, wait... by holding just ONE cup at a time, your hand is fine... oh, right - these guys have all forgotten one principle of good life science: conduct your study in a normal dosage range for the population you're trying to protect.
It's assholes like these guys in the study above that give scientists like myself a bad name. All they wanted to do was to shock and awe the world with a tale of aspartame-induced thyroid cell apoptosis (STILL, there is no mention of complete thyroid shutdown - just increased apoptosis which would likely still be in the ranges where the thyroid would be able to replace the cells in a controlled fashion) and try to gain some credibility for... wait for it... the Faculty of Integrated Arts and Sciences in Tokushima. Good for them.
Even in the scientific literature, be careful what you believe... context and procedure is ALWAYS important.
-M
aspartame shutting down thyroid function permanently? I want a citation for that. You can't just throw out a statement like that without citing the study; that's the way rumours get started.
===
Physiol Behav. 2002 Feb 1-15;75(1-2):41-7.
Effects of long-term ingestion of aspartame on hypothalamic neuropeptide Y, plasma leptin and body weight gain and composition.
Beck B, Burlet A, Max JP, Stricker-Krongrad A.
Centre de Recherches UHP/EA 3453, IFR no. 111, Systemes Neuromodulateurs des Comportements Ingestifs; 38, rue Lionnois, 54000 Nancy, France. [email protected]
The aim of this study was to determine the effects of the chronic ingestion of aspartame (ASP) on brain neuropeptide Y (NPY) concentrations, plasma hormones, food intake and body fat. Two groups of male Long-Evans rats, fed on a control (C) well-balanced diet, had to drink either a 0.1% ASP solution or water for a period of 14 weeks starting at weaning. Food intake and body weight were weekly recorded. At the end of the experiment, fat pads were sampled, leptin and insulin were measured in the plasma and NPY in several microdissected brain areas. Substituting ASP for water led to lower body weight (-8%; P<.004) and lower fat depot weight (-20%; P<.01) with no differences in energy intake or plasma insulin concentrations. Plasma leptin was significantly reduced by 34% (P<.05). Leptin concentrations were well-correlated with final body weight (r=.47; P<.025) and fat pad mass (r=.53; P<.01). NPY concentrations were 23% lower (P<.03) in the arcuate nucleus of ASP rats with no differences in other brain areas. The beneficial effects on body composition could be related to the decreased effects of NPY on lipid and energy metabolism, independently of insulin. The reasons for the NPY decrease (regulatory or toxicological) are not obvious. The constitutive amino acids of the ASP molecule might participate in the NPY regulation.
===
Physiol Behav. 2003 Apr;78(4-5):557-62.
Physiological mechanisms mediating aspartame-induced satiety.
Hall WL, Millward DJ, Rogers PJ, Morgan LM.
Centre for Nutrition and Food Safety, School of Biomedical and Life Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK. [email protected]
Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect. The effects of the constituents of aspartame, phenylalanine and aspartic acid, were also examined. Six subjects consumed an encapsulated preload consisting of either 400 mg aspartame, 176 mg aspartic acid+224 mg phenylalanine, or 400 mg corn flour (control), with 1.5 g paracetamol dissolved in 450 ml water to measure gastric emptying. A 1983-kJ liquid meal was consumed 60 min later. Plasma CCK, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, and insulin were measured over 0-120 min. Gastric emptying was measured from 0 to 60 min. Plasma GLP-1 concentrations decreased following the liquid meal (60-120 min) after both the aspartame and amino acids preloads (control, 2096.9 pmol/l min; aspartame, 536.6 pmol/l min; amino acids, 861.8 pmol/l min; incremental area under the curve [AUC] 60-120 min, P<.05). Desire to eat was reduced from 60 to 120 min following the amino acids preload (control, -337.1 mm min; aspartame, -505.4 mm min; amino acids, -1497.1 mm min; incremental AUC 60-120 min, P<.05). However, gastric emptying rates, plasma CCK, GIP, insulin, and glucose concentrations were unaffected. There was a correlation between the increase in plasma phenylalanine and decrease in desire to eat after the liquid meal following the constituent amino acids (r=-.9774, P=.004). In conclusion, it is unlikely that aspartame increases satiety via CCK- or GLP-1-mediated mechanisms, but small changes in circulating phenylalanine concentrations may influence appetite.
===
Now, if THIS is the paper to which you're referring:
J Pharmacol Sci. 2003 Jan;91(1):83-6.
Formaldehyde-induced shrinkage of rat thymocytes.
Nakao H, Umebayashi C, Nakata M, Nishizaki Y, Noda K, Okano Y, Oyama Y.
Laboratory of Cell Signaling, Faculty of Integrated Arts and Sciences, The University of Tokushima, Tokushima, Japan.
To test the possibility that micromolar formaldehyde, a metabolite of methanol derived from aspartame, exerts cytotoxicity, its effect on rat thymocytes was examined under the in vitro condition using a flow cytometer. Incubation of thymocytes with formaldehyde at 100 micro M or more for 24 h significantly increased the populations of shrunken cells and cells with hypodiploid DNA. The peak blood concentration of methanol in human subjects administered abuse doses of aspartame has been reported to exceed 2 mg/dL (625 micro M). It would increase the population of thymocytes undergoing apoptosis if formaldehyde at 100 micro M or more appears in the blood after administration of aspartame.
===
Then Nelson, you've been led astray. The amount of aspartame needed to generate a 100uM concentration of methanol in the human bloodstream is MASSIVE. When they talk of studies with 'abuse doses' of aspartame, they're talking about the equivalent of approximately 16 CASES of diet coke (or whatever your aspartame vehicle is; many aspartame-sweetened products contain generally the same amount of aspartame for the same sweetness) administered in a SINGLE dose. That's right - one dose. Furthermore, the formaldehyde (when they talk of formaldehyde, this is because methanol is metabolized to formaldehyde in the human body) was administered ARTIFICIALLY, in vitro! It was a one-shot, kick 'em in the ass deal, unlike normal metabolism which would have tapered the dosage of methanol (formaldehyde) up and down, allowing the cells to react in a graduated fashion, because of its time of action on the aspartame.
Now, if any of you sit down and chug 16 cases of diet coke (with or without lemon) after you workout, then MAYBE you'll approach the doses they're talking about. The fact is, the normal dietary intake of methanol is much higher than that produced by one's normal consumption of aspartame - these studies that quote 'abuse doses', or direct administration of 100uM methanol in vitro instead of in vivo are NOT relevant to normal consumption of the substance in question.
It's like saying that if one were to hold 100,000,000 coffe cups worth of heat at once, one's hand would MELT! AAAAAAAAAAHHHHH! STOP HOLDING YOUR COFFEE EVERYONE! Oh, wait... by holding just ONE cup at a time, your hand is fine... oh, right - these guys have all forgotten one principle of good life science: conduct your study in a normal dosage range for the population you're trying to protect.
It's assholes like these guys in the study above that give scientists like myself a bad name. All they wanted to do was to shock and awe the world with a tale of aspartame-induced thyroid cell apoptosis (STILL, there is no mention of complete thyroid shutdown - just increased apoptosis which would likely still be in the ranges where the thyroid would be able to replace the cells in a controlled fashion) and try to gain some credibility for... wait for it... the Faculty of Integrated Arts and Sciences in Tokushima. Good for them.
Even in the scientific literature, be careful what you believe... context and procedure is ALWAYS important.
-M
