Upcoming M-1-T Cycle

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  1. Now to complete my shameless post whoring, I'll start my M-1-T @ 20mg daily soon as well. I'm also running the anarchy stack, Guggulbolic Extreme, and UCP-1


  2. Now to complete my shameless post whoring, I'll start my stack soon as well. I'm also running the anarchy stack, Guggulbolic Extreme, and UCP-1
    Honestly, although you may not care, I think the Guggulbolic and the anarchy stack are rather redundant, if not outright unnecessary for an M-1-T cycle. I also question the uncoupler stacking as well, but, eh, who am I to dictate to others about their cycles; not to mention hijack others threads to do so. Apologies, but you might want to do at least a little more thinking before you dive in.
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  3. Originally posted by Method


    Honestly, although you may not care, I think the Guggulbolic and the anarchy stack are rather redundant, if not outright unnecessary for an M-1-T cycle.
    how do you figure Guggulsterones and the anarchy stack to be redundant? As i understand it Guggulsterones stimulate the thyroid gland. R-ALA is a nutrient partitioner and also a strong antioxidant. alcar transports fats into the mitochondria, and in the mitochondria these fats are converted to an energy source. CLA works by increasing AA and glucose transport into the muscle cells via insulin stimulated pathways, and therefore in hypocaloric diets acts as an anti-catabolic. CLA also keeps blood glucose levels more stable. In essence preventing preventing high blood glucose or hypoglycaemia after a carb meal.

  4. Originally posted by Method


    Honestly, although you may not care, I think the Guggulbolic and the anarchy stack are rather redundant, if not outright unnecessary for an M-1-T cycle. I also question the uncoupler stacking as well, but, eh, who am I to dictate to others about their cycles; not to mention hijack others threads to do so. Apologies, but you might want to do at least a little more thinking before you dive in.

    Originally posted by goldylight


    how do you figure Guggulsterones and the anarchy stack to be redundant? As i understand it Guggulsterones stimulate the thyroid gland. R-ALA is a nutrient partitioner and also a strong antioxidant. alcar transports fats into the mitochondria, and in the mitochondria these fats are converted to an energy source. CLA works by increasing AA and glucose transport into the muscle cells via insulin stimulated pathways, and therefore in hypocaloric diets acts as an anti-catabolic. CLA also keeps blood glucose levels more stable. In essence preventing preventing high blood glucose or hypoglycaemia after a carb meal.
    Well goldylight basically spelled that one out for me, for the most part. I do realize your point that cutting with M1T alone should be good, but these all work through different mechanisms that have different benefits.

    Why would you question uncoupler stacking exactly? And how would a strong anti-oxident be redundant when using an uncoupler, not to mention glucose control? Are the many benefits of ALCAR and Green Tea somehow magically not present with an AS cycle? This is news to me.

    I think what you may mean is that you would not spend the $$ to combine all of these together, if M1T will give benefits alone for cutting. I can respect that viewpoint, but don't insult my intelligence by insinuating I haven't thought about this at all. I will concede that this is certainly not the most cost-effective stack out there, but to say it will not be efficient or certain aspects are "redundant" seems rather unfounded to me.

    The anarchy stack is a year round thing for me now, regardless of cycling. The gglesterones I got a good deal on, and I have used them in the past and do not actually expect a dramaticsynergy or outstanding results from that one compound. As for UCP-1, I have done many cycle of that and SU in the past with success. Different strokes for different folks is one thing, but if you believe that one compund will negate the effects of another here or there is som specific reason to not do this, please post it.

     

    Sorry Bobo, this can be taken to another thread if need be.

  5. Now, have my responses just been moved? or have they now been completely deleted? (because I'd really rather not have to retype them...) Please feel free to delete this too once I get my answer...
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  6. jweave, any comments to methods questions? I also don't see why it is necessary to run all those supps _during_ a cycle seeing that M-1-T is pretty potent.

  7. Originally posted by jweave23
    Now to complete my shameless post whoring, I'll start my M-1-T @ 20mg daily soon as well. I'm also running the anarchy stack, Guggulbolic Extreme, and UCP-1
    have you ever thought of using the anarchy stack with guggul and 7-keto? Was thinking of using that for my next cutting cycle.

  8. Originally posted by MarcusG
    jweave, any comments to methods questions? I also don't see why it is necessary to run all those supps _during_ a cycle seeing that M-1-T is pretty potent.
    1. They aren't "necessary" by any means, as in "essential" for this cutting cycle, but then again what exactly is "necessary"? Again I think we're talking about cost-benfit here, which I understand may not be optimized with these supps taken together, but I wasn't going fot the most cost effective cycle this time around, necessarily.

    2. I'm running the anarchy stack indefinitely, for a multitude of reasons such as these from ALCAR alone, as posted in the anarchy stack thread in supps:

    Acetyl L-Carnitine

    ALC improves both Short-Term Memory and Long-Term Memory.

    ALC improves Mood [ALC improves Mood in 53% of healthy subjects].

    Acetyl L-Carnitine retards some aspects of the Aging Process in the Skin:

    ALC improves the reaction times of people afflicted with Cerebral Insufficiency.

    ALC (2-4 grams per day) improves walking distance without Pain in people afflicted with Intermittent Claudication.

    ALC prevents the age-related impairment of Eyesight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the Brain.

    ALC enhances the ability of Macrophages to function as Phagocytes.

    ALC improves Athletic Performance [ALC given prior to Exercise increased the maximum running speed of animals].

    ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).

    ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).

    ALC inhibits the damage caused by Hypoxia.
    ALC transports Lipids into the Mitochondria of Cells.

    ALC improves mood and memory in people with Age Associated Memory Impairment.

    ALC improves Mental Function where Alcohol induced cognitive Impairment exists.

    ALC increases Alertness.

    Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer’s Disease and slows the progression of Alzheimer’s Disease [people afflicted with Alzheimer’s Disease exhibited significantly less deterioration in Mental Function following the administration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].

    ALC increases Alertness in people afflicted with Alzheimer's Disease - 2,500-3,000 mg per day for 3 months].
    ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.

    ALC improves Attention Span in people afflicted with Alzheimer's Disease.

    ALC improves Short Term Memory in people afflicted with Alzheimer's Disease.

    High concentrations of ALC are naturally present in various regions of the Brain.
    ALC reverses the age-related decline that occurs in Cholinergic Receptors (i.e. the Receptors that receive Acetylcholine).

    ALC improves (eye to hand) Coordination [supplemental ALC @ 1.5 grams per day for 30 days improved eye to hand coordination in healthy, sedentary subjects by a factor of 300-400%].

    ALC improves the Interhemispheric Flow of Information across the Corpus Callosum of the Brain.

    ALC retards the decline in the number of Dopamine Receptors that occurs in tandem with the Aging Process and (more rapidly) with the onset of Parkinson's Disease.

    ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.

    ALC can prevent the destruction of Dopamine Receptors by MPTP (a neurotoxin capable of causing Parkinson's Disease via Dopaminergic Receptor death.

    ALC improves Attention Span and Memory in people afflicted with Down’s Syndrome.

    ALC retards the inevitable decline in the number of Glucocorticoid Receptors that occurs in tandem with the Aging Process.

    ALC enhances the recovery of people afflicted with Hemiplegia (Paralysis of one side of the body) and improves their Mood and Attention Span.

    ALC retards the age-related deterioration of the Hippocampus [research - rats].

    Acetyl-L-Carnitine (ALC) improves Learning ability [women aged 22 - 27 were supplemented with ALC for 30 days. Complex video game tests before and after supplementation concluded that supplemental ALC caused large increases in speed of Learning, speed of reaction and reduction in errors].

    ALC inhibits (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the Aging Process [scientific research - hyperglycemic mice treated with ALC for 16 weeks exhibited improved nerve conduction velocity and exhibited thicker Myelin Sheaths and larger myelinated Nerve Fibers].

    ALC retards the inevitable decline in the number of Nerve Growth Factor (NGF) Receptors that occurs in tandem with the Aging Process.

    ALC stimulates and maintains the growth of new Neurons within the Brain (both independently of Nerve Growth Factor (NGF) and as a result of preserving NGF) and helps to prevent the death of existing Neurons [ALC inhibits Neuron death in the Striatal Cortex, Prefrontal Cortex and the Occipital Cortex of the Brain].

    ALC inhibits the degeneration of Neurons that is implicit in Neuropathy.

    ALC rejuvenates and increases the number of N-Methyl-D-Aspartate Receptors (NMDA Receptors) in the Brain [even a single dose of ALC increases the number of functional NMDA Receptors]:

    ALC protects the NMDA Receptors in the Brain from the natural decline that occurs in tandem with the Aging Process [research - animals].

    ALC is presently being researched as a treatment for Parkinson's Disease.

    ALC inhibits the loss of Vision, degeneration of Neurons and damage to the Retina associated with Retinopathy (including Diabetic Retinopathy).

    ALC improves the quality of Sleep and reduces the quantity of Sleep required.

    ALC improves Spatial Memory (an aspect of Short Term Memory that involves remembering one’s position in space).

    ALC inhibits the excessive release of Cortisol in response to Stress and inhibits the depletion of Luteinising Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.

    ALC improves Verbal Fluency.

    ALC enhances the function of Cytochrome Oxidase (also called Complex IV) - an essential enzyme of the Electron Transport System.

    ALC normalizes Beta-Endorphin levels.
    ALC reduces Stress-induced Cortisol release [research - animals].

    ALC prevents the depletion of Luteinising Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.

    ALC retards the decline in the production of Nerve Growth Factor (NGF) that occurs in tandem with the Aging Process.

    ALC increases plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the Brain) and prevents the depletion of Testosterone caused by exposure to excessive Stress [research - rats].

    ALC increases the body's levels of circulating Thyrotrophin.

    ALC facilitates the production of Adenosine Triphosphate (ATP) [research - animals].

    ALC "shuttles" Long Chain Fatty Acids between the Cytosol and the Mitochondria of Cells.

    ALC facilitates both the release and synthesis of Acetylcholine.

    ALC's ability to increase the synthesis of Acetylcholine occurs as a result of it donating its Acetyl group towards the production of Acetylcholine.

    ALC increases the Brain's levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).

    ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.

    References

    De Falco, F. A., et al. Effect of the chronic treatment with L-acetylcarnitine in Down’s syndrome. Clin Ther. 144:123-127, 1994.

    Bowman, B. Acetyl-carnitine and Alzheimer’s disease. Nutr Rev. 50:142-144, 1992.

    Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord (USA). 9(3):128-131, 1995.

    Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Annals of the New York Academy of Sciences (USA). 663:483-486, 1993.

    Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer’s Disease? Annals of the New York Academy of Sciences (USA. 640:228-232, 1991.

    Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the efficacy of a pharmacological aid. Drugs under Experimental and Clinical Research. 14(11):715-718, 1988.

    Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. International Journal of Clinical Pharmacology Research. 10(1-2):75-79, 1990.

    Pettegrew, J. W., et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Aging. 16:1-4, 1995.

    Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine in patients with Alzheimer’s dementia. Current Medical Research and Opinion. 11(10):638-647, 1989.

    Sano, M., et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol. 49:1137-1141, 1992.

    Sinforiani, E., et al. Neuropsychological changes in demented patients treated with acetyl-L-carnitine. International Journal of Clinical Pharmacology Research. 10(1-2):69-74, 1990.

    Spagnoli, A. U., et al. Long-term acetyl-l-carnitine treatment in Alzheimer’s disease. Neurology. 41(11):1726-1732, 1991.


    I won't get on the soapbox too much regarding the anarchy stack.....anyone who reads the multitude of threads regarding it, especially here at AM, will see the obvious benefits of running it long-term. I will not justify the use of it anymore, and will simply refer people to that thread here, located at http://www.anabolicminds.com/forum/s...;thread****5553

    3. As for Guggulbolic Extreme: I have been using it for the past 5 days and just may stop until the cycle is over, or run it in between cycles of M-1-T if I decide to shorten them to several insted of one long one, which I may do.

    4. UCP-1 I happen to get good results from and am hoping that my results might be that much better if I do take it during this cycle as well. I have started M-1-T tonight, and haven't started UCP-1 yet, and again may run that inbetween shorter cycles.

    I hope that clarifies any questions as to my motivations behind this, and remember......everything is up for negotiation, lol!!

     

  9. Good luck. Be careful at 20mgs. I hear this stuff is potent

  10. Originally posted by goldylight


    have you ever thought of using the anarchy stack with guggul and 7-keto? Was thinking of using that for my next cutting cycle.
    I have been using the anarchy stack for a little while now, and have been using gugg for the past 5 days. I have used gugg in conjunction with 7-keto in the past and was happy with the results. Your idea is a good one, go with it IMO.

  11. Originally posted by NO MERCY
    Good luck. Be careful at 20mgs. I hear this stuff is potent
    Thanks, and I'm hoping it is!!

    My new idea is either 2 3 week cycles with 1.5 weeks inbetween or 3 2week cycles with 1 week inbetween.

    Between these cycles I would run the gugg and UCP-1. Again, if someone can convince me of a better plan, please do so

  12. I'm currently going to run it at 20mg a day for 30 days, then three weeks off and then 10mg a day for three weeks. It will be exactly one bottle. Of course I will probably take 8 weeks off then. But I will be stocking up while I'm off. I am on day 2 now. This **** is legit. Be prepared for the back cramps though. Mine are the worst at night.

  13. I don't want to sound like a hypocrit, because I take 2g of ALCAR daily as well, but a lot of the 'benefits' you tout mean very little IMO:

    ALC improves the reaction times of people afflicted with Cerebral Insufficiency.
    Wonderful, but do you have cerebral insufficiency?

    ALC (2-4 grams per day) improves walking distance without Pain in people afflicted with Intermittent Claudication
    Cool. But are you afflicted by this?

    ALC enhances the ability of Macrophages to function as Phagocytes.
    LOL...this one gets me; do you even know what this means?

    ALC improves Athletic Performance [ALC given prior to Exercise increased the maximum running speed of animals].
    Animal study. I'm not going to completely dismiss it because 5g of ALCAR and 10g of Choline Citrate also does the same thing in humans (can't find the study, but it's out there...). Still, you need to Choline to buffer the ALCAR with, otherwise, you're not seeing these benefits, and you need HIGH-dose ALCAR for this one. I should also add that Vallini-Gannon trial of high-dose Carnitine supplementation combined with aerobic training on dieting women from the 2000 Journal of Sports Nutrition & Exercise found that it improved performance "did not significantly alter the TBM or FM of overweight women, thereby casting doubt on the efficacy of L-C supplementation for weight loss."


    ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).

    ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).

    ALC transports Lipids into the Mitochondria of Cells.
    Okay, but the rate-limiting step in fat mobilization, utilization, and subsequently, oxidation at rest is still HSL, so this means very little from a dieting standpoint, although it does provide some insight into how ALCAR can improve exercise performance.


    ALC improves mood and memory in people with Age Associated Memory Impairment.

    Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer’s Disease and slows the progression of Alzheimer’s Disease [people afflicted with Alzheimer’s Disease exhibited significantly less deterioration in Mental Function following the administration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].

    ALC increases Alertness in people afflicted with Alzheimer's Disease - 2,500-3,000 mg per day for 3 months].
    ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.

    ALC improves Attention Span in people afflicted with Alzheimer's Disease.

    ALC improves Short Term Memory in people afflicted with Alzheimer's Disease.
    Same as above, none of this applies to you

    ALC improves Mental Function where Alcohol induced cognitive Impairment exists.
    This one is cool: I usually end up feeling obligated to bust some ALCAR and Silymarin extract damn-near every Saturday morning. But still, does this have any applications to dieting?

    See what I'm getting at? ALCAR is a phenominal supplement, but half of these things you've listed don't even apply to you, and about 90% of the rest won't do a damn thing for you on a diet. Now, there are some things related to dopamine and cortisol and cognitive function that will, so I would keep the ALCAR, but don't just umbrella a page of random and unrelated assertions together and then conclude its a convincing argument. But whatever, you like the anarchy stack, you say it works for you: if it's not broke, who am I to tell you to fix it. (Except the CLA portion. You're not bulking, so why even waste calories on it? It only really benefits untrained subjects and rodents, and you're neither. And, more to the point, CLA is absolutely worthless when cutting. The trans-10, cis-12 isomer only inhibits lipogenesis, it's worthless in regards to lipolysis. The 9,11 isomer will also do very little for you on a cutting cycle as well, because you're simply not operating with a caloric surplus. If I was less lazy I'd format a full rebuke, but instead, just check these out:

    Effects of CLA Supplementation During Resistance Training on Body Composition and Strength

    M. Ferreira¹, R. Kreider¹, M. Wilson¹, and A. Almada². Department of HMSE, University of Memphis¹, Memphis, TN 38152 & Experimental and Applied Sciences², Golden,
    CO 80401.

    Conjugated linoleic acids (CLA) are essential fatty acids that have been reported to possess anti-catabolic properties. Animal studies have found that CLA supplementation increases total body mass while reducing fat mass. This study investigated the effects of CLA supplementation during resistance training on markers of catabolism, body composition, and strength. In a double-blind and randomized manner, 27 experienced resistance-trained males were matchpaired according to total bodyweight and training volume and randomly assigned to supplement their diets with capsules containing either an olive oil placebo (P) or 5.6 g/day of CLA for 28 days. Fasting blood samples, total body mass, dual energy x-ray absorptiometry (DEXA) determined body composition, and 1RM bench press and leg press tests were performed on days 0 and 28 of supplementation. Data were analyzed by repeated measures ANOVA and are presented as mean ± SEM changes from day 0. No significant differences were observed in changes in total body mass (P: -0.10 ± 0.3; CLA: 0.02 ± 0.4 kg; P=0.77), DEXA scanned mass (P: 0.22 ± 0.3; CLA: 0.40 ± 0.3 kg; p=0.68), fat-free mass (P: 0.16 ± 0.2; CLA: 0.14 ± 0.2 kg; p=0.95), fat mass (P: 0.06 ± 0.1; CLA: 0.26 ± 0.2 kg; p=0.43), or percent bodyfat (P: 0.02 ± 0.2; CLA: 0.28 ± 0.3%; p=0.40). However, there was some evidence that CLA supplementation lessened changes in the ratio of blood urea nitrogen to creatinine, which is a general marker of catabolic state (P: 2.2 ± 1.0; CLA: -0.07 ± 0.9; p=0.10). Moreover, while not statistically significant, strength analysis revealed that 1RM bench press (P: -3.0 ± 2; CLA: 2.0 ± 2 kg; p=0.09), leg press (P: 7.3 ± 3; CLA: 11.9 ± 4 kg; p=0.41), and overall gains in 1RM strength (P: 4.3 ± 4; CLA: 13.9 ± 6 kg; p=0.17) were generally greater in the CLA group. Results indicate that 28 days of CLA supplementation (5.6 g/day) did not significantly alter body composition in resistance-trained males.



    Effect of conjugated linoleic acid supplementation after weight loss on appetite and food intake in overweight subjects.

    Kamphuis MM, Lejeune MP, Saris WH, Westerterp-Plantenga MS.

    1Department of Human Biology, Faculty of Health Sciences, Maastricht University, Maastricht, The Netherlands.

    OBJECTIVE:: To study the effects of 13 weeks conjugated linoleic acid (CLA) supplementation in overweight subjects on body-weight maintenance, parameters of appetite and energy intake (EI) at breakfast after weight loss. DESIGN:: This study had a double-blind, placebo-controlled randomized design. SUBJECTS:: A total of 26 men and 28 women (age 37.8+/-7.7 y; body mass index 27.8+/-1.5 kg/m(2)). INTERVENTIONS:: Subjects were first submitted to a very-low-calorie diet (VLCD; 2.1 MJ/day) for 3 weeks after which they started with the 13-week intervention period. They either received 1.8 g CLA or placebo per day or 3.6 g CLA or placebo per day. Additionally, subjects of the high dosage intervention replaced their habitual lunch by one meal of a protein-rich, low-energy supplement. EI was measured at breakfast and appetite profile after an overnight fast. RESULTS:: The mean body weight loss was 6.9+/-1.7% of their original body weight. Multiple regression analysis showed that at the end of the 13-week intervention, CLA did not have an effect on body weight regain. Feelings of fullness and satiety were increased and feelings of hunger were decreased after 13 weeks intervention by CLA compared to placebo, independent of %body weight regain. However, EI measured at breakfast was not affected by CLA. CONCLUSION:: Appetite (hunger, satiety and fullness) was favorably, dose-independently affected by a 13-week consumption of 1.8 or 3.6 g CLA/day. This did not result in a lower EI at breakfast or an improved body-weight maintenance after weight loss.European Journal of Clinical Nutrition (2003) 57, 1268-1274. doi:10.1038/sj.ejcn.1601684


    Conjugated linoleic acid supplementation in humans: effects on body composition and energy expenditure.

    Zambell KL, Keim NL, Van Loan MD, Gale B, Benito P, Kelley DS, Nelson GJ.

    U.S. Department of Agriculture/Western Human Nutrition Research Center, University of California, Davis 95616, USA.

    Recent animal studies have demonstrated that dietary conjugated linoleic acid (CLA) reduces body fat and that this decrease may be due to a change in energy expenditure. The present study examined the effect of CLA supplementation on body composition and energy expenditure in healthy, adult women. Seventeen women were fed either a CLA capsule (3 g/d) or a sunflower oil placebo for 64 d following a baseline period of 30 d. The subjects were confined to a metabolic suite for the entire 94 d study where diet and activity were controlled and held constant. Change in fat-free mass, fat mass, and percentage body fat were unaffected by CLA supplementation (0.18+/-0.43 vs. 0.09+/-0.35 kg; 0.01+/-0.64 vs. -0.19+/-0.53 kg; 0.05+/-0.62 vs. -0.67+/-0.51%, placebo vs. CLA, respectively). Likewise, body weight was not significantly different in the placebo vs. the CLA group (0.48+/-0.55 vs. -0.24+/-0.46 kg change). Energy expenditure (kcal/min), fat oxidation, and respiratory exchange ratio were measured once during the baseline period and during weeks 4 and 8 of the intervention period. At all three times, measurements were taken while resting and walking. CLA had no significant effect on energy expenditure, fat oxidation, or respiratory exchange ratio at rest or during exercise. When dietary intake was controlled, 64 d of CLA supplementation at 3 g/d had no significant effect on body composition or energy expenditure in adult women, which contrasts with previous findings in animals.


    Conjugated linoleic acid supplementation in humans: effects on fatty acid and glycerol kinetics.

    Zambell KL, Horn WF, Keim NL.

    USDA/Western Human Nutrition Research Center, Department of Exercise Science, University of California, Davis 95616, USA.

    Recent studies with mouse adipocytes have shown that dietary conjugated linoleic acid (CLA) may reduce body fat by increasing lipolysis. The present study examined the effect of CLA supplementation on fatty acid and glycerol kinetics in six healthy, adult women who were participating in a controlled metabolic ward study. These women were fed six CLA capsules per day (3.9 g/d) for 64 d following a baseline period of 30 d. The subjects were confined to a metabolic suite for the entire 94-d study, where diet and activity were controlled and held constant. The rate of appearance (Ra) of glycerol, which indicates lipolytic rates, was similar at baseline and after 4 wk of CLA supplementation at rest (1.87 +/- 0.21 and 2.00 +/- 0.39 micromol/kg/min, respectively) and during exercise (7.12 +/- 0.74 and 6.40 +/- 0.99 micromol/kg/min, respectively). Likewise, the Ra of free fatty acids (FFA) was not significantly different after 4 wk of dietary CLA at rest (2.72 +/- 0.06 and 2.74 +/- 0.12 micromol/kg/min, respectively) or during exercise (6.99 +/- 0.40 and 5.88 +/- 0.29 micromol/kg/min, respectively). CLA supplementation also had no effect on the percentage of FFA released from lipolysis that were re-esterified. The apparent rate of FFA re-esterification was 65.2 +/- 4.2% at rest and 32.1 +/- 3.44% during exercise. Four weeks of CLA supplementation had no significant effect on fatty acid or glycerol metabolism in healthy, weight-stable, adult women.

    Then there's also just the fact that CLA is a 'bastard' N-6, which means that it's going to be competing with (and kicking the ass of) your flax and fish oils for absorbption in the phospholipid membrane. Now, if you're proposing taking like 15-16g a day of the stuff as I've heard many Anarchy-guys advocate, you better be taking in a lot of flax to keep your N-3:N-6 ratios optimal for cutting. Which once again begs me to ask: why bother?

    As far as the UCP-1 goes, once again, I'd say save it until you're not running M-1-T. To explain why would, once again, take a lot of time which I'm not up to putting in. But read this, which gives a very good idea of how uncouplers act, and just think about how those sorts of conditions would affect tissue-turnover rates and protein synthesis in someone endeavoring to gain LBM.

    the article is here:

    http://www.blackwell-synergy.com/lin....00043.x/full/

  14. Is this place legit? I clicked the link and it put 199 cookies on my computer and then the page didn't even load.

    ~Todd

  15. Don't know, it works fine for me, and yes, the site is perfectly legit, it's the homepage for Blackwell Publishing Inc.

    If it really doesn't work for you, try going here, and scrolling down to article #255, then you can get it in PDF format

    http://www.blackwell-synergy.com/ser...2001&part=null

  16. Originally posted by Method
    I don't want to sound like a hypocrit, because I take 2g of ALCAR daily as well, but a lot of the 'benefits' you tout mean very little IMO:



    Wonderful, but do you have cerebral insufficiency?



    Cool. But are you afflicted by this?



    LOL...this one gets me; do you even know what this means?



    Animal study. I'm not going to completely dismiss it because 5g of ALCAR and 10g of Choline Citrate also does the same thing in humans (can't find the study, but it's out there...). Still, you need to Choline to buffer the ALCAR with, otherwise, you're not seeing these benefits, and you need HIGH-dose ALCAR for this one. I should also add that Vallini-Gannon trial of high-dose Carnitine supplementation combined with aerobic training on dieting women from the 2000 Journal of Sports Nutrition & Exercise found that it improved performance "did not significantly alter the TBM or FM of overweight women, thereby casting doubt on the efficacy of L-C supplementation for weight loss."




    Okay, but the rate-limiting step in fat mobilization, utilization, and subsequently, oxidation at rest is still HSL, so this means very little from a dieting standpoint, although it does provide some insight into how ALCAR can improve exercise performance.




    Same as above, none of this applies to you



    This one is cool: I usually end up feeling obligated to bust some ALCAR and Silymarin extract damn-near every Saturday morning. But still, does this have any applications to dieting?

    See what I'm getting at? ALCAR is a phenominal supplement, but half of these things you've listed don't even apply to you, and about 90% of the rest won't do a damn thing for you on a diet. Now, there are some things related to dopamine and cortisol and cognitive function that will, so I would keep the ALCAR, but don't just umbrella a page of random and unrelated assertions together and then conclude its a convincing argument. But whatever, you like the anarchy stack, you say it works for you: if it's not broke, who am I to tell you to fix it. (Except the CLA portion. You're not bulking, so why even waste calories on it? It only really benefits untrained subjects and rodents, and you're neither. And, more to the point, CLA is absolutely worthless when cutting. The trans-10, cis-12 isomer only inhibits lipogenesis, it's worthless in regards to lipolysis. The 9,11 isomer will also do very little for you on a cutting cycle as well, because you're simply not operating with a caloric surplus. If I was less lazy I'd format a full rebuke, but instead, just check these out:

    Effects of CLA Supplementation During Resistance Training on Body Composition and Strength

    M. Ferreira¹, R. Kreider¹, M. Wilson¹, and A. Almada². Department of HMSE, University of Memphis¹, Memphis, TN 38152 & Experimental and Applied Sciences², Golden,
    CO 80401.

    Conjugated linoleic acids (CLA) are essential fatty acids that have been reported to possess anti-catabolic properties. Animal studies have found that CLA supplementation increases total body mass while reducing fat mass. This study investigated the effects of CLA supplementation during resistance training on markers of catabolism, body composition, and strength. In a double-blind and randomized manner, 27 experienced resistance-trained males were matchpaired according to total bodyweight and training volume and randomly assigned to supplement their diets with capsules containing either an olive oil placebo (P) or 5.6 g/day of CLA for 28 days. Fasting blood samples, total body mass, dual energy x-ray absorptiometry (DEXA) determined body composition, and 1RM bench press and leg press tests were performed on days 0 and 28 of supplementation. Data were analyzed by repeated measures ANOVA and are presented as mean ± SEM changes from day 0. No significant differences were observed in changes in total body mass (P: -0.10 ± 0.3; CLA: 0.02 ± 0.4 kg; P=0.77), DEXA scanned mass (P: 0.22 ± 0.3; CLA: 0.40 ± 0.3 kg; p=0.68), fat-free mass (P: 0.16 ± 0.2; CLA: 0.14 ± 0.2 kg; p=0.95), fat mass (P: 0.06 ± 0.1; CLA: 0.26 ± 0.2 kg; p=0.43), or percent bodyfat (P: 0.02 ± 0.2; CLA: 0.28 ± 0.3%; p=0.40). However, there was some evidence that CLA supplementation lessened changes in the ratio of blood urea nitrogen to creatinine, which is a general marker of catabolic state (P: 2.2 ± 1.0; CLA: -0.07 ± 0.9; p=0.10). Moreover, while not statistically significant, strength analysis revealed that 1RM bench press (P: -3.0 ± 2; CLA: 2.0 ± 2 kg; p=0.09), leg press (P: 7.3 ± 3; CLA: 11.9 ± 4 kg; p=0.41), and overall gains in 1RM strength (P: 4.3 ± 4; CLA: 13.9 ± 6 kg; p=0.17) were generally greater in the CLA group. Results indicate that 28 days of CLA supplementation (5.6 g/day) did not significantly alter body composition in resistance-trained males.



    Effect of conjugated linoleic acid supplementation after weight loss on appetite and food intake in overweight subjects.

    Kamphuis MM, Lejeune MP, Saris WH, Westerterp-Plantenga MS.

    1Department of Human Biology, Faculty of Health Sciences, Maastricht University, Maastricht, The Netherlands.

    OBJECTIVE:: To study the effects of 13 weeks conjugated linoleic acid (CLA) supplementation in overweight subjects on body-weight maintenance, parameters of appetite and energy intake (EI) at breakfast after weight loss. DESIGN:: This study had a double-blind, placebo-controlled randomized design. SUBJECTS:: A total of 26 men and 28 women (age 37.8+/-7.7 y; body mass index 27.8+/-1.5 kg/m(2)). INTERVENTIONS:: Subjects were first submitted to a very-low-calorie diet (VLCD; 2.1 MJ/day) for 3 weeks after which they started with the 13-week intervention period. They either received 1.8 g CLA or placebo per day or 3.6 g CLA or placebo per day. Additionally, subjects of the high dosage intervention replaced their habitual lunch by one meal of a protein-rich, low-energy supplement. EI was measured at breakfast and appetite profile after an overnight fast. RESULTS:: The mean body weight loss was 6.9+/-1.7% of their original body weight. Multiple regression analysis showed that at the end of the 13-week intervention, CLA did not have an effect on body weight regain. Feelings of fullness and satiety were increased and feelings of hunger were decreased after 13 weeks intervention by CLA compared to placebo, independent of %body weight regain. However, EI measured at breakfast was not affected by CLA. CONCLUSION:: Appetite (hunger, satiety and fullness) was favorably, dose-independently affected by a 13-week consumption of 1.8 or 3.6 g CLA/day. This did not result in a lower EI at breakfast or an improved body-weight maintenance after weight loss.European Journal of Clinical Nutrition (2003) 57, 1268-1274. doi:10.1038/sj.ejcn.1601684


    Conjugated linoleic acid supplementation in humans: effects on body composition and energy expenditure.

    Zambell KL, Keim NL, Van Loan MD, Gale B, Benito P, Kelley DS, Nelson GJ.

    U.S. Department of Agriculture/Western Human Nutrition Research Center, University of California, Davis 95616, USA.

    Recent animal studies have demonstrated that dietary conjugated linoleic acid (CLA) reduces body fat and that this decrease may be due to a change in energy expenditure. The present study examined the effect of CLA supplementation on body composition and energy expenditure in healthy, adult women. Seventeen women were fed either a CLA capsule (3 g/d) or a sunflower oil placebo for 64 d following a baseline period of 30 d. The subjects were confined to a metabolic suite for the entire 94 d study where diet and activity were controlled and held constant. Change in fat-free mass, fat mass, and percentage body fat were unaffected by CLA supplementation (0.18+/-0.43 vs. 0.09+/-0.35 kg; 0.01+/-0.64 vs. -0.19+/-0.53 kg; 0.05+/-0.62 vs. -0.67+/-0.51%, placebo vs. CLA, respectively). Likewise, body weight was not significantly different in the placebo vs. the CLA group (0.48+/-0.55 vs. -0.24+/-0.46 kg change). Energy expenditure (kcal/min), fat oxidation, and respiratory exchange ratio were measured once during the baseline period and during weeks 4 and 8 of the intervention period. At all three times, measurements were taken while resting and walking. CLA had no significant effect on energy expenditure, fat oxidation, or respiratory exchange ratio at rest or during exercise. When dietary intake was controlled, 64 d of CLA supplementation at 3 g/d had no significant effect on body composition or energy expenditure in adult women, which contrasts with previous findings in animals.


    Conjugated linoleic acid supplementation in humans: effects on fatty acid and glycerol kinetics.

    Zambell KL, Horn WF, Keim NL.

    USDA/Western Human Nutrition Research Center, Department of Exercise Science, University of California, Davis 95616, USA.

    Recent studies with mouse adipocytes have shown that dietary conjugated linoleic acid (CLA) may reduce body fat by increasing lipolysis. The present study examined the effect of CLA supplementation on fatty acid and glycerol kinetics in six healthy, adult women who were participating in a controlled metabolic ward study. These women were fed six CLA capsules per day (3.9 g/d) for 64 d following a baseline period of 30 d. The subjects were confined to a metabolic suite for the entire 94-d study, where diet and activity were controlled and held constant. The rate of appearance (Ra) of glycerol, which indicates lipolytic rates, was similar at baseline and after 4 wk of CLA supplementation at rest (1.87 +/- 0.21 and 2.00 +/- 0.39 micromol/kg/min, respectively) and during exercise (7.12 +/- 0.74 and 6.40 +/- 0.99 micromol/kg/min, respectively). Likewise, the Ra of free fatty acids (FFA) was not significantly different after 4 wk of dietary CLA at rest (2.72 +/- 0.06 and 2.74 +/- 0.12 micromol/kg/min, respectively) or during exercise (6.99 +/- 0.40 and 5.88 +/- 0.29 micromol/kg/min, respectively). CLA supplementation also had no effect on the percentage of FFA released from lipolysis that were re-esterified. The apparent rate of FFA re-esterification was 65.2 +/- 4.2% at rest and 32.1 +/- 3.44% during exercise. Four weeks of CLA supplementation had no significant effect on fatty acid or glycerol metabolism in healthy, weight-stable, adult women.

    Then there's also just the fact that CLA is a 'bastard' N-6, which means that it's going to be competing with (and kicking the ass of) your flax and fish oils for absorbption in the phospholipid membrane. Now, if you're proposing taking like 15-16g a day of the stuff as I've heard many Anarchy-guys advocate, you better be taking in a lot of flax to keep your N-3:N-6 ratios optimal for cutting. Which once again begs me to ask: why bother?

    As far as the UCP-1 goes, once again, I'd say save it until you're not running M-1-T. To explain why would, once again, take a lot of time which I'm not up to putting in. But read this, which gives a very good idea of how uncouplers act, and just think about how those sorts of conditions would affect tissue-turnover rates and protein synthesis in someone endeavoring to gain LBM.

    the article is here:

    http://www.blackwell-synergy.com/lin....00043.x/full/
    Ok:

    1. That was a cut and paste from the anarchy stack thread. I did not say that all specific possible beneficial functions of ALCAR will benefit me. I did not "tout" these as all specifically benefitting me, again that was a copy and paste. You are being too presumptuous with your assertions of my intentions in posting that. What I did imply, however, is that with a rap sheet that long, and several benefits admitted above by yourself even, ALCAR should provide to be only beneficial to me, regardless of androgen use. Can you say that: a) taking ALCAR while on a cycle of M1T is a harmful and/or completely and totally ineffective thing (sans cost as mentioned above, that is not the major factor for me)? b) any possible benefits I may receive from using ALCAR while on cycle will be negated?

    2. I have not "umbrella-ed a blanket of random and unrelated assertions together to conclude a convincing argument". That is your slant on it. You seem to think that list was mine, and I back and represent every statement there. What I did was present what I thought to be a compelling list of possible benefits from using ALCAR, not imply that they all have a direct effect on me. There are many other things to consider with the anarchy stack, and I will not rehash them here. If you wish to argue the benefits of the anarchy stack, please do so in the anarchy thread in the supps section.

    3. I have posted this elsewhere, but I should clarify further apparently: I do not take CLA with the anarchy stack, for some reasons you have pointed out, as well as some things Nandi at CEM has brought to light, among many others at various boards.

    4. I can't access that article about uncouplers, I get a login page? You stated: "just think about how those sorts of conditions would affect tissue-turnover rates and protein synthesis in someone endeavoring to gain LBM". My point is that I am cutting, not specifically interested in major LBM gains.If they come, great, if I simply preserve mass while cutting, good enough for me.

    5. I completely understand your motivation in presenting that I may not "need" the anarchy stack while using this, but it isn't about "need" to me. With a proper diet I don't "need" any supplements at all, do I? As metnioned before, cost was not a paramount issue for me with this run. You unfortunately spent too much time on the CLA aspect BTW, as I do not take it, sorry for not clarfying that earlier. Now....consdering I don't believe my ideas to be completely idiotic and I think we've both proven some points here: get the hell of my nuts!!

     

     

  17. With that said I have to concede this:

    I think the best way to go about this would be:

    (3) 2 week cycles of M1T with 1.5 weeks off inbetween.
    Between cycles running the UCP-1 and Gugg, as well as Swole V2.

  18. no nolva - clomid or oxo in btw?

  19. Originally posted by goldylight
    no nolva - clomid or oxo in btw?
    Of course, yeah. I have plenty of both, probably use clomid

  20. Originally posted by Method
    Don't know, it works fine for me, and yes, the site is perfectly legit, it's the homepage for Blackwell Publishing Inc.

    If it really doesn't work for you, try going here, and scrolling down to article #255, then you can get it in PDF format

    http://www.blackwell-synergy.com/ser...&part=null
    Again, it says I need a subscription. Please upload the PDF file for us

  21. Again, it says I need a subscription. Please upload the PDF file for us
    My hunch is I can get it through my campus ethernet connection, and that's why no one else can. Since I seriously lack computer skills in that department, can somebody gimme a quick tutorial on uploading a PDF?


    4. I can't access that article about uncouplers, I get a login page? You stated: "just think about how those sorts of conditions would affect tissue-turnover rates and protein synthesis in someone endeavoring to gain LBM". My point is that I am cutting, not specifically interested in major LBM gains.If they come, great, if I simply preserve mass while cutting, good enough for me.
    Fine, but the point is that Bobo's cutting too, and he's gaining LBM and strength thanks to the M-1-T. Stacking an uncoupler with it will negate that though. Steroids alter your genetics so that you can lose fat and gain muscle simultaneously. That's why IMO taking an uncoupler is like shooting yourself in the foot gains-wise, because your body can't build muscle when it's 'fighting itself' to keep from overproducing energy.

  22. Originally posted by Method


    My hunch is I can get it through my campus ethernet connection, and that's why no one else can. Since I seriously lack computer skills in that department, can somebody gimme a quick tutorial on uploading a PDF?




    .
    Thats probably the reason. Its the same with many online publications (Journal of Endocrinology) that Universties get a free pass.
    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.

  23. Originally posted by Method


    My hunch is I can get it through my campus ethernet connection, and that's why no one else can. Since I seriously lack computer skills in that department, can somebody gimme a quick tutorial on uploading a PDF?




    Fine, but the point is that Bobo's cutting too, and he's gaining LBM and strength thanks to the M-1-T. Stacking an uncoupler with it will negate that though. Steroids alter your genetics so that you can lose fat and gain muscle simultaneously. That's why IMO taking an uncoupler is like shooting yourself in the foot gains-wise, because your body can't build muscle when it's 'fighting itself' to keep from overproducing energy.
    1. Save the file to your hard drive. The upload it as youwould any other attachment. We do accept .pdf files as attachments here.

    2. This seems tobe speculation, although not unfounded. I'll probably just run the UCP-1 during the 10 days off, although if one wanted to minimize the amount of lean mass lost, I would certainly think an anabolic agent would do so, no? (i.e like running one while on T3 for example, although I realize T3 and uncouplers do not share the same mechanism of action).

  24. Originally posted by Bobo


    Thats probably the reason. Its the same with many online publications (Journal of Endocrinology) that Universties get a free pass.
    Yep, we have many things here at the law school that require the student be on campus to utilize also 

  25. Originally posted by Method



    Fine, but the point is that Bobo's cutting too, and he's gaining LBM and strength thanks to the M-1-T. Stacking an uncoupler with it will negate that though. Steroids alter your genetics so that you can lose fat and gain muscle simultaneously. That's why IMO taking an uncoupler is like shooting yourself in the foot gains-wise, because your body can't build muscle when it's 'fighting itself' to keep from overproducing energy.

    I have a feedling with this, it just might be able too. Lets just say I have a *ahem* hunch


    It is DEFINETLY potent.
    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.
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