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vain68

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About vain68

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  • Birthday 06/26/1977

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  1. Changing your setpoint

    Also, for anyone who is further interested in what we are discussing here, in a rich and complex fashion, I encourage you to read: Berthoud, Hans-Rudolf. (2002). Multiple neural systems controlling food intake and body weight. Neuroscience and Biobehavioral reviews, 26, 393-428. An interesting note in this review that I seemed to have missed back in '02, was an outright rejection of the notion of a 'set-point.' Although we are well aware that we all seem to defend certain weights, this review takes a stance that I appreciate--a much more environmental approach to the study of body weight regulation. Drez, it's not as simple as drinking saltwater per se, as that will only impact one of the multiple systems discussed in the above paper. What we need are strategies and supplementation that take a parallel processing functional mentality. Thus, perhaps: ECA---centeral and peripheral effector mechanisms Nic---prefrontal systems (wanting and liking); cognitive input as discussed in my paper Something akin to leptigen---hypothalamic systems Fiber supps? ---more brainstem mechs...... it is about the total package of supplement and diet. It must be targeted. Vv
  2. Also, for anyone who is further interested in what we are discussing here, in a rich and complex fashion, I encourage you to read: Berthoud, Hans-Rudolf. (2002). Multiple neural systems controlling food intake and body weight. Neuroscience and Biobehavioral reviews, 26, 393-428. An interesting note in this review that I seemed to have missed back in '02, was an outright rejection of the notion of a 'set-point.' Although we are well aware that we all seem to defend certain weights, this review takes a stance that I appreciate--a much more environmental approach to the study of body weight regulation. Drez, it's not as simple as drinking saltwater per se, as that will only impact one of the multiple systems discussed in the above paper. What we need are strategies and supplementation that take a parallel processing functional mentality. Thus, perhaps: ECA---centeral and peripheral effector mechanisms Nic---prefrontal systems (wanting and liking); cognitive input as discussed in my paper Something akin to leptigen---hypothalamic systems Fiber supps? ---more brainstem mechs...... it is about the total package of supplement and diet. It must be targeted. Vv
  3. Changing your setpoint

    A very solid recent paper articulates quite well not only what I have been discussing as distinct circuitry to feeding mechanisms, but more importantly goes beyond typical hypothalamic-brainstem discussions to document and illustrate the important role of the forebrain, and in particular the rostral shell of the nucleus accumbens in controlling feeding. What we have are parallel circuits to a central regulator. The problem with supplementation offered here and vis a vis other formulators is that they attempt to affect a particular pathway, which does address the redundance issue and parallel circuitry. Take for example supplementation designed to sensitize or affect the 'leptin' pathway. While this idea is indeed a step forward towards a more credible science-supplement industry marriage, it does not address the fact that the forebrain, in conditions of powerful reward-incentive, can by itself strongly stimulate feeding. This parallels my commentary in my original contribution concerning the 'weakening' of inhibitory control during long-term and/or pre-contest dieting (for some reason, this article is not linked on MM and has appeared to have been 'lost'. Vv Watts, A. G., Salter, D. S., & Neuner, C. M. (2007). Neural-network interactions and ingestive behavior control during anorexia. Physiology and Behavior, 91, 389-396. Interestingly, one thing one could possibly take from their work is that slight drinking of a salt solution (perhaps warm water) may assist in promoting the anorexic state during pre-contest dieting.......VV Developmental_Regulatory_Model.pdf
  4. A very solid recent paper articulates quite well not only what I have been discussing as distinct circuitry to feeding mechanisms, but more importantly goes beyond typical hypothalamic-brainstem discussions to document and illustrate the important role of the forebrain, and in particular the rostral shell of the nucleus accumbens in controlling feeding. What we have are parallel circuits to a central regulator. The problem with supplementation offered here and vis a vis other formulators is that they attempt to affect a particular pathway, which does address the redundance issue and parallel circuitry. Take for example supplementation designed to sensitize or affect the 'leptin' pathway. While this idea is indeed a step forward towards a more credible science-supplement industry marriage, it does not address the fact that the forebrain, in conditions of powerful reward-incentive, can by itself strongly stimulate feeding. This parallels my commentary in my original contribution concerning the 'weakening' of inhibitory control during long-term and/or pre-contest dieting (for some reason, this article is not linked on MM and has appeared to have been 'lost'. Vv Watts, A. G., Salter, D. S., & Neuner, C. M. (2007). Neural-network interactions and ingestive behavior control during anorexia. Physiology and Behavior, 91, 389-396. Interestingly, one thing one could possibly take from their work is that slight drinking of a salt solution (perhaps warm water) may assist in promoting the anorexic state during pre-contest dieting.......VV Developmental_Regulatory_Model.pdf
  5. I anticipate rejoining this discussion sometime this weekend (have a boatload of items I need to write-up, analyze this week) with a detailed post reviewing and extending our discussion. Vv PS: Drez, your thoughts here, in a more elaborative framework, are greatly encouraged.
  6. On the nature of the physique game

    I anticipate rejoining this discussion sometime this weekend (have a boatload of items I need to write-up, analyze this week) with a detailed post reviewing and extending our discussion. Vv PS: Drez, your thoughts here, in a more elaborative framework, are greatly encouraged.
  7. I sense it is time to revist this thread, to continue to evolve with it; to mature within it. Vv
  8. On the nature of the physique game

    I sense it is time to revist this thread, to continue to evolve with it; to mature within it. Vv
  9. It just simply is not possible. Either the game, or the woman. Or the woman, and hit the iron when time permits. That is all. It's the same reason priests can't marry. Vv
  10. On the nature of the physique game

    It just simply is not possible. Either the game, or the woman. Or the woman, and hit the iron when time permits. That is all. It's the same reason priests can't marry. Vv
  11. Aspirin as an uncoupler

    Benson, I think Bayer has a timed release formula...I prefer their aspirin's to others........... I will check my bottle when I get home for the exact specifications. Vv
  12. Aspirin as an uncoupler

    The uncoupler issue aside for the moment, I have been extensively experimenting with regular aspirin or timed-release pre and post workout for its blood thinning properties which may be useful for cutting trouble areas and/or remaining allowing for optimal partitioning when remaining lean or going about a clean bulk. I have had some interesting results, and appear to stay leaner and partition refeeds much better when using additional aspirin around my workouts and along with ECA. Vv
  13. Research Highlight Nature Reviews Immunology 7, 87 (February 2007) | doi:10.1038/nri2026 Macrophages: Fat gets picky with macrophages Olive Leavy Three studies published in The Journal of Clinical Investigation show that in mouse models of atherosclerosis and obesity distinct subsets of monocytes are recruited, different chemokine receptors are used and a phenotypic switch in macrophage differentiation occurs at sites of lipid accumulation. These studies provide new insights into the heterogeneity of monocyte recruitment and macrophage phenotype in lipid-rich tissues. Atherosclerosis is an inflammatory disease that involves the accumulation of lipids and macrophages and the formation of plaques in the arteries. Mouse monocytes, the precursors of macrophages, can be divided into two main subsets on the basis of their expression of receptors that include Ly6C, GR1, CC-chemokine receptor 2 (CCR2) and CX3C-chemokine receptor 1 (CX3CR1). Ly6Chi monocytes (sometimes referred to as inflammatory monocytes) are GR1+CCR2+CX3CR1low, whereas Ly6Clowmonocytes are GR1-CCR2-CX3CR1hi. But what role do these circulating monocyte subsets have in the development of atherosclerosis? Both Swirski et al. and Tacke et al. examined the repertoire of monocytes in apolipoprotein E (APOE)-deficient mice that were fed a high-fat diet — a mouse model of atherosclerosis. They found that the Ly6Chi monocyte subset continuously expanded in the periphery compared with Ly6Clow monocytes. Interestingly, Ly6Chi monocytes were shown to efficiently accumulate in atherosclerotic lesions and Swirski et al. further showed that these cells differentiated into lesional macrophages. Owing to the differential expression of chemokine receptors by these monocyte subsets, Tacke et al. examined the role of the individual receptors in the accumulation of monocytes in atherosclerotic plaques. They found that the inflammatory Ly6Chi monocytes used CX3CR1 (as well as CCR2 and CCR5) to enter the plaques. Ly6Clow monocytes could also enter atherosclerotic plaques, albeit less frequently. But unlike Ly6Chi monocytes, Ly6Clow monocytes entered the plaques in a CCR2- and CX3CR1-independent, CCR5-dependent manner and were more likely to become CD11c+ dendritic-cell-like cells. Lumeng et al. examined the phenotype of macrophages that migrate to adipose tissue in diet-induced obese mice compared with those in lean mice that were fed a normal diet. Macrophages isolated from adipose tissue from lean mice expressed many hallmarks of alternatively activated macrophages — that is, they expressed genes encoding the anti-inflammatory molecules interleukin-10 (IL-10) and IL-1 decoy receptor. By contrast, adipose-tissue macrophages from obese mice undergo a phenotypic switch to express pro-inflammatory molecules, such as tumour-necrosis factor (TNF) and inducible nitric-oxide synthase (iNOS). Interestingly, macrophages from CCR2-deficient obese mice expressed alternatively activated macrophage markers at levels similar to macrophages from lean mice. This indicates that, in the absence of CCR2-dependent recruitment, adipose-tissue macrophages might have reduced inflammatory capacity. Collectively, these studies highlight potential targets to suppress the inflammatory response associated with lipid-associated diseases, such as obesity and atherosclerosis. Top of pageReferences and links ORIGINAL RESEARCH PAPERS Swirski, F. K. et al. Ly-6Chi monocytes dominate hypercholesterolemia-associated monocytosis and give rise to macrophages in atheromata. J. Clin. Invest. 117, 195–205 (2007) ArticlePubMedTacke, F. et al. Monocyte subsets differentially employ CCR2, CCR5, and CX3CR1 to accumulate within atherosclerotic plaques. J. Clin. Invest. 117, 185–194 (2007) ArticlePubMedLumeng, C. N. et al. Obesity induces a phenotypic switch in adipose tissue macrophage polarization. J. Clin. Invest. 117, 175–184 (2007) ArticlePubMedFURTHER READING Gordon, S. Macrophage heterogeneity and tissue lipids. J. Clin. Invest. 117, 89–93 (2007) ArticlePubMed
  14. As indicated. The Harris Benedict equation reevaluated: resting energy requirements and the body cell mass13 Allan M Roza, MD and Harry M Shizgal, MD, FRCS©, FACS ABSTRACT The Harris Benedict equations (HBE) were derived from indirect calorimetric data obtained in 239 normal subjects. Using these data and additonal data published by Benedict, which were obtained from subjects spanning a wider age range (n = 98), the present study evaluated the relationship between measured resting energy expenditure and age, sex, and predicted body cell mass (BCM). When the additional subjects from the subsequently published series are included, the regression equations, standard error ofthe estimate, and 95% confidence limits are similar to the original equations. The HBE estimate resting energy expenditure of a normal subject with a precision of 14%. Resting energy expenditure is directly related to the size of the 8CM and is independent of age and sex. The variables of height, weight, age, and sex in the HBE reflect the relationship between body weight and the BCM. Indirect calorimetry and body composition measurements were performed in both normally nourished and malnourished patients (n = 74) to assess the accuracy of the HBE in malnourished patients. Malnutrition is associated with an increase in resting oxygen consumption (V02) which becomes apparent only when V02 is expressed as a function of the BCM. There is no difference in resting VO2 between the sexes when expressed as a function of BCM. A regression equation was derived from the Harris Benedict data to predict resting V02 from age, height, weight, and sex. Predicted VO2 was not significantly different from measured VO2 for the normally nourished patients (n = 33) whereas in the malnourished (n = 41) predicted VO2 underestimated the measured value. The HBE accurately predict resting energy expenditure in normally nourished individuals with a precision of ±14%, but are unreliable in the malnourished patient. Am J Clin Nuir 1984;40: 168-182. KEY WORDS Basal metabolism, body composition, energy, malnutrition, metabolism Introduction Malnutrition is common in the hospitalized patient, developing as a complication of the disease process and/or as a result of diagnostic and therapeutic maneuvers. Aggressive nutritional support will both prevent and treat the malnourished state. The success of nutritional support depends on the delivery ofadequate calories and protein by either the enteral or parenteral route. Two methods are commonly used to determine the caloric or energy requirements of the individual patient. The first uses the Harris Benedict equations which give an estimate of resting energy expenditure (REE). The second method involves measurement of REE, by indirect calorimetry. In 1919, Harris and Benedict published their classic monograph on basal metabolism in normal subjects (1). Metabolic parameters were determined by indirect calorimetry on 136 men and 103 women. From these measurements they derived regression I From the Department of Surgery, McGill University and Royal Victoria Hospital, Montreal, Canada. 2 Supported by Medical Research Council of Canada. 3 Address reprint requests to: Harry M Shizgal, MD, Department of Surgery, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec, Canada H3A 1A1. The American Journal ofClinical Nutrition 40: JULY 1984, pp 168-182. Printed in USA © 1984 American Society for Clinical Nutrition
  15. Eclypz, If I might I just wanted to chime in here and say that a focus on single perceived 'rate-limiting' enzymes and their role in certain physiological processes may be leading a lot of us (as well as myself at times) astray. There is entirely too much focus on 'rate-limiting' and what this means for the supplementation etc. industry. This is becuase of something I have mentioned before 'redundant mechanisms.' In a paper which I tracked down through an original reference in a paper on fuel substrate utilization in starvation, we say the importance of redundant mechanisms and why a given substrate or enzyme can be rate-limiting or not depending on the millieu of the metabolic system. Here is a brief piece Strohman, 2002 (Science), Manuevering in the complex path from genotype to phenotype [a great title for our purposes I might add) My point is that the premise of your supplementation choice needs to be considered against a much broader backdrop, and, in my own mind, depending on your goals, is going to be at best, of limited effectiveness (assuming its bioavailability has been clearly demonstrated). Apologies if I have been confusing. Vv
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