Hooker's New Product, PyroGenX - More Bad Science

[Conciliator]

Some of you may remember my last post of this nature: Legal Gear's new product "Receptor" is a Fraud. In this post, I'll take a look at an aspect of Anthony Robert's new product, PyroGenX. Recently, Hooker said "I'm coming out with a fat burner within the next few weeks, which will be sold here on BB.com. PyroGenX is the name, and it's a mitochondrial uncoupler which works on UCP1."

Now anyone who knows anything about uncoupling protein 1 (UCP1) knows that 1) it's found only in brown adipose tissue (BAT), 2) that adult humans have very little BAT (they primarily have white adipose tissue or WAT), and 3) that pharmacological approaches to induce BAT formation and UCP1 expression/thermogenesis in humans (e.g. via beta-3 agonists) have been largely ineffective. So his product sounded like BS to me right off the bat. When I pressed him about it, he said "Sorry, son. It's based on WAT, not BAT, and it's already in production." Hooker is therefore claiming that his new product targets UCP1 in white adipose tissue (WAT). This post will take issue with that.

So what does the research say? Can PyroGenX "target" UCP1 in WAT, like Hooker claims? Or is this a BS marketing claim since UCP1 is found only in brown adipocytes (BAT)? Let's take a look at the research:

The uncoupling proteins, a review.
Eur J Endocrinol. 1998 Jul;139(1):1-9.

The uncoupling protein-1 (UCP1), cloned in 1985 (1?4) and called UCP until 1997, is an inner mitochondrial membrane protein (5) expressed exclusively in the brown adipocyte (6?8).

The human uncoupling protein-1 gene (UCP1): present status and perspectives in obesity research.
Obes Rev. 2000 Oct;1(2):61-72.

Uncoupling protein-1 is exclusively expressed in mitochondria of brown adipocytes where it uncouples respiration from ATP synthesis, dissipating the proton gradient as heat. In humans, although uncoupling protein-1 can be detected, the inability to quantify brown adipose tissue makes it difficult to argue for a role for uncoupling protein-1 in thermogenesis and energy expenditure.
...
In this context, the first indication came from the discovery of a regulated proton leak in the mitochondria from brown adipose tissue (BAT), which was catalysed by an uncoupling protein (UCP), now known as uncoupling protein-1 (UCP1). UCP1 is a 32-kDa protein exclusively expressed in mitochondria from BAT.
...
It has been clearly demonstrated that two types of adipose tissues exist: white adipose tissue (WAT), which stores triglycerides, and brown adipose tissue (BAT) (45). These two tissues differ in their anatomical localization, abundance, maintenance throughout the life of the animal, morphology and principally in their function (46).

Mitochondrial uncoupling as a target for drug development for the treatment of obesity.
Obesity Reviews, Volume 2, Number 4, 1 November 2001 , pp. 255-265(11)

UCP1 is restricted to brown adipocytes, and was originally thought to be the only transporter capable of uncoupling mitochondria (96?98)

Role of uncoupling proteins UCP1, UCP2 and UCP3 in energy balance, type 2 diabetes and obesity. Synergism with the thyroid.
Medicina (B Aires). 2005;65(2):163-9.

The discovery of brown adipose tissue (BAT) and its unique activity of heat production and dissipation through the action of uncoupling protein-1 (UCP1) during cold stress, showed the relevance of this tissue for energy expenditure in lower mammals. UCP1 is only expressed in BAT through the synergistic action of norepinephrine (NE) and thyroid hormones in animals exposed to cold and to a lesser degree after meals.

Life without UCP1: mitochondrial, cellular and organismal characteristics of the UCP1-ablated mice.
Biochem Soc Trans. 2001 Nov;29(Pt 6):756-63.

Within the family of proteins sharing high homology with the `original ' uncoupling protein (UCP1, thermogenin), UCP1 is characterized by being solely expressed in one tissue, mammalian brown adipose tissue.

UCP1: the only protein able to mediate adaptive non-shivering thermogenesis and metabolic inefficiency.
Biochim Biophys Acta. 2001 Mar 1;1504(1):82-106.

As UCP1 is only expressed in brown adipose tissue, and UCP3 only in brown adipose tissue and muscle, a rather comprehensive summary of the changes in expression of these UCPs can be made.

Mitochondrial proton leak and the uncoupling protein 1 homologues.
Biochim Biophys Acta. 2001 Mar 1;1504(1):144-58.

When UCP1 is fully inhibited by GDP, or when UCP1 expression has been knocked out, the proton conductance of BAT mitochondria is not essentially di?erent from that of mitochondria from other tissues [34,35]. These observations tell us that UCP1 activity accounts for only part of the total proton conductance of BAT mitochondria. And, as UCP1 is not expressed in other tissues, it cannot account for the proton conductance observed in all mitochondria. However, UCP1 can provide, and indeed has provided, a theoretical framework for the identification and study of other candidate uncoupling proteins.

Homologues of the uncoupling protein from brown adipose tissue (UCP1): UCP2, UCP3, BMCP1 and UCP4.
Biochim Biophys Acta. 2001 Mar 1;1504(1):107-19.

UCP1 was found to have the interesting property of being expressed only in specialised cells called brown adipocytes, constituting the brown adipose tissue of mammals. This peculiarity made the study of this protein and of its gene exceptionally attractive and, moreover, easier in several respects.

There are more where these came from, but I'm sure you get the idea: It's well established that UCP1 is found only in BAT. It's not present in white adipocytes. In the "recent" thread I linked to at the top, Hooker told me "Try not to talk unless you actually know something, this way you avoid looking like a moron." Well, who's looking like the moron now? Good luck with your fabulous new product. I'm sure it'll do an awesome job targeting UCP1 in WAT.

[cakedonkey]

I want to be just like Conciliator when I grow up.


In all seriousness: great collection of literature. Nice job debunking his [Anthony Roberts] bull**** claims. I never held the guy at too high of a regard anyhow, and this makes me think of even less of him. Will be interesting to see his rebuttal, considering all of the most recent papers disagree with his claim.

[Kernkraft]

seriously, saturday is officially drama day

[killerstack]

Hooker is the biggest fool ever in this industry. Everything about him is pure BS. No knowledge, no physique, no nothing. Just a big mouth.

[GeneGnomeX]

According to that other thread, AR may be required to terminate his existance?

[hooker]

Great job. You're wrong.

[Atheimetal]

Originally Posted by hooker

Great job. You're wrong.

...

Strong rebuttal.

[dtrain13]

Originally Posted by Atheimetal

...

Strong rebuttal.

My thoughts exactly.

[Conciliator]

This is another excellent paper on the topic: http://www.pubmedcentral.nih.gov/art...medid=16898874

It explains that "The thermogenic capacity of BAT is due to expression of UCP1 (uncoupling protein 1) exclusively in brown adipocytes." It goes on to discuss ways in which UCP1 expression can be induced in WAT, but this is described as "ectopic" (in an abnormal place or position) and actually as a result of brown adipocyte differentiation in that tissue. I'm guessing that his product is probably something like an activator of PGC-1α. As the conclusion states "The ability of PGC-1α to induce expression of UCP1 as well as mitochondrial biogenesis and activity in fat cells points to PGC-1α as the prime factor co-ordinating brown adipocyte differentiation and function.
...
Whether controlled recruitment of brown fat cells is a suitable strategy in the treatment of obesity and obesity-associated disorders remains to be shown. Nevertheless, designed interference of the balance between white and brown adipocyte differentiation requires a more detailed understanding of factors differentially regulating the formation of white and brown fat cells."

[DRP7]

BAT in humans occurs to a far less degree when compared with WAT, but its role for adiposity in humans appears to be higher than popular belief suggested.

here is a line of reasoning that could provide some rationale for the use of UCP-1 targeting in humans:

1. Recent imaging studies found surprisingly higher levels of BAT in humans than previously assumed

2. Certain polymorphisms of UCP-1 are associated with higher rates of obesity (and: specifically with abdominal WAT) in humans while other polymorphisms are associated with lower adiposity levels / higher rate of fat loss

3. It is a well known fact that even small deflections of RMR (resting metabolic rate) can have dramatic impact on the development of adiposity / obesity long-term-wise


4. Conclusion: Although BAT amount in humans is modest, changes of some of it's properties (here: UCP-1 functionality) may be a factor that contributes to the regulation of white adipose tissue-metabolism and accumulation. Since adiposity / obesity are multifactorial events, it is reasonable to target multiple regulatory factors in order to maximise the effects on fat-loss or prevention of adiposity. UCP1 in human BAT appears to have some promising potential to be one of those factors. It is reasonable to assume that successful anti-obesity treatment strategies will implement a multifactorial therapeutic approach and that UCP-1 holds some promise to be one part in those multi-pathways approaches (e.g. in combination with PPAR modulation, modulation ot TG formation, modulation of transmitochndrial FFA-transport, and fatty acid synthase - at the level of different tissues, such as WAT, muscles and - why not - BAT.


relevant studies:
------------------

Am J Physiol Endocrinol Metab. 2007 May 1; [Epub ahead of print] Links
Unexpected Evidence for Active Brown Adipose Tissue in Adult Humans.

Nedergaard J, Bengtsson T, Cannon B.
Stockholm University, The Wenner-Gren Institute, Stockholm, Sweden.

The contention that brown adipose tissue is absent in adult man has meant that processes attributed to brown adipose tissue in experimental animals (mainly rodents)--i.e. classical nonshivering thermogenesis, adaptive adrenergic thermogenesis, diet-induced thermogenesis, anti-obesity--should be either absent or attributed to alternative (unknown) mechanisms in man. However, serendipidously, as a consequence of the use of fluorodeoxyglucose positron emission tomography (FDG PET) to trace tumor metastasis, observations that may change that notion have recently been made. These tomography scans have visualised symmetrical areas of increased tracer uptake in upper parts of the human body; these areas of uptake correspond to brown adipose tissue. We examine here the published observations from a viewpoint of human physiology. The human depots are somewhat differently located from those in rodents, the main depots being found in the supraclavicular and neck regions with some additional paravertebral, mediastinal, para-aortic and suprarenal localizations (but no interscapular). Brown adipose tissue activity in man is acutely cold-induced, and is stimulated via the sympathetic nervous system. The prevalence of active brown adipose tissue in normal adult man can only be indirectly estimated but it would seem that the prevalence of brown adipose tissue in the population may be at least in the range of some tens of percent. We conclude that a substantial fraction of adult humans possess active brown adipose tissue which thus has the potential to be of metabolic significance for normal human physiology, as well as to become pharmaceutically activated in efforts to combat obesity. Key words: brown adipose tissue, fluorodeoxyglucose, adult man, thermogenesis, obesity.

PMID: 17473055 [PubMed - as supplied by publisher]


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J Med Invest. 2006 Aug;53(3-4):218-22.
A/G heterozygote of the A-3826G polymorphism in the UCP-1 gene has higher BMI than A/A and G/G homozygote in young Japanese males.

Nakano T, Shinka T, Sei M, Sato Y, Umeno M, Sakamoto K, Nomura I, Nakahori Y.
Department of Human Genetics and Public Health, Institute of Health Biosciences, The University of Tokushima Graduate School.

UCP-1 is suggested to have important roles for thermogenesis and energy expenditure. To elucidate whether the A-3826G polymorphism that is located in the 5' flanking region of the UCP-1 gene has roles in healthy young people, the polymorphism was genotyped among 251 young Japanese men whose mean age is 22.7 years old. We analyzed relationship between the A-3826G polymorphism and body mass index (BMI) or six biochemical parameters, serum concentration of total cholesterol (TC), high density lipoprotein (HDL) cholesterol, triglyceride (TG), asparatate aminotransferase (AST), alanine aminotransferase (ALT), fasting plasma glucose. The genotype frequencies were observed at the frequencies of 24.3% for AA, 48.2% for AG and 27.5% for GG, respectively. When BMI and the biochemical parameters were compared by ANOVA among individuals with each genotype, the statistical difference was observed only for BMI (P=0.016). Bonferroni's test demonstrated that the men with the AG genotype have higher BMI than those with the AA genotype (22.4+/-2.8 vs. 21.4+/-2.2) (P=0.04). The individuals with the AG genotype also showed trend to have higher BMI than those with the GG, although the difference was not statistically apparent (22.4+/-2.8 vs. 21.5+/-2.3) (P=0.07). Our results indicated that the young healthy Japanese men with the AG heterozygote showed higher BMI than those with other genotypes.

PMID: 16953057 [PubMed - indexed for MEDLINE]


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Biochem Biophys Res Commun. 2005 Sep 23;335(2):624-30.
The effects of UCP-1 polymorphisms on obesity phenotypes among Korean female subjects.Shin HD, Kim KS, Cha MH, Yoon Y.
SNP Genetics, Complex B, WooLim Lion's Valley, 371-28, Gasan-Dong, Geumcheon-Gu, Seoul 153-803, Republic of Korea.

Three SNPs of UCP-1 including A-3826G, A-1766G, and Ala64Thr (G+1068A) were genotyped among 453 overweight Korean female subjects recruited from an obesity clinic. Four common haplotypes with frequency greater than 0.04 were constructed with three SNPs. For an accurate evaluation of the effects of UCP-1 polymorphism on body fat accumulation, all subjects were tested using computerized tomography to measure the cross-sectional fat tissue areas at abdominal and distal part of the body. By statistical analyses, ht4[GAA] showed a significant association with decreased abdominal fat tissue area (P=0.02, dominant model), fat tissue area at thigh (P=0.008, dominant model), body fat mass (P=0.002, dominant model), and waist-to-hip ratio (P=0.01, dominant model). In addition, ht3[GAG] was associated with the accelerated reduction of waist-to-hip ratio and body fat mass by very low calorie diet among subjects who finished one-month-weight control program (P=0.05-0.006).

PMID: 16084837 [PubMed - indexed for MEDLINE]


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Biochim Biophys Acta. 2005 Jun 30;1741(1-2):149-55. Epub 2004 Dec 20.

The finding of new genetic polymorphism of UCP-1 A-1766G and its effects on body fat accumulation.

Kim KS, Cho DY, Kim YJ, Choi SM, Kim JY, Shin SU, Yoon YS.
Kirin Oriental Hospital, 38-25, Jamwon-dong, Seocho-gu, Seoul 137-905, Republic of Korea.

A-1766G polymorphism, for the first time, has been found in the sequencing of pooled and individual genomic DNA of Korean subjects at the 5' flanking region of the UCP-1 gene. The effects of new polymorphism on body fat were elucidated among 387 Korean female subjects. It was shown that the genotypes AA, AG, and GG were consisted of 57.4%, 37.7%, and 4.9%, respectively, which was in agreement with Hardy-Weinberg equilibrium (P=0.327). The frequency of major A allele was 0.762 and that of minor G allele was 0.238. It is found that the waist-hip ratio (WHR) (P=0.008), body fat mass (P=0.023), and percent body fat (P=0.014) are significantly higher in the AG/GG type compared to the AA type. When the subjects were analyzed using computerized tomography, there were significant increases in the AG/GG type compared to the AA type in the abdominal subcutaneous fat (P=0.015) and the abdominal visceral fat (P=0.013), respectively. A-1766G is approximately 2 kb downstream from the well-known A-3826G polymorphism, and no linkage between them was found (D'=0.929, R(2)=0.283). Three haplotypes (frequency >0.05) were examined from two polymorphisms and studied for their physiological effects. It was found that haplotype [GG] was significantly associated with increased body fat, while haplotype [GA] was associated with decreased body fat.

please note in the last study that I cited, that a certain UCP-1 polymorphisms was significantly correlated with visceral + subcutaneous abdominal adopise tissue (= WAT). So, the metabolic functionality of BAT - even if its total mass in the body is modest - appears to substantially influence the accumulation of abdominal WAT - in humans!!

beta-3 agonsits are pretty useless in humans, but to conclude from that that BAT and UCP1 per se are irrelevant targets in the regulation of human adposity / obesity IS BAD SCIENCE.

[DRP7]

on a side-note, I wish there would be a little less mob mentality here. (somebody said: "Well, who's looking like the moron now?").

Personally, I don't know who hooker is and I don't really care, but it's not fair to bash somebody based solely on the opinion of some other guy who presented only a fraction of the science that is relevant for the evaluation of the role of UCP-1 in adiposity and its treatment.

I really don't know which new product it might be that hooker is going to bring, possibly it will be crap, but possibly it will be of benefit - who knows?

when we look at the big picture, then UCP1 and BAT appear to not be that useless and certainly hold some promise. this is the message that science provides here. only the future will show in what way and how far these targets could potentially be used for therapeutical interventions.

[SCDiesel23]

Originally Posted by Dr.P

on a side-note, I wish there would be a little less mob mentality here. (somebody said: "Well, who's looking like the moron now?").

Personally, I don't know who hooker is and I don't really care, but it's not fair to bash somebody based solely on the opinion of some other guy who presented only a fraction of the science that is relevant for the evaluation of the role of UCP-1 in adiposity and its treatment.

It's not just that, and this isn't the first time he has done something outrageous like this.

Originally Posted by SCDiesel23

No, it is not like roids in terms of gains, no where close

Originally Posted by hooker

Actually...from my own bloodwork, I'd think that MyogenX is similar to about 100mgs/eod of testosterone propionate (which gets my bloodlevels to about 950 or so).

Here he is explaining to someone that they can get steroid-like gains by using his testosterone booster.

[IBE Labs]

Anthony likes to run when there is science involved.

[IBE Labs]

If you check out this link you will see why everyone hates him.

http://forums.steroid.com/showthread.php?t=305396

[DRP7]

O.K. guys, I am neither hooker's attorney nor his foster mother. If he did foolish things in the past then call him to account for those things.

but with regards to the current topic, it is absolutely unjustified to call an UCP-1/BAT-based approach for fat-loss "bad science" as the OP did.

[SCDiesel23]

Originally Posted by Dr.P

but with regards to the current topic, it is absolutely unjustified to call an UCP-1/BAT-based approach for fat-loss "bad science" as the OP did.

True, my fault, I did not understand what was going on when I made my previous post, but my opinion on the individual still stands.

Carry on.

[leonidas300]

It is funny that the only criticism I always see regarding Anthony is that he is an ass. People never really challenge his science or knowledge, just his general attitude. Personally I could care less how great of a personality the guy has as long as the products are legit or not, so for now lets stick with the science and see if he can back up these claims. WE all know how I feel about false claims, they make me very angry, but again, lets see what he has to say about this. I no nothing about this area at all so I am waiting to evaluate the arguments put forth.

[DRP7]

Originally Posted by leonidas300

It is funny that the only criticism I always see regarding Anthony is that he is an ass. People never really challenge his science or knowledge, just his general attitude. Personally I could care less how great of a personality the guy has as long as the products are legit or not, so for now lets stick with the science and see if he can back up these claims. WE all know how I feel about false claims, they make me very angry, but again, lets see what he has to say about this. I no nothing about this area at all so I am waiting to evaluate the arguments put forth.

the approach to target UCP-1 is legit and promising (as shown above). whether the actual product, however, will hold up to these promises, will turn out when we know what ingrediends it has and when we can review the existing literature on it. many substances that work well in animals often don't work well in humans, so we will see (e.g. CLA).
I am too very curious to hear more about the subject, but recent experiences with other companies suggest that we might not expect to get much information.

[Conciliator]

Originally Posted by Dr.P

beta-3 agonsits are pretty useless in humans, but to conclude from that that BAT and UCP1 per se are irrelevant targets in the regulation of human adposity / obesity IS BAD SCIENCE.

Dr. P, you're making the same error you have in the past: you fail to comprehend the argument and then you sound foolish when your conclusion is off topic. You really need to take a minute or two before posting to understand what is being said. You put in a whole lot of work into your straw man arguments, but it's just bad logic.

1) I bolded the sentence that "Hooker is therefore claiming that his new product targets UCP1 in white adipose tissue (WAT). This post will take issue with that." As you can see, my post (and all the quotes) is concerning this, the location of UCP1. All of your posts are on the potential for UCP1 in human BAT, an entirely different issue, even though I touched on it:

2) I said that "pharmacological approaches to induce BAT formation and UCP1 expression/thermogenesis in humans (e.g. via beta-3 agonists) have been largely ineffective."

3) You failed to comprehend my argument and committed a fallacious straw man, saying "but to conclude from that that BAT and UCP1 per se are irrelevant targets in the regulation of human adposity / obesity IS BAD SCIENCE."

No, this is not bad sciecne, this is more of your bad logic. It's pretty obvious that my conclusion was not that "BAT and UCP1 per se are irrelevant targets in the regulation of human adposity." It's sad that you would read my post and state that as the conclusion of my argument. That wasn't my conclusion at all. My conclusion was that UCP1 is found in brown adipocytes, not white adipocytes. I agree that there may be potential in BAT and UCP1 in humans, but that doesn't change the fact that "pharmacological approaches to induce BAT formation and UCP1 expression/thermogenesis in humans (e.g. via beta-3 agonists) have been largely ineffective." Go misinterpret arguments somewhere else. It wastes everyone's time and I'd prefer not to waste mine.

[Conciliator]

And of course, another neg from Dr. P: don't call other people "morons" based on incomplete science you are presenting.

No, I'm not presenting incomplete science, you're presenting a straw man of my position since you can't comprehend things too well. This happens all over the place with you. It's sad...

[Conciliator]

Originally Posted by Dr.P

but with regards to the current topic, it is absolutely unjustified to call an UCP-1/BAT-based approach for fat-loss "bad science" as the OP did.

No, that's what YOU claim I'm saying, even though I'm not. It amazes me how careless you are when interpreting arguments and forming your own. That's absolutely not what I said and that's absolutely not what my post was about. Geez.

[DRP7]

Conci, you are just a joke. we all know that you are the master of splitting hairs. but apparently you are responding to me without even reading what I wrote.
I will put it into some easier terms so you can comprehend it:


your thread / initial post had two obvious implications:

1. products that aim UCP-1 are pretty much worthless in humans
2. to bring as much evidence that UCP-1 is present only in BAT but not WAT


proof for point Nr.1:

Originally Posted by Conciliator

"Hooker's New Product, PyrogenX - More Bad Science"

Originally Posted by Conciliator

In this post, I'll take a look at an aspect of Anthony Robert's new product, PyroGenX. Recently, Hooker said "I'm coming out with a fat burner within the next few weeks, which will be sold here on BB.com. PyroGenX is the name, and it's a mitochondrial uncoupler which works on UCP1."

Now anyone who knows anything about uncoupling protein 1 (UCP1) knows that 1) it's found only in brown adipose tissue (BAT), 2) that adult humans have very little BAT (they primarily have white adipose tissue or WAT), and 3) that pharmacological approaches to induce BAT formation and UCP1 expression/thermogenesis in humans (e.g. via beta-3 agonists) have been largely ineffective. So his product sounded like BS to me right off the bat.

This is where your conclusion is not inline with current science. Targeing UCP-1 in humans is definitively no BS at all.

and with regards to point Nr.2: I don't care for your little 3-year-old-childish dispute with hooker about his alleged statment that UCP-1 occurs in WAT or not. I never commented on this.

so, stop talking crap and before insulting people next time 1. do a better research and 2. read people's posts before replying.

[Conciliator]

Originally Posted by Dr.P

Conci, you are just a joke. we all know that you are the master of splitting hairs. but apparently you are responding to me without even reading what I wrote.
I will put it into some easier terms so you can comprehend it:


your thread / initial post had two main implications:

1. products that aim UCP-1 are pretty much worthless in humans
2. to bring as much evidence that UCP-1 is present only in BAT but not WAT


proof for implication Nr.1:

This is where your conclusion is not inline with current science. Targeing UCP-1 in humans is definitively no BS at all.

and with regards to point /implic<tion Nr.2: I don't care for your little 3-year-old-childish dispute with hooker about his alleged statment that UCP-1 occurs in WAT or not. I never commented on this.

so, stop talking crap and before insulting people next time do a better research.


So product

Dr. P, this is called a straw man argument. This is a fallacy. It's sloppy reasoning and poor logic. I never argued that products that aim at UCP-1 are pretty much worthless in humans. I said they've largely been ineffective, and that's it. The rest of the post had nothing to do with their potential or their efficacy. Yet this is the conclusion you're trying to paint me as making so that you have something to attack. Do not do that to people. Do not waste people's time misrepresenting them

It's interesting that you think that me saying "his product sounded like BS to me right off the bat" is evidence that I'm claiming that "products that aim UCP-1 are pretty much worthless in humans". Those doesn't sound the same. Why don't you post what I said right after that: "When I pressed him about it, he said 'Sorry, son. It's based on WAT, not BAT, and it's already in production." Hooker is therefore claiming that his new product targets UCP1 in white adipose tissue (WAT). This post will take issue with that.'

Is that somehow unclear to you? How in the world do you come away saying that my conclusion is that "BAT and UCP1 per se are irrelevant targets in the regulation of human adposity / obesity". Give me a a break. It's obvious that I'm saying nothing of the sort. As I've said before, it's futile arguing with you since you're incapable of staying focused in an argument. You commit logical fallacies all over the place.

[DRP7]

Originally Posted by Dr.P

but with regards to the current topic, it is absolutely unjustified to call an UCP-1/BAT-based approach for fat-loss "bad science" as the OP did.

Originally Posted by Conciliator

No, that's what YOU claim I'm saying, even though I'm not. It amazes me how careless you are when interpreting arguments and forming your own. That's absolutely not what I said and that's absolutely not what my post was about. Geez.

oh, really?

VVVVVVV

Originally Posted by Conciliator

Let me guess, it's based on some great animal data, since only animals (and infants) have appreciable amounts of BAT, where UCP-1 is found. Just the fact that you say it works on UCP1 makes me skeptical as all hell.

Originally Posted by Conciliator

So his product sounded like BS to me right off the bat.

man, don't choke on your arrogance. I have seen other people lieing better than you.

[Conciliator]

Originally Posted by Dr.P

and with regards to point Nr.2: I don't care for your little 3-year-old-childish dispute with hooker about his alleged statment that UCP-1 occurs in WAT or not. I never commented on this.

If you don't care for it, then you never should have posted, since that's what the whole damn post is about. My guess is that you had nothing to post, but were itching to contradict me, so you invented a straw man you could take shots at. Well that's all nice and good, but it has nothing to do with me, my argument, or this thread.

Originally Posted by Dr.P

so, stop talking crap and before insulting people next time 1. do a better research and 2. read people's posts before replying.

Read people's posts before replying? That's what YOU need to do, hahah. You are such a tool, lol.

[DRP7]

Originally Posted by Conciliator

Dr. P, this is called a straw man argument. This is a fallacy. It's sloppy reasoning and poor logic. I never argued that products that aim at UCP-1 are pretty much worthless in humans. I said they've largely been ineffective, and that's it. The rest of the post had nothing to do with their potential or their efficacy. Yet this is the conclusion you're trying to paint me as making so that you have something to attack. Do not do that to people. Do not waste people's time misrepresenting them

It's interesting that you think that me saying "his product sounded like BS to me right off the bat" is evidence that I'm claiming that "products that aim UCP-1 are pretty much worthless in humans". Those doesn't sound the same. Why don't you post what I said right after that: "When I pressed him about it, he said 'Sorry, son. It's based on WAT, not BAT, and it's already in production." Hooker is therefore claiming that his new product targets UCP1 in white adipose tissue (WAT). This post will take issue with that.'

Is that somehow unclear to you? How in the world do you come away saying that my conclusion is that "BAT and UCP1 per se are irrelevant targets in the regulation of human adposity / obesity". Give me a a break. It's obvious that I'm saying nothing of the sort. As I've said before, it's futile arguing with you since you're incapable of staying focused in an argument. You commit logical fallacies all over the place.

hairsplitter, you have been cought and now you are trying to come out of this by all means. you are only making a public joke out of yourself. go on, it looks funny.

there is no "strawman argument". the case is obvious.

btw: since we are at hair-splitting: how about you show me where exactely hooker said: "UCP-1 is present in WAT"? It appears that you wanted to polish your ego on a boring weekend and searched someone to bash.

it appears that you are making straw-man arguments. it only is your interpretation that he said "UCP-1 occurs in WAT".

He said: "Itg's based on WAT". So, what is based on WAT? UCP-1? Or his product that via BAT-UCP-1 will influence WAT? I don't know what he meant. you don't know it either.

so much about Conci and his strawam arguments.

[Conciliator]

Originally Posted by Dr.P

man, don't choke on your arrogance. I have seen other people lieing better than you.

You can't take an excerpt from one thread, follow it with another excerpt from a different thread, and then try to make it sound like one is based on the other. Those are two seperate statements. Yes, if somone says he's targeting UCP1, I'm skeptical as hell. This has been largely ineffective in humans. That's not why I started a thread, though, or what I said was bad science. I started the thread attacking his claim that he was targeting UCP1 in WAT. That should be blatantly obvious from the content of my post. When I say his "product sounded like BS to me right off the bat", it's because "When I pressed him about it, he said 'Sorry, son. It's based on WAT, not BAT, and it's already in production.' Hooker is therefore claiming that his new product targets UCP1 in white adipose tissue (WAT). This post will take issue with that."

You've done this before, where you take my posts out of context, or place two different quotes back to back like one is referring to the other. That's just stupid, really. It's sloppy arguing. Read what I wrote: "When I pressed him about it, he said 'Sorry, son. It's based on WAT, not BAT, and it's already in production.' Hooker is therefore claiming that his new product targets UCP1 in white adipose tissue (WAT). This post will take issue with that." That was the scope of my argument. I ended the post saying "There are more where these came from, but I'm sure you get the idea: It's well established that UCP1 is found only in BAT. It's not present in white adipocytes." Get a clue Dr. P.

[DRP7]

Originally Posted by Conciliator

If you don't care for it, then you never should have posted, since that's what the whole damn post is about.

BS, the message of your post is very clear. and all your "UCP-1 is not present in WAT" was only a measure to prove your point how useless you find the UCP-1 approach.

Originally Posted by Concliator

My guess is that you had nothing to post, but were itching to contradict me, so you invented a straw man you could take shots at. Well that's all nice and good, but it has nothing to do with me, my argument, or this thread.
Read people's posts before replying? That's what YOU need to do, hahah. You are such a tool, lol.

Haha, yes, that's fine. whe you are cought and run out of arguments then you start with ad hominem. business as usual. Conci at his best.

[Conciliator]

Originally Posted by Dr.P

hairsplitter, you have been cought and now you are trying to come out of this by all means. you are only making a public joke out of yourself. go on, it looks funny.

It's not hair splitting, Dr. P, it's called thinking clearly, something you do not do.

Originally Posted by Dr.P

there is no "strawman argument". the case is obvious.

You wish the case was obvious. Nowhere in the post did I say anything that resembles what you claimed I was concluding. You set up a straw man argument.

Originally Posted by Dr.P

btw: since we are at hair-splitting: how about you show me where exactely hooker said: "UCP-1 is present in WAT"? It appears that you wanted to polish your ego on a boring weekend and searched someone to bash.

it appears that you are making straw-man arguments. it only is your interpretation that he said "UCP-1 occurs in WAT".

He said: "Itg's based on WAT". So, what is based on WAT? UCP-1? Or his product that via BAT-UCP-1 will influence WAT? I don't know what he meant. you don't know it either.

so much about Conci and his strawam arguments.

Hooker said his product targets UCP1 and that it's based on WAT, not BAT. I took this to mean that his new product targets UCP1 in WAT. I think this is a reasonable interpretation. If I misinterpreted him, he's more than welcome to clarify.

[DRP7]

Originally Posted by Conciliator

You can't take an excerpt from one thread, follow it with another excerpt from a different thread, and then try to make it sound like one is based on the other. Those are two seperate statements.

ou've done this before, where you take my posts out of context, or place two different quotes back to back like one is referring to the other.

haha, your defense sucks. your philosphy class will not be proud of you when they see you struggling that bad.
do you think I and all the other people out there are blind and dumbasses? You said in an earlier thread that you find this UCP-1 story BS and you said it again in this thread. these two threads and your statements in both threads are perfectly linked to each other and represent ONE context.

sucker!

Originally Posted by Conciliator

When I say his "product sounded like BS to me right off the bat", it's because "When I pressed him about it, he said 'Sorry, son. It's based on WAT, not BAT, and it's already in production.'

foul! this is just blatant lieing. step 3 in philosopher's handbook: "how to win a discussion even if you are wrong". you have absolutely been of the opinion that UCP-1 doesn't work in humans before you even started discussing with hooker. this is what I cited and what you got mad on.

Originally Posted by Conciliator

Hooker is therefore claiming that his new product targets UCP1 in white adipose tissue (WAT). This post will take issue with that."

foul! straw man argument from the philosphers handbook.
This is only your interpretation. hookers statement can be interpreted in different ways, as I have shown in my last post.

man, you just suck big time. grow up and admit when you see that you have been wrong on something.