You keep saying this about the "green tar" and I have yet to see a single valid source to support your statement. Can you provide some evidence to support your position?
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You keep saying this about the "green tar" and I have yet to see a single valid source to support your statement. Can you provide some evidence to support your position?
To think marijuana is not cancer causing you got to be blind or it cures cancer lol again this is just plain stupid thinking how many people you know that have CANCER and MJ cured it personally ??? not one fucking person i bet really in order to get a medical growing license one must be on his last legs literally thats a fact others use the major chronic pain it does not cure it just masks the pain Right
Oakley Ray, PhD, Emeritus Professor of Psychology and Pharmacology at Vanderbilt University, and Charles Ksir, PhD, Professor of Psychology at the University of Wyoming, noted in their 2004 textbook Drugs, Society and Human Behavior:
"The chemistry of Cannabis is quite complex, and the isolation and extraction of the active ingredient are difficult even today. The active agent in Cannabis is unique among psychoactive plant materials in that it contains no nitrogen and thus is not an alkaloid. Because Cannabis lacks nitrogen, the 19th century chemists who had been so successful in isolating the active agents from other plants were unable to identify its active component.
There are over 400 chemicals in marijuana, but only 61 [80 as of July 9, 2009; see Editor's Note below] of them are unique to the Cannabis plant -- these are called cannabinoids. One of them, delta-9-tetrahydrocannabinol (THC), was isolated and synthesized in 1964 and is clearly the most pharmacologically active.
Take special note that the relationship of THC to Cannabis is probably more similar to the relationship of mescaline to peyote then of alcohol to beer, wine, or distilled spirits. Alcohol is the only behaviorally active agent in alcoholic beverages, but there might be several active agents in Cannabis."
[Editor's Note: Mohamed M. Radwan, Mahmoud A. ElSohly, et al., researchers at the University of Mississippi, reported the discovery of nine new cannabinoids in their Apr. 3, 2009 study titled "Biologically Active Cannabinoids from High-Potency Cannabis Sativa," published in the Journal of Natural Products. This discovery brings the total number of cannabinoids to about 80, according to an Apr. 12, 2009 bulletin published by the International Association for Cannabis as Medicine.]
2004 - Charles Ksir, PhD
Oakley Ray, PhD
Americans for Safe Access, a medical marijuana advocacy group, stated in its website article "Research: Definitions and Explanations" (accessed Dec. 7, 2006):
"...[T]here are 483 different identifiable chemical constituents known to exist in cannabis. The most distinctive and specific class of compounds are the cannabinoids (66 known), that are only known to exist in the cannabis plant.
Other constituents of the cannabis plant are: nitrogenous compounds (27 known), amino acids (18), proteins (3), glycoproteins (6), enzymes (2), sugars and related compounds (34), hydrocarbons (50), simple alcohols (7), aldehydes (13), ketones (13), simple acids (21), fatty acids (22), simple esters (12), lactones (1), steroids (11), terpenes (120), non-cannabinoid phenols (25), flavonoids (21), vitamins (1) [Vitamin A], pigments (2), and elements (9).
The very most of these compounds are found in other plants and animals and are not of pharmacological relevance with regard to the effects exerted by cannabis preparations."
Dec. 7, 2006 - Americans for Safe Access (ASA)
The Mayo Clinic stated in its Aug. 25, 2006 article "Marijuana as Medicine: Consider the Pros and Cons," published on its website:
"Marijuana contains at least 60 chemicals called cannabinoids. Researchers are evaluating how effective some of these cannabinoids might be in controlling symptoms of certain medical conditions. For example:
THC. An abbreviation for delta-9-tetrahydrocannabinol, THC is the main component responsible for marijuana's mind-altering effect. It also may help treat signs and symptoms such as nausea and vomiting that are associated with a number of medical conditions.
Cannabinol and cannabidiol. These compounds have some of the properties of THC, but cause less psychoactive effects — the high. [...]
Also, marijuana smoke contains 50 percent to 70 percent more carcinogenic hydrocarbons than does tobacco smoke and has the potential to cause cancer of the lungs and respiratory tract. Marijuana smoke is commonly inhaled deeper and held longer than is tobacco smoke, increasing the lungs' exposure to carcinogens."
Oakley Ray, PhD, Emeritus Professor of Psychology and Pharmacology at Vanderbilt University, and Charles Ksir, PhD, Professor of Psychology at the University of Wyoming, noted in their 2004 textbook Drugs, Society and Human Behavior:
"The chemistry of Cannabis is quite complex, and the isolation and extraction of the active ingredient are difficult even today. The active agent in Cannabis is unique among psychoactive plant materials in that it contains no nitrogen and thus is not an alkaloid. Because Cannabis lacks nitrogen, the 19th century chemists who had been so successful in isolating the active agents from other plants were unable to identify its active component.
There are over 400 chemicals in marijuana, but only 61 [80 as of July 9, 2009; see Editor's Note below] of them are unique to the Cannabis plant -- these are called cannabinoids. One of them, delta-9-tetrahydrocannabinol (THC), was isolated and synthesized in 1964 and is clearly the most pharmacologically active.
Take special note that the relationship of THC to Cannabis is probably more similar to the relationship of mescaline to peyote then of alcohol to beer, wine, or distilled spirits. Alcohol is the only behaviorally active agent in alcoholic beverages, but there might be several active agents in Cannabis."
[Editor's Note: Mohamed M. Radwan, Mahmoud A. ElSohly, et al., researchers at the University of Mississippi, reported the discovery of nine new cannabinoids in their Apr. 3, 2009 study titled "Biologically Active Cannabinoids from High-Potency Cannabis Sativa," published in the Journal of Natural Products. This discovery brings the total number of cannabinoids to about 80, according to an Apr. 12, 2009 bulletin published by the International Association for Cannabis as Medicine.]
2004 - Charles Ksir, PhD
Oakley Ray, PhD
Americans for Safe Access, a medical marijuana advocacy group, stated in its website article "Research: Definitions and Explanations" (accessed Dec. 7, 2006):
"...[T]here are 483 different identifiable chemical constituents known to exist in cannabis. The most distinctive and specific class of compounds are the cannabinoids (66 known), that are only known to exist in the cannabis plant.
Other constituents of the cannabis plant are: nitrogenous compounds (27 known), amino acids (18), proteins (3), glycoproteins (6), enzymes (2), sugars and related compounds (34), hydrocarbons (50), simple alcohols (7), aldehydes (13), ketones (13), simple acids (21), fatty acids (22), simple esters (12), lactones (1), steroids (11), terpenes (120), non-cannabinoid phenols (25), flavonoids (21), vitamins (1) [Vitamin A], pigments (2), and elements (9).
The very most of these compounds are found in other plants and animals and are not of pharmacological relevance with regard to the effects exerted by cannabis preparations."
Dec. 7, 2006 - Americans for Safe Access (ASA)
The Mayo Clinic stated in its Aug. 25, 2006 article "Marijuana as Medicine: Consider the Pros and Cons," published on its website:
"Marijuana contains at least 60 chemicals called cannabinoids. Researchers are evaluating how effective some of these cannabinoids might be in controlling symptoms of certain medical conditions. For example:
THC. An abbreviation for delta-9-tetrahydrocannabinol, THC is the main component responsible for marijuana's mind-altering effect. It also may help treat signs and symptoms such as nausea and vomiting that are associated with a number of medical conditions.
Cannabinol and cannabidiol. These compounds have some of the properties of THC, but cause less psychoactive effects — the high. [...]
Also, marijuana smoke contains 50 percent to 70 percent more carcinogenic hydrocarbons than does tobacco smoke and has the potential to cause cancer of the lungs and respiratory tract. Marijuana smoke is commonly inhaled deeper and held longer than is tobacco smoke, increasing the lungs' exposure to carcinogens."
WaittillIdie
Member
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Okay, so you don't have any evidence to support your ridiculous assertions. I already knew that, but you could have saved yourself a lot of typing and me a lot of reading if you had just said that you're talking out of your ass from the start.
Again, you're doing no one any favors with this anti-intellectual approach to a discussion. You should consider becoming a politician as your double-speak and ability to ignore both concrete evidence as well as common sense while simultaneously deflecting actual points is really top notch.
people like you are a large part of the reason why cannabis is still illegal on a federal level. Let me know if you ever come out of your delusional fantasy world and want to have a real discussion.
WaittillIdie
Member
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WaittillIdie
Member
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Any facts. Any facts at all. Anything other than the same bullshit that you made up off the top of your head and have been repeating for months on this forum.
Your astounding lack of critical thinking skills and overall reasoning ability are offensive to me, but you don't see me asking for an apology.
At this point I don't know if I am talking to a child or someone with a mental disability.
WaittillIdie
Member
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Oh, I'm the one not making sense. My apologies. 
now I know why I got so many messages a week or two ago when I first started talking to you about this. You really are as insane as everyone said and this is indeed just as much of a waste of time as they said it would be.
By the way, to answer your above post, I just made this post and it is on the same page we are on. Put down the bong and answer the question or fuck off and stop spreading misinformation to support your own twisted worldview.
now I know why I got so many messages a week or two ago when I first started talking to you about this. You really are as insane as everyone said and this is indeed just as much of a waste of time as they said it would be. By the way, to answer your above post, I just made this post and it is on the same page we are on. Put down the bong and answer the question or fuck off and stop spreading misinformation to support your own twisted worldview.
WaittillIdie
Member
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Last edited:
WaittillIdie
Member
nvm
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all i know is that i smoke around 2 g daily, and I can still hop on my bike and ride 50 miles in less than three hrs no problem. haven't had bronchitis since i took a plane trip.
it is much more prudent to be worried about physical stagnation due to inactivity.
it is much more prudent to be worried about physical stagnation due to inactivity.
I see people asking for studies/ evidence of cannabis curative properties as the huge volume of anecdotal evidence is clearly not sufficient- so here's some.
Cannabis and Cannabinoids (PDQ®)
Laboratory/Animal/Preclinical Studies
Antitumor Effects
Appetite Stimulation
Analgesia
Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis species (e.g., Cannabis sativa L.) .[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.
Antitumor Effects
One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma (HCC) was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5-8]
Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.[9-12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents.[13,14] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. For example, these compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats, while they protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[9]
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC.[15] Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma [16] and breast cancer.[17]
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic mammary cells.[18] Other studies have also shown the antitumor effect of cannabinoids (i.e., CBD and THC) in preclinical models of breast cancer.[19,20]
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[21] In this experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation. In a subsequent study, the investigators found that the antiproliferative effect of CBD was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors.[22]
Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[12] ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.
In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[23] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[24,25]
In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation.[26] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[27-30]
CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine.[31] In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells. Also, CBD together with THC may enhance the antitumor activity of classic chemotherapeutic drugs such as temozolomide in some mouse models of cancer.[13,32]
Appetite Stimulation
Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[33] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[34]
Analgesia
Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in regions of the brain that regulate nociceptive processing.[35] CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[36,37]
Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.[38-40] One study reported that the efficacy of synthetic CB1- and CB2-receptor agonists were comparable with the efficacy of morphine in a murine model of tumor pain.[41]
References
Cannabis and Cannabinoids (PDQ®)
Laboratory/Animal/Preclinical Studies
Antitumor Effects
Appetite Stimulation
Analgesia
Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis species (e.g., Cannabis sativa L.) .[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.
Antitumor Effects
One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma (HCC) was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5-8]
Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.[9-12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents.[13,14] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. For example, these compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats, while they protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[9]
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC.[15] Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma [16] and breast cancer.[17]
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic mammary cells.[18] Other studies have also shown the antitumor effect of cannabinoids (i.e., CBD and THC) in preclinical models of breast cancer.[19,20]
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[21] In this experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation. In a subsequent study, the investigators found that the antiproliferative effect of CBD was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors.[22]
Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[12] ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.
In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[23] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[24,25]
In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation.[26] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[27-30]
CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine.[31] In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells. Also, CBD together with THC may enhance the antitumor activity of classic chemotherapeutic drugs such as temozolomide in some mouse models of cancer.[13,32]
Appetite Stimulation
Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[33] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[34]
Analgesia
Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in regions of the brain that regulate nociceptive processing.[35] CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[36,37]
Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.[38-40] One study reported that the efficacy of synthetic CB1- and CB2-receptor agonists were comparable with the efficacy of morphine in a murine model of tumor pain.[41]
References
mr. brunch, thanks for the links. I'm familiar with most of that info. What I was asking was pretty clearly stated in my post:
Specifically, I'm asking about statements such as these:
Once we get over that hurdle, I'll ask about some of the other comments. I'm trying to make this as simple as possible as the gentleman seems to have trouble following even a single argument, much less several at once.
Specifically, I'm asking about statements such as these:
Once we get over that hurdle, I'll ask about some of the other comments. I'm trying to make this as simple as possible as the gentleman seems to have trouble following even a single argument, much less several at once.
listen.
you stay there, and argue about which paid person writing things is talking truth,
me and dude are going to hop on our bikes, and live a real life, firsthand, without any dumbasses writing stuff we are supposed to think is true,
and at the end of the day, we'll have a pretty good idea about how we're doing. meanwhile, you can go check with your guy who writes stuff to find out if you're still healthy or not.
you stay there, and argue about which paid person writing things is talking truth,
me and dude are going to hop on our bikes, and live a real life, firsthand, without any dumbasses writing stuff we are supposed to think is true,
and at the end of the day, we'll have a pretty good idea about how we're doing. meanwhile, you can go check with your guy who writes stuff to find out if you're still healthy or not.
That's great, I hope you enjoy yourself. I'm not sure why my trying to get factual information and concrete evidence to support the statements made in this thread is so offensive to you, but this brand of oddly proud anti-intellectualism isn't doing anyone any favors, least of all you.
As I said in the other thread, you might want to try working on learning to divest your emotional arguments from your intellectual arguments if you want to be taken seriously and benefit from the huge amount of knowledge available to us. Otherwise, it is probably better for everybody if you stay out of the discussion that you have clearly stated you have no interest in participating in.
without reading your nonsense second paragraph, it's because
http://en.wikipedia.org/wiki/Epistemology
you might want to get one too. just make sure you buy a good one from an authorised retailer.
http://en.wikipedia.org/wiki/Epistemology
you might want to get one too. just make sure you buy a good one from an authorised retailer.
