Monday, January 2, 2012
Hemp Oil Used To Cure Diabetes
It is simply amazing what you can learn from others who study and show them selves approved.
Cannabis and the Christ: Jesus used Marijuana
Part 4 of "When Smoke Gets in my I" a series on the history of cannabis and human consciousness.
"If you know the truth, the truth will make you free." (John 8:32)
The very word "Christ", by the implication of its linguistic origins and true meaning, gives us the most profound evidence that Jesus did in fact use the same herb as his ancient semitic ancestors, and which is still used by people around the world for its enlightening and healing properties.
The Greek title "Christ" is the translation of the Hebrew word Messiah, which in English becomes "The Anointed" D. The Messiah was recognized as such by his being anointed with the holy anointing oil, the use of which was restricted to the instillation of Hebrew priests and kings. If Jesus was not initiated in this fashion then he was not the Christ, and had no official claim to the title.
The ancient recipe for this anointing oil, recorded in the Old Testament book of Exodus (30: 22-23) included over nine pounds of flowering cannabis tops, Hebrew "kaneh-bosm" B, extracted into a hind (about 6.5 litres) of olive oil, along with a variety of other herbs and spices. The ancient chosen ones were literally drenched in this potent cannabis holy oil.
From the time of Moses until that of the later prophet Samuel, the holy anointing oil was used by the shamanistic Levite priesthood to receive the "revelations of the Lord". At the dawn of the age of Kings, Samuel extended the use of the anointing oil to the Hebraic monarchs by anointing Saul (and later David) as "Messiah-king". These kings lead their people with the benefit of insights achieved through using the holy anointing oil to become "possessed with the spirit of the Lord."
Thursday, March 31, 2011
Romans 14
Romans 14 (King James Version)
Romans 14
1Him that is weak in the faith receive ye, but not to doubtful disputations.
2For one believeth that he may eat all things: another, who is weak, eateth herbs.
3Let not him that eateth despise him that eateth not; and let not him which eateth not judge him that eateth: for God hath received him.
4Who art thou that judgest another man's servant? to his own master he standeth or falleth. Yea, he shall be holden up: for God is able to make him stand.
5One man esteemeth one day above another: another esteemeth every day alike. Let every man be fully persuaded in his own mind.
6He that regardeth the day, regardeth it unto the Lord; and he that regardeth not the day, to the Lord he doth not regard it. He that eateth, eateth to the Lord, for he giveth God thanks; and he that eateth not, to the Lord he eateth not, and giveth God thanks.
7For none of us liveth to himself, and no man dieth to himself.
8For whether we live, we live unto the Lord; and whether we die, we die unto the Lord: whether we live therefore, or die, we are the Lord's.
9For to this end Christ both died, and rose, and revived, that he might be Lord both of the dead and living.
10But why dost thou judge thy brother? or why dost thou set at nought thy brother? for we shall all stand before the judgment seat of Christ.
11For it is written, As I live, saith the Lord, every knee shall bow to me, and every tongue shall confess to God.
12So then every one of us shall give account of himself to God.
13Let us not therefore judge one another any more: but judge this rather, that no man put a stumblingblock or an occasion to fall in his brother's way.
14I know, and am persuaded by the Lord Jesus, that there is nothing unclean of itself: but to him that esteemeth any thing to be unclean, to him it is unclean.
15But if thy brother be grieved with thy meat, now walkest thou not charitably. Destroy not him with thy meat, for whom Christ died.
16Let not then your good be evil spoken of:
17For the kingdom of God is not meat and drink; but righteousness, and peace, and joy in the Holy Ghost.
18For he that in these things serveth Christ is acceptable to God, and approved of men.
19Let us therefore follow after the things which make for peace, and things wherewith one may edify another.
20For meat destroy not the work of God. All things indeed are pure; but it is evil for that man who eateth with offence.
21It is good neither to eat flesh, nor to drink wine, nor any thing whereby thy brother stumbleth, or is offended, or is made weak.
22Hast thou faith? have it to thyself before God. Happy is he that condemneth not himself in that thing which he alloweth.
23And he that doubteth is damned if he eat, because he eateth not of faith: for whatsoever is not of faith is sin.
Romans 14
1Him that is weak in the faith receive ye, but not to doubtful disputations.
2For one believeth that he may eat all things: another, who is weak, eateth herbs.
3Let not him that eateth despise him that eateth not; and let not him which eateth not judge him that eateth: for God hath received him.
4Who art thou that judgest another man's servant? to his own master he standeth or falleth. Yea, he shall be holden up: for God is able to make him stand.
5One man esteemeth one day above another: another esteemeth every day alike. Let every man be fully persuaded in his own mind.
6He that regardeth the day, regardeth it unto the Lord; and he that regardeth not the day, to the Lord he doth not regard it. He that eateth, eateth to the Lord, for he giveth God thanks; and he that eateth not, to the Lord he eateth not, and giveth God thanks.
7For none of us liveth to himself, and no man dieth to himself.
8For whether we live, we live unto the Lord; and whether we die, we die unto the Lord: whether we live therefore, or die, we are the Lord's.
9For to this end Christ both died, and rose, and revived, that he might be Lord both of the dead and living.
10But why dost thou judge thy brother? or why dost thou set at nought thy brother? for we shall all stand before the judgment seat of Christ.
11For it is written, As I live, saith the Lord, every knee shall bow to me, and every tongue shall confess to God.
12So then every one of us shall give account of himself to God.
13Let us not therefore judge one another any more: but judge this rather, that no man put a stumblingblock or an occasion to fall in his brother's way.
14I know, and am persuaded by the Lord Jesus, that there is nothing unclean of itself: but to him that esteemeth any thing to be unclean, to him it is unclean.
15But if thy brother be grieved with thy meat, now walkest thou not charitably. Destroy not him with thy meat, for whom Christ died.
16Let not then your good be evil spoken of:
17For the kingdom of God is not meat and drink; but righteousness, and peace, and joy in the Holy Ghost.
18For he that in these things serveth Christ is acceptable to God, and approved of men.
19Let us therefore follow after the things which make for peace, and things wherewith one may edify another.
20For meat destroy not the work of God. All things indeed are pure; but it is evil for that man who eateth with offence.
21It is good neither to eat flesh, nor to drink wine, nor any thing whereby thy brother stumbleth, or is offended, or is made weak.
22Hast thou faith? have it to thyself before God. Happy is he that condemneth not himself in that thing which he alloweth.
23And he that doubteth is damned if he eat, because he eateth not of faith: for whatsoever is not of faith is sin.
Ditchweed Update: DEA Numbers 7/20/01
Last week, DRCNet reported on the Drug Enforcement Administration (DEA) Domestic Cannabis Eradication/Suppression Program (http://www.drcnet.org/wol/194.html#ditchweed), which appears primarily devoted to wiping out feral cannabis, or "ditchweed," descended from the "Hemp for Victory" program of World War II. Because the DEA was slow to respond to DRCNet requests for current information, we were unable to provide accurate recent figures.
The DEA has now responded. DEA figures confirm that the vast majority of cannabis plants destroyed by the eradication campaign are ditchweed, feral cannabis plants that do not contain enough THC to provide any psychoactive effects other than a headache.
According to the DEA, the eradication program destroyed 252, 717,000 cannabis plants in 2000. Of those, 250 million were ditchweed, 2.5 million were cultivated outdoor plants, and 717,000 were indoor cultivated plants. In other words, DEA's own data show that 98.92% of all cannabis plants destroyed under the program were harmless weeds whose destruction has absolutely no impact on drug use in the United States.
This year's program is funded at $13.2 million dollars, the DEA told DRCNet, with grants to state and local agencies ranging from $5,000 to over one million dollars per agency. The grants go to some 106 law enforcement agencies in all 50 states.
Surprisingly, the DEA also claimed to "have evidence that sample "ditchweed" plants submitted from each state contain THC in excess of the levels accepted for "getting high."
That was news to cannabis expert Chris Conrad (http://www.chrisconrad.com). "I don't know what their 'levels accepted for getting high' are," Conrad told DRCNet, "but I would place it at something above 2% THC concentration. Mexican brick weed averages about 3%, and according to the study done by the American Midland Naturalists in the mid-1970s, ditchweed averaged around 0.5%."
Readers should not be surprised, however, that the DEA claims that ditchweed can get you high. This is, after all, the same agency that has expressed serious concerns about people getting THC in their bodies from hemp-based lip balms and other body care products.
The DEA has now responded. DEA figures confirm that the vast majority of cannabis plants destroyed by the eradication campaign are ditchweed, feral cannabis plants that do not contain enough THC to provide any psychoactive effects other than a headache.
According to the DEA, the eradication program destroyed 252, 717,000 cannabis plants in 2000. Of those, 250 million were ditchweed, 2.5 million were cultivated outdoor plants, and 717,000 were indoor cultivated plants. In other words, DEA's own data show that 98.92% of all cannabis plants destroyed under the program were harmless weeds whose destruction has absolutely no impact on drug use in the United States.
This year's program is funded at $13.2 million dollars, the DEA told DRCNet, with grants to state and local agencies ranging from $5,000 to over one million dollars per agency. The grants go to some 106 law enforcement agencies in all 50 states.
Surprisingly, the DEA also claimed to "have evidence that sample "ditchweed" plants submitted from each state contain THC in excess of the levels accepted for "getting high."
That was news to cannabis expert Chris Conrad (http://www.chrisconrad.com). "I don't know what their 'levels accepted for getting high' are," Conrad told DRCNet, "but I would place it at something above 2% THC concentration. Mexican brick weed averages about 3%, and according to the study done by the American Midland Naturalists in the mid-1970s, ditchweed averaged around 0.5%."
Readers should not be surprised, however, that the DEA claims that ditchweed can get you high. This is, after all, the same agency that has expressed serious concerns about people getting THC in their bodies from hemp-based lip balms and other body care products.
Saturday, January 9, 2010
Effects of an Earth-strength magnetic field on electrical activity of pineal cells
Effects of an Earth-strength magnetic field on electrical activity of pineal cells
P. Semm, T. Schneider & L. Vollrath
University of Mainz, Department of Anatomy, Neurophysiology Laboratory, 6500 Mainz, Saarstr. 19/21, FRG
Although magnetic fields can influence biological systems, including those of man and other vertebrates1−5, no central nervous structure has been identified that might be involved in their detection. From a theoretical point of view, the pineal organ might be such a structure for the following reasons: (1) It is involved in the regulation of circadian rhythms6 and is thus essential for migratory restlessness ('Zugunruhe')7. Orientation at that time can be altered by an artificial magnetic field (MF) with a direction differing by 90° from that of the Earth. Circadian rhythms can be inhibited from phase shifting by compensation of the Earth's MF and can be influenced by an artificial MF8. (2) The pineal organ is strongly dependent on its sympathetic innervation6 and the sympatho-adrenergic system as a whole is sensitive to magnetic stimuli9. (3) The pineal organ is a light-sensitive time-keeping organ10,11 and could form part of a combined compass−solar-clock system, which has been postulated for maintaining orientation in birds12. We have therefore investigated the effect of a MF on electrophysiological activity of the guinea pig pineal organ, which is a useful system for such studies on individual cells11,13. We report here that activity was depressed by an induced MF and restored when the MF was inverted.
------------------
P. Semm, T. Schneider & L. Vollrath
University of Mainz, Department of Anatomy, Neurophysiology Laboratory, 6500 Mainz, Saarstr. 19/21, FRG
Although magnetic fields can influence biological systems, including those of man and other vertebrates1−5, no central nervous structure has been identified that might be involved in their detection. From a theoretical point of view, the pineal organ might be such a structure for the following reasons: (1) It is involved in the regulation of circadian rhythms6 and is thus essential for migratory restlessness ('Zugunruhe')7. Orientation at that time can be altered by an artificial magnetic field (MF) with a direction differing by 90° from that of the Earth. Circadian rhythms can be inhibited from phase shifting by compensation of the Earth's MF and can be influenced by an artificial MF8. (2) The pineal organ is strongly dependent on its sympathetic innervation6 and the sympatho-adrenergic system as a whole is sensitive to magnetic stimuli9. (3) The pineal organ is a light-sensitive time-keeping organ10,11 and could form part of a combined compass−solar-clock system, which has been postulated for maintaining orientation in birds12. We have therefore investigated the effect of a MF on electrophysiological activity of the guinea pig pineal organ, which is a useful system for such studies on individual cells11,13. We report here that activity was depressed by an induced MF and restored when the MF was inverted.
------------------
Sunday, November 29, 2009
Cannabis-Psychosis link not caused by dopamine increase
Klint Finley
There is now growing evidence that cannabis use causes a small but reliable increase in the chance of developing psychosis. Traditionally, this was explained by the drug increasing dopamine levels in the brain but a new study shortly to be published in NeuroImage suggests that the active ingredient in cannabis doesn’t effect this important neurotransmitter.
Despite some dissenting voices, disruption to the mesolimbic dopamine pathway is widely thought to be the key problem in the development of delusions, hallucinations and the other psychotic symptoms commonly diagnosed as schizophrenia.
This has led to the assumption that the small increased risk of psychosis reliably associated with cannabis use is due to the drug increasing dopamine levels in a deep brain structure called the striatum.
In itself, this is partly based on another assumption - the virtual mantra of recreational drug research that ‘all drugs of abuse increase dopamine levels in the reward system’ of which the striatum is a part.
This new study, led by neuroscientist Paul Stokes, tested dopamine levels by using a type of PET brain scan where participants are injected with a radioactive tracer that binds to free dopamine receptors. Higher dopamine levels will mean that there are less free dopamine receptors and, therefore, lower tracer levels.
Mind Hacks: The straight dopamine theory could be up in smoke
There is now growing evidence that cannabis use causes a small but reliable increase in the chance of developing psychosis. Traditionally, this was explained by the drug increasing dopamine levels in the brain but a new study shortly to be published in NeuroImage suggests that the active ingredient in cannabis doesn’t effect this important neurotransmitter.
Despite some dissenting voices, disruption to the mesolimbic dopamine pathway is widely thought to be the key problem in the development of delusions, hallucinations and the other psychotic symptoms commonly diagnosed as schizophrenia.
This has led to the assumption that the small increased risk of psychosis reliably associated with cannabis use is due to the drug increasing dopamine levels in a deep brain structure called the striatum.
In itself, this is partly based on another assumption - the virtual mantra of recreational drug research that ‘all drugs of abuse increase dopamine levels in the reward system’ of which the striatum is a part.
This new study, led by neuroscientist Paul Stokes, tested dopamine levels by using a type of PET brain scan where participants are injected with a radioactive tracer that binds to free dopamine receptors. Higher dopamine levels will mean that there are less free dopamine receptors and, therefore, lower tracer levels.
Mind Hacks: The straight dopamine theory could be up in smoke
Cognitive Training Can Alter Biochemistry Of The Brain
Klint Finley
Follow-up related to the dual n-back test and its use in intelligence amplification:
Researchers at the Swedish medical university Karolinska Institutet have shown for the first time that the active training of the working memory brings about visible changes in the number of dopamine receptors in the human brain. The study, which is published in the journal Science, was conducted with the help of PET scanning and provides deeper insight into the complex interplay between cognition and the brain’s biological structure. [...]
Professor Klingberg and his colleagues have previously shown that the working memory can be improved with a few weeks’ intensive training. Through a collaborative project conducted under the Stockholm Brain Institute, the researchers have now taken a step further and monitored the brain using Positron Emission Tomography (PET scans), and have confirmed that intensive brain training leads to a change in the number of dopamine D1 receptors in the cortex.
Science Daily: Cognitive Training Can Alter Biochemistry Of The Brain
Previously: Increase your intelligence with 20mins a day brain excerise
Follow-up related to the dual n-back test and its use in intelligence amplification:
Researchers at the Swedish medical university Karolinska Institutet have shown for the first time that the active training of the working memory brings about visible changes in the number of dopamine receptors in the human brain. The study, which is published in the journal Science, was conducted with the help of PET scanning and provides deeper insight into the complex interplay between cognition and the brain’s biological structure. [...]
Professor Klingberg and his colleagues have previously shown that the working memory can be improved with a few weeks’ intensive training. Through a collaborative project conducted under the Stockholm Brain Institute, the researchers have now taken a step further and monitored the brain using Positron Emission Tomography (PET scans), and have confirmed that intensive brain training leads to a change in the number of dopamine D1 receptors in the cortex.
Science Daily: Cognitive Training Can Alter Biochemistry Of The Brain
Previously: Increase your intelligence with 20mins a day brain excerise
HOW DRUGS AFFECT NEUROTRANSMITTERS
Dopamine appeared very early in the course of evolution and is involved in many functions that are essential for survival of the organism, such as motricity, attentiveness, motivation, learning, and memorization. But most of all, dopamine is a key element in identifying natural rewards for the organism. These natural stimuli such as food and water cause individuals to engage in approach behaviours. Dopamine is also involved in unconscious memorization of signs associated with these rewards.
It has now been established that all substances that trigger dependencies in human beings increase the release of a neuromediator, dopamine, in a specific area of the brain: the nucleus accumbens. Lien: Neurobiology of addiction and implications for treatment
But not all drugs increase dopamine levels in the brain in the same way.
* Some substances imitate natural neuromediators and take their place on their receptors. Morphine, for example, binds to the receptors for endorphin (a natural "morphine" produced by the brain), while nicotine binds to the receptors for acetylcholine.
* Other substances increase the secretion of natural neuromediators. Cocaine, for example, mainly increases the amount of dopamine in the synapses, while ecstasy mainly increases the amount of serotonin.
* Still other substances block a natural neuromediator. Alcohol, for example, blocks the NMDA receptors.
Click on the names of each of the following drugs to read about how they work and what effects they have.
Alcohol ----- Opiates (heroin, morphine, etc.) ----- Cocaine ----- Nicotine
Caffeine ----- Amphetamines ----- Cannabis ----- Ecstasy ----- Benzodiazepines
Alcohol
Alcohol passes directly from the digestive tract into the blood vessels. In minutes, the blood transports the alcohol to all parts of the body, including the brain.
Alcohol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate.
Click on the labels in the diagram to the right to see an animation about how alcohol affects a GABA synapse. GABA’s effect is to reduce neural activity by allowing chloride ions to enter the post-synaptic neuron. These ions have a negative electrical charge, which helps to make the neuron less excitable. This physiological effect is amplified when alcohol binds to the GABA receptor, probably because it enables the ion channel to stay open longer and thus let more Cl- ions into the cell.
The neuron’s activity would thus be further diminished, thus explaining the sedative effect of alcohol. This effect is accentuated because alcohol also reduces glutamate’s excitatory effect on NMDA receptors.
However, chronic consumption of alcohol gradually makes the NMDA receptors hypersensitive to glutamate while desensitizing the GABAergic receptors. It is this sort of adaptation that would cause the state of excitation characteristic of alcohol withdrawal.
Alcohol also helps to increase the release of dopamine, by a process that is still poorly understood but that appears to involve curtailing the activity of the enzyme that breaks dopamine down.
Cannabis
The sensations of slight euphoria, relaxation, and amplified auditory and visual perceptions produced by marijuana are due almost entirely to its effect on the cannabinoid receptors in the brain. These receptors are present almost everywhere in the brain, and an endogenous molecule that binds to them naturally has been identified: anandamide. We are thus dealing with the same kind of mechanism as in the case of opiates that bind directly to the receptors for endorphins, the body’s natural morphines.
Anandamide is involved in regulating mood, memory, appetite, pain, cognition, and emotions. When cannabis is introduced into the body, its active ingredient, Delta-9-tetrahydrocannabinol (THC), can therefore interfere with all of these functions.
THC begins this process by binding to the CB1 receptors for anandamide. These receptors then modify the activity of several intracellular enzymes, including cAMP, whose activity they reduce. Less cAMP means less protein kinase A. The reduced activity of this enzyme affects the potassium and calcium channels so as to reduce the amount of neurotransmitters released. The general excitability of the brain’s neural networks is thus reduced as well.
However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons.
In chronic consumers of cannabis, the loss of CB1 receptors in the brain’s arteries reduces the flow of blood, and hence of glucose and oxygen, to the brain. The main results are attention deficits, memory loss, and impaired learning ability.
It has now been established that all substances that trigger dependencies in human beings increase the release of a neuromediator, dopamine, in a specific area of the brain: the nucleus accumbens. Lien: Neurobiology of addiction and implications for treatment
But not all drugs increase dopamine levels in the brain in the same way.
* Some substances imitate natural neuromediators and take their place on their receptors. Morphine, for example, binds to the receptors for endorphin (a natural "morphine" produced by the brain), while nicotine binds to the receptors for acetylcholine.
* Other substances increase the secretion of natural neuromediators. Cocaine, for example, mainly increases the amount of dopamine in the synapses, while ecstasy mainly increases the amount of serotonin.
* Still other substances block a natural neuromediator. Alcohol, for example, blocks the NMDA receptors.
Click on the names of each of the following drugs to read about how they work and what effects they have.
Alcohol ----- Opiates (heroin, morphine, etc.) ----- Cocaine ----- Nicotine
Caffeine ----- Amphetamines ----- Cannabis ----- Ecstasy ----- Benzodiazepines
Alcohol
Alcohol passes directly from the digestive tract into the blood vessels. In minutes, the blood transports the alcohol to all parts of the body, including the brain.
Alcohol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate.
Click on the labels in the diagram to the right to see an animation about how alcohol affects a GABA synapse. GABA’s effect is to reduce neural activity by allowing chloride ions to enter the post-synaptic neuron. These ions have a negative electrical charge, which helps to make the neuron less excitable. This physiological effect is amplified when alcohol binds to the GABA receptor, probably because it enables the ion channel to stay open longer and thus let more Cl- ions into the cell.
The neuron’s activity would thus be further diminished, thus explaining the sedative effect of alcohol. This effect is accentuated because alcohol also reduces glutamate’s excitatory effect on NMDA receptors.
However, chronic consumption of alcohol gradually makes the NMDA receptors hypersensitive to glutamate while desensitizing the GABAergic receptors. It is this sort of adaptation that would cause the state of excitation characteristic of alcohol withdrawal.
Alcohol also helps to increase the release of dopamine, by a process that is still poorly understood but that appears to involve curtailing the activity of the enzyme that breaks dopamine down.
Cannabis
The sensations of slight euphoria, relaxation, and amplified auditory and visual perceptions produced by marijuana are due almost entirely to its effect on the cannabinoid receptors in the brain. These receptors are present almost everywhere in the brain, and an endogenous molecule that binds to them naturally has been identified: anandamide. We are thus dealing with the same kind of mechanism as in the case of opiates that bind directly to the receptors for endorphins, the body’s natural morphines.
Anandamide is involved in regulating mood, memory, appetite, pain, cognition, and emotions. When cannabis is introduced into the body, its active ingredient, Delta-9-tetrahydrocannabinol (THC), can therefore interfere with all of these functions.
THC begins this process by binding to the CB1 receptors for anandamide. These receptors then modify the activity of several intracellular enzymes, including cAMP, whose activity they reduce. Less cAMP means less protein kinase A. The reduced activity of this enzyme affects the potassium and calcium channels so as to reduce the amount of neurotransmitters released. The general excitability of the brain’s neural networks is thus reduced as well.
However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons.
In chronic consumers of cannabis, the loss of CB1 receptors in the brain’s arteries reduces the flow of blood, and hence of glucose and oxygen, to the brain. The main results are attention deficits, memory loss, and impaired learning ability.
Subscribe to:
Posts (Atom)