Canadense

Reductions in circulating endocannabinoid levels in individuals with post-traumatic stress disorder following exposure to the world trade center attacks. Hill MN , Bierer LM , Makotkine I , Golier JA , Galea S , McEwen BS , Hillard CJ , Yehuda R . Source The Hotchkiss Brain Institute, Department of Cell Biology & Anatomy and Psychiatry, University of Calgary, Calgary, AB, Canada; Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY, USA. Electronic address: mnhill@ucalgary.ca. Abstract Endocannabinoid (eCB) signaling has been identified as a modulator of adaptation to stress, and is integral to basal and stress-induced glucocorticoid regulation. Furthermore, interactions between eCBs and glucocorticoids have been shown to be necessary for the regulation of emotional memories, suggesting that eCB function may relate to the development of post-traumatic stress disorder (PTSD). To examine this, plasma eCBs were measured in a sample (n=46) drawn from a population-based cohort selected for physical proximity to the World Trade Center (WTC) at the time of the 9/11 attacks. Participants received a structured diagnostic interview and were grouped according to whether they met diagnostic criteria for PTSD (no PTSD, n=22; lifetime diagnosis of PTSD=24). eCB content (2-arachidonoylglycerol (2-AG) and anandamide (AEA)) and cortisol were measured from 8 a.m. plasma samples. Circulating 2-AG content was significantly reduced among individuals meeting diagnostic criteria for PTSD. The effect of reduced 2-AG content in PTSD remained significant after controlling for the stress of exposure to the WTC collapse, gender, depression and alcohol abuse. There were no significant group differences for AEA or cortisol levels; however, across the whole sample AEA levels positively correlated with circulating cortisol, and AEA levels exhibited a negative relationship with the degree of intrusive symptoms within the PTSD sample. This report shows that PTSD is associated with a reduction in circulating levels of the eCB 2-AG. Given the role of 2-AG in the regulation of the stress response, these data support the hypothesis that deficient eCB signaling may be a component of the glucocorticoid dysregulation associated with PTSD. The negative association between AEA levels and intrusive symptoms is consistent with animal data indicating that reductions in AEA promote retention of aversive emotional memories. Future work will aim to replicate these findings and extend their relevance to clinical pathophysiology, as well as to neuroendocrine and molecular markers of PTSD. Copyright © 2013 Elsevier Ltd. All rights reserved. KEYWORDS: 2-Arachidonoylglycerol, Anandamide, Anxiety, Cortisol, Endocannabinoid, HPA axis, N-arachidonylethanolamine, PTSD, Stress, Trauma PMID: 24035186 [PubMed - as supplied by publisher] http://www.ncbi.nlm.nih.gov/pubmed/24035186

nao e de maconha.

.... compra um assim

FILTRO DE CARBONO... por mim esse topico deveria ta fechado.... um monte de "curas caseiras" que mal funcionam.... filtro de carbono e um fan inline e 100%... o resto, e resto...

http://www.nytimes.com/2013/09/17/science/the-rational-choices-of-crack-addicts.html?ref=science&_r=3&pagewanted=all& The Rational Choices of Crack Addicts Long before he brought people into his laboratory at Columbia University to smoke crack cocaine, Carl Hart saw its effects firsthand. Growing up in poverty, he watched relatives become crack addicts, living in squalor and stealing from their mothers. Childhood friends ended up in prisons and morgues. Those addicts seemed enslaved by crack, like the laboratory rats that couldn’t stop pressing the lever for cocaine even as they were starving to death. The cocaine was providing such powerful dopamine stimulation to the brain’s reward center that the addicts couldn’t resist taking another hit. At least, that was how it looked to Dr. Hart when he started his research career in the 1990s. Like other scientists, he hoped to find a neurological cure to addiction, some mechanism for blocking that dopamine activity in the brain so that people wouldn’t succumb to the otherwise irresistible craving for cocaine, heroin and other powerfully addictive drugs. But then, when he began studying addicts, he saw that drugs weren’t so irresistible after all. “Eighty to 90 percent of people who use crack and methamphetamine don’t get addicted,” said Dr. Hart, an associate professor of psychology. “And the small number who do become addicted are nothing like the popular caricatures.” Dr. Hart recruited addicts by advertising in The Village Voice, offering them a chance to make $950 while smoking crack made from pharmaceutical-grade cocaine. Most of the respondents, like the addicts he knew growing up in Miami, were black men from low-income neighborhoods. To participate, they had to live in a hospital ward for several weeks during the experiment. At the start of each day, as researchers watched behind a one-way mirror, a nurse would place a certain amount of crack in a pipe — the dose varied daily — and light it. While smoking, the participant was blindfolded so he couldn’t see the size of that day’s dose. Then, after that sample of crack to start the day, each participant would be offered more opportunities during the day to smoke the same dose of crack. But each time the offer was made, the participants could also opt for a different reward that they could collect when they eventually left the hospital. Sometimes the reward was $5 in cash, and sometimes it was a $5 voucher for merchandise at a store. When the dose of crack was fairly high, the subject would typically choose to keep smoking crack during the day. But when the dose was smaller, he was more likely to pass it up for the $5 in cash or voucher. “They didn’t fit the caricature of the drug addict who can’t stop once he gets a taste,” Dr. Hart said. “When they were given an alternative to crack, they made rational economic decisions.” When methamphetamine replaced crack as the great drug scourge in the United States, Dr. Hart brought meth addicts into his laboratory for similar experiments — and the results showed similarly rational decisions. He also found that when he raised the alternative reward to $20, every single addict, of meth and crack alike, chose the cash. They knew they wouldn’t receive it until the experiment ended weeks later, but they were still willing to pass up an immediate high. These findings made Dr. Hart rethink what he’d seen growing up, as he relates in his new book, “High Price.” It’s a fascinating combination of memoir and social science: wrenching scenes of deprivation and violence accompanied by calm analysis of historical data and laboratory results. He tells horrifying stories — his mother attacked with a hammer, his father doused with a potful of boiling syrup — but then he looks for the statistically significant trend. Yes, he notes, some children were abandoned by crack-addicted parents, but many families in his neighborhood were torn apart before crack — including his own. (He was raised largely by his grandmother.) Yes, his cousins became destitute crack addicts living in a shed, but they’d dropped out of school and had been unemployed long before crack came along. “There seemed to be at least as many — if not more — cases in which illicit drugs played little or no role than were there situations in which their pharmacological effects seemed to matter,” writes Dr. Hart, now 46. Crack and meth may be especially troublesome in some poor neighborhoods and rural areas, but not because the drugs themselves are so potent. “If you’re living in a poor neighborhood deprived of options, there’s a certain rationality to keep taking a drug that will give you some temporary pleasure,” Dr. Hart said in an interview, arguing that the caricature of enslaved crack addicts comes from a misinterpretation of the famous rat experiments. “The key factor is the environment, whether you’re talking about humans or rats,” Dr. Hart said. “The rats that keep pressing the lever for cocaine are the ones who are stressed out because they’ve been raised in solitary conditions and have no other options. But when you enrich their environment, and give them access to sweets and let them play with other rats, they stop pressing the lever.” Drug warriors may be skeptical of his work, but some other scientists are impressed. “Carl’s overall argument is persuasive and driven by the data,” said Craig R. Rush, a psychologist at the University of Kentucky who studies stimulant abuse. “He’s not saying that drug abuse isn’t harmful, but he’s showing that drugs don’t turn people into lunatics. They can stop using drugs when provided with alternative reinforcers.” A similar assessment comes from Dr. David Nutt, a British expert on drug abuse. “I have a great deal of sympathy with Carl’s views,” said Dr. Nutt, a professor of neuropsychopharmacology at Imperial College London. “Addiction always has a social element, and this is magnified in societies with little in the way of work or other ays to find fulfillment.” So why do we keep focusing so much on specific drugs? One reason is convenience: It’s much simpler for politicians and journalists to focus on the evils of a drug than to grapple with the underlying social problems. But Dr. Hart also puts some of the blame on scientists. “Eighty to 90 percent of people are not negatively affected by drugs, but in the scientific literature nearly 100 percent of the reports are negative,” Dr. Hart said. “There’s a skewed focus on pathology. We scientists know that we get more money if we keep telling Congress that we’re solving this terrible problem. We’ve played a less than honorable role in the war on drugs.”

Sei que e a tua opiniao, mas na minha opiniao, VC e um ignorante total quando referente ao assunto cannabis estude mais, faz mais, fale menos...

Eu num tomo cafe com acucar mas a patroa sim, entao compramo aucar de coco... de côco

esses msm

pior IMO sao os nectares... que tem a msm quantidade de acucar e povo acha que faz bem... EDIT: falando como um ex obeso, ta explicado pq foi facinho parar heroina... agora o açucar mermao, essa é uma batalha constante. Nem diaria, é coisa de minuto. Tem um dairy queen na esquina de casa... o vicio

http://www.telegraph.co.uk/news/worldnews/europe/netherlands/10314705/Sugar-is-addictive-and-the-most-dangerous-drug-of-the-times.html Sugar is 'addictive and the most dangerous drug of the times' Soft drinks should carry tobacco-style warnings that sugar is highly addictive and dangerous, a senior Dutch health official has warned. Paul van der Velpen, the head of Amsterdam's health service, the Dutch capital city where the sale of cannabis is legalised, wants to see sugar tightly regulated. "Just like alcohol and tobacco, sugar is actually a drug. There is an important role for government. The use of sugar should be discouraged. And users should be made aware of the dangers," he wrote on an official public health website. "This may seem exaggerated and far-fetched, but sugar is the most dangerous drug of the times and can still be easily acquired everywhere." Mr Van der Velpen cites research claiming that sugar, unlike fat or other foods, interferes with the body's appetite creating an insatiable desire to carry on eating, an effect he accuses the food industry of using to increase consumption of their products. "Sugar upsets that mechanism. Whoever uses sugar wants more and more, even when they are no longer hungry. Give someone eggs and he'll stop eating at any given time. Give him cookies and he eats on even though his stomach is painful," he argued. "Sugar is actually a form of addiction. It's just as hard to get rid of the urge for sweet foods as of smoking. Thereby diets only work temporarily. Addiction therapy is better." The senior health official wants to see sugar taxes and legal limits set on the amount that can added to processed food. He also wants cigarette-style warnings on sweets and soft drinks telling consumers that "sugar is addictive and bad for the health". "Health insurers should have to finance addiction therapy for their obese clients. Schools would no longer be allowed to sell sweets and soft drinks. Producers of sports drinks that are bursting with sugar should be sued over misleading advertising and so on," he said. The number of obese people in the Netherlands has doubled over the last two decades meaning that more than half of Dutch adults and one in seven children are overweight in a country famed for its deep fried croquettes. Obesity hit the headlines in July when police arrested three people from the town of Alkmaar for abusing Shetland ponies by filming them while they ridden by obese women clad in erotic clothing and wielding whips.

Medical Marijuana: Will Colorado's "green rush" last? http://www.cbsnews.com/video/watch/?id=50133577n http://cnettv.cnet.com/av/video/cbsnews/atlantis2/cbsnews_player_embed.swf

GARDAI are hunting a dopey drugs gang after discovering a botched cannabis growing operation with no drugs. Detectives were delighted when 150 plants were found hidden in two grow houses at the rear of a home in rural Co Donegal. Officers found the blooming plants up a lane near the village of Kilmacrennan. But those behind the operation hadn't done their homework. All the plants were male. Male plants are usually dumped early into the cultivation process because they don't contain any of the chemicals which give the user the 'high'. It now means gardai have had to downgrade the value of the seizure from €120,000 – to nothing. "There wasn't enough cannabis leaf for a single joint," one source revealed. Some of the plants may have taken up to a year to grow. Gardai seized various equipment including heat lamps, gardening tools and boxes of the fertiliser MiracleGro. It's understood gardai have interviewed one man and wish to talk to at least three others. A file will be sent to the Director of Public Prosecutions (DPP) recommending prosecution for the attempted cultivation of cannabis. However, those behind the operation may have spared themselves some time behind bars. Anyone found with €120,000 of cannabis can expect to get seven years in prison. "It won't spare any blushes, but it will spare them some jail time," said a legal source. http://www.independent.ie/irish-news/dopey-gang-spent-months-growing-cannabis-but-used-wrong-plant-29573180.html

entao, pelo que eu tou vendo acho que esse medicamento e uma composto, pq o idebenone e CoQ10.... so que que num vira auto-oxidante. Tem que ver msm com a fonte.

Valeu!!! http://medicalmarijuana.com/medical-marijuana-treatments/Friedreich-s-Ataxia Friedreich's Ataxia--Medical Marijuana for Symptom Relief Published by Jan Friedreich’s Ataxia Friedreich's ataxia is an inherited disease that causes progressive damage to the nervous system, resulting in symptoms ranging from gait disturbance to speech problems; it can also lead to heart disease and diabetes. The ataxia of Friedreich's ataxia results from the degeneration of nerve tissue in the spinal cord, in particular sensory neurons essential (through connections with the cerebellum) for directing muscle movement of the arms and legs. Friedreich's ataxia (also called FA or FRDA) is a rare inherited disease that causes nervous system damage and movement problems. It usually begins in childhood and leads to impaired muscle coordination (ataxia) that worsens over time. The disorder is named after Nicholaus Friedreich, a German doctor who first described the condition in the 1860s. In Friedreich’s ataxia the spinal cord and peripheral nerves degenerate, becoming thinner. The cerebellum, part of the brain that coordinates balance and movement, also degenerates to a lesser extent. This damage results in awkward, unsteady movements and impaired sensory functions. The disorder also causes problems in the heart and spine, and some people with the condition develop diabetes. The disorder does not affect thinking and reasoning abilities (cognitive functions). Friedreich’s ataxia is caused by a defect (mutation) in a gene labeled FXN. The disorder is recessive, meaning it occurs only in someone who inherits two defective copies of the gene, one from each parent. Although rare, Friedreich’s ataxia is the most common form of hereditary ataxia, affecting about one in every 50,000 people in the United States. Both male and female children can inherit the disorder The spinal cord becomes thinner and nerve cells lose some of their myelin sheath (the insulating covering on some nerve cells that helps conduct nerve impulses). Studies have revealed that frataxin is an important mitochondrial protein for proper function of several organs. Yet in people with the disease, the amount of frataxin in affected cells is severely reduced. It is believed that the loss of frataxin makes the nervous system, heart, and pancreas particularly susceptible to damage from free radicals (produced when the excess iron reacts with oxygen). Once certain cells in these tissues are destroyed by free radicals, they cannot be replaced. Nerve and muscle cells also have metabolic needs that may make them particularly vulnerable to this damage. Free radicals have been implicated in other degenerative diseases such as Parkinson's and Alzheimer's diseases. Symptoms Symptoms are caused by the wearing away of structures in areas of the brain and spinal cord that control coordination, muscle movement, and some sensory functions. Symptoms generally begin in childhood before puberty, and may include: • Abnormal speech • Changes in vision, particularly color vision • Decrease in ability to feel vibrations in lower limbs • Foot problems, such as hammer toe and high arches • Hearing loss -- occurs in about 10% of patients • Jerky eye movements • Loss of coordination and balance, which leads to frequent falls • Muscle weakness • No reflexes in the legs • Unsteady gait and uncoordinated movements (ataxia) -- gets worse with time Muscle problems lead to changes in the spine, which may result in scoliosis or hyphoscoliosis. Heart disease usually develops and may lead to heart failure. Death may result from heart failure or dysrhythmias that do not respond to treatment. Diabetes may develop in later stages of the disease What are the signs and symptoms? Symptoms typically begin between the ages of 5 and 15 years, although they sometimes appear in adulthood and on rare occasions as late as age 75. The first symptom to appear is usually gait ataxia, or difficulty walking. The ataxia gradually worsens and slowly spreads to the arms and the trunk. There is often loss of sensation in the extremities, which may spread to other parts of the body. Other features include loss of tendon reflexes, especially in the knees and ankles. Most people with Friedreich's ataxia develop scoliosis (a curving of the spine to one side), which often requires surgical intervention for treatment. Dysarthria (slowness and slurring of speech) develops and can get progressively worse. Many individuals with later stages of Friedreich’s ataxia develop hearing and vision loss. Other symptoms that may occur include chest pain, shortness of breath, and heart palpitations. These symptoms are the result of various forms of heart disease that often accompany Friedreich's ataxia, such as hypertrophic cardiomyopathy (enlargement of the heart), myocardial fibrosis (formation of fiber-like material in the muscles of the heart), and cardiac failure. Heart rhythm abnormalities such as tachycardia (fast heart rate) and heart block (impaired conduction of cardiac impulses within the heart) are also common. About 20 percent of people with Friedreich's ataxia develop carbohydrate intolerance and 10 percent develop diabetes. Most individuals with Friedreich’s ataxia tire very easily and find that they require more rest and take a longer time to recover from common illnesses such as colds and flu. The rate of progression varies from person to person. Generally, within 10 to 20 years after the appearance of the first symptoms, the person is confined to a wheelchair, and in later stages of the disease, individuals may become completely incapacitated. Friedreich's ataxia can shorten life expectancy, and heart disease is the most common cause of death. However, some people with less severe features of Friedreich's ataxia live into their sixties, seventies, or older. The triplet repeat expansion greatly disrupts the normal production of frataxin. Frataxin is found in the energy-producing parts of the cell called mitochondria. Research suggests that without a normal level of frataxin, certain cells in the body (especially peripheral nerve, spinal cord, brain and heart muscle cells) cannot effectively produce energy and have been hypothesized to have a buildup of toxic byproducts leading to what is called “oxidative stress.” It also may lead to increased levels of iron in the mitochondria. When the excess iron reacts with oxygen, free radicals can be produced. Although free radicals are essential molecules in the body's metabolism, they can also destroy cells and harm the body. Based upon this information, scientists and physicians have tried to reduce the levels of free radicals, also called oxidants, using treatment with “antioxidants”. Initial clinical studies in Europe suggested that antioxidants like coenzyme Q10, vitamin E, and idebenone might offer individuals some limited benefit. However, recent clinical trials in the United States and Europe have not revealed effectiveness of idebenone in people with Friedreich’s ataxia, but more powerful modified forms of this agent and other antioxidants are in trials at this time. There is also a clinical trial to examine the efficacy of selectively removing excess iron from the mitochondria. Scientists also are exploring ways to increase frataxin levels through drug treatments, genetic engineering and protein delivery systems. Several compounds that are directed at increasing levels of frataxin may be brought to clinical trials in the near future. As with many degenerative diseases of the nervous system, there is currently no cure or effective treatment for Friedreich's ataxia. However, many of the symptoms and accompanying complications can be treated to help individuals maintain optimal functioning as long as possible. Doctors can prescribe treatments for diabetes, if present; some of the heart problems can be treated with medication as well. Orthopedic problems such as foot deformities and scoliosis can be corrected with braces or surgery. Physical therapy may prolong use of the arms and legs. Advances in understanding the genetics of Friedreich's ataxia are leading to breakthroughs in treatment. Research has moved forward to the point where clinical trials of proposed treatments are presently occurring for Friedreich’s ataxia. Complications • Diabetes • Heart failure or heart disease • Loss of ability to move around Low intensity strengthening exercises should also be incorporated to maintain functional use of the upper and lower extremities. Stretching exercises can be prescribed to help relieve tight musculature due to scoliosis and pes cavus deformity (hollow foot)-deformity of foot where instep is very high. Surgery because of difficulty is only done if there is severe pain. A person suffering from Friedreich's Ataxia may require some surgical interventions (mainly for the spine and heart). Friedreich's ataxia slowly gets worse and causes problems performing everyday activities. Most patients need to use a wheelchair within 15 years of the disease's start. The disease may lead to early death. Currently, there is a medication approved in Canada called idebenone. This prescription medicine is also under regulatory review in Europe and Switzerland. In both the United States and in Europe there are two Phase III clinical trials on going with idebenone. As of 2009, Persons with Friedreich’s ataxia may also benefit from a conservative treatment approach for the management of symptoms How Can Medical Marijuana Help? Cannabinoids act as antioxidants to reduce free radical levels. Cannabinoids are pain relievers. Suppress transmission of pain signals in the brain. Marijuana has a neurochemical effect on pain. Cannabinoids relieve “jerky eye movements” Cannabinoids relax tight muscles (spine) Cannabinoids help relieve depression. Cannabinoids help relieve muscle spasms and leg cramps Cannabinoids help relieve stress So far, there is no effective treatment ( except medical marijuana for symptom relief) and there is no cure for Friedreich’s ataxia. Researchers around the world are getting closer to finding the answers. Best Strain: Sweet Cheese References: 1. Johnston MV. Movement disorders. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson Textbook of Pediatrics. 18th ed. Philadelphia, Pa: Saunders Elsevier, 2007: chap 597. 2^ The Friedreich ataxia AAG triplet repeat: permutation and normal alleles L Montermini, E Andermann, M Labuda, A Richter, M Pandolfo, F Cavalcanti, L Pianese, L Iodice, G Farina, A Monticelli, M Turano, A Filla, G De Michele and S Cocozza. Human Molecular Genetics, Vol. 6, 1261-1266 3^ http://emedicine.medscape.com/article/1150420-overview 4^ Delatycki M, Williamson R, Forrest S (2000). "Friedreich ataxia: an overview". J Med Genet 37 (1): 1–8 As. doi: 10.1136/jmg.37.1.1.PMC 1734457. PMID 10633128. 5^ http://www.clinicaltrials.gov/ct2/results?term=idebenone+friedreich%27s+idebenone 6^ Boesch S, Sturm B, Hering S, Goldenberg H, Poewe W, Scheiber-Mojdehkar B (November 2007). "Friedreich's ataxia: clinical pilot trial with recombinant human erythropoietin". Ann. Neurol. 62 (5): 521–4. doi: 10.1002/ana.21177. PMID 17702040. 7^ Boesch S, Sturm B, Hering S, et al (October 2008). "Neurological effects of recombinant human erythropoietin in Friedreich's ataxia: a clinical pilot trial". Mov. Disord. 23 (13): 1940–. doi: 10.1002/mds.22294. PMID 18759345. 8^ a b c d e Powers, Wendy (2007-01-01). "Holding Steady: How physical therapy can help patients with Friedreich's Ataxia". Advance 18 (1): 26. Retrieved 2011-05-16. 9^ a b "Facts About Friedreich's Ataxia (FA)". Muscular Dystrophy Association. 2011. Archived on 2011-05-16. Error: If you specify|archivedate=, you must also specify |archiveurl=. Retrieved 2011-05-16. 10^ Lodi R, Tonon C, Calabrese V, Schapira AH (2006). "Friedreich's ataxia: from disease mechanisms to therapeutic interventions". Antioxid. Redox Signal. 8 (3-4): 438–43. doi: 10.1089/ars.2006.8.438. PMID 16677089. 11^ Barbeau A, Sadibelouiz M, Roy M, Lemieux B, Bouchard JP, Geoffroy G (1984). "Origin of Friedreich's disease in Quebec". The Canadian journal of neurological sciences. Le journal Canadian des sciences neurologiques 11 (4 Suppl): 506–9. PMID 6391645. 12^ Friedreich N (1863). "Ueber degenerative Atrophie der spinalen Hinterstränge". Arch Pathol Anat Phys Klin Med 26 (3–4): 391–419.doi: 10.1007/BF01930976. 13^ Friedreich N (1863). "Ueber degenerative Atrophie der spinalen Hinterstränge". Arch Pathol Anat Phys Klin Med 26 (5–6): 433–459.doi: 10.1007/BF01878006. 14^ Friedreich N (1863). "Ueber degenerative Atrophie der spinalen Hinterstränge". Arch Pathol Anat Phys Klin Med 27 (1-2): 1–26.doi: 10.1007/BF01938516. 15^ Friedreich N (1876). "Ueber Ataxie mit besonderer Berücksichtigung der hereditären Formen" (PDF). Arch Pathol Anat Phys Klin Med 68 (2): 145–245. doi: 10.1007/BF01879049.

li e reli todas as materias, onde fala o nome do remedio? so se a dyslexia hj ta muito braba e num tou vendo

e agora? como procede?

SEM FLAGRANTE NAO HA TRAFICANTE!!

descriminalizacao nao! LEGALIZACAO.... num faremos pela metade pls....

porra, na boa... amador msm... deixar bagulho junto... porra, isso e aula; 101.... iniciante.

Num seja por isso... O tio ainda tem seus 15 anos de vida, vai, 10 de utilidade..... Utilidade na vida de lavoura digo, obvio... EDIT: Todos que me conhecem sabem que eu adoro velhinhos, criança e que eu num sou muito aliado

O pior que isso vai pra ficha do caboclo forévis bom, se vc acha que ser normal de 70 anos tem melhores reflexos e visao de que alguem com 16, entao boa sorte pro senhor... O resto é só aprender

coitado, tao fazendo a msm coisa que fizeram com o Marl Emery

tinha que ter limite de carteira, proibido para maiores de 70 anos. porra, eu confio bem mais num moleque de 16 guiando do que um velho com 70

eu fazia direto o pren, mas agora melhor fazer oleo e depois taco no leite... EDIT: pra falar verdade, eu faço oleo e ponho em capsulas de gelatina. ae, uma ou duas capsulas tou passando bem.