Wiet gebruik tijdens bodybuilding

MeDieViL · 1 dec 2010

Cancer Res. 2005 Mar 1;65(5):1635-41.
Cannabinoid receptor as a novel target for the treatment of prostate cancer.
Sarfaraz S, Afaq F, Adhami VM, Mukhtar H.

Department of Dermatology, University of Wisconsin, Madison, Wisconsin 53706, USA.
Abstract
Cannabinoids, the active components of Cannabis sativa Linnaeus (marijuana) and their derivatives have received renewed interest in recent years due to their diverse pharmacologic activities such as cell growth inhibition, anti-inflammatory effects and tumor regression. Here we show that expression levels of both cannabinoid receptors, CB1 and CB2, are significantly higher in CA-human papillomavirus-10 (virally transformed cells derived from adenocarcinoma of human prostate tissue), and other human prostate cells LNCaP, DUI45, PC3, and CWR22Rnu1 than in human prostate epithelial and PZ-HPV-7 (virally transformed cells derived from normal human prostate tissue) cells. WIN-55,212-2 (mixed CB1/CB2 agonist) treatment with androgen-responsive LNCaP cells resulted in a dose- (1-10 micromol/L) and time-dependent (24-48 hours) inhibition of cell growth, blocking of CB1 and CB2 receptors by their antagonists SR141716 (CB1) and SR144528 (CB2) significantly prevented this effect. Extending this observation, we found that WIN-55,212-2 treatment with LNCaP resulted in a dose- (1-10 micromol/L) and time-dependent (24-72 hours) induction of apoptosis (a), decrease in protein and mRNA expression of androgen receptor (b), decrease in intracellular protein and mRNA expression of prostate-specific antigen (c), decrease in secreted prostate-specific antigen levels (d), and decrease in protein expression of proliferation cell nuclear antigen and vascular endothelial growth factor (e). Our results suggest that WIN-55,212-2 or other non-habit-forming cannabinoid receptor agonists could be developed as novel therapeutic agents for the treatment of prostate cancer.

In vitro onderzoek, dus mss is er nog hoop

growlikeweed · 1 dec 2010

syntax zei:
wat mij betreft is een vreetkick ideaal voor de bulk

Blowen ontregelt de spijsvertering. Op langere termijn vallen veel blowers alleen maar af en worden mager als een sprietje.

syntax · 1 dec 2010

growlikeweed zei:
Blowen ontregelt de spijsvertering. Op langere termijn vallen veel blowers alleen maar af en worden mager als een sprietje.

hoor ik jou nou net toegeven dat op korte termijn blowen goed voor je is

Anoniem_1985_1 · 1 dec 2010

Dit is dan toch vooral bij dagelijks gebruik? 1 keer in de week lijkt me niet zoveel kwaad kunnen..

MeDieViL · 1 dec 2010

Exp Neurol. 2010 Jul;224(1):15-22. Epub 2010 Mar 29.
Alcohol and endocannabinoids: neuroendocrine interactions in the reproductive axis.
Rettori V, De Laurentiis A, Fernandez-Solari J.

Centro de Estudios Farmacológicos y Botánicos, CEFYBO-CONICET-UBA, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, piso 16, 1121ABG, Buenos Aires, Argentina. vrettori@yahoo.com
Abstract
Marihuana and alcohol consumption affect adversely reproduction by inhibiting the hypothalamic-pituitary-gonadal axis. The endocannabinoid system, present in the central nervous system and in peripheral tissues, participates in the regulation of hormones involved in the reproductive physiology such as luteinizing hormone, prolactin and oxytocin. This system is activated in response to pathophysiological conditions such as stress and inflammatory/infectious states as well as alcoholism and drug consumption acting as a negative modulator of reproductive function. The secretion of luteinizing hormone from the adenohypophysis is reduced, mainly through hypothalamic inhibitory action of cannabinoids and alcohol on luteinizing hormone releasing hormone release from its nervous terminals in the median eminence. This inhibitory effect is mediated, at least in part, by the activation of cannabinoid type 1 receptors. Cannabinoids also inhibit prolactin release from the lactotropes in the adenohypophysis acting locally and by increasing the release of hypothalamic dopamine mainly from tuberoinfundibular dopaminergic neurons in the external layer of the median eminence. On the contrary, ethanol stimulates prolactin release from the adenohypophysis as well as oxytocin from the neurohypophysis. Besides, endocannabinoids modulate oxytocin synthesis and release from the hypothalamic magnocellular neurons and neurohypophysis. In summary, all the results exposed in the present review suggest that there is interplay between the endocannabinoid system, hormones and neuropeptides in the control of reproduction and that this system mediates, at least in part, ethanol adverse effects on reproductive function.

Copyright 2010 Elsevier Inc. All rights reserved.

Exp Neurol. 2010 Jul;224(1):37-47. Epub 2010 Mar 29.
Modulation of the endocannabinoid system: neuroprotection or neurotoxicity?
Fowler CJ, Rojo ML, Rodriguez-Gaztelumendi A.

Department of Pharmacology and Clinical Neuroscience, Umeå University, SE-901 87 Umeå, Sweden. cf@pharm.umu.se
Abstract
There is now a large volume of data indicating that compounds activating cannabinoid CB(1) receptors, either directly or indirectly by preventing the breakdown of endogenous cannabinoids, can protect against neuronal damage produced by a variety of neuronal "insults". Given that such neurodegenerative stimuli result in increased endocannabinoid levels and that animals with genetic deletions of CB(1) receptors are more susceptible to the deleterious effects of such stimuli, a case can be made for an endogenous neuroprotective role of endocannabinoids. However, this is an oversimplification of the current literature, since (a) compounds released together with the endocannabinoids can contribute to the neuroprotective effect; (b) other proteins, such as TASK-1 and PPARalpha, are involved; (c) the CB(1) receptor antagonist/inverse agonist rimonabant has also been reported to have neuroprotective properties in a number of animal models of neurodegenerative disorders. Furthermore, the CB(2) receptor located on peripheral immune cells and activated microglia are potential targets for novel therapies. In terms of the clinical usefulness of targeting the endocannabinoid system for the treatment of neurodegenerative disorders, data are emerging, but important factors to be considered are windows of opportunity (for acute situations such as trauma and ischemia) and the functionality of the target receptors (for chronic neurodegenerative disorders such as Alzheimer's disease).

Expert Opin Ther Targets. 2010 Apr;14(4):387-404.
The endocannabinoid system as a target for the treatment of neuronal damage.
Fernández-Ruiz J, García C, Sagredo O, Gómez-Ruiz M, de Lago E.

Departamento de Bioquímica y Biología Molecular III, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, Facultad de Medicina, Universidad Complutense, Ciudad Universitaria s/n, 28040-Madrid, Spain. jjfr@med.ucm.es
Abstract
IMPORTANCE OF THE FIELD: Cannabinoids have been proposed as clinically promising neuroprotective molecules, based on their capability to normalize glutamate homeostasis, reducing excitotoxicity, to inhibit calcium influx, lowering intracellular levels and the subsequent activation of calcium-dependent destructive pathways, and to reduce the generation of reactive oxygen intermediates or to limit their toxicity, decreasing oxidative injury. Cannabinoids are also able to decrease local inflammatory events by acting on glial processes that regulate neuronal survival, and to restore blood supply by reducing vasocontriction produced by several endothelium-derived factors.

AREAS COVERED IN THIS REVIEW: Current literature supporting these neuroprotective effects, particularly evidence generated during the last ten years, concentrating on targets within the cannabinoid signaling system that facilitate these effects. Acute or chronic neurodegenerative disorders where cannabinoids have shown neuroprotective effect.

WHAT THE READER WILL GAIN: Most of the information reviewed here relates to preclinical studies. However, these molecules may progress from the present preclinical evidence to clinical applications.

TAKE HOME MESSAGE: Treatment of neurodegenerative disorders is a challenge for neuroscientists and neurologists. Unhappily, the efficacy of available medicines is still poor and there is an urgent need for novel neuroprotective agents. Cannabinoids can serve this purpose given their recognized antiexcitotoxic, antioxidant and anti-inflammatory properties.

Neuroimmunomodulation. 2010;17(3):153-6. Epub 2010 Feb 4.
Endocannabinoid system participates in neuroendocrine control of homeostasis.
De Laurentiis A, Fernández Solari J, Mohn C, Zorrilla Zubilete M, Rettori V.

Centro de Estudios Farmacológicos y Botánicos, CEFYBO-CONICET-UBA, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina. andredelaurentiis@yahoo.com
Abstract
The hypothalamo-neurohypophyseal system plays a role in homeostasis under a variety of stress conditions, including endotoxemia. Oxytocin (OXT) and vasopressin (VP) are important hormones synthesized by neurons in the hypothalamic paraventricular and supraoptic nuclei and released into different brain regions and from the neurohypophyseal terminals into the blood in response to many patho-physiological stimuli. However, the mechanism that controls OXT and VP secretion has not been fully elucidated. Nitric oxide (NO) is a known mediator that regulates the release of these hormones. The endocannabinoid system is a new intercellular system that modulates several neuroendocrine actions. Endocannabinoids (eCB) are released as retrograde messengers by many neurons, including hypothalamic magnocellular neurons and cannabinoid receptors are localized within these neurons, as well as in the anterior and posterior pituitary lobes, suggesting an eCB role in the production and release of OXT and VP. Lipopolysaccharide (LPS) injection is a model used as immune challenge. LPS causes a neuroendocrine response that is mediated by cytokines, tumor necrosis factor-alpha being one of them. We focused on NO and endocannabinoid system participation on OXT and VP production and secretion during basal and stress conditions and found that eCB affect basal OXT and VP secretion by acting differently at each level of the hypothalamo-neurohypophyseal system. After LPS, there is an increase in eCB synthesis that enhances OXT secretion.

Prog Neuropsychopharmacol Biol Psychiatry. 2010 Jun 30;34(5):791-7. Epub 2009 Nov 10.
Involvement of the endocannabinoid system in the neurobehavioural effects of stress and glucocorticoids.
Hill MN, McEwen BS.

Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10065, USA. mhill@rockefeller.edu
Abstract
The endocannabinoid system is a neuroactive lipid signaling system that functions to gate synaptic transmitter release. Accumulating evidence has demonstrated that this system is responsive to modulation by both stress and glucocorticoids within the hypothalamus and limbic structures; however, the nature of this regulation is more complex than initially assumed. The aim of the current review is to summarize the research to date which examines the effects of acute stress and glucocorticoid administration on endocannabinoid signaling in limbic-hypothalamic-pituitary-adrenal (LHPA) axis, and in turn the role endocannabinoid signaling plays in the neurobehavioural responses to acute stress and glucocorticoid administration. The majority of research suggests that acute stress produces a mobilization of the endocannabinoid 2-arachidonoylglycerol (2-AG) while concurrently reducing the tissue content of the other endocannabinoid ligand anandamide. Genetic and pharmacological studies demonstrate that the reduction in anandamide signaling may be involved in the initiation of HPA axis activation and the generation of changes in emotional behaviour, while the increase in 2-AG signaling may be involved in terminating the stress response, limiting neuronal activation and contributing to changes in motivated behaviours. Collectively, these studies reveal a complex interplay between endocannabinoids and the HPA axis, and further identify endocannabinoid signaling as a critical regulator of the stress response.

CNS Neurol Disord Drug Targets. 2009 Dec;8(6):432-9.
Cannabinoids and Parkinson's disease.
García-Arencibia M, García C, Fernández-Ruiz J.

Departamento de Bioquímica y Biología Molecular and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Facultad de Medicina, Universidad Complutense, 28040-Madrid, Spain.
Abstract
Cannabinoid-based medicines have been proposed as clinically promising therapies in Parkinson's disease (PD), given the prominent modulatory function played by the cannabinoid signaling system in the basal ganglia. Supporting this pharmacological potential, the cannabinoid signaling system experiences a biphasic pattern of changes during the progression of PD. Thus, early and presymptomatic stages, characterized by neuronal malfunctioning but little evidence of neuronal death, are associated with desensitization/downregulation of CB(1) receptors. It was proposed that these losses may be part of the pathogenesis itself, since they can aggravate different cytotoxic insults which are controlled in part by cannabinoid signals, mainly excitotoxicity but also oxidative stress and glial activation. By contrast, intermediate and, in particular, advanced stages of parkinsonism characterized by a profound nigral degeneration and occurrence of major parkinsonian symptoms (e.g. bradykinesia), are associated with upregulatory responses of CB(1) receptors, possibly CB(2) receptors too, and the endocannabinoid ligands for both receptor types. This would explain the motor inhibition typical of this disease and the potential proposed for CB(1) receptor antagonists in attenuating the bradykinesia typical of PD. In addition, certain cannabinoid agonists have been proposed to serve as neuroprotective molecules in PD, given their well-demonstrated capability to reduce excitotoxicity, calcium influx, glial activation and, in particular, oxidative injury that cooperatively contribute to the degeneration of nigral neurons. However, the potential of cannabinoid-based medicines in PD have been still scarcely studied at the clinical level despite the existence of solid and promising preclinical evidence. Considering the relevance of these preclinical data, the need for finding treatments for motor symptoms that may be alternative to classic dopaminergic replacement therapy, and the lack of efficient neuroprotective strategies in PD, we believe it is of major interest to develop further studies that allow the promising expectations generated for these molecules to progress from the present preclinical evidence towards a real clinical application.

CNS Neurol Disord Drug Targets. 2009 Dec;8(6):440-50.
Cannabinoids and neurodegenerative diseases.
Romero J, Orgado JM.

Laboratorio de Investigación, Hospital Universitario Fundación Alcorcón and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED). C/o Budapest 1. 28922. Alcorcón, Spain. jromerop@fhalcorcon.es
Abstract
Although significant advances have taken place in recent years on our understanding of the molecular mechanisms of different neurodegenerative diseases, its translation into effective therapeutic treatments has not been as successful as could be expected. There is still a dramatic lack of curative treatments for the most frequent disorders and only symptomatic relief for many others. Under this perspective, the search for novel therapeutic approaches is demanding and significant attention and efforts have been directed to studying additional neurotransmission systems including the endocannabinoid system (ECS). The neuroprotective properties of exogenous as well as endogenous cannabinoids have been known for years and the underlying molecular mechanisms have been recently unveiled. As discussed later, antioxidative, antiglutamatergic and antiinflammatory effects are now recognized as derived from cannabinoid action and are known to be of common interest for many neurodegenerative processes. Thus, these characteristics make cannabinoids attractive candidates for the development of novel therapeutic strategies [1]. The present review will focus on the existing data regarding the possible usefulness of cannabinoid agents for the treatment of relevant neurological pathologies for our society such as Alzheimer's disease, multiple sclerosis, Huntington's disease and amyotrophic lateral sclerosis.

Horm Behav. 2010 Jun;58(1):100-10. Epub 2009 Oct 9.
Cannabinoid-hormone interactions in the regulation of motivational processes.
López HH.

Department of Psychology, Neuroscience Program, Skidmore College, 815 N. Broadway, Saratoga Springs, NY 12866, USA. hlopez@skidmore.edu
Abstract
There is a bi-directionality in hormone-cannabinoid interactions: cannabinoids affect prominent endocrine axes (such as the hypothalamic-pituitary-gonadal), and gonadal hormones modulate cannabinoid effects. This review will summarize recent research on these interactions, with a specific focus upon their implications for motivated behavior. Sexual behavior will serve as a "case study." I will explore the hypothesis that ovarian hormones, in particular estradiol, may serve to release estrous behavior from endocannabinoid inhibition. Hormonal regulation of the endogenous cannabinoid system also affects processes that underlie drug abuse. This review will briefly discuss coïtus differences in behavioral responses to cannabinoids and explore potential mechanisms by which gonadal hormones alter cannabinoid reward. An examination of this research informs our perspective on how hormones and endocannabinoids may affect drug-seeking behavior as a whole and the development of addiction.

Gastroenterol Hepatol. 2010 Apr;33(4):323-9. Epub 2009 Sep 16.
[Endogenous cannabinoids in liver disease: Many darts for a single target]
[Article in Spanish]

Reichenbach V, Ros J, Jiménez W.

Servicio de Bioquímica y Genética Molecular, CIBEREHD, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínico, Universitat de Barcelona, Barcelona, España.
Abstract
Endogenous cannabinoids are ubiquitous lipid-signaling molecules able to partially mimic the actions produced by Delta(9)-tetrahydrocannabinol, the compound responsible for most of the psychological effects of marijuana. Endocannabinoids are derived from arachidonic acid and are involved in many physiological effects. This family of substances includes anandamide (arachidonylethanolamide), 2-arachydonylglycerol, noladin ether and virodhamine. The interaction of these substances with CB1 and CB2 receptors results in most of their biological effects. The endocannabinoid system is involved in the pathogenesis of the cardiovascular dysfunction occurring in advanced liver disease and also plays a role in the pathogenesis of portal hypertension and liver fibrosis. Moreover, this system is also altered in other processes associated with hepatic dysfunction, including encephalopathy, obesity and steatosis. These findings indicate that the endocannabinoid system may open new avenues for the therapeutic regulation of fibrosis and portal hypertension in advanced liver disease.

J Opioid Manag. 2009 May-Jun;5(3):153-68.
Medicinal use of cannabis in the United States: historical perspectives, current trends, and future directions.
Aggarwal SK, Carter GT, Sullivan MD, ZumBrunnen C, Morrill R, Mayer JD.

Medical Scientist Training Program, University of Washington, Seattle, WA, USA.
Abstract
Cannabis (marijuana) has been used for medicinal purposes for millennia, said to be first noted by the Chinese in c. 2737 BCE. Medicinal cannabis arrived in the United States much later, burdened with a remarkably checkered, yet colorful, history. Despite early robust use, after the advent of opioids and aspirin, medicinal cannabis use faded. Cannabis was criminalized in the United States in 1937, against the advice of the American Medical Association submitted on record to Congress. The past few decades have seen renewed interest in medicinal cannabis, with the National Institutes of Health, the Institute of Medicine, and the American College of Physicians, all issuing statements of support for further research and development. The recently discovered endocannabinoid system has greatly increased our understanding of the actions of exogenous cannabis. Endocannabinoids appear to control pain, muscle tone, mood state, appetite, and inflammation, among other effects. Cannabis contains more than 100 different cannabinoids and has the capacity for analgesia through neuromodulation in ascending and descending pain pathways, neuroprotection, and anti-inflammatory mechanisms. This article reviews the current and emerging research on the physiological mechanisms of cannabinoids and their applications in managing chronic pain, muscle spasticity, cachexia, and other debilitating problems.

Changes in the endocannabinoid system may give insight into new and effective treatments for cancer.
Alpini G, Demorrow S.

Department of Medicine, Texas A&M Health Science Center, College of Medicine, Temple, Texas, USA.
Abstract
The endocannabinoid system comprises specific cannabinoid receptors such as Cb1 and Cb2, the endogenous ligands (anandamide and 2-arachidonyl glycerol among others) and the proteins responsible for their synthesis and degradation. This system has become the focus of research in recent years because of its potential therapeutic value several disease states. The following review describes our current knowledge of the changes that occur in the endocannabinoid system during carcinogenesis and then focuses on the effects of anandamide on various aspects of the carcinogenic process such as growth, migration, and angiogenesis in tumors from various origins.

(positief effect op kanker ^^).

**** it, wat een focus ik krijg van dexedrine, en normaal ben ik zo'n zwaar ADHD geval.

Kom maar op met die karma :roflol:

---------- Toegevoegd om 12:21 ---------- De post hierboven werd geplaatst om 12:19 ----------

Tante Jans zei:
Dit is dan toch vooral bij dagelijks gebruik? 1 keer in de week lijkt me niet zoveel kwaad kunnen..

Dat kan idd geen kwaad, heel het weekend doorsmoren zal ook wel goed meevallen

growlikeweed · 1 dec 2010

syntax zei:
hoor ik jou nou net toegeven dat op korte termijn blowen goed voor je is

Als dat jou interpretatie is dan zou ik vanavond nog 1 dikke zak wiet van een eurotje of 20 halen, een film erbij pakken, een flinke koelkast vol met bulkvoedsel, jezelf helemaal panja smoken, vreetkick houden, vergeet niet de extra plak spacecake voor een extra "ontspannen" gevoel, lekker gaan slapen en morgenvroeg jou ervaring hier met ons delen

Sinds je een diehard stoner bent op korte termijn maak je vast de gains van je leven

Ik kan niet wachten tot je bevindingen

Retired · 1 dec 2010

skinnie zei:
omdat ik amper op mijn eten let, wat zouden jullie groeien als je door blowen na de training je cortisolaanmaak vermindert

Teveel Cortisol verhoogd je hongergevoel en vetopslag.

MeDieViL · 1 dec 2010

Het gaat hier trouwens vooral wel om rattenonderzoek, en de effecten zullen wss erg miniem zijn op mensen, maar het is goed om hier mee rekening te houden indien je een hoger risico hebt op diabetis ofzo.

Als weed enorm negatieve effecten veroorzaakte dan wisten we dat nu wel al. Maar compleet onschadelijk is het ook niet.

syntax · 1 dec 2010

growlikeweed zei:
Als dat jou interpretatie is dan zou ik vanavond nog 1 dikke zak wiet van een eurotje of 20 halen, een film erbij pakken, een flinke koelkast vol met bulkvoedsel, jezelf helemaal panja smoken, vreetkick houden, vergeet niet de extra plak spacecake voor een extra "ontspannen" gevoel, lekker gaan slapen en morgenvroeg jou ervaring hier met ons delen

Sinds je een diehard stoner bent op korte termijn maak je vast de gains van je leven

Ik kan niet wachten tot je bevindingen

uhu dat kan ik je wel nu vertellen hoor.... want dat was zo ongeveer me vorge weekend

growlikeweed · 1 dec 2010

syntax zei:
uhu dat kan ik je wel nu vertellen hoor.... want dat was zo ongeveer me vorge weekend

Uit mijn ervaringen kan ik je wel vertellen dat ik er niet beter op ben geworden in het verleden

goede ouwe tijd :rolleyes:

syntax · 1 dec 2010

growlikeweed zei:
Uit mijn ervaringen kan ik je wel vertellen dat ik er niet beter op ben geworden in het verleden

goede ouwe tijd

je bent er nix beter op geworden tog was het de GOEDE ouwe tijd

Roth · 1 dec 2010

Die hele negatieve lading die loskomt als je het over wiet hebt is sowieso bullshit. Ik gain en rook wiet :trollface:

http://www.youtube.com/watch?v=CROgZki_eCU

growlikeweed · 1 dec 2010

Ja ligt er maar net aan vanuit welk perspectief je het bekijkt

Lekker? jazeker
Functioneel? niet echt nee

Het werd op een gegeven moment dagelijkse gang van zaken. Het werd meer een sleur dan dat ik er nog echt plezier van had. Het begon gewoon voor de lol, op een gegeven moment ging ik zelf maar kweken, dat werd meer een hobby maar die 2 bij elkaar liepen nogal uit de hand. Ik rookte zelf teveel en de rest verkocht ik dan weer. Op een gegeven moment werd het toch maar tijd om er een einde aan te maken.

helboy · 1 dec 2010

Van wiet smoren wordt je droog

growlikeweed · 1 dec 2010

helboy zei:
Van wiet smoren wordt je droog

droge humor?

daniel20 · 1 dec 2010

helboy zei:
Van wiet smoren wordt je droog

Het is maar net hoe je je gedraagt imo... ik bedoel, als ik heb gesmookt ga ik echt niet als een lamme dwaas voor me uit zitten kijken, of lachen om de gaarste dingen.. dat stadium ben ik al ver voorbij.

(no e-hero praat)

CoD · 1 dec 2010

daniel20 zei:
Het is maar net hoe je je gedraagt imo... ik bedoel, als ik heb gesmookt ga ik echt niet als een lamme dwaas voor me uit zitten kijken, of lachen om de gaarste dingen.. dat stadium ben ik al ver voorbij.

(no e-hero praat)

Als je dat stadium voorbij bent kun je net zo goed stoppen met blowen

(want dan is het meer een gewoonte dan dat je er nog iets aan hebt. Ik word bijvoorbeeld niet meer stoned als ik een tijdje flink blow, dan kan ik echt de een na de ander roken zonder gaar te worden (of eigenlijk ben je gewoon de hele dag gaar en daarom merk je er niks meer van

))

Gelukkig ben ik nu overal mee gestopt.

growlikeweed · 1 dec 2010

CoD zei:
Als je dat stadium voorbij bent kun je net zo goed stoppen met blowen
(want dan is het meer een gewoonte dan dat je er nog iets aan hebt. Ik word bijvoorbeeld niet meer stoned als ik een tijdje flink blow, dan kan ik echt de een na de ander roken zonder gaar te worden (of eigenlijk ben je gewoon de hele dag gaar en daarom merk je er niks meer van ))

Gelukkig ben ik nu overal mee gestopt.

Ja precies. Na een tijdje wordt het gewoon een sleur en het erge ervan is: je hebt het zelf vaak niet eens door. Ik ziet het aan een paar maten van me altijd wel heel duidelijk. Voordat ze hebben gesmoked nog helemaal fit, altijd overal zin in, hele plannen maken. Even later als de joint op is worden dingen uitgesteld en komt het er vaak niet meer van. En maar zeggen dat het er niks mee te maken heeft. Merk het aan mezelf ook sinds ik ermee gestopt bent veel fitter, veel meer buiten onder de mensen enzow.

thomastog · 1 dec 2010

daniel20 zei:
Elke dag, daarna met je vreetkick die-hard bulken, wat is het probleem? als je maar niet zo'n domme slome gozer word en je zelf vertrouwen gaat verliezen is alles goed.

Weet niet van andere mensen maar ik heb niet zin in bakken met rijst en kip als ik een vreetkick krijg, dan wil ik echt suiker hebben.

MeDieViL · 1 dec 2010

CoD zei:
Als je dat stadium voorbij bent kun je net zo goed stoppen met blowen
(want dan is het meer een gewoonte dan dat je er nog iets aan hebt. Ik word bijvoorbeeld niet meer stoned als ik een tijdje flink blow, dan kan ik echt de een na de ander roken zonder gaar te worden (of eigenlijk ben je gewoon de hele dag gaar en daarom merk je er niks meer van ))

Gelukkig ben ik nu overal mee gestopt.

Hahaha, dat ik dat geen meemaken, cod trots vertellen dat hij met alles gestopt is :roflol:

Wiet gebruik tijdens bodybuilding

Monstrous Giant

Advanced Bodybuilder

Dutch Bodybuilder

Dutch Bodybuilder

Monstrous Giant

Advanced Bodybuilder

Advanced Bodybuilder

Monstrous Giant

Dutch Bodybuilder

Advanced Bodybuilder

Dutch Bodybuilder

Freaky Bodybuilder

Advanced Bodybuilder

Dutch Bodybuilder

Advanced Bodybuilder

Colossal Veteran

Colossal Veteran

Advanced Bodybuilder

Huge Freak

Monstrous Giant

Soortgelijke topics