Deleted member 576750
Discord Sr. Moderator
does anyone here use cannabis for ADHD or find that it helps you focus?
if so, how do you use it for this purpose?
if so, how do you use it for this purpose?
-
CD Moderators: nepalnt21
Cannabis and ADHD
- Thread starter Deleted member 576750
- Start date
lavalamplynx
Greenlighter
- Joined
- Nov 8, 2025
- Messages
- 4
i have never heard of it but i imagine that if cannabis were to be used for such it would be low doses seeing as high doses impair concentration. Maybe a more stimulating cannabinoid like THC-V would be better
Deleted member 576750
Discord Sr. Moderator
I've tried THCv and it is helpful but I typically prefer oral THC. sometimes with CBD but many times that isn't stimulating enough for me
Bleaney
Bluelighter
- Joined
- Mar 13, 2021
- Messages
- 2,755
I think it affects everyone differently. Whenever I had more than a couple of relatively small hits on a dry weed vape, my attention span would be completely destroyed.
To the extent that I could not even watch a 5 minute yotube video as my mind would be all over the place. As for audiobooks just forget it, there was no chance I'd be able to concentrate and focus.
I guess I'm highly sensitive to the effects of weed as I have Autism as well as ADHD. Autistic people tend to be either hypersensitive or hyposensitive to a variety of things.
Tbh I cant understand how cannabis could help with ADHD based on my experiences, but I have to try to remember that everyone reacts differently to different things.
To the extent that I could not even watch a 5 minute yotube video as my mind would be all over the place. As for audiobooks just forget it, there was no chance I'd be able to concentrate and focus.
I guess I'm highly sensitive to the effects of weed as I have Autism as well as ADHD. Autistic people tend to be either hypersensitive or hyposensitive to a variety of things.
Tbh I cant understand how cannabis could help with ADHD based on my experiences, but I have to try to remember that everyone reacts differently to different things.
Deleted member 576750
Discord Sr. Moderator
I also have autism and ADHD and I'd agree om too much making things worse. theres definitely a dosi g sweet spot where my attention is improve but too much destroys it
Allylbenzene
Bluelighter
- Joined
- Jul 25, 2025
- Messages
- 982
Yes, alongside some long-term strategies which i've outlined here.
From a biochemistry perspective cannabinoids help to alleviate ADHD symptoms by activating the body's inhibitory (calming) system. This in turn reduces the excitatory (stimulating) system which includes adrenaline, cortisol and glutamate.
Adrenaline gives people intelligence and enhances creativity but in excess causes hyperactivity, impulsivity and puts you in fight-or-flight mode which can be pretty disruptive (eg overstimulation, racing thoughts, unfocused, anxiety, panic, brain fog etc).
Without excess levels of adrenaline then most ADHD symptoms disappear. Since stress (cortisol) triggers adrenaline, if you've got an "overactive stress response" then this causes high adrenaline (which is pretty disruptive).
Interestingly, all ADHD medications counteract adrenaline whether directly (eg guanfacine via α2A adrenergic agonism) or indirectly (eg amphetamine, methylphenidate, atomoxetine, viloxazine). The "indirect drugs" operate primarily via DRI and/or NRI:
• Dopamine inhibits the ACTH-glucocorticoid system (ACTH triggers cortisol which triggers adrenaline, less ACTH = less adrenaline);
• Noradrenaline activates the α2A adrenergic receptors which in turn lowers adrenaline release (and boosts endogenous GABA which also helps).
This quote gives some context for the role of dopamine in all this, and that of 2 key inhibitory neurotransmitters (GABA and adenosine):
Quote on the role of noradrenaline:
eg, the ADHD drug atomoxetine (Strattera) is a pure NRI (noradrenaline reuptake inhibitor) which boosts noradrenaline levels.
With the understanding of how excess adrenaline causes ADHD symptoms - and why calming things like guanfacine or THC can temporarily alleviate symptoms - we can start to see why stimulants aren't appropriate for ADHD. Just because modern medicine has adopted them as a way to manage ADHD symptoms doesn't mean that they're appropriate. Modern medicine is a bad influence for many reasons.
In some ways ADHD medications (particularly stimulants) are quite crude and none address the fundamental issues (cue: why is the ACTH-glucocorticoid system hyperactive). You could apply this criticism to most prescription drugs, it's a key characteristic of corporate healthcare.
Last edited:
emkee_reinvented
Bluelighter
Cannabis is sort of a adaptogen right ? Endo-Cannabinoid system is a sort of balancing system 
. For me It is basically the lubricant that keep s my system going smooth. Was out a few day not persee bad.
But way harder to control my impulses. Get a lot more fiery without it.
Been smoking it for ages 2nd drug that reached my brain consciously.
ADD or ADHD well depends what day you meet me. Bit Autistic to.
No way as hardcore as my son though. He can literally floor the room.
With one polite sentence.
Autisme interestingly bizar. Do people with it benefit from stimulant s ?
THC doesn t really knock me out. But taking ADHD medication with it.
Not a to high dose 20 mg dextro-Amphetamine seem s to make live endurable.
A lot more bearable. Not a cure but useful tools.
. For me It is basically the lubricant that keep s my system going smooth. Was out a few day not persee bad.But way harder to control my impulses. Get a lot more fiery without it.
Been smoking it for ages 2nd drug that reached my brain consciously.
ADD or ADHD well depends what day you meet me. Bit Autistic to.
No way as hardcore as my son though. He can literally floor the room.
With one polite sentence.
Autisme interestingly bizar. Do people with it benefit from stimulant s ?
THC doesn t really knock me out. But taking ADHD medication with it.
Not a to high dose 20 mg dextro-Amphetamine seem s to make live endurable.
A lot more bearable. Not a cure but useful tools.
Are you using an LLM to write this?
Also where are you getting this info? It is pretty fringe, and I would just be interested in seeing what has led you to these conclusions.
Also to clarify, when you talk about adrenaline, you are referring to the hormone epinephrine, or something else?
Allylbenzene
Bluelighter
- Joined
- Jul 25, 2025
- Messages
- 982
I prefer not to use those.
It's a synthesis of metabolic (eg thyroid, mitochondrial) & endocrine concepts contextualised with the MOA of drugs used for ADHD. Papers on the individual elements exist, eg
• on noradrenaline activating α2A adrenergic receptors
• α2-adrenergic agonists reducing noradrenaline & excitatory signalling via GABA
• dopamine mitigating cortisol release (and thus adrenaline)
Broadly speaking ADHD drugs either increase noradrenaline, increase dopamine or activate α2-adrenergic receptors.
I'm aware of the official story of ADHD involving executive dysfunction, framing it as a neurodevelopmental disorder which requires continued symptom management.
Yes, adrenaline = epinephrine. Calling it a hormone can be misleading for some people due to the connotations of the word; but yes, a hormone or phenethylamine-based psychoactive drug.
Last edited:
I think some of those conclusions feel like they are made in isolation.
I agree that norepinephrine activates a2 adrenergic receptors, but am unsure of the sufficience or necessity of GABA in this response. That paper mentioned that clonidine effects gaba levels but the citation for that is buried so there isn’t much context. The presynaptic a2 receptors are Gi coupled and are sufficient on their own to decrease catecholamine release. Expressing a2 receptors on cells is sufficient to drive an inhibitory response from its agonists.
The dopamine paper you cited has more to do with corticosteroids not impacting d2 receptor levels. They cite a paper demonstrating that d2 selective agonists reduce aberrant cortisol release in Cushing’s Syndrome, but I would advise the caveats that this is a pathological state, and selective d2 agonism does not occur subsequent to dopamine release.
D2 receptors are inhibitory towards adenylyl cyclase, but D1 receptors stimulate it. D1 receptors are expressed in adrenal glands as well as the d2 family, making dopamine unlikely to selectively inhibit release of adrenal hormones.
Are there any papers which discuss this theory of adhd directly? I am wary of drawing conclusions based on tangential interpretations of papers reporting other findings.
Allylbenzene
Bluelighter
- Joined
- Jul 25, 2025
- Messages
- 982
If there are such papers then I'd be amazed. I'm currently searching.
...
Finds so far:
This seems an appropriate primer on the role of cortisol although I wouldn't necessarily agree with some of the conclusions & rationale:
https://scibrief.blog/cortisol-adhd-hpa-axis
On ACTH:
— "Our express goal is a technical discussion about ADHD from a scientific perspective"
https://www.adxs.org/en/page/130/acth
Last edited:
Bleaney
Bluelighter
- Joined
- Mar 13, 2021
- Messages
- 2,755
Yes. Because around 70% of Autistic people also have ADHD, according a consensus of studies.
It is known as AuDHD.
And living with both conditions is a constant inner struggle. For example my Autistic side likes order, organisation, tidyness etc. But my ADHD renders me completely incapable of implementing that as consistently and thoroughly as I would like, especially when it comes to household chores. And that's even with being on stimulant medication. I guess that most of my mental energy is used up by work, and I'm all out and recovering during my free time, or on the internet, chasing dopamine. So the household chores pile up. If I didn't work, I think I would be on top of everything as much as I'd like. As I found during 3 or 4 months of Furlough during the Covid lockdown. And I wasn't on any stimulant meds, or taking any substances at all during that period.
Last edited:
emkee_reinvented
Bluelighter
Hmm ... ... ... joggling with 7 ball s. Wanna throw one in.
Distraction s, random occurring can totally disrupt my live. Happened a lot lately.
Seem s a bit like like a internal battle. It s been 18 year s ago i worked for a boss.
These disruption s alone well i do water my plant s they florish but the leaves are collecting dust
You are juggling with 7 ball s while thing s pile up.My house just the same, i rather type this somehow my brain think s it is of more importance. 100 % agree with it.
With DIY diagnosing i am AuD[H]D.The Autisme that at times balances the ADHD. And sometimes not. Makes sense.
Cortisol and attention deficit hyperactivity disorder
There is a link between cortisol levels and attention deficit hyperactivity disorder (ADHD), though this relationship is intricate and not elusive. Children with ADHD tend to have lower basal salivary cortisol levels in comparison to healthy counterparts. However, no distinct relation between cortisol levels and the severity of ADHD symptoms has been established [34]. Moreover, low hair cortisol concentrations (HCC) have been linked to inattentive ADHD (ADHD-I) symptoms and impaired working memory. Additionally, lower HCC was found at age four to five years to predict the development of ADHD by age eight [35].A meta-analysis has concluded that children and adolescents with ADHD experience lower morning, random, and cumulative daily cortisol levels in comparison to healthy controls. This suggests that diurnal cortisol may not be a biomarker of ADHD [36]. In contrast, other studies have found no differences in cortisol levels between ADHD and control groups [37, 38]. Children and adolescents with ADHD, especially the combined subtype (ADHD-C) and predominantly hyperactivity-impulsive subtype (ADHD-HI), tend to have lower morning and evening cortisol levels compared to healthy controls. This blunted cortisol response may be related to an underactive behavioral inhibition system, which is closely associated with deficits in self-regulation, working memory, and other core ADHD symptoms [39, 40]. ADHD-I appears to show an elevated cortisol response to psychosocial stress, in contrast to the blunted response seen in ADHD-C [40]. Also, a study reported a trend towards higher cortisol responses in the ADHD-I subtype compared to controls [38]. Long-term cortisol secretion, assessed through HCC, was found to be significantly lower, particularly in boys with ADHD-I. This association persisted even after accounting for the presence of comorbid oppositional defiant disorder, conduct disorder, and anxiety or depressive disorders [35].
In children with ADHD who experience gastrointestinal symptoms, altered cortisol profiles were found. Both hair and salivary cortisol levels were found to be elevated in children with gastrointestinal symptoms [41], indicating a potential link between stress and gastrointestinal issues in these populations. Chronic stress may contribute to or exacerbate gastrointestinal symptoms. Moreover, children with gastrointestinal symptoms showed greater externalizing, e.g., aggression, hyperactivity, and internalizing, e.g., anxiety, depression problems compared to those without gastrointestinal symptoms. The HPA axis-ADHD relationship seems to be complicated and not fully understood. The HPA axis dysfunction may manifest differently across ADHD subtypes. The lower cortisol levels in ADHD, particularly in the ADHD-HI, were found to be more strongly associated with the core symptoms of hyperactivity, impulsivity, and inattention rather than cognitive deficits [39].
Evidence suggests a complex and inconsistent relationship between cortisol regulation and ADHD. This indicates that cortisol alone may not serve as a reliable biomarker as it depends on the disease subtype. Comorbid conditions, such as gastrointestinal issues, appear to further alter cortisol levels and may exacerbate behavioral symptoms. The effects of stimulant medication on cortisol are mixed—some studies show increases, particularly in boys and the combined subtype, while others report no significant changes. Animal studies on prenatal stress support the idea that maternal cortisol exposure may contribute to ADHD-like traits in offspring.
Overall, these findings point to substantial heterogeneity in cortisol patterns across ADHD presentations. Future research should consider ADHD subtypes, sex differences, and comorbidities to better understand the role of HPA axis dysfunction in ADHD.
In their study, VarmiŞ et al. [42] reported that cortisol levels in patients with ADHD measured before and after six months of methylphenidate (MPH) treatment, which inhibits the reuptake of dopamine and norepinephrine, were markedly elevated. In addition, sex differences affect this phenomenon, which was more pronounced in boys with ADHD relative to girls. A significant increase in serum levels of dehydroepiandrosterone (DHEA) and its sulphate ester (DHEA-S) was found after three months of MPH treatment in children with ADHD, but no significant changes in cortisol levels [43]. There is limited evidence that directly targeting cortisol levels can improve ADHD symptoms. It was found that stimulant medications like MPH used to treat ADHD may increase cortisol levels in certain patients, especially boys and those with the ADHD-C subtype. However, the effects are mixed, with other studies finding no significant changes in cortisol with MPH treatment [36].
Children and adolescents with ADHD typically show lower basal morning cortisol, compared to the corresponding controls. The lower activity of the HPA axis and the blocked diurnal cortisol rhythm are linked to physiological under-arousal and may contribute to symptoms such as fatigue and delayed awakening. The stimulant drugs may occasionally normalize cortisol levels, but they tend to revert after long-term treatment [38].
Maternal stress during pregnancy is linked to adverse effects on fetal development and can lead to psychiatric issues in children, including ADHD. Increased cortisol levels in mothers are associated with dysregulation of the HPA axis, which affects both maternal and infant health. Jeon et al. [44] found that administering corticosterone (20 mg/kg/day) to pregnant rats exhibited significantly higher cortisol levels compared to control groups, in both moms and their pups. Moreover, pups displayed hyperactivity and impulsivity, characteristic of ADHD, as evidenced by increased activity in the forced swimming and open field tests, greater exploration in the open arms of the elevated plus maze test, and longer swimming distances in the Morris water maze test, indicating cognitive impairments. In addition, it was found that cortisol-induced pups revealed lower body weight compared to the control ones, suggesting that maternal cortisol exposure adversely affected fetal growth.
Kim et al. [45] treated pregnant rats with corticosterone. Corticosterone treatment affected the offspring’s learning and memory abilities. Furthermore, this memory and learning impairment was linked to a delay in the development of synapses in the CA1 region of the hippocampus. Specifically, corticosterone treatment caused structural and functional alterations in the postsynaptic density and dendritic spines, which are essential for synaptic transmission and plasticity.
In their article, Kozłowska et al. [46] explored the differences in serum steroid hormone levels in the blood of spontaneously hypertensive rats (SHR) as an animal model for ADHD. SHR rats exhibit altered levels of key steroid hormones, including corticosterone, testosterone, and estradiol, compared to control rats. The altered corticosterone levels, indicative of a dysregulated stress response, are particularly significant, as elevated corticosterone is often associated with hyperactivity and attention deficits, common traits in ADHD. These findings suggest that hormonal imbalances in SHR rats may play a role in ADHD-like behaviors, providing insights into the physiological mechanisms that could underlie the condition in humans. The study highlights the importance of hormonal regulation in ADHD pathology and offers a potential avenue for future therapeutic strategies targeting these imbalances.
Combined exposure to deltamethrin, a common pesticide, and corticosterone, during neurodevelopment, resulted in epigenetic changes in male mice. This may be examined by the effects on the Nr3c1 gene, a gene that encodes the GR in the midbrain region. Male mice exposed to both deltamethrin and corticosterone during critical periods of brain development showed increased hypermethylation of the Nr3c1 gene. Hypermethylation generally leads to reduced gene expression [47], suggesting that the GR function may be diminished in these mice. The changes in Nr3c1 methylation are associated with alterations in stress response regulation, which could contribute to the development of neurodevelopmental disorders or affect stress-related behaviors in adulthood.
Together, these studies suggest that cortisol and its regulatory mechanisms—both hormonal and epigenetic—play a significant role in shaping ADHD-related neurodevelopment. While therapeutic interventions targeting cortisol regulation are still in early stages, this line of research may offer promising avenues for novel ADHD treatments, particularly those tailored to stress axis dysfunction. For drugs targeting cortisol in the treatment of ADHD, see Table 2.
At the end of the section there is a table which states “Atomoxetine, methylphenidate, and dexmethylphenidate for regulating attention deficit hyperactivity disorder symptoms by increasing cortisol levels.
From the second link
“
3. Details about
- In children with ADHD, no altered basal ACTH levels were found in any subtype.
- Augmentative (supportive) treatment with an ACTH 4-9 analog (Semax) for ADHD is discussed. Studies show that MPH (alone) shows significantly greater improvements than an ACTH 4-9 analog (alone).
Taken together theses two sources which comment directly on adrenal hormones and ADHD, quite fundamentally disagree with your prior statements regarding how ADHD medication function, and rather disagree about the role of adrenal hormones in the etiology of ADHD, as they are complicated enough to suggest multiple other factors are at play.
Allylbenzene
Bluelighter
- Joined
- Jul 25, 2025
- Messages
- 982
Yes I noticed.
As I wrote in my previous post, the info from the links is useful but I wouldn't necessarily agree with the conclusions/rationale. Just because those drugs temporarily relieve ADHD symptoms by increasing cortisol doesn't mean this is an appropriate long-term solution.
I've noticed in academia that it's fairly common for researchers to confidently arrive at questionable conclusions based on limited or incomplete data. Imo this is partly due to a compartmentalised understanding of biology which overlooks certain things. You see the same shortcomings in other areas of research involving SSRIs and statins. I do not question the researchers personally but moreso the environment which they are participating in.
I'd propose that the more fundamental factors at play in ADHD include mitochondrial dysfunction, thyroid dysregulation and excessive aromatase activity.
I still prefer academic publishing to anecdotal conjectures despite all of the issues with academia, because they go through peer review (in good journals at last), and have experiments that can be assessed. This renders academic research inherently more conservative (as in resists progress) so that the needle of progress only inches forward under an extremely strong foundation.
Look at SSRI and statin research. There has been an explosion in the past ten years of people understanding the different ways SSRIs modulate BDNF, and I was taught in classes that statins function to protect the heart through inducing hormesis mediated by increased ROS production.
I personally think your ideas are undeniably interesting, but they are often extremely heterodox. In fact, this heterodoxy is the single most consistent element of most of your posts around here (a second that they are well written and include citations, both of which I greatly thank you for).
Allylbenzene
Bluelighter
- Joined
- Jul 25, 2025
- Messages
- 982
I'd agree with you as much of my understanding is based on academic research. This paper on biophotons is excellent for example. But in some ways the corporate element of healthcare has grossly undermined the quality of modern medicine and the care that it provides. The outcome is temporary symptom management, long-term prescriptions and a corporate healthcare industry which ensures a continued return on investments.
A rhetorical question:
— Why offer an ADHD treatment that succeeds in say 2 years, when they can offer a treatment that requires 30+ years of continued adherence? (equally SSRIs, statins, anti-epileptics)
A rhetorical answer:— Because it's the best we have based on the most recent expert understanding of biology. Just because it alligns with corporate business practice doesn't mean that treatments are based on financially-oriented goals.
As an aside, this thread is in Cannabis Discussion. The corporate healthcare appropriation of cannabinoids like THC (Dronabinol), CBD (Epidyolex), Sativex and Rimbonant gives some insights into how things work (or in the case of rimbonant, don't).
Last edited:
Allylbenzene
Bluelighter
- Joined
- Jul 25, 2025
- Messages
- 982
Imo the "research branch" of corporate healthcare is problematic. This impacts everything including ADHD and cannabis medications (eg Dronabinol, Epidyolex, Sativex, Rimbonant).
The origins of corporate healthcare are outlined here, some excerpts:
https://meridianhealthclinic.com/how-rockefeller-created-the-business-of-western-medicine/
Last edited: