cbd oil cortisol

December 15, 2021 By admin Off

CBD is a cannabinoid that interacts with your endocannabinoid system, which is a complex system that manages psychological processes such as mood and appetite. This endocannabinoid system in your body is also involved in managing endocrine processes. In short, with all of these systems working together, by stimulating the endocannabinoid system, CBD and other cannabinoids can directly affect hormone levels in the body.

It’s recommended that anyone taking CBD for the first time starts small with somewhere between 20-40 mg the first time and gradually increases it by 5 mg every week. You can keep increasing it until you feel that your symptoms are being properly treated because it takes different amounts for everyone and there is no exact science on the amount to ingest.

Many people have spoken about going into “flight or fight” mode when they’re stressed out or threatened. While this is just a saying, there is a hormone called cortisol, also known as the stress hormone, that’s responsible for this type of reaction in stressful situations. Cortisol was an essential hormone when humans were hunting for meals every day and running from predators because it allowed an extra boost of energy in that high-stress situation so we could either outrun the predator or catch the prey.

CBD and cortisol.

If you ‘re using a product that is mostly CBD with very low levels of THC, then you should not experience any side effects that you would from ingesting THC, such as the stereotypical high that people associated with cannabis.

Keep track of your dosages every day and the corresponding symptoms of what you are trying to treat to figure out what works for you. Some studies have shown that 300 mg is most effective for the short-term effects of CBD on anxiety but always start small first.

CBD has been highly studied as a way to fight against these high cortisol levels. The results have been encouraging because they’ve found that CBD interacts with your endocrine system to regulate hormone production. Your endocrine system is a variety of glands that produce the hormones in your body and these hormones are powerful chemicals that sustain major effects on your body.

While cortisol is good in high-stress situations to trigger our flight or fight and get us out safely, too much of it can have detrimental effects on our health including developing long-term chronic diseases. These health effects can include poor sleeping habits, high blood pressure, and even gastrointestinal issues. Chronic cortisol release can also result in diabetes, obesity, and other autoimmune issues.

Since the endocrine system is in charge of managing stress and thus producing cortisol, CBD can be used to directly manage cortisol production. By using CBD, you can avoid the psychoactive effects of THC and gain the benefits of regulating hormone production.

When calculating how many mg of CBD to take for treating any symptoms including lowering cortisol levels, there are a few aspects to factor in. You will want to consider your body weight, your condition, your treating, and the concentration of CBD in whatever form you are taking it in. It’s important to discuss this with your doctor before taking anything to make sure that it is safe for your specific health issues.

There are many ways to ingest CBD available on the market today. There are oils, capsules, drops, tea, vapors, candies, and more. Make sure the product you buy indicates how many milligrams of CBD is in a serving; for example, if it comes in capsule form and the bottle says there are 5 mg per capsule.

The recommended dosage.

Nowadays, cortisol can be triggered by things beyond hunting for our meals. Stress can be something we experience all too often, especially with the world we are currently living in. Those with a busy lifestyle are also more prone to high cortisol levels because they’re not getting the relaxation and downtime required to lower those levels.

Overall, CBD can be an effective way to reduce cortisol levels by lowering the body’s inflammatory response to stress. This in turn can reduce anxiety, depression, and insomnia, which can lead to a much healthier lifestyle!

How cortisol works.

Due to the increasing opioid crisis in America, researchers struggle to find ways to alleviate pain while also avoiding compounds that are habit-forming and harmful.

CBD can significantly lower cortisol levels, improving your mood, sleep, blood pressure, and even helping with weight loss.

When they’re harvested, the extract is then purified even further to create the CBD product. CBD is a cannabinoid that binds to receptors in your brain (all cannabinoids can bind to those receptors), causing the health benefits that so many people love. It also isn’t associated with some of the side effects of the THC found in marijuana.

Cortisol is the hormone your body secretes when you’re stressed. It’s not bad in and of itself; in fact, it’s there to help you.

Hemp plants contain over eighty cannabinoids, and CBD makes up 40 percent of that. In order to produce more CBD, the plants are strategically grown to increase the CBD to THC ratio.

5. Reduce Pain & Need For Pain Medication.

When insulin levels remain high due to a high carbohydrate diet, your body eventually becomes resistant to it. More and more insulin is required until your body can’t keep up. Loss of blood sugar levels ensues and the result is diabetes.

A recent study by the Hadassah University Hospital in Israel showed that CBD lowered insulin levels enough to reverse diabetes in mice; the improvement was statistically significant.

However, in our fast-paced world we’re often flooded with cortisol, and that’s not a good thing. High levels of cortisol can cause chronic anxiety, high blood pressure, headaches, and weight gain (particularly in your abdomen, where we need it the least).

Opioid receptors in the body will bind to CBD, meaning that it can provide the significant pain relief of strong medication, without being an addictive substance.

Inflammation is the body’s response to injury.

CBD is 100 percent legal in all of the US and, while many people still confuse the two, it’s important to note the difference. CBD is not psychoactive. In fact, it can actually be quite beneficial for your health. As it becomes increasingly popular, more and more people are turning to the plant-based oil to find relief from aches, pains, and more.

One of CBD’s most talked-about benefits is its impact on stress and anxiety. Earlier we talked about cortisol, the body’s response to stress. Not only does CBD reduce cortisol levels in those already dealing with chronic stress, but it also improves your ability to be calm and centered, which prevents stress and anxiety in the first place.

However, what you may not realize is that marijuana contains two compounds: THC (its psychoactive component that gives you the “high”) and CBD (the non-psychoactive component.)

Remember when we talked about how cannabinols bind to certain receptors in your brain? There are certain receptors that CBD binds to, specifically, that regulate fear and anxiety. This is especially good news for those dealing with chronic anxiety, PTSD, and generalized anxiety disorder.

Unfortunately with inflammatory diseases like arthritis, multiple sclerosis, and asthma, the body’s inflammation response is in overdrive, causing pain and chronic illness. Like the receptors that regulate fear and anxiety, there are receptors in your immune system that regulate inflammation. CBD binds to these receptors causing a significant decrease in inflammation.

2. Decrease Insulin Levels.

It’s no secret that modern humans struggle with our sleep quality. Millions of people take some sort of sleep aid in order to get a good night’s sleep. These drugs can be addictive, make you drowsy the next day, and some even have serious long term side effects.

Type II diabetes is a debilitating disease that impairs your body’s ability to process sugar, and it is at an all-time high. In fact, over 30 million people in the US are affected.

Due to CBD’s effects on stress, anxiety, inflammation, and pain, all these combine to really calm your brain and nervous system, providing you with some of the best sleep you have ever had.

Truthfully, CBD has so many reported health benefits that to touch on all of them would take far more than one blog post. Here, we’re going to focus on the top six benefits that will help just about anyone.

There has been a lot of media hype in recent years over the legalization of marijuana and the possible health benefits it can provide. While these benefits may or may not be true, the fact of the matter is that although many states have legalized the drug, many have not. There is still quite a bit of controversy over the subject and it’s not likely to die down anytime soon.

If you have wondered about the legality or addictive qualities of CBD due to the fact that it comes from the hemp plant, rest assured that it’s safe and legal.Make sure you purchase it from a respectable source with purity testing results available. If you’re dealing with anxiety, sleeplessness, or any of the other issues highlighted above, CBD may be able to help. It may even be a safer alternative than medications for some individuals.*

If you want to explore this topic in more depth, check out Ben Greenfield’s great podcast on the subject. He delves into the science in greater detail. And if you would like to learn more about how to live a long, healthy life, schedule a consultation with Matrix Age Management. Our customized age management programs, peptide treatments, hormonal replacement therapy treatments, and sexual vitality treatments can help you live you feel better, now.

How Can CBD Help Me?

These procedures were approved by Psychiatry, Nursing and Midwifery Research Ethics Committee at King’s College, London (Approval number PNM/13/14-22), and NHS ethics 13/LO/0243. All participants gave written informed consent before taking part in the study and completed anonymised questionnaires in private.

Group-dependent cortisol reaction.

Dr. Appiah-Kusi was supported by the National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care South London at King’s College Hospital NHS Foundation Trust when this work was carried out.

Dr. Bhattacharyya was supported by the National Institute for Health Research (NIHR) through a NIHR Clinician Scientist Award (NIHR CS-11-001) when this work was carried out and funding from the Medical Research Council (MRC) (MR/J012149/1) supported this work.

The harmful effects of cannabis have been mainly attributed to the effects of its main psychoactive ingredient, delta-9-tetrahydrocannabinol (THC), which has been shown under experimental conditions to induce psychotic and anxiety symptoms in healthy individuals (D’Souza et al. 2005) and exacerbate psychotic symptoms in patients with pre-existing psychosis (D’Souza et al. 2005). In contrast, cannabidiol (CBD), is a safe and well-tolerated (Bergamaschi et al. 2011a) constituent of cannabis and has antipsychotic (Iseger and Bossong 2015; Leweke et al. 2012; McGuire et al. 2017; Bhattacharyya et al. 2010) and anxiolytic (Bergamaschi et al. 2011b) properties. Importantly, preclinical evidence suggests that CBD may attenuate the effects of experimentally induced stress in lab animals following both acute (Guimarães et al. 1990; Campos and Guimarães 2008; Gomes et al. 2011; Gomes et al. 2012) and chronic treatments (Campos et al. 2013). Consistent with this, other data has accumulated that CBD may also block anxiety symptoms induced by THC (Zuardi et al. 1982) or social stress under experimental conditions in healthy volunteers (Zuardi et al. 1993) or patients with social anxiety (Bergamaschi et al. 2011b). Furthermore, CBD has broadly opposite effects to that of THC, both at the behavioural and neural levels (Bhattacharyya et al. 2010; Bhattacharyya et al. 2015; Bhattacharyya et al. 2012) in healthy volunteers and evidence from double-blind randomised clinical trials point towards efficacy as an antipsychotic in patients with established psychosis (Leweke et al. 2012; McGuire et al. 2017). More recently, we have shown that a single dose of CBD may partially normalise dysfunction in the key neural substrates implicated in psychosis in CHR patients (Bhattacharyya et al. 2018). However, whether CBD could attenuate the effects of stress under experimental conditions in patients with CHR has never been tested before. This is of particular importance due to the lack of evidence of a beneficial effect of currently available antipsychotic treatments on the dysregulated neuroendocrine stress response. Therefore, the main objective of the present study was to investigate whether cannabidiol, a non-psychoactive substance present in the extract of the cannabis plant, has potential to mitigate the harmful effects of exposure to stress under experimental conditions in CHR patients.

Funding Information.

Table ​ Table2 2 outlines the descriptive statistics for each time point for all of the measures of response to stress.

The Trier Social Stress Test (TSST) (Kirschbaum et al. 1993) is a well-validated stress induction paradigm that has been shown to reliably induce stress as reflected in changes in cortisol levels, under experimental conditions over the past couple of decades. This stress induction paradigm involves a social evaluative element, which make it comparable to the social stressors which individuals experience in their daily lives and arguably ecologically more valid. Participants were told they will take part in a public speaking exercise. The experimenter takes the participant into a separate room where a panel of two people were assembled and the standardised TSST instructions were read to them (see additional materials; see Fig. ​ Fig.1 1 for explanation of timing of procedures). They were then taken to a different room for the 10-min preparation period. They were informed that they would be given 10 min to prepare for a 5-min speech where they had to imagine they had an interview for their ideal job and they needed to deliver the speech to convince the panellists as to why they were ideal for that job, they were then led to an empty room to prepare. After the 10-min preparation period in a different room, participants returned to the panel to deliver their speech. Once they had completed the speech, they were informed they would take part in a mental arithmetic task as per the TSST protocol (see additional materials for details of mental arithmetic task).

Notwithstanding its limitations, the present study provides a strong rationale for future studies to investigate whether CBD may have potential to mitigate the harmful effects of stress in the course of daily life by attenuating the altered neuroendocrine and psychological responses to acute stress in CHR participants.

There was a significant effect of group (HC, CHR-P, CHR cannabidiol; CBD F (2,54) = 5.78, p  = .005) on cortisol reactivity (measured as the change in the level of cortisol at 0 min relative to baseline; − 60 min). Across the three participant groups, there was a significant F (1,54) = 9.46, p  = .003 linear decrease in cortisol reactivity, such that the change in cortisol (cortisol at time 0 min relative to baseline; − 60 min) associated with experimental stress exposure was greatest in HC controls and least in CHR-P patients, with CHR-CBD patients exhibiting an intermediate response (Fig.  2 ). Planned contrasts revealed that the cortisol reactivity was significantly different ( t (54) = 3.08, p  = .003; HC v CHR-P mean difference = 117.67, 95% CI 25.45–209.88, d  = 1.31) in HC ( M  = 77.08 nmol/L, s.d. = 122.54) compared with CHR-P ( M  = − 40.59 nmol/L, s.d. = 136.98), and in HC compared with CHR-CBD ( M  = − 23.67, s.d. = 99.82; t (54) = 2.53, p  = .014, mean difference = 100.75, 95% CI 4.94–196.55, d  = 0.90) but was not different between CHR-P and CHR-CBD ( t (54) = − .39, p  = .70, mean difference = 16.92, 95% CI − 86.99–120.84, d  = 0.14)).

We investigated whether CBD would normalise the neuroendocrine and anxiety responses to stress in clinical high risk for psychosis (CHR) patients.

One-way analysis of variance (ANOVA) revealed a significant effect of group (HC, CHR-P, CHR-CBD ( p  = .005) on cortisol reactivity as well as a significant ( p  = .003) linear decrease. The change in cortisol associated with experimental stress exposure was greatest in HC controls and least in CHR-P patients, with CHR-CBD patients exhibiting an intermediate response. Planned contrasts revealed that the cortisol reactivity was significantly different in HC compared with CHR-P ( p  = .003), and in HC compared with CHR-CBD ( p  = .014), but was not different between CHR-P and CHR-CBD ( p  = .70). Across the participant groups (CHR-P, CHR-CBD and HC), changes in anxiety and experience of public speaking stress (all p ’s < .02) were greatest in the CHR-P and least in the HC, with CHR-CBD participants demonstrating an intermediate level of change.

In line with our main hypothesis, we also found that CHR-CBD displayed intermediate levels of neuroendocrine (cortisol reactivity) and psychological [anxiety and perception of stress (negative self-statements)] response to experimental stress comparedwith CHR-P and HC. Collectively, these findings suggest that CHR participants under placebo displayed abnormal neuroendocrine and psychological responses to experimental stress compared with HC participants, and that 7-day treatment with CBD may potentially help partially attenuate these altered responses to experimental stress in CHR participants. However, one needs to be cautious in considering this interpretation, as the significant linear relationship across the 3 participant groups was mainly driven by the significant difference between HC and CHR-P on these measures. Therefore, further research is needed to investigate whether CBD may be used to influence the stress response in early psychosis. Differences in cortisol reactivity and anxiety response to stress in pairwise comparisons between CHR-P and CHR-CBD were not statistically significant, although this difference approached significance when change in perception of stress (negative self-statements) was compared between them. Future longitudinal studies in larger samples taking into account confounders are necessary to independently confirm whether CBD treatment can significantly attenuate altered responses to experimental stress in CHR participants relative to placebo treatment.

Some participants had incomplete data for the different time points and could not realistically be transposed and were therefore not entered into certain analyses. In the cortisol analysis, this occurred in one CHR-CBD participant. For the STAI analysis, this occurred in four healthy controls, five CHR-P participants and two CHR-CBD participants. For the SSDPS-N analysis, this occurred in three healthy controls, five CHR-P participants and two CHR-CBD participants.

There was a significant effect of group (HC, CHR-P, CHR-CBD F (2,44) = 4.57, p  = .016) on SSDPS-N AUC scores. There was a significant F (1,44) = 9.11, p  = .004 linear increase in SSDPS-N AUC scores indicating that the experience of negative statements was greatest in CHR-P, and least in HC, with CHR-CBD patients exhibiting an intermediate response. Planned contrasts revealed that the SSDPS-N was significantly different ( t (44) = − 1.07, p  = .004; HC v CHR-P mean difference = − 169.36, 95% CI − 309.01–− 29.71, d  = 0.94) in HC ( M  = 333.50, s.d. = 135.82) compared with CHR-P ( M  = 502.86, s.d. = 217.12), but not when compared with CHR-CBD ( M  = 394.62, s.d. 121.58; t (44) = −1.12, p  = .27; mean difference = − 61.12, 95% CI − 203.89–81.66, d  = 0.47) and approached a significant difference between CHR-P and CHR-CBD ( t (44) = − 1.75, p  = .088 mean difference = 108.24, 95% CI − 46.12–262.60, d  = 0.62).

Therefore, we investigated whether CHR patients had a blunted neuroendocrine and exaggerated anxiety response to acute exposure to social stress compared with healthy controls. Our main aim was to assess whether short-term treatment with CBD would partially normalise the altered acute neuroendocrine and anxiety response stress exposure in CHR patients. We hypothesised that relative to healthy controls, CHR patients under the influence of placebo would display the most severe alterations in the neuroendocrine and psychological responses to stress, while CBD treatment would attenuate some of these effects such that CHR patients under CBD would display an intermediate level of stress response.

Statistical analysis.

Dr. Matthijs Bossong was supported by a Veni fellowship from the Netherlands Organisation for Scientific Research.

There was a significant effect of group (HC, CHR-P, CHR-CBD F (2,43) = 3.68, p  = .034) on STAI-S AUC scores. Across the three participant groups, there was a significant ( F (1,43) = 6.85, p  = .012) linear increase in STAI-S scores, indicating that the experience of anxiety in response to the TSST was greatest in CHR-P and least in HC, with CHR-CBD exhibiting an intermediate response (Fig.  3 ). Planned contrasts revealed that the STAI-S AUC was significantly different ( t (43) = − 2.62, p  = .01; HC v CHR-P mean difference = − 373.75, 95% CI − 720.52–− 26.98, d =  0.92) in HC ( M  = 1428.33, s.d. = 413.26) compared with CHR-P( M  = 1802.08, s.d. = 397.16), but not when compared with CHR-CBD ( M  = 1656.54, s.d. = 359.41, t (43) = −1.64, p  = .11; HC v CHR-CBD mean difference = −228.21, 95% CI − 566.38–109.97, d =  0.59) and was also not different between CHR-P and CHR-CBD ( t (43) = − .92, p  = .36, mean difference = − 145.54, 95% CI − 529.16–238.07, d =  0.38) (see Fig. ​ Fig.3 3 ).

This study represents independent research supported by the National Institute for Health Research (NIHR)/Wellcome Trust King’s Clinical Research Facility and the NIHR Biomedical Research Centre and Dementia Unit at South London and Maudsley NHS Foundation Trust and King’s College London.

In the case of missing data for outcomes that were measured repeatedly, the last observation carried forward method was used to impute missing values. This was used in three instances of missing data in HC and once in CHR-P for the SSDPS-N and once for CHR-P for cortisol.

Stress is a risk factor for psychosis and treatments which mitigate its harmful effects are needed. Cannabidiol (CBD) has antipsychotic and anxiolytic effects.

Nevertheless, our results provide preliminary evidence that CBD may affect the altered neuroendocrine as well as the psychological responses to acute stress in daily life in CHR patients. Therefore, in contrast to atypical antipsychotics, which have been shown to reduce elevated diurnal cortisol levels (Zhang et al. 2005; Cohrs et al. 2006; Mondelli et al. 2010), but not correct the blunted cortisol response observed in psychosis (Mondelli et al. 2010), CBD may potentially attenuate abnormalities in some of the main components of the acute stress response in the CHR state, future research using larger samples would be required to confirm this suggestion. These results are in line with previous research, which suggests that CBD may have anxiolytic (Bergamaschi et al. 2011b) and antipsychotic effects (Bhattacharyya et al. 2018; Leweke et al. 2012; McGuire et al. 2017).

Group-dependent experience of anxiety.

Discussion.

We would like to thank all the participants for taking part in this study, as well as the students and staff past and present for their help in the collection and entering of data, particularly Ewa Klamerus, Enrico Foglia, Eimear Leyden, Sita Parmar, Liam Embliss, Rupa Ramesh, Anand Beri, Maria Calem, Irene Wuersch, Cordelia Watson, Efisia Sais, Noah Yogo and Tabea Schoeler.

Furthermore, in this study, we used venous blood sampling, which in itself can be quite stressful. However, in order to mitigate the effects of venepuncture, we used an atraumatic needle and employed an intravenous cannula that enabled us to avoid repeated venepuncture. While we cannot completely rule out the possibility that the stress of venepuncture may have added to the stress of participants, we do not believe that this would have confounded our results as such stress would have acted across all participants and only added to the social evaluative stress induced by the public speaking task, thereby contributing to how stressed participants felt overall. Furthermore, there was a gap of approximately 50 min between venepuncture and stress exposure, by which time any effects of stress from the venepuncture would have reduced substantially.

Our findings show that it is worthwhile to design further well powered studies which investigate whether CBD may be used to affect cortisol response in clinical high risk for psychosis patients and any effect this may have on symptoms.

Descriptives for reactions to stress.

The mechanism underlying the potential anti-stress effect of CBD is currently unclear, with multiple potential mechanisms being posited. Antipsychotic effects of CBD have been linked to its effects on levels of the endogenous cannabinoid anandamide (AEA) potentially by inhibiting its catalytic enzyme fatty acid amide hydrolase (FAAH). Recent preclinical work has also suggested that CBD may block the anxiogenic effects of chronic stress that was associated with a concomitant decrease in the expression of FAAH following CBD treatment (Fogaça et al. 2018). Anxiolytic effects of CBD were blocked by cannabinoid receptor (type 1 and type 2) antagonists but not by the serotonergic 5HT-1A receptor antagonist. However, other preclinical work suggests an effect of CBD on 5-HT 1a receptors (Fogaça et al. 2016; Bih et al. 2015; Russo et al. 2005) may underlie its anxiolytic effects.

To the best of our knowledge, this is the first study to have investigated the effects of short-term treatment with CBD on experimentally induced stress in the context of psychosis risk. We employed a well-validated stress induction task that has a long history (Kudielka et al. 2007a) of use for experimental stress induction. This experimental stress paradigm employed social evaluative stress, which may arguably be considered more similar to the kind of life-stress that has been linked with psychosis. While the use of a laboratory task may undermine ecological validity compared with other approaches such as experience sampling techniques, it does allow for more stringent control and standardised stress exposure. Furthermore, the task of speaking in public can be said to be life-like in that it is formed as part of a mock job interview, which is a situation that most people who experience it perceive as stressful. Further, in the healthy population sample, we recruited participants such that they were matched to the at-risk participants.

Anxiety was assessed using the State Trait Anxiety Inventory (STAI) (Spielberger et al. 1970). We employed the ‘state’ subscale of the questionnaire to measure change in anxiety induced by experimental exposure to stress (STAI-S). Reactions to public speaking were measured using the Self-Statements during Public Speaking Scale (SSDPS) (Hofmann and DiBartolo 2000). This measures individuals’ perception of performance in relation to public speaking. It has 5 items evaluating negative thoughts and 5 evaluating positive thoughts, each rated on a 5-point Likert scale. We employed the negative subscale for this study. Both of these scales were collected at baseline (− 60 min) and at 0, + 10 and + 20 min after the Trier Social Stress Test (TSST).

Accumulating evidence suggests that a dysfunction in the HPA-axis might underlie the psychosis continuum (Pruessner et al. 2017). A recent review of the evidence (Appiah-Kusi et al. 2016) suggests that in response to a stressor, patients with established psychosis and those at clinical high risk (CHR) for psychosis (Day et al. 2014; Pruessner et al. 2013) tend to exhibit a blunted cortisol response to both social stress and awakening. Similarly, evidence has shown that individuals at CHR of psychosis also have an impaired psychological response to stress. Another study also found that impaired tolerance to stress was more predictive of transition to psychosis than attenuated psychotic symptoms (Yung et al. 2005), showing that the psychological response to stress is an important predictor for psychosis. While atypical antipsychotics have been shown to reduce elevated diurnal cortisol levels (Zhang et al. 2005; Cohrs et al. 2006; Mondelli et al. 2010), antipsychotic treatment has not been shown to correct the blunted cortisol response observed in psychosis (Mondelli et al. 2010).