I have been totally off the effexor and all anti-depressants for 2 weeks now. The dizziness is getting much better however my emotions/agitation are horrible. I cry at everything and am extremely crabby/agitated. I realize most of this has to do with the withdrawal. I really want to see this through to find out if I can live without anti-depressants but at the same time I know it's very hard on my family. I have another doctor appt beginning of April and she says that if I don't feel better by then I most likely will need to go back on an anti-depressant. For the most part I agree with her. My hopes of proving her wrong as getting slim however. I'd like to know how long it took some of you who have withdrawn from anti-depressants to feel somewhat 'normal' or you knew you had to go back on them? I guess I'm asking if another month is a good amount of time for me to determine what I should do. In some ways I feel like I should start on them again now but I'm not going there yet? BTW, I am in no way feeling suicidal. Mornings seem to be my worst time and by early evenings I feel somewhat better – is this strange too? I haven't tried the CBD living water yet but did find a place near me to get it. Just havent had the time to get there. I also have the Ativan which I take one night to help with sleep. I'm trying not to take it unless really necessary. Tomorrow I have a huge even that my husband and I are in charge of so I'm planning to take an Ativan in the morning to get me through the day without falling apart (crying scene) in front of everyone (or yelling at them) :)! Thanks for all your input!!
Multiple types of anxiety: A limitation associated with CBD research is that it hasn’t been tested extensively among patients with a specific diagnostic subtype of anxiety (e.g. generalized anxiety). That said, studies note that CBD is likely efficacious in treating symptoms of many different types of anxiety including: social phobia, PTSD, panic disorder, OCD, and generalized anxiety disorder.  Therefore, individuals may derive anxiolytic benefit from CBD – regardless of their specific type of anxiety.
Again, with all things, each person will react differently so you will have to know yourself well and maybe experiment with a few different concentrations to know what is right for you.  My friend used an equal ratio of CBD to THC and after just a week, his blood pressure was down, his bowel movements were much more regular, and it helped with his lactose intolerance.
Preliminary research indicates that cannabidiol may reduce adverse effects of THC, particularly those causing intoxication and sedation, but only at high doses.[24] Safety studies of cannabidiol showed it is well-tolerated, but may cause tiredness, diarrhea, or changes in appetite as common adverse effects.[25] Epidiolex documentation lists sleepiness, insomnia and poor quality sleep, decreased appetite, diarrhea, and fatigue.[3]
Duchess was diagnosed with cancer in her right anal gland. When the cancer was removed it had spread to her left anal gland and was attached to her bowels. She was given 3 months to live. Since then I have had 2 vets check her glands and have had complete physical. She has a clean bill of health. I am so grateful to you. We are going to start on a maintenance program. I tell everyone how she has done. Thanks

Following cloning of the endogenous receptor for THC, namely the CB1R, endogenous CB1R ligands, or “endocannabinoids” (eCBs) were discovered, namely anandamide (AEA) and 2-arachidonoylglycerol (reviewed in [22]). The CB1R is an inhibitory Gi/o protein-coupled receptor that is mainly localized to nerve terminals, and is expressed on both γ-aminobutryic acid-ergic and glutamatergic neurons. eCBs are fatty acid derivatives that are synthesized on demand in response to neuronal depolarization and Ca2+ influx, via cleavage of membrane phospholipids. The primary mechanism by which eCBs regulate synaptic function is retrograde signaling, wherein eCBs produced by depolarization of the postsynaptic neuron activate presynaptic CB1Rs, leading to inhibition of neurotransmitter release [23]. The “eCB system” includes AEA and 2-arachidonoylglycerol; their respective degradative enzymes fatty acid amide hydroxylase (FAAH) and monoacylglycerol lipase; the CB1R and related CB2 receptor (the latter expressed mainly in the periphery); as well as several other receptors activated by eCBs, including the TRPV1 receptor, peroxisome proliferator-activated receptor-γ, and G protein-coupled 55 receptor, which functionally interact with CB1R signaling (reviewed in [21, 24]). Interactions with the TRPV1 receptor, in particular, appear to be critical in regulating the extent to which eCB release leads to inhibition or facilitation of presynaptic neurotransmitter release [25]. The TRPV1 receptor is a postsynaptic cation channel that underlies sensation of noxious heat in the periphery, with capsacin (hot chili) as an exogenous ligand. TRPV1 receptors are also expressed in the brain, including the amygdala, periaqueductal grey, hippocampus, and other areas [26, 27].


A review published in 2017 in the journal Frontiers in Pharmacology described how CBD may work to protect the hippocampus — the part of the brain responsible for several important functions, such as learning, memory and navigation — during times of stress, and may also help prevent brain-cell destruction that results from schizophrenia. Another 2017 review published in the journal Annals of Palliative Medicine summarized a handful of studies that suggest cannabis oils containing THC or CBD, or both, may help with chronic pain management, but the mechanism is unclear.

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