Phone Therapy, Exercise Helpful in Chronic Widespread Pain

Megan Brooks www.medscape.com

November 22, 2011 — Both brief cognitive behavioral therapy (CBT) delivered by telephone and exercise can yield "substantial, significant, and clinically meaningful" improvements in global health in adults with chronic widespread pain, according to a new study from the United Kingdom.

The study, by John McBeth, PhD, from the Arthritis Research UK Primary Care Centre, Keele University, Staffordshire, and colleagues, was published online November 14 in the Archives of Internal Medicine.

Non-opioid-based alternatives to chronic pain management are "desperately needed," Seth A. Berkowitz, MD, and Mitchell H. Katz, MD, from the Los Angeles County Department of Health Services, California, point out in an accompanying editorial. The current study makes "an important contribution" to that goal, they write.

"An Important Contribution"

In their article, the researchers note that no drugs are currently approved in the United Kingdom for chronic, widespread pain, the cardinal feature of fibromyalgia. In addition, none of the 3 drugs currently approved in the United States (duloxetine hydrochloride, milnacipram hydrochloride, and pregabalin) adequately controls the multiple symptoms of fibromyalgia.

Current guidelines recommend pharmacological, physical, and psychological therapies, although the value of individual therapies is unclear. Traditional CBT has shown promise for fibromyalgia, and telephone-based CBT (TCBT) is potentially more acceptable, accessible, and cost-effective.

Dr. McBeth's team randomly assigned 442 patients meeting American College of Rheumatology criteria for chronic widespread pain to 6 months of TCBT, graded exercise, both interventions, or usual care (control group).

TCBT was delivered by a trained therapist and involved an initial assessment and 7 weekly sessions, each lasting 30 to 45 minutes, plus 1 session 3 and 6 months after randomization. The exercise intervention involved 6 monthly sessions led by a fitness instructor who took a 1-day training session on exercise for chronic pain. Exercisers were also encouraged to be physically active and work out at least twice a week on their own.

Usual care was delivered by the patients' family physician, and the precise nature of the care was not known.

TCBT, Exercise Bests Usual Care

At the end of the intervention (6 months), and at 9 months after randomization, significantly more patients in the TCBT, exercise, and combined groups reported a positive outcome compared with those patients the usual care group. A positive outcome was defined as feeling "much better" or "very much better" on a standard self-rated global assessment scale.

....

"Receiving both interventions was associated with a slight improvement in outcome but were not substantially better than single treatments," Dr. McBeth and colleagues note in their report.

"It's interesting that the TCBT continued to show improvements over time, while the benefits of exercise began to decrease with time (as is usual in exercise interventions)," Dr. McBeth told Medscape Medical News.

After adjusting for age, sex, center, and baseline predictors of outcome, the likelihood of a positive outcome was significantly higher with TCBT, exercise, or both, relative to usual care.

....

Despite meaningful improvements in self-rated global health with TCBT and exercise, there was no apparent effect on chronic pain grade, the investigators report.

Increased Availability at Lower Cost

Although CBT and physical exercise are recommended for patients with chronic widespread pain, evidence to date in support of these modalities is equivocal, Dr. McBeth and colleagues note in their article.

"I think this has risen, in part, due to methodological limitations in some previous studies," such as small sample sizes, Dr. McBeth told Medscape Medical News. "However, the results of 2 recently published meta-analyses were also equivocal."

He says there are several possible reasons why CBT and exercise had a significant effect in their study.

"Our study was conducted among patients presenting to primary, rather than secondary, care, with possibly lower levels of factors such as psychological distress that may influence response to treatment," he explained. Also, "the therapists delivering treatment were very experienced, and adherence to the treatment was very high possibly due to the nature of treatment delivery (ie, patients weren't required to get to a therapists office)."

Delivering CBT by telephone should "increase treatment availability at lower costs," Dr. McBeth predicted.

Although an economic analysis suggested that in the short follow-up period TCBT was not more cost-effective than usual care, "there was a trend towards cost-effectiveness. It will be interesting to follow these patients up for a longer period to determine whether, over the longer term, TCBT is a more cost-effective option," Dr. McBeth said.

Dr. Katz told Medscape Medical News that CBT "done in person or by phone could save money because patients will get fewer unnecessary tests and medications and specialty visits."

Putting Patients in Charge

In their commentary, Dr. Katz and Dr. Berkowitz note that CBT and exercise "represent a management strategy that puts patients firmly in charge. The skills learned in CBT, for example, are available after hours and over long weekends and do not require monthly refills. Moreover, because CBT can be administered by telephone, this intervention is convenient and can be made available to a wide range of patients."

"As practicing physicians who treat many patients with chronic pain, we welcome additional research that seeks to minimize the use of pharmacotherapy, with its unclear efficacy and attendant consequences, in favor of a regimen that focuses, in a truly patient-centered way, on teaching skills for self-management of symptoms and return to meaningful lives," they write.

....

Arch Intern Med. Published online November 14, 2011. Abstract, Editorial

http://www.medscape.com/viewarticle/754047

I know there are already tons of tips on here, but I thought it’d be good to see them in an actual person’s day.

While we respect our members' attempts to make sense of withdrawal, this site follows a model of withdrawal syndrome in which there is an acute neurobiological phase that may transition within a month or so to a protracted neurobiological phase that may last years. (Many people will recover in the acute phase.) Of course, along the way, a person suffering withdrawal syndrome may have opinions and emotions about their distressing symptoms and possible disability that may become habits of mind, generating their own distress, but we hold withdrawal syndrome is not primarily psychological, it is biological.

Over all psychotropics, including addictive drugs and prescription psychotropics, acute withdrawal symptoms last a few weeks. This is explained in 

Hi Everyone!  I felt it was important to give a quick understanding about what I have learned through withdrawal and how to possibly break the cycle of the extended withdrawal loop.

I believe withdrawal is only 2-6 weeks in length.  I am not a doctor, but when the doctor says that withdrawal is only this long, I believe they are right.  The issue they don’t understand is the loops our brains go into that keep the symptoms going for much longer.

What happens is our nervous system and our brain becomes hypersensitive during this process.  As I have learned, withdrawal is basically emotional/physical trauma according to our brains.  When you go through such a difficult period of brain zaps, bad digestion, insomnia, headaches, and the list can go on and on.   I haven’t even mentioned the completely weird symptoms that make no sense that every doctor thinks you have some serious condition.   So now our brain has gone through some serious trauma of symptoms that a lot of us have never had or maybe haven’t had in a long time.   What is happening right now is your subconscious is sending these alerts to conscious brain that we are “under attack”, “something bad is happening”, “be hyper vigilant”!  So the conscious brain starts to worry, trys to fix it, starts googling, starts focusing on symptoms, fear, fear, fear, fear (creates neural pathways), go on forums and see if people have the same symptoms (which is fear).  It then goes back to our subconscious and reaffirms this which then starts firing up the defense system AKA fight or flight.  When you are in fight or flight guess what happens, more symptoms and then the loops start all over again.

So how do we break this loop?  For me, these are the biggest things that have helped.

1.       Mindfulness.  You have to first be aware of your thoughts in the conscious stage of this loop.  You can’t fix the symptoms, but the thoughts/feelings you can rewire which will eventually stop the symptoms.

2.       Find a program like Gupta Programme, or  DNRS.  These are both neural retraining programs that help you catch the loop and rewire it.

3.       Realize that nothing is wrong with you and that you can heal and that you are just in a loop in your brain.  The more we are stuck in the in fear (angry, jealousy, inner critic, shame, etc) the more our bodies are pumping us with stress hormones that create symptoms.  The more we are in the feeling of LOVE, the happy chemicals that heal us like serotonin, dopamine, etc.  Our bodies have a internal pharmacy that can heal anything IMO, we just need to put ourselves in the rest and digest mode in order to have our bodies heal ourselves.  Also of course diet and other things.  This bullet point is important that you are 100% believe this.

4.       Meditation.  This really helps to calm your nervous system down.  But you really need to do it for 20-30 minutes a day.

Here is just a small sample of something I have learned on my journey.  I hope to one day possibly be a coach where I can guide people through what exactly I did.  Most of my information is all from the retraining programs I took.   I still get into loops but I can quickly get myself out of them because I no longer fear my body.  I realize that once I get IBS, or if I get a headache my body is just telling me something.  Its always because I am not aligned with love which I have found is always the emotional cause of it.    When I am aligned with worry or fear my body is sensitive and I get symptoms.   It’s a reminder to get back to my true nature.  Joy and happiness.

Ferritin is a universal intracellular protein that stores iron and releases it in a controlled fashion. The protein is produced by almost all living organisms, including archaea, bacteria, algae, higher plants, and animals. In humans, it acts as a buffer against iron deficiency and iron overload. Wikipedia 

Sorry i posted this somewhere else and just copying and pasting for some advise. My doctor said its normal but im beginning to doubt anything she is saying (Always misdiagnosing me)

 i have severe fatigue, always feel run-down, losing hair, nails brittle etc etc The results:

IRON 26.2 (Ref 10-30)
TRANSFERRIN 2.9 (Ref 2-3.6)
TRANSFERRIN SATURATION 36% (Ref 15-50)

This is concerning me:

FERRITIN 23 (Ref 11-306.80)

I know the reference rage for the ferritin is 11-306.8 but 23 is really low and i read online its very low for anyone and it means i might have anemia.

Weighted blankets & Bed Tents for restlessness, akathisia, insomnia and anxiety

Blog: My Akathisia Experience by akathisiainfo contains many reports of drug-induced akathisia and recovery from it

NOTICE This is a poster circulating on Facebook. It is inaccurate and not endorsed by the Akathisia Alliance. The symptoms it attributes to akathisia mostly do NOT describe akathisia.

Addition September 15, 2022:

Due to the tireless work of patient advocates over the last several years, akathisia has become a better known adverse effect of drugs. However, I have seen more drug-induced activation than akathisia. Quite frequently, members report here they have "akathisia" when they're taking too many "brakes" (sedating drugs such as benzodiazepines, antipsychotics, sleep drugs, etc.). This is not what I would call akathisia but activation from the paradoxical effect of sedating drugs at doses that are too high. 

If you take too many "brakes", your nervous system rebels against being so pressed down, responding with symptoms of activation that might be taken for akathisia. That is a paradoxical reaction, because the drugs are supposed to be calming rather than activating. You have control over a paradoxical reaction, because you can eliminate it by reducing the drug.

You do not have control over akathisia, which is related to a movement disorder, and may persist or emerge after you reduce the drug.

- Altostrata

There's an interesting discussion of akathisia buried in this May 25, 2011 post by psychiatrist Steve Balt http://carlatpsychiatry.blogspot.com/2011/05/horizant-second-coming-of-gabapentin.html

".... However, the symptoms of RLS (restless leg syndrome) are rather nonspecific: "an urge to move the limbs, which improves with activity and worsens with rest." That's about it. Which leads to yet another problem (a problem that GSK and Xenoport don't see as a problem, that's for sure): with such vague and common symptoms (who among us hasn't felt somewhat restless at times, with interrupted sleep?), a lot of people might get diagnosed with RLS when their symptoms are actually due to something else.

A while back, a fellow blogger directed me to the RLS "patient page" on the National Institutes of Health (NIH) web site, where RLS was—and still is—referred to as "akathisia." However, these may be two entirely different things. Akathisia (from the Greek for "not sitting still") has long been recognized as a side effect of some—perhaps most—psychiatric medications, from antipsychotics to antidepressants. It is often described as an "inner restlessness," a "need to keep moving." Sometimes it's associated with extreme emotional distress. In terms of severity, it can range from a mild nuisance to—in some cases—aggressive tendencies. (Indeed, the psychiatrist David Healy has even linked psychotropic-induced akathisia to suicide attempts and violent behavior.)

Psychiatrists really don't know exactly what causes akathisia, and disagree on how to treat it. It may have something to do with dopamine blockade, or something completely independent. Treatment might consist of benzodiazepines (like Ativan or Valium), beta blockers (like propranolol), or discontinuing the drug that caused it in the first place.

Unlike RLS, which seems to bother people most when they are lying down (hence its tendency to disrupt sleep), drug-induced akathisia is worse when people are awake and moving around. Sounds like a simple distinction. But nothing is quite this simple, particularly when psychiatric drugs—and real people—are involved. In fact, many psychiatric meds can cause other motor side effects, too, involving (theoretically) yet other neural pathways, such as "parkinsonian" side effects like rigidity and tremor. In fact, some antipsychotic drug trials show "restlessness" and "akathisia" as entirely separate side effects (and when I've tried to ask experts to explain the difference, I have never received a straightforward answer.) ...."

Im quite in a bad spot right now, just looking for others who have had a setback far out and made it to the other side.

Had an extremely severe setback 6 months ago and it hasnt let up yet. Im afraid and feeling quite hopeless and tired since its been going on for so long now. I have also developed new symptoms and as usual my tests are all normal.

That procedure is supposedly extremely expensive and of course invasive, so I've been looking up other ways of stimulating the vagus nerve. Apparently, you can do this just through deep, slow belly breathing. Click here for one method.

Over the past year I have sometimes been able to do deep breathing, usually when I am walking, that leaves me feeling with a sense of relief and well-being. Almost like a bit of a high. Not a too-much-oxygen high, but more like a sense of deep calm and well-being nearing on pleasure (like swimming in the ocean and then lying on a warm beach). I can't always get it right, but right now I tried deep belly breathing and felt it again. I don't know how well it would work if I was deep in AM anxiety, but I'm going to try it. As soon as I stop doing the breathing the feeling disperses, but I think if I did this a few times a day I could probably get my anxiety levels down.

Apparently you can also stimulate vagus nerve endings in your ear with your finger, by doing the Valsava maneuver, and by carotid sinus pressure (which can be dangerous).

Google for more info! There is everything from how yoga helps stimulate the vagus nerve to interest in it in relation to Kundalini awakening. (Not sure what to think about kundalini awakening, but the link is a good read anyway.)

From Wikipedia, the free encyclopedia

"Phe" redirects here. For other uses, see Phe (disambiguation).

Phenylalanine

IUPAC name[hide]

Phenylalanine

Other names[hide]

2-Amino-3-phenylpropanoic acid

Identifiers

CAS number 150-30-1 (DL) , 63-91-2 (L)

PubChem 994

ChemSpider 5910

UNII 8P946UF12S

DrugBank DB00120

KEGG D00021

ChEBI CHEBI:58095

ChEMBL CHEMBL301523

Jmol-3D images Image 1

SMILES

[show]

InChI

[show]

Properties

Molecular formula C9H11NO2

Molar mass 165.19 g mol−1

Acidity (pKa) 1.83 (carboxyl), 9.13 (amino)[1]

Hazards

MSDS External MSDS

NFPA 704

120

Supplementary data page

Structure and

properties n, εr, etc.

Thermodynamic

data Phase behaviour

Solid, liquid, gas

Spectral data UV, IR, NMR, MS

(verify) (what is: /?)

Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)

Infobox references

Phenylalanine (pron.: /fɛnəlˈəlɒˈniːn/) (abbreviated as Phe or F)[2] is an α-amino acid with the formula C6H5CH2CH(NH2)COOH. This essential amino acid is classified as nonpolar because of the hydrophobic nature of the benzyl side chain. L-Phenylalanine (LPA) is an electrically neutral amino acid, one of the twenty common amino acids used to biochemically form proteins, coded for by DNA. The codons for L-phenylalanine are UUU and UUC. Phenylalanine is a precursor for tyrosine, the monoamine signaling molecules dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), and the skin pigment melanin.

Phenylalanine is found naturally in the breast milk of mammals. It is used in the manufacture of food and drink products and sold as a nutritional supplement for its reputed analgesic and antidepressant effects. It is a direct precursor to the neuromodulator phenylethylamine, a commonly used dietary supplement.

Contents [hide]

1 Other biological roles

1.1 In plants

2 Phenylketonuria

3 D-, L- and DL-phenylalanine

4 Commercial synthesis

5 History

6 See also

7 References

8 External links

[edit]Other biological roles

L-Phenylalanine is biologically converted into L-tyrosine, another one of the DNA-encoded amino acids. L-tyrosine in turn is converted into L-DOPA, which is further converted into dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline). The latter three are known as the catecholamines.

Phenylalanine uses the same active transport channel as tryptophan to cross the blood–brain barrier, and, in large quantities, interferes with the production of serotonin.

[edit]In plants

Phenylalanine is the starting compound used in the flavonoid biosynthesis. Lignan is derived from phenylalanine and from tyrosine. Phenylalanine is converted to cinnamic acid by the enzyme phenylalanine ammonia-lyase.[3]

[edit]Phenylketonuria

Main article: Phenylketonuria

The genetic disorder phenylketonuria (PKU) is the inability to metabolize phenylalanine. Individuals with this disorder are known as "phenylketonurics" and must regulate their intake of phenylalanine. A (rare) "variant form" of phenylketonuria called hyperphenylalaninemia is caused by the inability to synthesize a coenzyme called biopterin, which can be supplemented. Pregnant women with hyperphenylalaninemia may show similar symptoms of the disorder (high levels of phenylalanine in blood) but these indicators will usually disappear at the end of gestation. Individuals who cannot metabolize phenylalanine must monitor their intake of protein to control the buildup of phenylalanine as their bodies convert protein into its component amino acids.

Phenylketonurics often use blood tests to monitor the amount of phenylalanine in their blood. Lab results may report phenylalanine levels in different units, including mg/dL and μmol/L. One mg/dL of phenylalanine is approximately equivalent to 60 μmol/L.

A non-food source of phenylalanine is the artificial sweetener aspartame. This compound, sold under the trade names Equal and NutraSweet, is metabolized by the body into several chemical byproducts including phenylalanine. The breakdown problems phenylketonurics have with protein and the attendant build up of phenylalanine in the body also occurs with the ingestion of aspartame, although to a lesser degree. Accordingly, all products in Australia, the U.S. and Canada that contain aspartame must be labeled: "Phenylketonurics: Contains phenylalanine." In the UK, foods containing aspartame must carry ingredient panels that refer to the presence of "aspartame or E951"[4] and they must be labeled with a warning "Contains a source of phenylalanine." In Brazil, the label "Contém Fenilalanina" (Portuguese for "Contains Phenylalanine") is also mandatory in products which contain it. These warnings are placed to aid individuals who suffer from PKU so that they can avoid such foods.

Geneticists have recently sequenced the genome of macaques. Their investigations have found "some instances where the normal form of the macaque protein looks like the diseased human protein" including markers for PKU.[5]

[edit]D-, L- and DL-phenylalanine

The stereoisomer D-phenylalanine (DPA) can be produced by conventional organic synthesis, either as a single enantiomer or as a component of the racemic mixture. It does not participate in protein biosynthesis although it is found in proteins in small amounts - particularly aged proteins and food proteins that have been processed. The biological functions of D-amino acids remain unclear although some, such as D-phenylalanine, may have pharmacological activity.[citation needed] D-phenylalanine, in particular, has been postulated to inhibit the enzymes that breakdown enkephalins, giving it a potential analgesic profile.

DL-Phenylalanine (DLPA) is marketed as a nutritional supplement for its supposed analgesic and antidepressant activities. DL-Phenylalanine is a mixture of D-phenylalanine and L-phenylalanine. The reputed analgesic activity of DL-phenylalanine may be explained by the possible blockage by D-phenylalanine of enkephalin degradation by the enzyme carboxypeptidase A.[6] The mechanism of DL-phenylalanine's supposed antidepressant activity may be accounted for by the precursor role of L-phenylalanine in the synthesis of the neurotransmitters norepinephrine and dopamine. Elevated brain levels of norepinephrine and dopamine are thought to have an antidepressant effect. D-Phenylalanine is absorbed from the small intestine and transported to the liver via the portal circulation. A small amount of D-phenylalanine appears to be converted to L-phenylalanine. D-Phenylalanine is distributed to the various tissues of the body via the systemic circulation. It appears to cross the blood–brain barrier less efficiently than L-phenylalanine, and so a small amount of an ingested dose of D-phenylalanine is excreted in the urine without penetrating the central nervous system[citation needed].

L-Phenylalanine is an antagonist at α2δ Ca2+ calcium channels with a Ki of 980 nM.[7] At higher doses, this may play a role in its analgesic and antidepressant properties.

In the brain, L-phenylalanine is a competitive antagonist at the glycine binding site of NMDA receptor[8] and at the glutamate binding site of AMPA receptor.[9] At the glycine binding site of NMDA receptor L-phenylalanine has an apparent equilibrium dissociation constant (KB) of 573 µM estimated by Schild regression[10] which is considerably lower than brain L-phenylalanine concentration observed in untreated human phenylketonuria.[11] L-Phenylalanine also inhibits neurotransmitter release at glutamatergic synapses in hippocampus and cortex with IC50 of 980 µM, a brain concentration seen in classical phenylketonuria, whereas D-phenylalanine has a significantly smaller effect.[12]

[edit]Commercial synthesis

L-Phenylalanine is produced for medical, feed, and nutritional applications, such as aspartame, in large quantities by utilizing the bacterium Escherichia coli, which naturally produces aromatic amino acids like phenylalanine. The quantity of L-phenylalanine produced commercially has been increased by genetically engineering E. coli, such as by altering the regulatory promoters or amplifying the number of genes controlling enzymes responsible for the synthesis of the amino acid. [13]

[edit]History

The first description of phenylalanine was made in 1879, when Schulze and Barbieri identified a compound with the empirical formula, C9H11NO2, in yellow lupine (Lupinus luteus) seedlings. In 1882, Erlenmeyer and Lipp first synthesized phenylalanine from phenylacetaldehyde, hydrogen cyanide, and ammonia.[14][15]

The genetic codon for phenylalanine was first discovered by J. Heinrich Matthaei and Marshall W. Nirenberg in 1961. They showed that by using m-RNA to insert multiple uracil repeats into the genome of the bacterium E. coli, they could cause the bacterium to produce a polypeptide consisting solely of repeated phenylalanine amino acids. This discovery helped to establish the nature of the coding relationship that links information stored in genomic nucleic acid with protein expression in the living cell.

[edit]See also

Hyperphenylalanemia

[edit]References

^ Dawson, R. M. C. et al. (1959). Data for Biochemical Research. Oxford: Clarendon Press.

^ IUPAC-IUBMB Joint Commission on Biochemical Nomenclature (1983). "Nomenclature and Symbolism for Amino Acids and Peptides". Recommendations on Organic & Biochemical Nomenclature, Symbols & Terminology etc.. Retrieved 2007-05-17.

^ Nelson, D. L.; Cox, M. M. (2000). Lehninger, Principles of Biochemistry (3rd ed.). New York: Worth Publishing. ISBN 1-57259-153-6.

^ "Aspartame". UK: Food Standards Agency.

^ Gibbs, R. A. et al. (2007). "Evolutionary and Biomedical Insights from the Rhesus Macaque Genome" (pdf). Science 316 (5822): 222–234. doi:10.1126/science.1139247. PMID 17431167.

^ Christianson, D. W.; Mangani, S.; Shoham, G.; Lipscomb, W. N. (1989). "Binding of D-Phenylalanine and D-Tyrosine to Carboxypeptidase A" (pdf). Journal of Biological Chemistry 264 (22): 12849–12853. PMID 2568989.

^ Mortell KH, Anderson DJ, Lynch JJ, et al. (March 2006). "Structure-activity relationships of alpha-amino acid ligands for the alpha2delta subunit of voltage-gated calcium channels". Bioorganic & Medicinal Chemistry Letters 16 (5): 1138–41. doi:10.1016/j.bmcl.2005.11.108. PMID 16380257.

^ Glushakov, AV; Dennis, DM; Morey, TE; Sumners, C; Cucchiara, RF; Seubert, CN; Martynyuk, AE (2002). "Specific inhibition of N-methyl-D-aspartate receptor function in rat hippocampal neurons by L-phenylalanine at concentrations observed during phenylketonuria.". Molecular psychiatry 7 (4): 359–67. doi:10.1038/sj.mp.4000976. PMID 11986979.

^ Glushakov, AV; Dennis, DM; Sumners, C; Seubert, CN; Martynyuk, AE (2003 Apr 1). "L-phenylalanine selectively depresses currents at glutamatergic excitatory synapses.". Journal of neuroscience research 72 (1): 116–24. doi:10.1002/jnr.10569. PMID 12645085.

^ Glushakov, AV; Glushakova, O; Varshney, M; Bajpai, LK; Sumners, C; Laipis, PJ; Embury, JE; Baker, SP; Otero, DH; Dennis, DM; Seubert, CN; Martynyuk, AE (2005 Feb). "Long-term changes in glutamatergic synaptic transmission in phenylketonuria.". Brain : a journal of neurology 128 (Pt 2): 300–7. doi:10.1093/brain/awh354. PMID 15634735.

^ Möller, HE; Weglage, J; Bick, U; Wiedermann, D; Feldmann, R; Ullrich, K (2003 Dec). "Brain imaging and proton magnetic resonance spectroscopy in patients with phenylketonuria.". Pediatrics 112 (6 Pt 2): 1580–3. PMID 14654669.

^ Glushakov, AV; Dennis, DM; Sumners, C; Seubert, CN; Martynyuk, AE (2003 Apr 1). "L-phenylalanine selectively depresses currents at glutamatergic excitatory synapses.". Journal of neuroscience research 72 (1): 116–24. doi:10.1002/jnr.10569. PMID 12645085.

^ Sprenger, G. A. (2007). "Aromatic Amino Acids". Amino Acid Biosynthesis: Pathways, Regulation and Metabolic Engineering (1st ed.). Springer. pp. 106–113. ISBN 978-3-540-48595-7.

^ Thorpe, T. E. (1913). A Dictionary of Applied Chemistry. Longmans, Green, and Co.. pp. 191–193. Retrieved 2012-06-04.

^ Plimmer, R. H. A. (1912) [1908]. Plimmer, R. H. A.; Hopkins, F. G.. ed. The Chemical Composition of the Proteins. Monographs on Biochemistry. Part I. Analysis (2nd ed.). London: Longmans, Green and Co.. pp. 93–97. Retrieved 2012-06-04.

[edit]External links

Phenylalanine at ChemSynthesis

Food Sources of Phenylalanine

[show] v t e

The 20 common amino acids

[show] v t e

Amino acid metabolism metabolic intermediates

[show] v t e

Analgesics (N02A, N02B)

[show] v t e

Antidepressants (N06A)

[show] v t e

Anxiolytics (N05B)

[show] v t e

Dopaminergics

[show] v t e

Phenethylamines

Categories: Animal productsProteinogenic amino acidsGlucogenic amino acidsKetogenic amino acidsAromatic amino acidsEssential amino acidsEnkephalinase inhibitors

Mushrooms provide a vast array of potential medicinal compounds. Many mushrooms -- such as portobello, oyster, reishi and maitake -- are well-known for these properties, but the lion's mane mushroom, in particular, has drawn the attention of researchers for its notable nerve-regenerative properties.

Lion's mane mushrooms are not your classic looking cap-and-stem variety. These globular-shaped mushrooms sport cascading teeth-like spines rather than the more common gills. From these spines, white spores emerge. Lion's mane mushrooms also have other common names: sheep's head, bear's head and the Japanese yamabushitake. I like the clever name "pom pom blanc" -- a reference to their resemblance to the white pom-poms cheerleaders use. The Latin name for lion's mane is Hericium erinaceus; both names mean "hedgehog."*

2012-08-08-Images1and2.jpg

Lion's mane mushrooms are increasingly sold by gourmet food chains. This nutritious mushroom is roughly 20 percent protein, and one of the few that can taste like lobster or shrimp (Stamets, 2005). Lion's mane is best when caramelized in olive oil, deglazed with saké wine, and then finished with butter to taste. Lion's mane can be bitter if not cooked until crispy along the edges. It takes some practice to elicit their full flavor potential.

Lion's mane mushrooms are increasingly studied for their neuroprotective effects. Two novel classes of Nerve Growth Factors (NGFs) -- molecules stimulating the differentiation and re-myelination of neurons -- have been discovered in this mushroom so far. These cyathane derivatives are termed "hericenones" and "erinacines." The levels of these compounds can vary substantially between strains, based on the measurements our team has conducted.

About a dozen studies have been published on the neuroregenerative properties of lion's mane mushrooms since 1991, when Dr. Kawagishi first identified NGFs in Japanese samples. Since his original discovery, in vitro and in vivo tests have confirmed that hericenones and erinacines stimulate nerve regeneration. In 2009, researchers at the Hokuto Corporation and the Isogo Central and Neurosurgical Hospital published a small clinical study. Giving lion's mane to 30 Japanese patients with mild cognitive impairment resulted in significant benefits for as long as they consumed the mushrooms:

"The subjects of the Yamabushitake group took four 250 mg tablets containing 96 percent of Yamabushitake dry powder three times a day for 16 weeks. After termination of the intake, the subjects were observed for the next four weeks. At weeks eight, 12 and 16 of the trial, the Yamabushitake group showed significantly increased scores on the cognitive function scale compared with the placebo group. The Yamabushitake group's scores increased with the duration of intake, but at week four after the termination of the 16 weeks intake, the scores decreased significantly." (Mori, 2009)

Recently, mice were injected with neurotoxic peptides in an experiment to assess the effects of lion's mane on the type of amyloid plaque formation seen in Alzheimer's patients. The mice were then challenged in a standard "Y" maze, designed for testing memory. Mice fed with a normal diet were compared to those supplemented with lion's mane mushrooms. As the peptide-induced plaque developed, the mice lost the ability to memorize the maze. When these memory-impaired mice were fed a diet containing 5 percent dried lion's mane mushrooms for 23 days, the mice performed significantly better in the Y maze test. Interestingly, the mice regained another cognitive capacity, something comparable to curiosity, as measured by greater time spent exploring novel objects compared to familiar ones.

The reduction of beta amyloid plaques in the brains of mushroom-fed mice vs. the mice not fed any mushrooms was remarkable. The formation of amyloid plaques is what many researchers believe is a primary morphological biomarker associated with Alzheimer's. Plaques linked to beta amyloid peptide inflame brain tissue, interfere with healthy neuron transmission, and are indicated in nerve degeneration.

The medical community is bracing for an increase of patients with Alzheimer's and senile dementia as the baby boomer population ages. Mortality trends related to Alzheimer's are outpacing death rates of many other diseases. This makes preventive and curative treatments of age-related cognitive diseases hot subjects of research. In the past 10 years, deaths from Alzheimer's disease have surged roughly 66 percent, while deaths from other primary diseases have generally declined.

The influence of lion's mane influence on neurological functions may also have other added benefits -- making you feel good. In another small clinical study (n=30), post-menopausal women who consumed lion's mane baked into cookies vs. those without showed less anxiety and depression yet improved in their ability to concentrate (Nagano et al., 2010).

2012-08-08-Image3.jpg

Dusty Yao with lion's mane cultivated three months from the time the wild specimen, featured in photograph, was collected.

Is this data conclusive thus far? No.

Is this data suggestive of positive outcomes? Absolutely.

In another small Japanese study with a randomized sample of 30 women, ingesting lion's mane showed that "HE intake has the possibility to reduce depression and anxiety, and these results suggest a different mechanism from NGF-enhancing action of H. erinaceus." (Nagano et al. 2010).

In light of the numerous diseases related to neurodegeneration, lion's mane deserves more clinical attention. If lion's mane enhances memory and is an antidepressant, can consuming this mushroom alter the course of Alzheimer's and other neurodegenerative diseases? Could this mushroom help Parkinson's patients or those with multiple sclerosis, or maybe maintain your mental acumen as you age? Lion's mane is a relatively inexpensive, easily-cultivated fungal food that may prove to be therapeutic in ways beyond being tasty.

Lion's mane may be our first "smart" mushroom. It is a safe, edible fungus that appears to confer cognitive benefits on our aging population. Unfortunately, lion's mane is not available in most grocery stores. But you can buy kits to grow them at home, and organic lion's mane supplements are available at some health food stores. If you are skilled enough and looking for adventure, you can forage for them by hunting in the hardwood forests of North America, Europe and Asia during the summer and fall.**

2012-08-08-Images4and5.jpg

Left: Fresh, organically grown lion's mane ready for sale. Right: Close up of spore-producing spines.

*Hedgehog is a name more commonly associated with Hydnum species, specifically the edible Hyndum repandum.

**Before consuming any wild mushroom, make positively sure that it is accurately identified. For a list of mycological societies, which may be able to help you, go to the North American Mycological Association website: www.namyco.org.

References:

Kawagishi, H., Ando, M., Sakamoto, H., Yoshida S., Ojima, F., Ishiguro, Y., Ukai, N., Fukukawa, S. 1991. "Hericenone C, D and E, stimulators of nerve growth factor (NGF) synthesis from the mushroom Hericium erinaceum." Tetrahedron Lett 32, 4561-4564.

Ma, Bing-Ji , Jin-Wen Shen, Hai-You Yu, Yuan Ruan, Ting-Ting Wu & Xu Zhao, 2010. "Hericenones and erinacines: stimulators of nerve growth factor (NGF) biosynthesis in Hericium erinaceus." Mycology: An International Journal on Fungal Biology. 1(2): 92-98.

Mori, K., Inatomi, S., Ouchi, K. Azumi, Y and Tuchida T. 2009. "Improving effects of the mushroom Yamabushitake (Hericium erinaceus) on mild cognitive impairment: a double blinded, placebo controlled clinical trial." Phytother Res. 23:367-372.

Mori, K., Obara, Y., Moriya, T., Inatomi, S., Nakahata, N. 2011. "Effects of Hericium erinaceus on amyloid β(25-35) peptide-induced learning and memory deficits in mice." Biomed Res. 32(1):67-72.

Nagano, M., Shimizu, K., Kondo, R., Hayashi, C., Sato, D., Kitagawa, K., Ohnuki, K. 2010. "Reduction of depression and anxiety by 4 weeks Hericium erinaceus intake." Biomed Res. 31(4):231-7.

Stamets, P., "Notes on nutritional properties of culinary-medicinal mushrooms." International Journal of Medicinal Mushrooms. 2005; 7:109-116.

Thal, L.J., Kantarci, K., Reiman, E.M., Klunk, W.E., Weiner, M.W., Zetterberg, H., Galasko, D., Praticò, D., Griffin, S., Schenk, D., Siemers, E. 2006. "The role of biomarkers in clinical trials for Alzheimer disease." 20(1):6-15.

For more by Paul Stamets, click here.

For more on natural health, click here.

Non-drug techniques to cope with emotional symptoms

Deep emotional pain and crying spells, spontaneous weeping

Health anxiety, hypochondria, and obsession with symptoms

Shame, guilt, regret, and self-criticism

Dealing With Emotional Spirals

What is happening in your brain?

Withdrawal dialogues & encouragement

If you feel you cannot manage your thoughts and are actually suicidal, seek face-to-face help immediately, see For those who are feeling desperate or suicidal

For many reasons, our emotions are on a hair-trigger, amplified, and perseverative. We probably don't even know all of what's going on physically yet, but it includes diminished prefrontal lobe executive functions, rebound amygdala, dysregulated HPA, over-active adrenals, etc.

The neuro-emotions include --

neuro-fear

neuro-anger

neuro-guilt

neuro-shame

neuro-hurt

neuro-regret

neuro-self-criticism

neuro-grudge-holding

...and more!

It is very, very confusing to have these intense neuro-emotions and try to remember that they are not what they appear to be. Emotions are compelling. Emotions during recovery from psych meds are even more compelling.

Sometimes, the neuro-emotion is really totally artificial. Some of my neuro-fears have been so unlikely to come to pass as to bear no resemblance to reality or to my personal history.

But, I think a lot of the time, part of what makes it so confusing is that there is a grain of reality to the neuro-emotion. For example, some situation might make you a bit angry under normal circumstances, but the neuro-anger is huge. This is when it's very difficult to 1) catch it in the first place and notice this is a neuro-emotion, 2) convince ourselves, yes, this is really a neuro-emotion, not a real emotion, 3) contain the emotion, try not to act on it, or channel the energy into something safe and constructive -- like exercise or journaling or building a birdhouse.

Whenever you're having an intense, disturbing feeling, try to remind yourself that, right now -- even if it does have something to do with reality -- it is largely a neuro-emotion that you wouldn't be feeling if you were fully healed. And you *will* be fully healed. It's happening! Get ready!

For me, when the cortisol starts to rise in the early morning, (2 to 3 AM), this happens as a sharp spike instead of a gentle rise, because my nervous system is still not fully healed from PAWS, and the FASD.  So my brain interprets this as a danger signal.  If the cortisol spike is sharp enough, this then triggers a release of adrenaline, which causes my C-PTSD brain to start scanning for danger.  High sodium and high glutamate in my system will amplify this effect.  If my blood sugar is low, it perceives this as an energy crisis, and the body quickly releases glucagon, cortisol, adrenaline, which jolts me into high alert at 3 AM.  I could have never figured this out on my own, without AI.  And, the doctors don't have time to unravel these complex issues.  

Gemini has suggested that I limit carbohydrates, and emphasize heavy proteins and healthy fats.  It also suggests that I eat a high fat and high protein snack before bedtime, and again when I wake up at 3 AM.  This alone has helped me a lot.  I also limit/avoid foods high in glutamates, sugar, simple carbs, sodium, and chemicals.  It’s a minefield when going out to eat.  I ate at a Mexican restaurant 2 days ago, and it really affected me.  But, I will use AI next time I eat out to help me select a healthy choice.  I’m limiting how much I eat out.

Just this morning, Gemini walked me through some supplements I can try, to further support and help my neurodivergent and sensitive nervous system, and help me to relax and sleep.  I will try them one at a time, to make sure I don’t react badly to them.  The ones they suggested are magnesium taurate, L-theanine, and glycine.  I have been taking a quality reishi mushroom supplement for the past week, and we will see if that helps too.  AI also made me aware that I needed to use magnesium glycinate in the evening, instead of magnesium citrate.  I was also able to import a spreadsheet with my supplements, and it tweaked that, and made sure I wasn’t taking ones at the same time that would compete with each other for absorption - for example, taking calcium at a different time than magnesium.

I’ve already experienced a big improvement in my sleep, just with the dietary changes, the changes in my magnesium, and adding the reishi mushroom extract.  It will be interesting to see how the other supplements help me.

I want to make everyone aware of how helpful AI can be in managing withdrawal, and especially when it is combined with other health and neurological issues and differences.  It is super easy to use.  Here is the link to Google’s Gemini AI. It is free to use!  There is also a paid option, which I haven’t needed yet.  I'm sure ChatGPT or other AI systems would be very helpful too.  Please realize that AI makes mistakes, so double check it and use it with discretion. 

https://gemini.google.com/app

On 12/19/2020 at 6:39 AM, MarieR said:

 

There is no such thing as an OCD person. Only OCD thoughts. All thoughts come and go. I think the point is that there is some truth to what we resists persists, to some degree. If we keep looking a those thoughts and being afraid of them, they get recognized by the brain as something important because we attach energy to them and they get cycled back a bit. Regardless, over time, they will fade. It's just so much easier on us if we relax into them as much as possible. They are only thoughts and nothing to be afraid of. Bottom line, underneath the thoughts you are mentally healthy and well. Always.

 

ADMIN NOTE

The term "OCD" has become slang for normal preoccupations or unwelcome thoughts that keep on returning. Most of these situations are not true  Obsessive Compulsive Disorder (OCD) but nagging doubts or worries, or a self-sabotaging habit of mind that can be resolved. (Still, you might have gotten a drug prescription to treat this pseudo-OCD.)

Withdrawal symptoms can bring up intense, shocking thoughts and feelings out of nowhere and are unprecedented in the person's experience. Ordinarily, we dismiss these thoughts, but the neurological condition of withdrawal seems to exacerbate them or dredge up primal fears. These arise with withdrawal symptoms and fade in the recovery process. This is not true OCD. See Neuro-emotion

However, some people have repetitive intrusive thoughts or behaviors that existed before going on drugs, even from childhood. These can be very distressing, impairing the ability to conduct a normal life. This is true Obsessive Compulsive Disorder (OCD).

Nobody on this site thinks any psychological disorders magically go away by going off psychiatric drugs. If you think the drugs are controlling certain symptoms, such as true OCD, you will need to learn to manage those symptoms without drugs.

Taking responsibility for your own health and behavior is key to going off psychiatric drugs. If you cannot do that, and the symptoms are hampering your life, perhaps tapering to the lowest effective dosage rather going off drugs should be your goal.

If you have a tendency towards obsessive anxiety about your health, no amount of reassurance from others here will have an effect on it. You must do the work yourself. Read Health anxiety, hypochondria, and obsession with symptoms

Cognitive Behavior Therapy (CBT), Dialectical Behavior Therapy (DBT), other types of psycotherapy, and meditation are non-drug ways to manage habits of obsessive thinking. People also find their own effective self-treatments, such as taking up various sports or hobbies. See Non-drug techniques to cope with emotional symptoms

SurvivingAntidepressants.org is not a general mental health support site. If you wish to talk about your obsessive preoccupations, you may wish to visit http://www.depressionforums.org/or other general mental health support sites, and post on SurvivingAntidepressants.org only when you have questions about tapering.

I would love to discuss this, as it has been one of my worst issues since I've weaned. I've struggled off and on with ocd since about 2000. Was on zoloft for a year when it first started. Was told at the time I had ppd/ocd. After that time period I'd spent many years managing it without the use of medication. Ocd became a little more bothersome after I'd learned of my husband's affair in 2009. Hello prozac. On it, things felt more calm but the issues were still there. kind of felt like they were paused. Like they were in waiting. I think the med made it feel like I didn't have to work on it because I had the buffer. It didn't bother me the way it should have. Still, it was there and I just sort of carried it around with me. The prozac numbed out the need to to truly work on it. I hope that made sense. It's kinda hard to explain. Now I'm here....in withdrawal. The ocd I'm experiencing now is so vastly different than the ocd of my past. It kind of makes a lot of what I'd once dealt with seem like a mere annoyance. (although the ppd was no picnic) (This must be the neuro-emotion that I've seen talked about here?) The ocd has become relentless. It really likes to focus on the things I love most. I would love to hear from those here that deal with obsessive thoughts and behaviors in withdrawal. How do you cope with them? What helps?

I am slowly recovering and weaning myself off Paroxetine (Paxil) after four years of hardship. 

It has been 24 months since I went cold turkey. I have suffered a lot, but I feel like I can see the light at the end of the tunnel !

I am starting to dream again, to enjoy my activities, my passions, my hobbies, and as you know, that is priceless after months/years of mental fog.

But for the past few days, I have been feeling a strange sensation in my throat, as if something were stuck there and I have a discomfort in the throat (without pain).

Add to that the fact that I'm coughing a LOT more than before, and chronically. I did some research on the internet (thanks Chat GPT) and concluded that it was probably related to laryngopharyngeal reflux !

I've never had symptoms like this before ! Yes, right now I'm eating a lot of junk food since I've regained my appetite, but I was quite surprised to have this all of a sudden.

I'm obviously going to rebalance my diet in the next few days to calm the symptoms, but I was wondering: could this be related to (another) window/wave of withdrawal ?

We know that 90% to 95% of serotonin is produced in the stomach, and the brain-gut axis has been proven to play a role in mental and physical well-being. Hence the recent research on microbiota and mental illness symptoms. Especially since gastroesophageal reflux and laryngopharyngeal reflux are linked to a problem with the upper stomach closing… via the nervous system.

With everything I've learned about the nervous system and its recovery/regeneration during withdrawal from psychiatric medication, I wondered: is it possible that it will gradually go away on its own ?

Could this problem just be a nervous system issue ? Like, my brain is trying to rewire its entire system, and it made a little mistake, and now my stomach is acting up ?

If anyone has experienced these kinds of symptoms, whether related to withdrawal or not, and could share their experience, testimony, recovery, with me, that would be great. 

Thank you guys !

There's a description of her approach here: https://www.eleanorsteinmd.ca/blog/what-is-neuroplasticity-and-how-does-it-work

and an assessment to see if you have the kind of pain she deals with: https://www.eleanorsteinmd.ca/neuroplastic-pain-assessment

She's giving a free talk and Q/A on 17th May https://momence.com/Nourish-Therapeutic-Yoga/Paths-to-Wellness%3A-Two-Holistic-Approaches-for-Chronic-Complex-Conditions/101497922?syclid=cop908sh33ns73epma3g

and there's a 55-minute youtube interview with her here :

Disclaimer: I don't know anything more about her work than I've said above. There's a fee to attend her courses.

See journal articles about PSSD in Papers about Post-SSRI Sexual Disorder (PSSD)

If you wish to discuss symptoms, theories, and treatment of PSSD, please go to these sites:

PSSD Network pssdnetwork.org 

PSSDforum https://pssdforum.org/

Yahoo group SSRIsex (log in to http://Yahoo.com to join)

Facebook group (log into Facebook.com to join)

Various pages on Rxisk.org

Please note the following:

On 6/15/2011 at 11:45 AM, Altostrata said:

Graphic descriptions of sexual organs or functioning. This is offensive to some of our members and not appropriate for this site.

SEE ALSO:

Non-drug techniques to cope with emotional symptoms

Stabilising After a Reduction - What Does That Mean?

Withdrawal Normal Description

npanth blog on Waves and Windows in SSRI Withdrawal

On 3/9/2019 at 5:08 AM, bubble said:

 

when we are in a wave it feels like we have always been unwell and like we will always be unwell.

 

___________________________________________________________________________________________

Topic Summary by KarenB June 11, 2017:

Windows and waves occur in a stair-step pattern, with a general upwards trend.

                                        After a year, a little better.

Awful

Alto:  I've experienced waves. I'll have a window when I feel better, then a wave, which feels as bad as ever, except a little different. Over time, the windows have gotten more frequent and longer and the troughs not as deep, and shorter. So, on average, I've gotten slowly better. Kind of like 1 step forward and 5 steps back, then 2 steps forward and 5 steps back, then 3 steps forward and 4 steps back, then 2 steps forward and 3 steps back, then 3 steps forward and 3 steps back....uh, where was I?

Waves mean your nervous system is struggling to heal. It moves in the right direction for a bit then falls back a bit. This is normal. You can view the "better" part of the wave as when your nervous system is finding its balance. These periods will get longer and more frequent as time goes on.

Rather than damaged receptors, I've found it more accurate to visualize post-acute withdrawal syndrome as autonomic dysregulation. The effects are generalized and when the nervous system is under stress, symptoms can reappear -- and go away again, as is common with autonomic issues.

Our nervous systems are so complicated they repair themselves in patches. Some parts recover then the whole thing needs to re-balance again. Rinse and repeat.

The windows are part of the pattern of healing. They are when your autonomic (and other) systems are working in harmony.

Withdrawal Cycles vs Other Cycles
Alto:  There are regular biological cycles, daily, monthly, seasonally etc, and there are the waves from withdrawal syndrome. Withdrawal syndrome can exacerbate some normal cycles, e.g. early morning cortisol, menstrual symptoms, or seasonal sadness. Waves from withdrawal syndrome can also come out of the blue and have no apparent relationship to any other biological pattern.

Fast Tapering and Waves
Alto: If you are tapering too fast and get withdrawal symptoms, they may fluctuate in a windows and waves pattern. This leads a lot of people to ignore the warning signs of going too fast. If you continue to taper, withdrawal symptoms probably will get worse. It's the nature of withdrawal symptoms to fluctuate, because the nervous system is trying to correct itself.

It's important to treat yourself gently. You may not be able to handle difficult situations that you've always handled before. Focus on stress reduction. Learning how to protect your nervous system from abrasive people is a good skill and will serve you well in the long run. Being pushed to take care of ourselves is, I guess you could say, one of the benefits of this awful condition.

The Importance of Flowing with the Waves

JanCarol:  There was a DIRECT CORRELATION between how hard I worked during my window / hypo-mania, and HOW LONG and DEEP my ensuing depression was.  If I got to washing the dog and mowing the lawn, it might be 3 weeks or more before I'd see the light of day.  This is a cautionary tale:  when in a window, learn to relax and flow.  Don't push.  I know, things aren't getting done, and you are tired of it - but if you push too hard, the wave will crash deeper.  See entire post - Flow with the Waves

Video
Healing from Antidepressants: Patterns of Recovery

Members' Theories on what Windows and Waves are all about
Healing:  I have heard of people having long-lasting setbacks even very far out. It's extremely upsetting. In some cases, it seems like the setback is triggered by stressful life events. My theory is that, even after we have healed a lot, we are still very fragile for a time after that. If life happens to be fairly smooth, we can function pretty well, but if life hands us a big stressor or two, we become really autonomically dysregulated. We're still more sensitive to conditions than we will be when we have healed further.

Eventually.....eventually.....we heal even more, become more robust, and stressful life events can no longer knock our nervous systems off balance so easily.

Jemima:  Because antidepressants change brain functioning by destroying serotonin receptors, recovery goes in fits and starts as these receptors regenerate. (From what I've read, this is my understanding of what getting back to health after withdrawal is all about.)

Starlitegirlx I have a theory that it's a healing process where our body is adapting and adjusting to not having the meds.  Pain or hellish days come into play, then we feel better for a bit until our body finds a new way to heal and recover which triggers the pain/suffering cycle again.

The body knows how to heal from just about anything, but often we interfere or things interfere with it (like stress, other meds or other health issues that compound one another). I like the idea of trusting in my body and believing it knows how to find its way back to its wellness.

Bad days are awful but if they mean my body is going through some kind of adaption as it heals, I feel they are worth enduring. Like when you are tired and just want to go home but traffic and bad weather slow you down and frustrate you.  Those things pass and you will get home eventually. So accepting the traffic/ bad weather as par for the course makes the journey home easier on you emotionally. It’s a simple analogy but it holds the truth of what is happening – there are storms and delays when we just want to be home (well again).

Recoveries are rarely as smooth and linear as we would like. I think it has to do with how the body has to adapt to a new status quo. Any healing is change which brings about a new status quo. So maybe this new status quo throws the workings of our systems off balance - and that's why we have waves. The body is saying 'wait, this is different than it was. Adjust! Adjust! Then as it adjusts we have the suffering we call waves. Those adjustments are probably system stressors, and we all know how sensitive we are to stressors.

I think it's why windows get longer as we progress and have healed more.  The adjustments we need to make are less because we are closing in on our original normal so the healing isn't as dramatic.  Like how a cut stings, then the scab forms and it hurts and tends to itch. That's a healing cycle. At the end, the itch is minor - like how some people who are further into recovery have less dramatic and shorter wanes.

A clear description of the healing pattern

ADMIN NOTE Original post:

In other words, when you go through a period of symptoms getting worse, and then that draws to an end, is it followed pretty obviously by a period of new gains? Are you now better than you were before the wave?

People have reported this pattern. I have never been able to discern it clearly in myself, but I'm open to the possibility. What is your experience of this yourself? Or observation of others? Or opinion?

Vitamin D3 (cholecalciferol) is the preferred form for supplementation. It is the kind naturally found in humans and easiest to absorb (from Dr. Weil http://www.drweil.com/drw/u/ART02812/vitamin-d ).
 
Adequate vitamin D is necessary to good health. It is a pro-hormone for various hormones.
 
While research is limited regarding which form is best, it seems vitamin D3 in oil is better absorbed than that in tablet form http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033429/ Sublingual may be the best way to take it; you can keep a caplet in your mouth or under your tongue until it dissolves. It also available as a liquid, with vitamin D3 in olive oil.

From US National Institutes of Health MedLine Plus http://www.nlm.nih.gov/medlineplus/ency/article/002405.htm
 

Quote

Vitamin D
Vitamin D is a fat-soluble vitamin. Fat-soluble vitamins are stored in the body's fatty tissue.

Function
Vitamin D helps the body absorb calcium. Calcium and phosphate are two minerals that are essential for normal bone formation.

Throughout childhood, your body uses these minerals to produce bones. If you do not get enough calcium, or if your body does not absorb enough calcium from your diet, bone production and bone tissues may suffer.

Vitamin D deficiency can lead to osteoporosis in adults or rickets in children.

Food Sources
The body makes vitamin D when the skin is directly exposed to the sun. That is why it is often called the "sunshine" vitamin. Most people meet at least some of their vitamin D needs this way.

Very few foods naturally contain vitamin D. As a result, many foods are fortified with vitamin D. Fortified means that vitamins have been added to the food.

Vitamin D is found in the following foods:

Dairy products

• Cheese
• Butter
• Cream
• Fortified milk (all milk in the U.S. is fortified with vitamin D)

Fatty fish (such as tuna, salmon, and mackerel)
Oysters
Fortified breakfast cereals, margarine, and soy milk (check the Nutrition Fact Panel on the food label)

It can be very hard to get enough vitamin D from food sources alone. As a result, some people may need to take a vitamin D supplement. Vitamin D found in supplements and fortified foods comes in two different forms:

• D2 (ergocalciferol)
• D3 (cholecalciferol)

Side Effects
Too much vitamin D can make the intestines absorb too much calcium. This may cause high levels of calcium in the blood. High blood calcium can lead to:

• Calcium deposits in soft tissues such as the heart and lungs
• Confusion and disorientation
• Damage to the kidneys
• Kidney stones
• Nausea, vomiting, constipation, poor appetite, weakness, and weight loss

Recommendations
Ten to 15 minutes of sunshine three times weekly is enough to produce the body's requirement of vitamin D. The sun needs to shine on the skin of your face, arms, back, or legs (without sunscreen). Because exposure to sunlight is a risk for skin cancer, you should use sunscreen after a few minutes in the sun.

People who do not live in sunny places may not make enough vitamin D. Skin that is exposed to sunshine indoors through a window will not produce vitamin D. Cloudy days, shade, and having dark-colored skin also cut down on the amount of vitamin D the skin makes.
....

In general, people over age 50 need higher amounts of vitamin D than younger people.....

Vitamin D toxicity almost always occurs from using too many supplements.

The safe upper limit for vitamin D is:

• 1,000 to 1,500 IU/day for infants
• 2,500 to 3,000 IU/day for children 1 - 8 years
• 4,000 IU/day for children 9 years and older, adults, and pregnant and breast-feeding teens and women

One microgram of cholecalciferol (D3) is the same as 40 IU of vitamin D.

Alternative Names
Cholecalciferol; Vitamin D3; Ergocalciferol; Vitamin D2

 

NOTE: Vitamin D is a daytime vitamin. Even if you take it in the morning, it can keep you awake at night. Be sure to start low and don't take too much.
 
What about dosage? According to respected naturopath Chris Kresser in his Aug. 2, 2016 article Vitamin 😧 More Is Not Better http://chriskresser.com/vitamin-d-more-is-not-better/

Quote

Vitamin D status is measured by 25(OH)D in blood....

 

There is little to no evidence showing benefit to 25(OH)D levels above 50 ng/mL, and increasing evidence to suggest that levels of this magnitude may cause harm.

....

Beyond vitamin 😧 The many benefits of sunlight

Vitamin D is really just the tip of the iceberg when it comes to the benefits of sunlight. A recent 20-year study following 29,518 subjects found that those individuals avoiding sun exposure were twice as likely to die from all causes (21). While this study did not assess vitamin D levels, findings from other epidemiological studies suggest that this cannot be accounted for by the increase in vitamin D production alone.

Indeed, humans make several important peptide and hormone “photoproducts” when our skin is exposed to the UVB wavelength of sunlight (22). These include:

• β-Endorphin: a natural opiate that induces relaxation and increases pain tolerance (23, 24)
• Calcitonin Gene-Related Peptide: a vasodilator that protects against hypertension, vascular inflammation, and oxidative stress (25)
• Substance P: a neuropeptide that promotes blood flow and regulates the immune system in response to acute stressors (26)
• Adrenocorticotropic Hormone: a polypeptide hormone that controls cortisol release by the adrenal glands, thus regulating the immune system and inflammation (27)
• Melanocyte-Stimulating Hormone: a polypeptide hormone that reduces appetite, increases libido, and is also responsible for increased skin pigmentation (27)

Exposure to the UVA wavelength of sunlight has also been shown to have benefits, including increasing the release of nitric oxide from storage (28). Nitric oxide is a potent cellular signaling molecule that dilates the blood vessels and thus reduces blood pressure (29).

 

In addition to the production of photoproducts and release of nitric oxide, sunlight also entrains circadian rhythms. Exposure to bright light during the day activates neurons in the suprachiasmatic nucleus of the hypothalamus, which sends signals to the pineal gland that regulate melatonin production. Disruption of circadian rhythm has been associated with mood disorders, cognitive deficits, and metabolic syndrome (30, 31).

....

 

Based on my assessment of the literature and my own clinical experience, I believe the functional range for 25(OH)D is around 35 to 60 ng/mL. However, I can’t stress enough that there is significant variation among populations. For those with non-white ancestry, the optimal range may be a bit lower. For those with autoimmune disease, the optimal range might be a bit higher (45 to 60 ng/mL) to maximize the immune-regulating benefits of vitamin D. Here are a few recommendations for optimizing your vitamin D level.

1. Don’t supplement blindly.
   If your 25(OH)D level is:

• less than 20 ng/mL: you likely need some combination of UV exposure, cod liver oil, and a vitamin D supplement
• 20 to 35 ng/mL: get your PTH tested. If PTH is adequately suppressed (less than 30 pg/mL), supplementing is probably unnecessary.
• 35 to 50 ng/mL: continue your current diet and lifestyle for maintaining adequate vitamin D
• greater than 50 ng/mL: try reducing your vitamin D supplements, and make sure you are getting adequate amounts of the other fat-soluble vitamins to protect against toxicity

2. Get retested!
   Check your levels after three to four months to see if you have achieved or maintained adequate levels of vitamin D. If not, adjust your diet, lifestyle, or supplements accordingly and check again in another three to four months.

3. Get sunlight or UV exposure as your primary form of vitamin D.
   Reap the many benefits of sunlight beyond just subcutaneous production of vitamin D, and reduce your chance of achieving toxic levels. Spend about 15 to 30 minutes, or about half the time it takes your skin to turn pink, in direct sunlight. Sunscreens not only block production of vitamin D, but also all of the other beneficial photoproducts produced in the skin in response to UVB.

4. Mind your micronutrients to protect against toxicity.
   Try cod liver oil as a good source of vitamins A and D and high-vitamin butter oil or pastured butter and ghee for vitamin K. Sweet potatoes, bananas, plantains, and avocados all contain significant amounts of potassium. Consider supplementing with magnesium as it is very difficult to get adequate amounts of this micronutrient from food due to soil depletion.

 

The entire article bears reading, as it indicates how much good health depends on integration of many nutrients and human experience in the natural environment.

Here are some topics discussing tests, supplements, herbs, and treatments that may answer your questions.

No matter what you read about "natural" supplements or herbs, or even if an alternative practitioner, naturopath, or integrative doctor recommends them, you cannot treat withdrawal syndrome as though it is "natural" depression.

In "natural" depression, your nervous system is normal and it is operating your body properly. In withdrawal syndrome, your nervous system is struggling to get back to normal operation. Don't try to speed this along with anything that may be stimulating, or you may further unbalance it.

SAM-E and other supplements that act on serotonin, including St. John's Wort, are not recommended for people with withdrawal syndrome. They tend to be stimulating in a way that most of us really do not need.

Many herbs also have unusual side effects in people with withdrawal syndrome.

Whatever you try, understand you may be hypersensitive to that particular substance or treatment. If you are trying an herb or supplement, take a tiny fraction of a normal dose and see how you react. Don't think you're going to smack a symptom down with a big dose of anything. More is not better when your system is sensitized by withdrawal.

Try herbs or supplements one by one. Don't take a bunch of supplements at once. If you have a bad reaction, you won't know which substance caused it. For this reason, we don't recommend "mixed" supplements, such as B vitamin supplements or sleep supplements with multiple ingredients.

We also don't recommend programs that promise you a fast recovery. Generally, they are overpriced and contain common supplements you can find yourself at lower prices. You will want to try those supplements one by one anyway, as taking them all together may cause unpleasant reactions.
 
See Don't waste your money on these supplements

Click on the links and add to these topics if you wish:

_______________________________________
CHECK FOR DRUG AND SUPPLEMENT INTERACTIONS !!!!!!!

Drug Interactions Checker -- use it to reduce your drug burden
 
_______________________________________
BASIC SUPPLEMENT TOOLKIT

King of supplements: Omega-3 fatty acids (fish oil)

Magnesium, nature's calcium channel blocker

_______________________________________
REDUCING CORTISOL, THE ANXIETY HORMONE
 

Waking with panic or anxiety -- managing cortisol spikes*

_______________________________________
AMINO ACIDS

5-HTP (5-hydroxytryptophan) and l-tryptophan

L-arginine An amino acid good for sleep?

L-glycine for sleep?

Update on milk peptides for sleep: Our friend Lactium again *

SAM-e (S-adenosyl-L-methionine)

Taurine (L-taurine amino acid)
 
L-Theanine for anxiety, insomnia

Be careful with l-tyrosine

whey protein isolate *

_______________________________________
SUPPLEMENTS AND HERBS
 
Can you take too many supplements?
 
Supplements - how long should I give them?
 
CoQ10

Curcumin -- helps neurons to recover? Supplement derived from Indian spice turmeric

Magnesium, nature's calcium channel blocker *

Melatonin for sleep: Many people find it helpful *

King of supplements: Omega-3 fatty acids (fish oil) *

Valerian Root

_______________________________________
TESTS

What lab testing is reasonable prior to starting or tapering?

Genetic testing: "Personalized medicine," liver enzymes, genotypes, GeneSightRx, Genomind, etc.

The importance of MTHFR, methylation, and B vitamins: Eat leafy green veggies!

The trouble with brain scans -- fMRI, QEEG, or SPECT -- for psychiatric problems
 
Invalid: Urine testing for neurotransmitters in the brain

Thyroid symptoms
 
_______________________________________
TREATMENTS

Liver detox, gallbladder flush, internal cleansing, enemas, fasting, & other detoxification methods

Ask Shanti about homeopathy

One theory of antidepressant withdrawal syndrome

Lamictal to calm post-discontinuation withdrawal symptoms

_______________________________________
VITAMINS

Vitamin A and beta-carotene

Vitamin B3 (niacin, niacinamide)
 
Vitamin B8 (inositol)

Vitamin B12: essential for mood, nervous system
Vitamin D3 (cholecalciferol or calcitriol)

Got too much vitamin D - Now what?

Deplin -- the L-methylfolate swindle

_______________________________________
DIET AND DIGESTION
 
That acid reflux pill may be causing your health problems
 
Digestive problems: Nausea, Diarrhea, Bloating, GERD

Avoid hypokalemia: Eat high-potassium foods and take magnesium
 
Food sensitivities
 
Gluten Sensitivity Vs. Celiac Disease Vs. Gluten Intolerance...
 
Histamine food intolerance

Elimination or exclusion diets for reactions to food (food intolerance)

SCD/GAPS/Paleo Diets
 
Probiotics and gut health
* Many people find this helpful for withdrawal symptoms. Always try a small amount first to see how your system reacts.

Because of its ability to stimulate new neuronal connections, psilocybin may also be effective in the treatment of depression. According to Higher Perspective, people who are depressed typically have an overactive prefrontal cortex, an area of the brain that is directly affected by psilocybin. Related research out of the U.K. confirms this, having found that psilocybin literally switches off the anterior cingulate cortex, allowing depressed individuals to experience relief.

"People with depression have overactive default mode networks and so ruminate on themselves, on their inadequacies, on their badness, that they are worthless, that they have failed -- to an extent that is sometimes delusional," says Professor David Nutt from Imperial College London's neuropsychopharmacology department. "[P]silocybin appears to block that activity and stops this obsessive rumination."

Be sure to check out Dr. Sanchez-Ramos' presentation at the Horizons 2011 gathering entitled "Effects of Psilocybin and other Selective Serotonin Agonists on Hippocampal Neurogenesis," which discusses in further depth how psilocybin affects brain function:
http://vimeo.com.

Sources for this article include:

http://vimeo.com

http://altering-perspectives.com

http://www.theguardian.com

http://science.naturalnews.com

http://www.naturalnews.com/043214_psychedelic_mushrooms_psilocybin_brain_cells.html

😊

https://baylissa.com/withdrawal-resources/

The above website, created by a person connected with Recovery Road, has some excellent resources available including some videos and audios.

This link goes straight to the resources page.  There might be other things on the site that might be helpful.  If you find anything that helps you or might help other members, please post in this topic and provide the link.

https://baylissa.com/family-videos/

^ has a series of short videos for family members and carers, including Impact of Withdrawal on Family and Friends and How to Best Give and Receive Support.   Parents, Partners, Adult Children, and Loved ones impacted by WD.

______________________________________________________

PLEASE NOTE

31.10.2021:  Unfortunately these videos are no longer available to the public on YouTube.

Please see this post which provides the explanation.

☹️ Following videos no longer available.

Withdrawal Dialogues - Impact of Withdrawal

https://www.youtube.com/watch?v=fODeaH-bFU4

Withdrawal Dialogues - Benzos & Antidepressants

No longer available

Withdrawal Dialogues - Acceptance

https://www.youtube.com/watch?v=rxY4MrQoTjE

Withdrawal Dialogues - Family & Carers

https://www.youtube.com/watch?v=m0Pzbl1jZGQ

Withdrawal Dialogues - Doctor's Visit Pt. 1 - typical

https://www.youtube.com/watch?v=iwZuvo_au1M

Withdrawal Dialogues - Doctor's Visit Pt. 2 - a keeper

https://www.youtube.com/watch?v=AF2vmb8XbHw

high-cortisol-and-ssris

This seems to be a very common symptom of withdrawal syndrome. Many people report waking up with a surge of panic or anxiety, or a feeling of anxiety early in the morning. People generally feel this around 3:30-4:30 a.m. or closer to dawn.

The first glimmers of morning light signal the nervous system to start the morning cycle with a normal rise in cortisol. This is a normal part of your circadian rhythm. Normally, cortisol gives you energy. When you have withdrawal syndrome, your system is on "high alert" all the time.

For people whose nervous systems have been sensitized by going on and off psychiatric drugs, the normal morning peak of cortisol is felt as exaggerated. What you would normally feel as "wake up" becomes a surge of unease, panic, anxiety, or dread at the start of the day.

Since the cortisol increase is signaled by early morning light, you can reduce the stimulation by reducing light in your bedroom with the use of blackout shades and curtains and a sleep mask to shield your eyes. Strengthening your sleep also helps. See

What is the sleep cycle?

Tips to help sleep -- so many of us have that awful withdrawal insomnia

Sleep and withdrawal

Path to Better Sleep FREE online for everyone from the US Veterans Administration

Music for self-care: Calms hyperalertness, anxiety, aids relaxation and sleep

Melatonin for sleep: Many people find it helpful

TV or computer use in evening can disrupt sleep: Bright light signals the brain that it's daytime

Also see:
Overwhelmed, demotivated, apathetic? Cannot get going on interest or action

Memories without emotions

Creating a new self after withdrawal

Post by BrassMonkey

How many of you, apart from the whole gamut of other symptoms, are suffering from emotional numbness as of present? How does it manifest in your case?

Adaptation progressing to psychotropic tolerance is a universal, inexorable biological process. It is possible that some people do not feel the effects of tolerance, but adaptation has occurred regardless. Often tolerance is felt as a loss of drug effect or even mild withdrawal.

Psychiatry calls this loss of drug effect "tachyphylaxis" or even "breakthrough depression" or "relapse" while taking the drug. Colloquially, it's called drug "poop-out".

Doctors' common response to poop-out is to prescribe a higher dosage of the drug, a different drug, or an additional (adjunct) drug to obtain the desired effect. However, studies show that people have a diminishing positive response to antidepressants as they try them one after the other. 

Loss of beneficial antidepressant effect is not due to any characteristic of the patient. The natural biological mechanism of adaptation leading to tolerance decrees every drug will eventually lose effect. The misnomer "treatment-resistant" is often applied in these situations, but there's only so much a drug can squeeze out of neuroreceptors.

Also see this post by Brassmonkey who successfully tapered out of poop out from Paxil and developed the Brassmonkey Slide taper method and his post  Tachyphylaxis, Reaching Tolerance or as It's Lovingly Known “Poop-Out”

2 examples:

• a person who takes paxil 12 years and weans one year (never in tolerance)
• my example : 6 years ok + 6 years in "tolerance"

the difference is during my six years tolerance, i feel my body deteriorate, and in fact after my tapering i was and am very deteriorate

i think if i would not be six years in "tolerance", i would be much better

12 years without "tolerance" is much more healthier than 12 (6 in "tolerance")

testimonies with years in "tolerance" seem more damaged

Hypersensitivity and Kindling   

What causes hypersensitivity? 

Some people may experience minor difficulty in stopping a psychiatric drug one time, but the next time they start, startup symptoms are much worse,  and the next time they stop, the withdrawal symptoms are worse. The nervous system can become destablilzed or sensitized from repeated adverse drug effects and withdrawal events.

If someone goes on and off multiple psychiatric drugs, they may be in a state of overlapping withdrawal reactions and often a persistent hypersensitivity.

 In One Theory of Antidepressant Withdrawal, Altostrata writes:

On 5/24/2011 at 8:59 PM, Altostrata said:

My guess is: The first phase of withdrawal, the acute phase, is the initial shock of withdrawal at the target receptors, with the most defined symptoms, such as brain zaps and nausea and possibly waves of unusually intense "depression" and "anxiety" -- actually, emotions generated by the neurological upset. Later, hyper-reactivity and autonomic instability take over. Often the autonomic instability causes wide hypersensitivity to drugs, supplements, and even foods.

What is kindling? 

Kindling is a neurological reaction that comes about after repeated withdrawal or adverse drug reactions cause hypersensitivity. When the same drug or a different drug is introduced, there is a hyper-reaction. That is the kindling response: An exaggerated adverse reaction to exposure to a drug, due to pre-established hypersensitive. 

You may be vulnerable to kindling if you have a history of repeated rapid taper or cold turkey withdrawal and / or a history of heavy or chronic alcohol use, especially binge drinking -- in effect, going on and off the drug, with hyper-reaction when the drug is taken again.  

Generally, kindling is an activation reaction -- a sense of overstimulation, which may be an inner electrical feeling, anxiety, nervousness, panic, or at the extreme, akathisia, which includes an urge to move to relieve intense inner agitation.

Here is an excellent explanation on the Benzodiazepine International Coalition website: Benzo Kindling. 

While the exact mechanism of kindling is unknown, some of the details on kindling have been written about in papers on alcohol withdrawal, which like benzodiazepines, affects GABA (here is one such paper - Kindling in Alcohol Withdrawal).

While this phenomenon has been documented in the scientific literature for benzodiazepines for a long time, any drug that effects the nervous system and causes dependency can have a traumatic impact on the nervous system when changes are made often and abruptly. Research is now also pointing to kindling in antidepressant use. In the article Expertise from outside the Academy: tapering off antidepressants, Dr. Mark Horowitz cites a study by Dr. Giovanni Fava:

Quote

Kindling: a phenomenon observed with illicit psychotropic medications may be relevant to antidepressants – whereby repeated rounds of trialling different medications, or stopping and starting medications makes withdrawal increasingly more difficult (Fava, 2020). (This may help explain why people who use a single antidepressant for a short period of time often do not experience difficulty in stopping, whereas those who have years of complex regimes often do.)

Example: Hypersensitivity when tapering a benzodiazepine

A benzo works by increasing GABA. Long-term exposure to benzos causes GABA receptor down-regulation and glutamate receptor up-regulation. For a more thorough description of GABA and glutamate during benzo withdrawal, see What is happening in your brain?

A slow and careful taper makes it easier for the receptors to gradually return to their pre-benzo state. But when there's a history of prior withdrawal, hypersensitivity may result in increased neuro-excitability, creating worsening withdrawal symptoms upon even very small dosage reduction.

The risk of this is much higher with a rapid or cold turkey benzo withdrawal.

When tapering a benzo, this withdrawal reaction can even include seizures due to a lowered seizure threshold. Stimulants and some antidepressants (such as Wellbutrin) also lower the seizure threshold. 

If someone is dealing with antidepressant withdrawal in addition to benzo withdrawal, neurological hyper-reactivity may be even more intense. And with serotonin needed to release GABA and glutamate (see Serotonin as a Modulator of Glutamate- and GABA-Mediated Neurotransmission), the interplay of all of this neurotransmitter dysregulation can make hypersensitivity more likely. 

Example: Kindling in benzodiazepine use

Some short half-life benzos (such as Halcion) and z-drugs used for sleep may cause kindling because much of the drug is eliminated in between nightly doses, a mini-withdrawal effect. Over time, this can sensitize the nervous system with repeated exposure and withdrawal in between doses. When a dose is introduced again or increased, it may paradoxically cause kindling -- an activation instead of sedating effect.

Repeated instances of going on and off drugs, adverse reactions, cold turkey, etc. seem to build neurological hypersensivity to drug and dosage changes, resulting in worsening adverse reactions, usually some form of activation.

The same may be true of the short half-life antidepressants. After a gap in dosing, a new dose, even if tolerated before, can cause a hyper-reaction. Skipping doses to taper may have the same effect, every re-introduction of the drug causing progressively worse withdrawal symptoms. (See How about taking my medication every other day to reduce my dosage? and NEVER SKIP DOSES TO TAPER).

Hopefully, more research will be published in the future regarding kindling in antidepressants, antipsychotics, drugs used as mood stabilizers, and drugs for pain. Kindling in antidepressants, for example, may involve the damage caused to the serotonin receptors by repeated on and off use of one or more of these types of drugs and the effect this has on the overall nervous system. 

Here is a more recent article Kindling in psychopharmacology: Unveiling an overlooked clinical challenge with significant implications.

A note on dopamine receptor supersensitivity

If you've been exposed to neuroleptics (antipsychotics), you can become hypersensitive to endogenous dopamine (the dopamine your body makes naturally) when the drug's dopamine blockage is removed. As opposed to benzo and antidepressant withdrawal caused by down-regulation of receptors, dopamine receptor supersensitivity is caused by up-regulation. However, dopamine receptor supersensitivity is not kindling - the symptoms of dopamine supersensitivity can occur without additional introduction or reinstatement of a drug or substance. You may experience dopamine receptor supersensitivity after coming off only one neuroleptic but not experience kindling. For more on dopamine receptor supersensitivity, see:

Chouinard, 2017 Antipsychotic-Induced Dopamine Supersensitivity Psychosis: Pharmacology, Criteria, and Therapy

While dopamine supersensitivity psychosis is specifically a neuroleptic withdrawal symptom, switching neuroleptics or making abrupt dose changes to the same neuroleptic can also lead to kindling. So it's important for people tapering neuroleptics to taper slowly to decrease the chances of both dopamine receptor supersensitivity and kindling. 

A note on limbic or psychological kindling

In this article on limbic (or psychological) kindling, the concept of being "hard-wired" for hypersensitivities is explored. If in addition to psychiatric drugs, you are also dealing with trauma, exposure to other drugs, pollutants, or chemicals, etc., you may already be in a state of chronic stress or what is also called the "flight or fight" state.  Whether this directly translates to kindling is not clear - it may be related to learned responses, especially for those who have a history of trauma. Either way, learning how to self-soothe and calm the limbic system can be very helpful. See Non-drug techniques to cope with emotional symptoms.

Steps to reduce the damage and mitigate hypersensitivity and kindling:

• Come off stimulating drugs first.
   Taking multiple psych drugs? Which drug to taper first?
   
• Consider a slow and mindful symptoms-based micro-taper.
   Micro-taper instead of 10% or 5% decrease
  The Brassmonkey Slide Method of Micro-tapering
  The slowness of slow tapers
   
• Allow withdrawal symptoms or adverse reactions to settle down before attempting another drug change.
   
• If you reinstate a drug or introduce a new drug, start at a very low dose.
  About reinstating and stabilizing to reduce withdrawal symptoms 
  The Windows and Waves Pattern of Stabilization 
  The rule of 3KIS: Keep it simple. Keep it slow. Keep it stable.

I think of it as a deep transformative process happening to us...we are being made...

http://wp.me/p5nnb-9M0

Also see:   ways-to-cope-with-daily-anxiety

This topic has some links to helpful things, as well as a detailed explanation of how anxiety affects different areas of the body

VIDEO:  The FASTEST Way to Stop a Panic Attack - Dr. Berg

Excellent Youtube video

______________________________________

can anyone explain why I get extreme feelings of fear when there is nothing going on, I am ironing or just pottering about at home. It is dreadful! I can almost feel the adrenaline gushing around my body . It makes my stomach feel tender.I am 6 years off the drug.

See also one member's description of a bad reaction:  magnesium-sensitivity-bad-reaction

PLEASE NOTE:  Some magnesium tablets contain additional ingredients. B vitamins can be activating, especially vitamin B6.

Calcium cancels the calming effect of magnesium and the 2 should be taken at least 2 hours apart.

On 5/25/2012 at 7:46 PM, tezza said:

 

Taking magnesium at the same time as Neurontin/ gabapentin decreases the absorption of gabapentin.

 

Avoid taking aluminum or magnesium containing products (such as antacids) for 2 hours before your gabapentin.

 

Magnesium can be calming and reduce anxiety, like a calcium channel blocker.
 
Our diets often don't supply us with enough magnesium, which is important for nervous system health and autonomic regulation, as well as just about every operation in the body.
 
Don't overdo taking magnesium -- too much will give you diarrhea. Start with 25mg. (I was never able to take more than 50mg-75mg at a time, but others can take much more.) To start, you will want to get 100mg tablets you can cut up or 100mg capsules you can open, so you can try a lower dose and gradually increase if you wish.
 
Drug stores most often carry magnesium carbonate, but magnesium citrate is a type that's gentler on your stomach and absorbs well.

I found if I dissolved magnesium citrate in ice water and sipped it, this reduced withdrawal anxiety quite a bit.

Some people think magnesium glycinate, a chelate, has even better absorption, is easier on the gut, and has other health benefits. See Chris Kresser http://chriskresser.com/handouts/natural_prevention.pdf

Albion process magnesium glycinate chelate is a good-quality magnesium supplement. These products are carried by Bluebonnet, Designs for Health, Life Zone, Metagenics, Olymp Laboratories (Poland), Optimal Nutrients, Solgar, Swanson, Trophic (Canada), and other brands.

Doctor's Best also offers a high-quality chelated magnesium glycinate.

Some people get magnesium by taking hot baths in Epsom salts (magnesium sulfate), See Epsom salts baths -- another way to relax with magnesium

Others rub on magnesium oil. It's not really an oil; under high pressure, magnesium is dissolved in water. The magnesium is absorbed through the skin. This is a another way of taking magnesium. Some find it gentler than taking magnesium by mouth.

Another option is homemade magnesium bicarbonate water, see Instructions For Making Homemade Magnesium Water

If you take too much magnesium, you will know because you'll get stomach cramps or diarrhea. Reduce the amount you're taking if these things occur.

NOTE: Magnesium is more effective taken in divided doses throughout the day. There's no need to take one large daily dose, you'll absorb it poorly. You might find you can take 50mg or 100mg magnesium 4 times a day or so and it will help you relax. Build up slowly.

ADMIN NOTE: Summary of the topic, up until post # 372

(Mod note 2019 December,  some of the links below are not working at present, most of the information is in this topic though, 14 pages now, and we'll get to work on the hyperlinks ASAP, thanks for your patience, mmt)

How to make creams and sprays

Studies on blood brain barriers

Mag for achy knees

When Magnesium makes you Worse

Magnesium Supplementation Article

Recipe for magnesium spray

Recipe for magnesium water

How to Change Your Life with Magnesium by Dr Carolyn Dean

Descriptions of many forms of magnesium

Answers to many questions by Jan Carol

A detailed post from Jan Carol

Results one member had from a variety of magnesium forms.

Many members noticed improvements in w/d symptoms.  Some of the specifics reported were:  improved short-term memory; general withdrawal improved by 90% for one member; improved restless legs; less cramps; nerve-damage pain was eased; depression lessened; akathisia improved.

Mag chloride oil helped with joint pain and reduced constipation

Mag oil stopped pins and needles.  GiaK also had good results with magnesium oil

Mag maleate helped with relaxation

Epsom salt lotion relaxed muscles, and helped with cortisol spikes

Mag citrate cream helped achy knees and was calming

Chelated mag was found to be good for sleep.  (In general, Magnesium may be better taken in the evening if it makes you sleepy.)

Some members noticed worsened side-effects.   These included:  dizziness; disorientation; worse short-term memory; tingly skin; tired; heart palpitations; worse sleep; agitation; lip twitching; brain zaps, twitching body; facial tingling; ear pain; racing heart.   

When taking magnesium glycinate, a member noticed increased sleep-apnoea and worsening of all their other symptoms; a member noticed anxiety from Epsom salts. 

However, in nearly all cases, worsening symptoms was a result of taking TOO MUCH magnesium.  In some cases members found they could tolerate some forms of magnesium better than others.  Overall it seems to be well worth following the ‘start low’ advice, and trying out different types to see what you might tolerate.

Mag oxide is less well absorbed than other forms.

Magnesium citrate and magnesium glycinate are supposed to be the most biologically available and effective, but may be more expensive.

Useful Excerpts from the thread

From Dave, a moderator:  ‘I tried most of the mags. Malate, citrate, glycinate, etc. Glycinate was the one that really resonated with me as well. It's the one I take consistently. It is the ultimate chill pill. I will take 200mg before an aspirin for a headache. If I have very high anxiety or trouble settling in the evening, 200mg will cut into the negative feelings and stabilize me - soothe me. I've taken up to 800mg of Doctor's Best mag glycinate in a single day w/ no adverse reactions. That was in acute withdrawal. I took it 200mg at a time spread throughout the day. It really helped me. We are all so very deficient in magnesium as it is. Stress further depletes us. It is truly a supplement well-worth trying while navigating withdrawal. Glycinate reigns supreme amongst the mags for me, but I do like Natural Calm mixed into seltzer water with a splash of cranberry juice.

Moderator JanCarol compared the following types of magnesium

‘Magnesium chloride crystals - 1 cup - 20 min soak - was almost sedating, very relaxing, very calming, very "all is well with the world."  

Magnesium Sulfate (Epsom Salts) - 1 cup - 20 min soak - was mildly relaxing, felt good on the muscles, but didn't feel like it affected emotion much at all.  I was glad I took the bath, but it didn't feel nearly like the "secret weapon" the magnesium chloride is.  I think the effects of the Epsom Salts were not as long acting, either.

I have had fewer headaches upon starting the citrate and maleate.  No change in emotional output or anxiety - unless I would take a mag chloride bath!’

What is Chelation?  By Scallywag:  ‘Chelation is a process used to trick the body into treating a mineral like a food by bonding the mineral with an amino acid such as L-glycine. When minerals aren't chelated, our body sees them as the "rocks" they are and is more likely to excrete them unused. A chelated mineral is more likely to be absorbed because our body sees it and treats is as food.  Foods are far better absorbed than rocks.  All magnesium glycinate products are magnesium chelated with L-glycine. I've never seen a magnesium lysinate product before, but that doesn't mean anything. Lysine is an essential amino acid, meaning we can't make it on our own so we have to get it from food.’

I have found paracetamol very helpfull in combating the tremor / akathesia / tension side of withdrawal.

However when taken regulally for a long period of time that actually make you feel really anxious and depressed.

Once you stop taking taking them the anxiety / depression they cause ceases within 48h in my experience.

If you scour the internet you will fing details of several experiments with rats and paracetamol that seem to suggest short term use of paracetamol increases seretonin in the brain and prolonged use suppresses the production of seretonin in the brain.

This seems to fit with my experience.

I would not suggest anyone else abuses pain killers in this way but sometimes any relief is welcome no matter what.

I have also experimented with codeine and dyhydroceine.

Both, in my experience, help greatly with the symptoms of A.D withdrawal, however both are highly addictive and are opiates, as is heroin !!

I have a long history of recreation drug abuse, including over the counter opiates and the negatives of these far outway any positives !!

After taking a theraputic dose of dyhydrocodeine recently I found myself with crippling anxiety the next day. This lasted a number of weeks !!

has anyone else had any similar experiences ?

I'm wondering whether anyone has experienced nocturnal vocalisations in withdrawal?  Mine commenced a couple of years ago, together with myoclonic jerking at night.  The jerking has become less intense but the shouting, which can be extremely loud (I now sleep with my windows shut tight) has continued and is often preceded by a strange crawling/ squeezing sensation in my eyeballs.  It is distressing and embarrassing and can happen 30-40 times a night.

Any advice or observations would be most welcome please.  I have become accustomed to this but it is very wearing and difficult and I'd like it to go away!

pecanut

So I've always been this way, add to it someone playing their music or TV too loudly and I am near to choking the life out of them.

I am adding it here because since recovering from WD syndrome, my reaction is not so 'going for the throat' with noise but cutting me off in traffic makes me want to go into ramming mode.

Some stuff more easily angers me, some stuff not. But to find this article was great: I always thought it was me and I 'learned' it from my dad.

Um, the chewing thing will have me leaving you at the restaurant alone to save my sanity, however (and likely saving you from a fork in your eye).

Has anyone else gotten a flu shot while tapering? Did you react differently compared with when you'd previously had the shot? Did it aggravate your WD symptoms?

Thanks for your thoughts and feedback.

-Mtnbkr