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Monday, February 9, 2015

TAL; Taltirelin (TA-0910) - A potent Dopamine Secretagogue and "SuperAgonist" at the human thyrotropin-releasing hormone receptor (TRH-R1)

This article has been exclusively written for TrueLIFE Research - TeamTLR.com and to foster further progress within research with the valuable compound Taltirelin; TA-0910.
It can be purchased at their home page > http://teamtlr.com/anti-aginglongevity-research/98-taltirelin-98.html


Out of all the innovative nootropics and certainly worthy to be placed in the most popular Dopaminergic Pot of Gold article, nothing stirs quite the amount of attention as the dedicated science behind a new superagonist at the human thyrotropin-releasing hormone receptors (TRH-R1) - TALTIRELIN , abbreviated as TAL.

Though Taltirelin (marketed under the tradename Ceredist) is a thyrotropin-releasing hormone (TRH) analog - it has a much longer half-life and duration of action than natural TRH(2).

One of the first cited studies back in 2002 shows this chemical, taltirelin, to be neuroprotective(3).
This effect was exerted even with models of ischemia (!) and other conditions that are hard to treat.
However, studies on it's neuroprotective, and moreover, pro-cognitive / nootropic effects date back to 1997 ; where it was demonstrated to have ameliorated consiousness impairment, memory impairment and motor dysfunction in several models(!).

In 2007, a much larger study showed taltirelin to be a potent antinociceptive ( (pain relieving) ) as well, an effect at least partly, but certainly not solely - dependent on the indirect activation of serotonin 5-HT(1)A receptors(SEE STUDY HERE).

The larger wonders of this chemical began in 2013,with tests showing marvelous anti-depressant effects(4) and even more significant, the demonstrations of it being almost unprecedented, and even comparable to methamphetamine (but not dangerous and without adverse events) in inducing/increasing dopamine release(!).

It was also demonstrated to have acute and chronic memory enhancement effects, and could ameliorate memory impairment on a central hypothalamic level, and by directly modulating cholinergic neurotransmission in the hippocampuls ; a brain area largely involved with spatial, active and declarative memory(!).

An anti-ataxic effect of taltirelin was noted as well - an effect that probably has to do with NMDA-glutamate receptor modulation/activation, as this benefit was blocked by an NMDA-antagonist; MK-801-------------(5)(6).

Taltirelin was also revealed to have neurotropic; brain cell increasing and synapse regenerating effects - this occurred at the molecular and central level - and most profound effects were seen in the spinal cord - though it was also noted to reverse nerve damage in other tissues/brain regions(7).


---------------------------------------Taltirelin's effects on NEUROTRANSMISSION-----------------------------------------
----------------------------------------------------------------------------------------------------------------------------------------------------




  • Taltirelin increases extracellular levels of acetylcholine in the hippocampus, but modulates turnover if levels are already high (potentially protecting against excesses of ACh as well).
  • Taltirelin increases noradrenaline in the hypothalamus.
  • Taltirelin super-potently increases dopamine release in the striatum and nucleus accumbens - which are area's involved in motivation and as such this is likely the responsible action for it's pungent anti-depressant effects.
  • The compound also can regulate/increase serotonin levels in the brain stem. nucleus accumbens and striatum. 
  • Taltirelin may increase neurite outgrowth via distinct modulation of neurotrophic factors and via positive effects on blood flow.



In summary, TALTIRELIN; marketed as  Ceredist and often referred to as TA-0910 - has the following effects/benefits.

  • As an anti-depressant(!)(!).
  • As a nootropic(!).
  • Ameliorating memory deficits, and increasing retention(!).
  • As a novel analgesic/pain reliever(!).
  • As a stimulant - with motivation increasing effects(!) (!).
  • Regenerating spinal cord nerves and treating spinal muscular atrophy(!). 
  • Rapidly increasing dopamine, noradrenaline, serotonin and acetylcholine(!)  (!).








The Birth and Ascendence of N-PEA; A non-addictive Endocannibinoid and Ultimate Nemesis of THC (From a Rhetorical Competition standpoint)

This article has been exclusively written for TrueLIFE Research - TeamTLR.com and to foster further progress within research with the valuable endocannabinoid substrate N-PEA
-------------------------------------------------------------PURCHASABLE AT LINK BELOW---------------------------------
http://teamtlr.com/analgesia-research/92-n-palmitoylethanolamide-99-n-pea.html
------------------------------------------------------------------------------------------------TeamTLR HomePage--------------------

While THC certainly is the "cannabinoid" most are more familiar with - another cannabinoid has been sparking much more scientific appeal and attention - this cannabinoid is not "traditional" by any means, but certainly has demonstrated itself worthy in pain and inflammation, among other disorders.

The name of it is Palmitoylethanolamide (also known as N-PEA, and referred to as simply "PEA" within medical study). This chemical is NOT the same as PHENYL-ETHYLAMINE; another unrelated chemical (a stimulant) with the same "PEA" as it's acronym.




The chemical was discovered in the late 1950's...


Significant studies on this chemical began before the 1980's; and the heat of it's research was published in "The Lancet" - an older but respectable, and somewhat notorious worldwide medical journal(1) (2)

Notably, when 1.8 grams of N-PEA was compared to 3 grams of aspirin - it was seen to have similar analgesic efficacy, and very potent influence on mast cell overexcitation.
In the 1990s, the relation between anandamide and PEA was described, and the expression of receptors sensitive for those two molecules on mast cells was first demonstrated by the group of Nobel prize winner Rita Levi-Montalcini.(3)

Specifically, one group of researchers; published promising (and additive) evidence -  demonstrating that PEA could alleviate, in a dose-dependent manner, pain behaviors elicited in mice-pain models and could downregulate hyperactive mast cells.(4)(5) PEA and related compounds such as anandamide also seem to have synergistic effects in models of pain and analgesia.(6)

The effects on mast cells are remarkable, because there aren't many remedies at all with as good as scientific background and follow-up studies as Palmitoylethanolamide (N-PEA).



In a variety of animal models PEA seems promising, and researchers could demonstrate relevant clinical activity in a variety of disorders, from multiple sclerosis to neuropathic pain.(7)(8).

It also was seen as an effective natural anti-convulsant(!).


2011; another highlight for N-PEA - demonstrates it having potent anti-depressant effects comparable to the popular anti-depressant Fluoxetine AKA Prozac(9).

Even more significantly, attentiveness to it's neuroprotective abilities became even more powerful when it was demonstrated to directly counter reactive astrogliosis induced by beta-amyloid peptides(SEE HERE).
Now, astrogliosis is an abnormal increase in the number of astrocytes (specific glial cells in the brain and spinal cord) due to the destruction of nearby neurons from CNS trauma, infection, ischemia, stroke, autoimmune responses, and neurodegenerative disease. Astrocyte excess can cause nerve/tissue damage and impair axon regeneration(!).

More research on it's anti-inflammatory, neuroprotective, and pain - relieving effects were confirmed in the following year; 2012(10)(11).

                                    2012 STUDIES on N-PEA

Palmitoylethanolamide exerts neuroprotective effects in mixed neuroglial cultures and organotypic hippocampal slices via peroxisome proliferator-activated receptor-α

Therapeutic utility of palmitoylethanolamide in the treatment of neuropathic pain associated with various pathological conditions: a case series


Research on N- PEA , again, has taken quite the spotlight research years , a 2013 article with a bold title - (Evolution in pharmacologic thinking around the natural analgesic palmitoylethanolamide)  confirms N-PEA's mechanism of action as a PPAR agonist. It's described as a unique and very effective nutraceutical - something memorable as nutraceuticals have gained notoriety in many places in the scientific community.

An excerpt from the same article was also INCREDIBLY significant in the identification and worth of N-PEA.


The history of the development of insights into the biological role of PEA after its identification in 1957 is worth telling because it demonstrates the close interrelationship between the scientific context and the development of scientific facts.

Thus the discovery of and testing of N-PEA was not only a checkpoint for science, but also an important vehicle for later defined guidelines and a coming scientific revolution , of sorts.



Messina , Italy - an area known for it's A+ medical schooling and criteria standards( University of Messina), also became a part of N-PEA's growing interest, which is quickly turning into a phenomenon of sorts , in the scientific community. Emanuela Esposito and Salvatore Cuzzocrea published a review to CNS & Neurological Disorders - Drug Targets, 2013, 12, 55-61 - the study was principally overseen in Department of Biological and Environmental Sciences, University of Messina(!).




The conclusions came up to confirm and reiterate it's neuroprotective potential.


Here's a quote.




"PEA appears to exert its protective effect by decreasing the development of cerebral edema, down-regulating the inflammatory cascade, and limiting cellular necrosis and apoptosis. All these are plausible mechanisms of neuroprotection."



If this wasn't enough, an article/study in Med Hypothesis; (a well-respected medical journal noted for it's deposits/studies of information that would later be utilized in a significant manner or that remain a poster child for studies to come) - soon was the site of the resonating ability of N-PEA to yet again emerge as a fundamental and yet rare breakthrough in science .

It was demonstrated to prove useful in treating cannabis dependence (12) (go figure, an endocannibinoid like chemical could drift people away from the gaping hole of cannabis dependence).

Another study (13) goes on to prove N-PEA as an antioxidant that has prevented kidneys from succumbing to hypertensive damage, and direct protective effects against hypertension related disorders.

JUNE 2013, a year where influenza is certainly more talked about, what with the swine flu warning flag being aired in past years and up to, certainly was the right timing for N-PEA to come up YET AGAIN; this time as the new hero in fighting influenza and the common cold(14)

Amazing..., and then a NOVEMBER 2013 study shows that N-PEA is able to correct or modulate gut homeostasis, helping to ALLEVIATE gut disorders such as IRRITABLE BOWEL SYNDROME(I.B.S) and INFLAMMATORY BOWEL DISEASES (I.B.D).

Finally , in 2014 - the wand of science yielded yet another justification for N-PEA, again proving it's neuroprotective effects - this time in a more suitable model ; ALZHEIMER'S DISEASE(14). This study was published in the prestigious  "Cell Death and Disease" publications. 

Many other studies, including with major research companies like Pfizer have published serene and worthwhile data on N-PEA - which has further skyrocketed it's overall interest, appeal and it's magnitude on those awaiting more plausible, and safer treatments for the following disorders.



  • Pain and inflammation.
  • Neurodegenerative disorders; including Alzheimer's,
  • Gut disorders (I.B.S / I.B.D)
  • Depression
  • Metabolic Disorders / Leptin sensitivity (!)
  • Cold / Flue and infection treatment/recovery.
AND ADDITIONALLY, SUCH INTEREST HAS BEEN SHOWN IT TO BE EFFECTIVE....
  • As an anti-convulsant.
  • As a cellular activity modulator ; and to demonstrate the significance of the PPAR-A ; peroxisome proliferator-activated receptor alpha - in multiple disorders.
  • As an add-on or augmentor  of traditional analgesics.
  • As an investigate or comparative tool in finding cures for neurodegenerative diseases - even though it is quite efficient and powerful by itself - this speaks for it's significance even more as it becomes the new "gold-standard" in scientific / medical advancement, one likely to stay with the pace as we accelerate to the next phase in scientific enlightenment and advancement.

Sunday, February 8, 2015

Natural NOREPINEPHRINE Only Reuptake INHIBITORS (Natural NET Inhibitors)

In my quest to find natural norepinephrine transporter inhibitors - AKA NorAdrenaline reuptake inhibitors AKA natural NET Inhibitors - I have come across three easily obtainable "remedies" that also have a fair amount of LEGIT, unquestionable science behind them.

But real quickly , why would one want a norepinephrine inhibitor, and not a dopamine reuptake inhibitor, or serotonin reuptake inhibitor?


  • Norepinephrine is a form of adrenaline, thus if you have low blood pressure - it may be one part of one means to increase it.
  • NorAdrenaline can be made more efficient by increasing it's activity; and thus can be a side-kick to a formidable natural anti-depressant.
  • Norepinephrine (NORadrenaline) is involved in attentiveness to detail, in particular lights, smells and colors. 
  • Low levels of norepinephrine often result in  "depressive like symptoms" with sensory deficiency and low enthusiasm / quality of life. 
  • Rasing the activity of norepinephrine may improve energy levels and treat SOME** ADD symptoms and may help to counter the lethargy associated with many anti-psychotic/mood stabilizing drugs.
  • It may help in increments to restore normal visual processing capacity, naturally!


The first natural norepinephrine reuptake inhibitor would be ginkgo biloba extract; however, it is not purely so - it also antagonizes GABA-A and affects receptor expression across the board. Mainly influencing the 5-HT1A receptors (preventing loss of) and increasing muscarinic receptors if they are decreased by age.


 2009 Jul;60(1):68-73. doi: 10.1016/j.phrs.2009.02.012. Epub 2009 Mar 21.

Ginkgo biloba extract (EGb761) influences monoaminergic neurotransmission via inhibition of NE uptake, but not MAO activity after chronic treatment.

Abstract

In order to explain cognition-enhancing effects of standardized Ginkgo biloba extract (EGb761), an increase of central monoaminergic neurotransmission has been suggested, but the underlying mechanisms have not yet been elucidated. Here, we confirm that the norepinephrine (NET), the serotonin (SERT), the dopamine (DAT) uptake transporters and MAO activity are inhibited by EGb761 in vitro, although rather high concentrations are required for inhibition of MAO-A and MAO-B activity. However, after 14 days of daily oral treatment with 100mg/kg EGb761 only NE uptake is significantly decreased in NMRI mice, while 5-HT uptake and MAO activity are not affected. As synaptic dopamine clearance in the frontal cortex is mediated by NET, not DAT, these findings may give an explanation for the enhancement of dopaminergic neurotransmission by EGb761 seen in animal models, presumably linked to its positive effects on cognition and attention.
PMID:
 
19427589
 
[PubMed - indexed for MEDLINE]





MY RECOMMENDED GINKGO BILOBA EXTRACT PRODUCT  IS BELOW
                                                                   



The Second natural NORADRENALINE REUPTAKE INHIBITOR ; PSORALEA CORYLIFOLIA!

"This one is a real gem, with additional dopamine reuptake inhibiting properties and listed as an MAO-Inhibiting herb."

It's mentioned on a discussion forum called "DR.BOB" and reiterated as the new "god-tier herb" and future phenomenon on longecity!

http://www.dr-bob.org/babble/alter/20090727/msgs/924490.html
--------------------------------------------------------------------------------------------------------------------------
http://www.longecity.org/forum/topic/45332-psoralea-corylifolia-a-soon-to-be-herbal-phenomenon/


 2009 May;66(9):1617-29. doi: 10.1007/s00018-009-9030-9.

In vitro dopaminergic neuroprotective and in vivo antiparkinsonian-like effects of Delta 3,2-hydroxybakuchiol isolated from Psoralea corylifolia (L.).

Abstract

Cocktail recipes containing Psoralea corylifolia seeds (PCS) are used to empirically treat Parkinson disease. A PCS isolate Delta(3),2-hydroxybakuchiol (BU) can inhibit dopamine uptake in dopamine transporter (DAT) transfected Chinese hamster ovary (CHO) cells, and dopamine reuptake blockade may provide an alternative approach for ameliorating parkinsonism. Here, we assessed the potential dopaminergic neuroprotective, and antiparkinsonian-like activity of BU. BU sample size was increased by using a scale-up extraction paradigm. Pharmacologically, BU significantly protected SK-N-SH cells from 1-methyl-4-phenylpyridinium (MPP(+)) insult, produced striking inhibitory actions on dopamine/norepinephrine uptake and WIN35,428 binding in synaptosomes on in vivo administration, and significantly preventing poor performance on rotarod and dopaminergic loss in substantia nigra in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mice. BU acts by protecting dopaminergic neurons from MPP(+) injury and preventing against MPTP-induced behavioral and histological lesions in the Parkinson's disease (PD) model, possibly by inhibiting monoamine transporters. These findings suggest that BU could be meaningful in PD treatment.
                                                            

Antidepressant-like effects of psoralen isolated from the seeds of Psoralea corylifolia in the mouse forced swimming test.


Bakuchiol analogs inhibit monoamine transporters and regulate monoaminergic functions.


Saturday, February 7, 2015

How I Cured my OCD Naturally (With Herbal Remedies)

This is going to be a little lengthy, but I'll make it understandable and formidable. 

Fact is, I've suffered from OCD (Obsessive-Compulsive-Disorder) for many years, since age 11 when the symptoms became really profound. 

The symptoms consisted of 


  • Repeated lock turning and checking of locks.
  • Device Power on/Off checking.
  • Walking over dividers/cracks in sidewalks.
  • Doing multiple things in intervals of 7.
  • Turning my head in 3's when I was alone.
  • " Intrusive Thoughts" (irrational,but often subjugated fears and scenarios)

A fragment of my willpower was able to keep these things fairly in check when around people or in a public place , this ability became more necessary to internalize and adapt to as I aged between 16-17.

In my adult life - I still suffered from continuous intrusive thoughts, that seemed to get worse - especially in times of ANTICIPATION or STRESS.

However, publicly I was able to tone them down or mostly eliminate them. 
However, at times I didn't want to leave or go anywhere because the thoughts would be repetitive and severely disturbing. 

Yet I found going out to alleviate these thoughts by shifting my attention to something more worthwhile; hence I was often "living inside my head".

The biggest strain was in small rooms, closed in especially, intrusive thoughts would be hastened.

Additionally - I often had other more reclusive thoughts, but especially more irritating - mainly centered around things or events that I would be therefore SIMULATING a fear of.

I ended up taking part in writing online, as I do here - to give a sense of responsibility and to shift my thoughts away for a while, well....really to channel them into something minimally stressful. Yet, with WiFi even, certain signal interruptions and slow load times would be enough to trigger yet another "SIMULATED STRESS RESPONSE" - which would include rapidly merging intrusive thoughts and then a not-so-fun adrenaline response which would leave me in a state of almost CONSTANT IRRITATION and being intensely unsettled.

I tried over 50 different herbs and supplements over the course of years.

  • Kanna ( a reported natural serotonin reuptake inhibitor)
  • Kava Kava (an herb with psychoactive properties)
  • Magnesium Citrate ( a mineral with calming properties )
  • D-Aspartic Acid (NMDA-glutamate agonists are reported to help compulsions)
  • N-Acetyl-Cysteine (antioxidant with anti-glutamate properties)
  • Ashwagandha (tonic with relaxing effects)
  • Methyl B12 (methyl groups supposedly can help excessive stimulation)
  • Switching caffeine with yerba mate.
  • American Ginseng (calming "cold" ginseng) (Panax quinquefolius)
  • Inositol (supposedly enhances serotonin)

All of these were either only mildly tuning down the intrusive thoughts, or mildly decreasing compulsions, but not necessarily obsessions. 

NAC; N-Acetyl-Cysteine - definitely halted most of the thoughts, but I found it too sedating and it made it hard to concentrate.

Magnesium I still use today, and it helps some aspects - and definitely tunes it down but not super significantly.

The rest were mildly helpful, at best.

I also tried several diets.

  • ANTI-HISTAMINE DIET (more fruits, less protein and more fiber and sulfur containing foods DAILY; such as beets, onions, garlic etc) (Helped a good amount, but I was hesitant to believe that it had all to do with lowering histamine, as studies are mixed regarding it.
  • PRO-HISTAMINE DIET; My lack of ever catching a cold or flu, and/or not producing symptoms of such made me think I may actually have low histamine...even though I matched only some of the qualitative traits of high histamine described in this article.

***Much to my surprise (or maybe not), the high histamine diet actually seemed to relieve some symptoms with less of a crash - so I guess science hasn't really wrapped their head around the true cause of OCD quite yet; although, generalizations tend to be foolish anyhow!**


All was only mildly helpful, and in this time span of years and searching for new treatments - I became addicted to multiple stimulants (as they reduced symptoms for a small period of time, gave some relief)....eventually though, I began again - relentlessly searching for other supplements. 

I ventured away from embracing the serotonergic hypothesis of deficient serotonin levels - thinking in absolutes for a while. 

I ended doing a hella lot more research, and found, that serotonin is NOT NECESSARILY A GOOD THING FOR OCD - IT ALL DEPENDS ON WHAT RECEPTOR SEROTONIN BINDS TO - SOME ACTUALLY MAKE IT WORSE!!!

Interestingly, me stumbling upon a cure (or at least what would be MY CURE) actually was completely unintentional. 

I was looking for cognitive enhancing supplements with serotonin BLOCKING properties; and decided to test the waters with a supplement called MAGNOLIA OFFICINALIS. An herb with nootropic and anxiolytic; anxiety relieving properties. AGAIN, I didn't think it would have much a positive effect on OCD due to it's serotonin antagonist properties (even despite what I learned) , plus it had been shown to actually deplete serotonin levels in some studies - thus inhibiting any POTENTIALLY positive effect any remaining serotonin would have.

The herb also had GABA-ergic properties, and acetylcholine boosting properties.
It acts specifically as a NATURAL POSITIVE ALLOSTERIC MODULATOR OF GABA-A receptors (which is the mechanism of klonopine/benzodiazepine drugs).

Anyway, the first night I took this - I felt a calm I haven't felt in years, then as each day I continued it - I noticed my intrusive thoughts had become substantially less repetitive. 

At the end of the second week - I no longer felt need for most of my compulsions - and I could just as easily dismiss any remaining partitions of them.

By WEEK THREE - Almost all of my intrusive thoughts were either non-existent or manageable or easily ignorable like a raindrop dropping on my shoulder. 

It amazed me that a remedy with SEROTONIN BLOCKING properties would be able to manage symptoms to such an extent. 

NOW I'M NOT SAYING THAT WAS THE REASON WHY, IN FACT....It most likely had more to do with the GABA-A enhancement. 

But there are tons of chemicals in any given plant or herb - so it's hard to tell really what exactly did it - but something in MAGNOLIA OFFICINALIS CERTAINLY DID!!!

Now it's been a year and I still take it today - and the effects DO linger - and without adverse effects as with drugs or with other supplements that would crash me or easily reduce my productivity / creativity.

Finally, I noticed something interesting ---- ADDING GOTU KOLA to the regimen seemed to balance out the effect provide an additional sense of mental clarity without being too stimulating.

BOTH OF THESE ARE ADRENAL STABILIZING AND / OR ANTI-STRESS HERBS.

Both are also considered NOOTROPICS (cognitive enhancers or "BRAIN-BOOSTERS".

So it's a win-win situation, you get COGNITIVE ENHANCEMENT with OCD-TREATMENT - AND EFFECTIVELY DOING BOTH AT AN UNPRECEDENTED RATE.

The particular brands / supplements I used to cure my OCD NATURALLY are below.

They were both very cheap as you can see below - which is relieving in itself. 

The Magnolia Product I bought is "Genesis Today" Magnolia Bark Capsules which I still take today as of (6/10/2016) & as well with Swanson Gotu Kola Extract which I also still take.

On study days, I do only one magnolia capsule per day, and two gotu kola. :-)





                                                       


click here now

Natural Treatment for ADD/ADHD - Is it possible ? Overview and Comparison to Drug Treatment


Attention deficit hyperactivity disorder (ADHD) is a developmental disorder characterized by inattention, hyperactivity, and impulsivity(!).


{ SCROLL PAST THIS CHART FOR DIRECT  } {DISCUSSION OF ALTERNATIVE REMEDIES }

Signs and Symptoms

A person is diagnosed with ADHD if they have at least 6 symptoms from the following categories, lasting for at least 2 months. In diagnosing children, the symptoms must appear before age 7, and pose a significant challenge to everyday functioning in at least 2 areas of life (usually home and school). Most children do not show all the symptoms, and they may be different in boys and girls (boys may be more hyperactive and girls more inattentive).

  • Inattention
  • Fails to pay close attention to details or makes careless mistakes
  • Has difficulty sustaining attention in tasks or play activities
  • Does not seem to listen when spoken to directly
  • Does not follow through on instructions and fails to finish tasks
  • Has difficulty organizing tasks and activities
  • Avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (such as school work)
  • Loses things needed for tasks or activities
  • Is easily distracted
  • Is forgetful in daily activities
  • Hyperactivity and Impulsivity
  • Fidgets with hands or feet or squirms when seated
  • Does not remain seated when expected to
  • Runs or climbs excessively in inappropriate situations (in teens or adults, may be feelings of restlessness)
  • Has difficulty playing or engaging in leisure activities quietly
  • Acts as if "driven by a motor"
  • Talks excessively
  • Blurts out answers before questions are completed
  • Has difficulty waiting his or her turn
  • Interrupts or intrudes on others





Current treatment of Attention-Deficit-Hyperactivity-Disorder (ADHD) consists of stimulant medication aimed at restoring dopaminergic function . Interestingly, a stimulant may, in some cases also further hyperactivity issues - although the notion that stimulants "balance out" ADD sufferers is well-accepted.

The current hypothesis and / or conclusions that medical science and neuropharmacological publications have elaborated on - is that ADD/ADHD sufferer's have alterations in dopamine and norepinephrine transporter activity which often results in increased recylcling of neurotransmitters and thus less efficiency for one to use them(!)(!). 

In simpler terms, and also outlined with the picture below, a normal brain will utilize dopamine and it will stay in the synapse a specific amount of time - whereas an ADD/ADHD sufferer uses up the dopamine/norepinephrine too quickly , because the increased levels of transporters are quickly moving it out of the synapse (which is considered a measure of overall neurotransmission and activity).

Additionally, norepinephrine levels may be elevated but poorly used, which may be responsible for the common comorbidity of anxiety disorders with ADHD. Interestingly, the NET (norepinephrine transporter) is also capable of itself binding to and inactivating dopamine in the frontal cortex(!), exclusively - meaning although the NET mainly recycles the norepinephrine neurotransmitter, it can also in that one area of the brain (but not elsewhere) recycle dopamine!


This explains why NET inhibition produces positive effects in the affected, despite the capacity to increase anxiety - because it results in an extra dopamine boost in the prefrontal cortex, an area highly associated with both cognitive and attention disorders. Thus balancing out the rush! (dopamine has inhibitory or calming effects as well)

THE PROBLEM with current pharmaceutical medications for ADD/ADHD goes well beyond the reports and concerns of "stunted growth" - current studies are identifying that long-term use of ADHD/ADD stimulant medications actually INCREASE dopamine transporter mRNA - which as mentioned before, the whole purpose is to DECREASE the activity of this transporter (!).

Therefore , current drug treatments lack in efficacy and effects wear off after continuous treatment. 

BUT, to make matters worse, they are also associated with a number of disturbing side-effects.
  •                                                  SLEEP PROBLEMS
  • mood swings
  • loss of appetite
  • heart problems
  • suicidal thoughts or actions




All or most of these side-effects come from the fact that all this stimulation comes in such a short-period of time, and as the body gets stimulated - a compensatory effort is made by the body to "normalize" or lessen the amount of stimulation - so therefore, the body actually does the opposite in response of the medication, over time.



How do we BYPASS this?




One plausible option is to use a natural reuptake inhibitor that doesn't bind as quickly or as fast - and thus doesn't force the body into negative feedback.


I recommend a product called  PSORALEA CORYLIFOLIA; a natural dopamine and norepinephrine reuptake inhibitor(!).

Additionally, because this product "presses the buttons a little lighter" it is ideal for those who have become tolerant to their ADHD Medication/s, and the product also has a second benefit; inhibiting the breakdown of neurotransmitter at the enzymatic/systemic level.

Finally, the herb is also NEURO-PROTECTIVE instead of neuro-degradative like drugs are, meaning, instead of causing the loss of brain cells with time of treatment, this will actually increase them and their resistance to degradation.(!)



                                                                  
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Another alternative remedy for ADHD/ADD would be FLOWERING QUINCE; also known as MU GUA!  

This herb is a natural DOPAMINE REUPTAKE INHIBITOR (!) - with a high potency but has virtually no affinity for NET/Norepinephrine transporter - ----- --- and thus less stimulatory or ANXIOGENIC (anxiety provoking) effects.
You can buy it with the link below from amazon, this one can be easily steeped in tea, or put with juice, as it does not have a bad taste - and tastes a bit like a cross between a plum and an apple.


Here's a discussion below on FQ  

Re: Quince DARI - Confirmation: this stuff works



                                                                     





**SIMILAR ARTICLES/CITATIONS**

Does Serotonin raise Dopamine, or lower it? Does dopamine raise serotonin, or lower it? INTERACTIONS With Dopaminergic-Serotonergic Systems Explored

HOW DOES DOPAMINE AFFECT SEROTONIN, OR HOW DOES SEROTONIN AFFECT DOPAMINE?
{ CLICK ON THE IMAGES TO GET A BETTER VIEW }
TEXT VERSION IS AFTER THEM



It's not so simple as to say dopamine raises serotonin, or serotonin raises dopamine - but if you're gonna go with such an assumption - you should at least hear the ODDS THAT SEROTONIN WILL RAISE DOPAMINE ARE INCREDIBLY LOW!!!

  • Dopamine inhibits dopamine at the D(2) receptors expressed as autoreceptors, whereas the post-synaptic D(2) receptors play a separate role in initiating endocrine responses and in controlling spasms and jerky movements.

  • Dopamine at D(2) and D(3) receptors interact with AMPA-glutamate pathway, and have secondary effects on GABA-ergic neurons.

  • Dopamine D(4) are similar to the two above, but may have a distinct or more specific action in depression and also on behavioral phenotypes.

  • Dopamine D(1) and dopamine D(5) stimulate locomotion (an indice of anti-depressant effects & general QOL scores) .
QuoteNow here's the biggest point to remember, no matter which neurotransmitter you are talking about. 
ALWAYS KNOW WHETHER THE RECEPTOR IS POSITIVELY OR NEGATIVELY COUPLED TO G-PROTEINS AND THUS ADENYLATE CYCLASE...


BECAUSE.....

If it's positively coupled it will have stimulatory effects and will increase basal and active metabolism as well as increase thyroid output and dopamine production. It will also signal HOMEOSTATIC mechanisms particularly signaling to serotonin 5-HT(1) autoreceptors to then decrease in moderation, the level of cAMP that was just increased...hence , this second messenger's all - important role in determining WHICH receptors get to handle the homeostatic feedback and partially determining the NET RATE of serotonin synthesis and activity. AKA that which is released in the blood stream or into the synapse BY THE MEANS of indirect autoreceptor activation that is the result of activating the conditional second messenger system of CYCLIC ADENOSINE MONOPHOSPHATE

If it's negatively coupled then we have an opposite array of effects, seeing instead of stimulation, we get depression, a decrease in dopamine synthesis and activity, and instead of 5-HT inhibitory signaling we get the potential CROSS-ACTIVATION of type 2 like serotonin receptors.

Additionally, those negatively coupled HAVE A TENDENCY to induce histamine and nitric oxide release, as well as GABA activity.

NOW LET'S GO BACK TO DOPAMINE AND SEROTONIN...IF YOU'VE ABSORBED THE ABOVE; then you're good!

Serotonin inhibits dopamine activity and release the type 1 receptors, as well as type 2, type 6 and type 5A receptors.
Whereas 5-HT3/4 have mixed effects , in some studies showing an enhancement in frontal lobe transmission, and in hippocampus mixed effects TRENDING WITH A DECREASE.

Therefore, all in all, there is a PROPENSITY & HIGHER LIKELIHOOD of serotonin to INHIBIT dopamine, than to raise it.
The NET effect of ANY neurotransmitter, especially MONOAMINES - is based on which receptors are available and the NET RATIO of heterodimized pairings and coincidentally, the ratio of NEGATIVE;POSITIVE FEEDBACK.

In other words, it simply comes down to more or less, if there is more positively coupled G-protein receptors being activated or more negatively coupled receptors being activated by premise or by consequence!

OR, IN EVEN SIMPLER TERMS....HOW MUCH CYCLIC AMP ONE HAS IS THE PRIMARY DETERMINANT TO TOTAL NERVOUS SYSTEM ACTIVITY AND THE BALANCE BETWEEN PARASYMPATHETIC AND SYMPATHETIC ACTIVITY THAT DETERMINES CENTRAL HOMESTASIS AND THUS THE PLAUSIBLE EXISTANCE OF DEPRESSIVE DISORDERS AND/OR THE TENDENCY TO SUCCUMB TO SUCH DISORDERS!


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