Fake Profiles on FaceBook, Twitter, Dating Sites; What Gives?

Well this is going to be a fairly anticipated discussion. Fake Profiles.

People who either have nothing better to do with their time or people obsessed with harassing their target....

Is it really that simple though?

I could go on and on about the exact differences between specific fake profiles...but I'm going to make it real simple.

Fake Profiles are often but not always the idea of some 'perv' behind the screen..and , for the ladies, they aren't always a jealous ex or a friend you have recently 'cut-off'. In fact, many fake profiles are people that either were on your friends list or still are, and are using your pictures or one of your friends pictures for some malicious practice. 

It could also be very benign, fake profiles are known to be used for anything from aggressively accumulating likes on someone's profile or to re-inforce the esteem of a given crowd...or organization!

THINK of those product ads or company sites and their advertisements, where a nutritional product is just bathing in testimonials from supposedly, hundreds or thousands of happy customers...well, fake profiles can be there in effort to - figuratively, or literally; provide those "testimonials". 

Fake profiles are deceivers no matter which way you look at it. They are a lie. But , they can be a simple lie or a sophisticated con. 

Therefore in more communicable terms, there is a division between fake profiles, almost a hierarchy. 

~DATING SITES~

Dating sites, especially the large , paid and structured variants. Are especially prone to fake profiles and other forms of abuse. They are literally hammered with fake profiles. Much more than free sites. 

Why?

Because in part, the administrators or at least the faculty within the marketing department are fascinated with the idea of using 'sensor bots' and 'magical profiles' to entice and gauge customers who may then go forth and buy other products by means of request within personal message.

This seems to happen on adultfriendfinder like sites and other sites that are qualified to be , extremely enticing. XXX select, mingle , passion search are all examples of sites flooded with illegitimate profiles. Some may simply be estranged wives, eh, div-orc-e's - that may be really.that.desperate, but this can not be attributed to all of them .

Of course, to some extent or another..this will be an issue on every site, because wherever there is a chance to profit, there will be cons of all sizes, small or large, fanatic or stable.

A good buddy of mine, a psychotherapist once elaborated on the inhumanity in these fellows. How clear it is that there is either financial incentive or a disturbed mind behind the screens of whom post fake profiles, but..... 

It doesn't take a psychologist or human behavior specialist to know that fake profiles altogether, are created for the following reasons.

• To exploit ordinary people for a diverse marketing purpose, as in financial incentive. 
• To extract information or entice an individual to gain information.
• To reinforce the esteem or distort perceived popularity of a person, organization or fan page.
• To harass either an ex-girlfriend, boyfriend, wife, or husband .
• To test a spouse if he or she may cheat when given the opportunity.
• For other forms of sabotage or disruption where fake characters may play a supplemental role.

Specific Effects of Vitamins and Minerals on Neurotransmitters : Interactions Defined (including serotonin, dopamine , glutamate, histamine, GABA, acetylcholine etc)

          

Although I hate generalizing, with science (or really neurobiology) there comes a time where consistency in rapport (between studies and researchers) leads to comfortability. Oh there comes a time when we need the most straightforward, fairly simple consistencies to elevate our understanding of such things. 

Well, now is that time. 

                              ::  ::  :: VITAMINS   ::  ::  ::
................................................................................................................
Vitamin A: Decreases acetylcholine synthesis (except when correcting deficiency)(1)(2), increases growth factors and essential to maturation of hippocampus and other important brain regions(3), protects against beta-amyloid in the brain(4), maintains dopamine D(2) receptor expression(5).

Vitamin B1 (THIAMINE) : essential to forming serotonin-ergic neuronal networks/mossy fibres and to maintaining integrity of glutamate-networks(6)(7), increases acetylcholine and corrects acetylcholine deficiency(8)(9)(10), increases dopamine in the striatum(11), modulates/inhibits serotonin synthesis(12), essential to brain norepinephrine function and cognitive processes(13)(14), necessary for both glutamate and GABA production(15).

Vitamin B2 (RIBOFLAVIN) : affects sensitivity of the MAO-A enzyme to inhibition(16), increases acetylcholine at high doses but does not affect at low doses(17), decreases glutamate from cortical nerves(18). may improve some symptoms of ADD by impacting central alpha & beta wave performance(19)

Vitamin B3 : may increase histamine and serotonin as well as nitric oxide levels(20)(21), increases BDNF and may improve brain cell growth(22).

Vitamin C : (ascorbic acid/ascorbate) ; decreases striatal dopamine(6), increases norepinephrine production from dopamine(7)(8), increases acetylcholine at high doses(9)(10), protects against NMDA and glutamate related cell death(11)(12), decreases histamine release(13)(14), necessary for serotonin synthesis(15), necessary for dopamine production(16).

Vitamin D - Increases serotonin production rates and general serotonin synthesis (17)(18) as well as dopamine synthesis(19) (formation), protects against glutamate neurotoxicity(20), inhibits inducible nitric oxide synthase which may reduce inflammation and cell death(21), does not notably reduce other forms of nitric oxide however, increases glutathione and concentrations of antioxidant enzymes(22), necessary for glutamate decarboxylase (GAD) which is responsible for converting Glutamate into GABA; meaning Vitamin D is essential for creating GABA and moderating glutamate exposure(23), Vitamin D regulates muscarinic 3 receptor expression and prevents excess expression in Diabetes (24), decreases acetylcholine in high doses(25).

Vitamin E : increases acetylcholine release at low or high doses (26 ), attenuates/decreases excitotoxicity/protects against excess glutamate effect on neurons(27), increases glutamate when low, prevents excess GABA accumulation(28)

Vitamin  K  : decreases acetylcholine in low or high doses (29), regulates cell proliferation in olfactory bulb inputs and subventricular stem cells(30), maintains normal insulin sensitivity and helps offset diabetes (31), necessary for protein production in human hypothalamus, hippocampus, pons medulla and other brain regions - and helps maintain . increase mitochondrial energy production(32)(33)(34)(35).


Iron : Essential for glutamate binding and GABA transaminase activities( ). 
Increases nAChR's (nicotinic-Acetylcholine-Receptors) and massively increases NMDA-Receptors in Hippocampus (!) (!!)
Iron is also needed for TH and TPH as well as both monoamine oxidases; thus ,  IRON is necessary for production of DOPAMINE, SEROTONIN, glutamate AND GABA as well as the breakdown of the former two (*!!!*)


Magnesium : Necessary for 5-HT(1)A Serotonin Receptor Expression (!) (!!) (!!!) (!!!!)
Blocks NMDA Receptors (!!!!!)

Zinc(Zn): negative allosteric modulator of 5-HT1A receptors and signaling; may improve memory theoretically by lessening inhibitory serotonin influence( ),  negative allosteric modulator of GABA-(A) function; this may explain anxiogenic effects of high dose Zinc therapy, however, it also may explain it's memory and synaptic improving events(!).
Zinc amplifies and induces supersensitivity of MUSCARINIC acetylcholine Receptors; in part by upregulating the receptors in all major brain regions..thus , Zinc is essential for maintenance of Acetylcholine-receptor function and can be categorized as one of the major minerals involved in receptor expression. {<see here>}

• Zinc also amplifies and potentiates Beta-2-Adrenoreceptors (B2) by acting as a PAS (Positive Allosteric Modulator) ; this means Zinc (Zn2+) can improve the efficacy / benefits of ASTHMA Medications that use this pathway (ALBUTEROL, CLENBUTEROL, FORMOTEROL etc)... (<see here>)
• CAUTION:  Moderate-High dose Zinc is then expected to also INCREASE one's sensitivity to BOTH Caffeine and Albuterol / other asthma drugs that act as BETA-AGONISTS.

ZINC is involved in NMDA-Receptor regulation; it blocks the uptake of Glutamate and Aspartate into the HIPPOCAMPUS (~*~) and directly blocks NMDA-Receptors (*C-Here*)

http://www.ncbi.nlm.nih.gov/pubmed/16513220

tags :: NMDA-receptor binding, glutamate ion channels, minerals affecting glutamate neurotransmission, minerals affecting n.o synthesis, minerals affecting histamine, nos free radicals, the effects of zinc on l-glutamate binding, effects on serotonin receptors by minerals, 

GABA-Transaminase Inhibitors (GABA-Reuptake Inhibitors) (How to Enhance GABA & Prevent it's Breakdown)

While monoamine neurotransmitters such as dopamine, serotonin and norepinephrine are metabolized (broken down, cleared & made useless) primarily by MAO enzymes and & COMT , amino acid transmitters which are much more abundant, are broken down by totally separate enzymes.


Additionally, transporters that take their respective neurotransmitters 'out of operation' as in DAT to dopamine, and SERT to serotonin, are structurally different than their amino acid transmitter counterparts.


GABA-T or GABA Transaminase; is the enzyme that transports GABA out of the synaptic cleft and acts as a 'SHUNT' (also referred to as the GABA shunt enzyme or shunt scenario), effectively diverting (or really sending away) active GABA currents. 

GABA-T, also known as 4-aminobutyrate transaminase is what DAT is to dopamine and SERT is to serotonin, it degrades neuronal GABA preventing it from accumulating and thus reaching a higher order of consistency.

Inhibiting the enzyme may lead to not only sustained GABA levels but also potentiation of all substances that act on the GABA system and thus inhibiting the enzyme will amplify the effects of alcohol and other depressants.

There are a few Active and human compatible transaminase inhibitors that may enhance the activity of GABA and thus prolong it's effects.

Natural GABA transaminase inhibitors (GABA Reuptake Inhibitors) would be. 

• Lemon Balm Extract (!) (!). 
• Rosemarinic Acid Extract (!).
• Gastrodin (!)

**Gastrodin is a known neuroprotective agent which is primarily marketed by Life Extension, a great deal of research has been conducted in the life extension community and by some practicing naturopathic doctors as well as UA researchers, however, it is not strictly a GABA-T inhibitor.**

~My recommended brands of each respective product are below~

Lemon Balm
              


ROSEMARINIC ACID EXTRACT w/ Butterbur
(helps anxiety, allergies and asthma)




Brand Name Gastrodin
("BRAIN SHIELD")

Pharmaceutical Transmaninase Inhibitors

Vigabitrin; an anti-epileptic drug marketed as Sabril. 

Vigabatrin, a GABA Transaminase Inhibitor, Reversibly Eliminates Tinnitus in an Animal Model

Vigabatrin decreases cholecystokinin-tetrapeptide (CCK-4) induced panic in healthy volunteers.




****REFERENCES/CITATIONS/SOURCES****
The GABA shunt: an attractive and potential therapeutic target in the treatment of epileptic disorders.

Broad-Spectrum Protection Against Brain Aging : By Arlan Myerson

Gastrodin Discussion @ Longecity 

Use of inhibitors of gamma-aminobutyric acid (GABA) transaminase for the estimation of GABA turnover

Chronic administration of the antidepressant phenelzine and its N-acetyl analogue: effects on GABAergic function.

GABA-elevating effects of the antidepressant/antipanic drug phenelzine in brain: effects of pretreatment with tranylcypromine, (-)-deprenyl and clorgyline.

Vigabatrin, a GABA Transaminase Inhibitor, Reversibly Eliminates Tinnitus in an Animal Model


Vigabatrin decreases cholecystokinin-tetrapeptide (CCK-4) induced panic in healthy volunteers.

Serotonin Role in Stimulant Addiction (Does Serotonin Increase or Decrease Stimulant Cravings?)

Serotonin is a powerful neurotransmitter that affects a number of systemic and behavioral processes. It's effects in the Central Nervous System extend to blood pressure regulation as well as affecting heart rate. Behaviorally, serotonin has differential effects depending on the receptor activated.

In regards to stimulant addiction, serotonin doesn't necessarily go one way or another. However, serotonin is shown in the following study to lead to a proclivity to stimulant addiction/dependence when it activates the 5-HT1A autoreceptor. This makes perfect sense, because that particular receptor is inhibitory whereas many other serotonin receptors are stimulatory (such as 2A,3A,4A,7A). 

Oddly though, 5-HT1A post-synaptic receptors are the complete opposite to the autoreceptors in that they may inhibit the expression of addiction like behaviors(1). 

Despite serotonin's stimulatory effects at other receptors...this does not mean that activating them is a proper resort to reducing stimulant addiction, because many serotonin receptors increase stress hormones - paradoxically the stimulatory subtypes may actually create an addiction-prone-atmosphere..thus it is wise to not utilize the serotonergic system to treat addiction, aside from autoreceptor specific antagonists that have no affinity/attachment to other receptors(2)(3)(4)(5). 


More evidence for the above, when serotonin activates the type 2A receptor(6), or when there is a polymorphism of the receptor(7), addiction-related behavior for smoking specifically is INCREASED - this provides evidence that multiple serotonin receptors may promote addiction related behavior. With a tendency towards cocaine and tobacco addiction . This implicates serotonin as an anti-target for treating certain forms of addiction.

Area-1255: Optimal Smoking Cessation Therapy (O.S.C.T) (Best Supplements/Drugs to Quit Smoking)

There's been a lot of disinformation and erroneous conclusions over the years regarding smoking cessation strategies and the aides to go with them. Particularly confusing are the inconsistent, or downright confusing performances of the market aimed at smokers and want-to-be-non-smokers. 

For instance, if nicotine is supposed to be so helpful and the total all-in-one package for replacing the psychostimulant effects of smoking..then we would see better statistics than this.

But let's be honest, nothing in life - or at least in Science is that simple. 

So where are we with real mean-uvers in the smoking cessation movement? 

I'd say we're about here.

If you go by a realistic, comprehensive approach actually based on real facts. Scientific facts.

Nicotine replacement is not dumb, but it is weak alone.

The two psychoactive chemicals in tobacco, the ones that actually provide a mood lift - are nicotine and some form of a beta-carboline alkaloid (!)..which act to prevent the breakdown of dopamine by inhibiting the MAO-B enzyme(!!). 

So common sense would tell ya nicotine should at least* be paired with a safe form of a beta-carboline(!!!), or at least an MAO-B inhibitor(!!!!)..which is why these types of studies have been conducted but unfortunately, aren't always brought to the surface..at least not from a marketing perspective.

So would an MAO inhibitor + nicotine be ideal?
(not just better, but ideal)

Not exactly, not ideal, but definitely better. ;)

 

Miscellaneous / Undocumented Effects of Anti-Depressants ( Hidden / Obscure Effects of Psych Meds )

This is going to be my one of my most delightful articles yet, and over a period of weeks will be wholly complete. 

Often one question people will ask - what are the 'other' mechanisms of anti-depressants...the 'hidden' effects which may correlate to drug efficacy and / or neurological side-effects.

Let's start off with an example, one that isn't shown in pharmacy booklets. MAPROTILINE sold as Deprilept, Ludiomil, Psymion; is an anti-depressant medication cited as being a norepinephrine reuptake inhibitor (NET Inhibitor) (1) , OK so it enhances norADRENALINE levels creating sensory and motor effects and stimulation. Second to this, it also antagonizes serotonin 7A receptors (2) - or simply the 7th serotonin receptor...which can result in a decrease in cAMP and an increase in dopaminergic neurotransmission(3)(4). 

The part not cited, even on the wiki, is maprotiline's ability to inhibit K+ (POTASSIUM) inward rectifying currents (5) (6). Inhibiting these currents would provide additional stimulation parallel to or mimicking histamine activity(7). AND IT'S NOT JUST MAPROTILINE FOLKS, it's also imipramine, desipramine, amitriptyline, nortriptyline, clomipramine,, and citalopram that inhibit potassium channels(8). < CLICK IMAGE TO GET BETTER VIEW >

Another not well-known mechanism of some anti-depressants - is the unspecified action on histamine H2 receptors...some anti-depressants have such a weak potency for the receptor that it may not matter - however, some like mianserin(9)(10), amitryptiline(11) and trimipramine/imipramine(12) have relative effects and can to a moderate extent, inhibit histamine H2-related responses(13).

If, in process, cAMP is reduced effectively by H2 inhibition - this may be a mechanism in which some* anti-depressants can exacerbate psychosis(14)(15)(16).

However, not all anti-depressants will have these side-effects, it is mainly amitryptiline, noritryptiline, imipramine and trimipramine, mianserin is less likely to cause these specific side-effects, and mirtazapine is on average, much safer than all of the above and has seemingly zero affinity for H2R's, as opposed to it's cousin drug mianserin.

How to Reverse Gynecomastia (Reverse Gyno) (AntiPsychotic Induced , AAS Induced, Misc, Pubertal)

Let me start off by saying, there is no 100% effective way besides surgery to completely eliminate severe cases of gynecomastia(male-breast-growth, 'gyno'). While some sups can help treat a mild to moderate case of gyno, this won't happen with most oral sups.

Your best bets for OTC gyno treatment are the following.

1.) YOHIMFLAME; a yohimbine containing gel. Use alone or with the other products mentioned in this article. Can be applied to chest area directly.

Click image to be brought to site.

<STUDIES ON YOHIMBINE>

<TOPICAL FAT REDUCTION W YOHIMBINE>

2.) Andractim DHT Gel; A DHT product that directly counteracts estrogen on the receptor-RNA level(!), helping to revert glandular growth and fat gain in the chest area(!). Can be used alone but preferably with yohimflame shown above. Click image to buy Andractim online.  Also treats pubertal gynecomastia(!).
Can decrease prolactin secretion and increase libido as well(!).

              

                                                    

3.) Tamoxifen + Arimidex (oral combination)

Using a SERM such as Tamoxfien along with a classical aromatase inhibitor such as Arimidex is a powerful , comprehensive strategy and perhaps the only oral combination effective for gyno treatment. It can be done alone or with the above implemented into the regimen. May also help avert side-effects from testosterone replacement therapies. Click the words above to go to site and buy.

Treatment of gynecomastia with tamoxifen: a double-blind crossover study.

Management of physiological gynaecomastia with tamoxifen.

Reversing gyno with arimidex?

SERM + AROMATASE INHIBITORS

How to : Treat Anti-Psychotic Induced Weight Gain (Reverse / Prevent AntiPsychotic Weight Gain)

Anti-Psychotic drug induced weight gain is a very common occurrence, especially in those taking Zyprexa ( OLANZAPINE ) and Risperdal ( RISPERIDONE ) (1) (2) ...

Anti-histamine effects are a huge contributing factor in anti-psychotic induced weight gain(3) (4) (5), and the anti-serotonin property (specifically the 2C antagonist effects) also play a huge role(5). Belviq ( LORCASERIN ) works as a direct opposite to this effect, acting instead as a serotonin 2C agonist(6). However, during anti-psychotic treatment, the effects of serotonin agonists will be blocked or minimized in most cases. 

Can Belviq help anti-psychotic induced weight gain?

Most likely, No.

What to use instead?

Use a histamine H3 antagonist like betahistine (7) or KUTAJ (8) (9) extract to counter weight gain and some of the sedation of antipsychotic drugs.

Betahistine can be purchased here, it is legal and not a controlled substance anywhere. > http://www.internationaldrugmart.com/betahistine.shtml

Hollarhena (KUTAJ) can be purchased below. 

                                                                     





Additionally, ginkgo biloba can be used to minimize prolactin increases (10) (11) which may be caused by anti-psychotic drugs which (prolactin) may also lead to weight gain, ginkgo is also very synergistic with KUTAJ and betahistine(12)(13)(14).

                                                                  

ANDRACTIM DHT Gel (shown below) is a gel you can apply to your chest area to help prevent & reverse anti-psychotic induced gynecomastia and estrogen and prolactin related issues.

Click the image below to buy DHT Gel.

Mechanisms of Anti-Psychotic Drug Induced Sedation (sleepiness,grogginess) (Management and Reversal of AntiPsychotic Sedation)

Sedation is a common side-effect associated with anti-psychotic drugs, both typical and atypical(1)(2). Zyprexa ( OLANZAPINE ), Seroquel ( QUETIAPINE ) and Clozapine tend to a more pronounced sedative effect than Risperdal (Risperidone) and Haldol ( HALOPERIDOL ) , depending on the dose and method of administration(3). Thorazine is typically regarded as the strongest sedative out of all of them(4)(5) (6). 

However, there is debate and controversy about this, given the administration is almost always intramuscular or subcutaneous and is not typically used orally in contrast to the other medications available for typical events.

In regards to anti-histamine effects solely, Hydroxyzine AKA Vistaril seems to be the most potent.

Amisulpride and Abilify seem to be the least on the sedation scale, so substituting the above medications with either amisulpride or abilify seems like a reasonable mediation.

The mechanisms of sedation are generally, in ranked order, H1 antagonism (anti-histamine activity) (7), Alpha-1-adrenergic blockade (blocking stimulant effects of adrenaline)(8)(9), serotonin 2A antagonism (10) (blocking stimulatory effects and hallucinogenic effects of serotonin) - finally, anticholinergic effects as in with clozapine mediate the high rate of remission and sedative effects as well as weight gain(11)(12)(13).

A collaborative effort is necessary to improve patient well-being and cognitive functions in those taking sedative psychotropic medications. The mechanisms should be taken into consideration based on the patients history and individual need assessment. Adjunct treatments should be discussed to help eliminate daytime drowsiness in patients.

Some of these treatments may include.

Histamine H3 Antagonists(!); though it may not fully eliminate the sedative effects - it can certainly reduce the sedation and improve cognitive function in patients with schizophrenia and other psychiatric disorders such as ADHD(14) (15).

An example may be something as simple as supplementing with Hollarhena extract which contains a natural H3R antagonist compound(16). Patient should be monitored and the supplement should be taken during the day.

Additionally, histamine H3 antagonists like betahistine may target and attenuate anti-psychotic induced weight gain(17).

ALPHA-2-ANTAGONISTS; Caution in those with bipolar disorder or those taking clonidine, as alpha-2-antagonists will also block the effects of clonidine, not just the sedative effects(18).

A2-Antagonists may also improve cognitive function and symptoms of depression(19), especially that which is induced by adrenergic blocker drugs. They also may improve treatment outcomes and symptoms of psychosis(20)(21).

One, Idazoxan may help counter sedative effects however it is unavailable in most areas except by special order, custom synthesis or a compound pharmacy.

Alternatively, yohimbine (USA), or mianserin (U.K) could be used but careful observation and caution must be exercised. 

GABA-A Antagonism; very very risky, but will provide an almost definite reduction / reversal in anti-psychotic induced sedation. However, it can not be done in patients who have a risk of seizures or previous seizure disorder and can not be used by those with anxiety disorders..which severely limits the therapeutic application indices and restricts the the number of target patients(!).

Ginkgo biloba possesses a wakefulness effect as well as a GABA-A antagonist effect (!) - and it may exert a pro-histamine effect (!) as well which may be a very effective method to reduce antipsychotic sedation however the doses may be tricky to gauge in many patients(!).

Finally, opiate antagonist drugs such as naltrexone may help to reverse or treat anti-psychotic induced weight gain as well as tardive dyskinesia(22)(23). They may also improve/reduce sedation to a degree(24).