809 replies to this topic

[ScienceGuy]

I also wonder about... Chamomile

CHAMOMILE (MATRICARIA CHAMOMILLA)

CHAMOMILE’s mechanism of action in relation to its ANXIOLYTIC effects appears to involve both GABA RECEPTOR AGONISM and weak GABA TRANSAMINASE INHIBITION; and as such, prolonged usage will to an extent induce a down-regulation of the GABA RECEPTORS

Therefore, prolonged usage of CHAMOMILE for the medium to long-term should be avoided; and usage should be restricted to short-term usage and/or CYCLING ON/OFF

See the following:

Phytotherapy Res. 1996;10:177–179.

Benzodiazepine-like compounds and GABA in flower heads of Matricaria chamomilla.

Avallone, R.; Zanoli, P.; Corsi, L.; Cannazza, G.; Baraldi, M.

Source

Department of Pharmaceutical Sciences, Modena University, Via Campi 183, 41110 Modena (Italy)

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Planta Med. 1995 Jun;61(3):213-6.

Apigenin, a component of Matricaria recutita [and Matricaria chamomilla] flowers, is a central benzodiazepine receptors-ligand with anxiolytic effects.

Viola H, Wasowski C, Levi de Stein M, Wolfman C, Silveira R, Dajas F, Medina JH, Paladini AC.
Source

Instituto de Biología Celular, Facultad de Medicina, Buenos Aires, Argentina.
Abstract

The dried flower heads of Matricaria recutita L. (Asteraceae) are used in folk medicine to prepare a spasmolytic and sedative tea. Our fractionation of the aqueous extract of this plant led to the detection of several fractions with significant affinity for the central benzodiazepine receptor and to the isolation and identification of 5,7,4'-trihydroxyflavone (apigenin) in one of them. Apigenin competitively inhibited the binding of flunitrazepam with a Ki of 4 microM and had no effect on muscarinic receptors, alpha 1-adrenoceptors, and on the binding of muscimol to GABAA receptors. Apigenin had a clear anxiolytic activity in mice in the elevated plusmaze without evidencing sedation or muscle relaxant effects at doses similar to those used for classical benzodiazepines and no anticonvulsant action was detected. However, a 10-fold increase in dosage produced a mild sedative effect since a 26% reduction in ambulatory locomotor activity and a 35% decrement in hole-board parameters were evident. The results reported in this paper demonstrate that apigenin is a ligand for the central benzodiazepine receptors exerting anxiolytic and slight sedative effects but not being anticonvulsant or myorelaxant.
PMID: 7617761
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Canadian Journal of Physiology and Pharmacology, Volume 85, Number 9, September 2007 , pp. 933-942(10)

Effects of traditionally used anxiolytic botanicals on enzymes of the γ-aminobutyric acid (GABA) system

Awad, R.; Levac, D.; Cybulska, P.; Merali, Z.; Trudeau, V.L.; Arnason, J.T.

Source

NRC Research Press.

Abstract

In Canada, the use of botanical natural health products (NHPs) for anxiety disorders is on the rise, and a critical evaluation of their safety and efficacy is required. The purpose of this study was to determine whether commercially available botanicals directly affect the primary brain enzymes responsible for γ-aminobutyric acid (GABA) metabolism. Anxiolytic plants may interact with either glutamic acid decarboxylase (GAD) or GABA transaminase (GABA-T) and ultimately influence brain GABA levels and neurotransmission. Two in vitro rat brain homogenate assays were developed to determine the inhibitory concentrations (IC₅₀) of aqueous and ethanolic plant extracts. Approximately 70% of all extracts that were tested showed little or no inhibitory effect (IC₅₀ values greater than 1mg/mL) and are therefore unlikely to affect GABA metabolism as tested. The aqueous extract of Melissa officinalis (lemon balm) exhibited the greatest inhibition of GABA-T activity (IC₅₀ = 0.35mg/mL). Extracts from Centella asiatica (gotu kola) and Valeriana officinalis (valerian) stimulated GAD activity by over 40% at a dose of 1mg/mL. On the other hand, both Matricaria recutita (German chamomile) and Humulus lupulus (hops) showed significant inhibition of GAD activity (0.11-0.65mg/mL). Several of these species may therefore warrant further pharmacological investigation. The relation between enzyme activity and possible in vivo mode of action is discussed.

[ScienceGuy]

I also wonder about... Hops

HOPS (HUMULUS LUPULUS)

HOPS’ mechanism of action in relation to its ANXIOLYTIC effects appears to be that of MELATONIN RECEPTOR AGONIST (like AFOBAZOLE) and weak GABA TRANSAMINASE INHIBITION (like LEMON BALM and CHAMOMILE)

Since GABA TRANSAMINASE INHIBITION induces an INCREASE in GABA LEVELS, prolonged usage theoretically will to an extent induce a down-regulation of the GABA RECEPTORS.

However, to put things into perspective, it is important to note that HOPS' GABA TRANSAMINASE INHIBITION effects are WEAK (much weaker in fact than that of LEMON BALM); and as such the potential for down-regulation of the GABA RECEPTORS is small.

Consequently, after weighing up all the evidence I have placed HOPS onto the ‘POSSIBLY TO AVOID’ list

If one wanted to be ‘absolutely safe’, prolonged usage of HOPS for the medium to long-term should be avoided; and usage should be restricted to short-term usage only and/or CYCLING ON/OFF

See the following:

HerbalGram. 2010; 87: 44-57

Hops (Humulus lupulus): A Review of its Historic and Medicinal Uses
Uwe Koetter, Martin Biendl

Source

American Botanical Council

Extract from Full Text

Recent in vitro experiments on sedative activity indicated activity on the melatonin receptor. Melatonin, a hormone secreted by the pineal gland in humans, through binding to its receptor, is responsible for maintaining the diurnal circadian rhythm in vertebrates.
Hops extracts had significant hypothermic effects in vivo in male mice analog melatonin. This effect was antagonized with the competitive melatonin receptor antagonist luzindole. The data suggest that potential sleep-inducing effects of hops extract are possibly centrally mediated through activation of melatonin receptors.

Other in vitro and in vivo research points towards involvement of the GABA-_A receptor. The fraction containing beta-acids of a lipophilic CO₂ hops extract was investigated in a benzodiazepine receptor-binding assay. Hops beta-acids affected the plateau of the GABA currents dose dependently without mediating this effect via the benzodiazepine receptor.

Another study examined the effects of beer, hop oils, and fragrance components on the GABA-_A response using the Xenopus oocyte expression system and an electrophysiological method. The 2 hops oils alpha-humulene and mycrene caused only a small potentiation of the GABA-_A receptor response. However, these compounds did not work as agonists. More pronounced were the effects of fragrances, which caused a potentiation of the GABA-_A receptor response.

In mice, the sedating activity of hops could be attributed to alpha-bitter acids as the most active constituents. Beta-bitter acids and the volatile oil contributed to the activity in ethanolic and carbon dioxide extracts of hops. Spontaneous locomotor activity was reduced, ketamine-induced sleeping time increased, and body temperature was reduced, thus confirming a central sedating effect.

Most promising are the results from Butterweck et al. (2007), as they provide direction for future isolation and structure elucidation work. With the mode of action potentially linked to melatonin, structural analog substances or precursors may now be identified in hops.
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J Agric Food Chem. 2006 Apr 5;54(7):2514-9.

Effects of beer and hop on ionotropic gamma-aminobutyric acid receptors.

Aoshima H, Takeda K, Okita Y, Hossain SJ, Koda H, Kiso Y.

Source
Department of Physics, Biology and Informatics, Faculty of Science, Yamaguchi University, Yoshida, Yamaguchi 753-8512, Japan.

Abstract
Beer induced the response of the ionotropic gamma-aminobutyric acid receptors (GABA(A) receptors) expressed in Xenopus oocytes, indicating the presence of gamma-aminobutyric acid (GABA)-like activity. Furthermore, the pentane extract of the beer, hop (Humulus lupulus L.) oil, and myrcenol potentiated the GABA(A) receptor response elicited by GABA. The GABA(A) receptor responses were also potentiated by the addition of aliphatic esters, most of which are reported to be present in beer flavor. Aliphatic esters showed the tendency to decrease in the potentiation of the GABA(A) receptor response with an increase in their carbon chain length. When myrcenol was injected to mice prior to intraperitoneal administration of pentobarbital, the pentobarbital-induced sleeping time of mice increased additionally. Therefore, the beer contained not only GABA-like activity but also the modulator(s) of the GABA(A) receptor response.
PMID: 16569037
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Canadian Journal of Physiology and Pharmacology, Volume 85, Number 9, September 2007 , pp. 933-942(10)

Effects of traditionally used anxiolytic botanicals on enzymes of the γ-aminobutyric acid (GABA) system

Awad, R.; Levac, D.; Cybulska, P.; Merali, Z.; Trudeau, V.L.; Arnason, J.T.

Source

NRC Research Press.

Abstract

In Canada, the use of botanical natural health products (NHPs) for anxiety disorders is on the rise, and a critical evaluation of their safety and efficacy is required. The purpose of this study was to determine whether commercially available botanicals directly affect the primary brain enzymes responsible for γ-aminobutyric acid (GABA) metabolism. Anxiolytic plants may interact with either glutamic acid decarboxylase (GAD) or GABA transaminase (GABA-T) and ultimately influence brain GABA levels and neurotransmission. Two in vitro rat brain homogenate assays were developed to determine the inhibitory concentrations (IC₅₀) of aqueous and ethanolic plant extracts. Approximately 70% of all extracts that were tested showed little or no inhibitory effect (IC₅₀ values greater than 1mg/mL) and are therefore unlikely to affect GABA metabolism as tested. The aqueous extract of Melissa officinalis (lemon balm) exhibited the greatest inhibition of GABA-T activity (IC₅₀ = 0.35mg/mL). Extracts from Centella asiatica (gotu kola) and Valeriana officinalis (valerian) stimulated GAD activity by over 40% at a dose of 1mg/mL. On the other hand, both Matricaria recutita (German chamomile) and Humulus lupulus (hops) showed significant inhibition of GAD activity (0.11-0.65mg/mL). Several of these species may therefore warrant further pharmacological investigation. The relation between enzyme activity and possible in vivo mode of action is discussed.

Edited by ScienceGuy, 16 February 2012 - 04:02 PM.

[Ampa-omega]

scienceguy, i have a question for you, do you know of any good natural mood stabilizers since you do not recommend lithium?

Please kindly note that whilst I do not specifically recommend using LITHIUM, I do not as such specifically recommend against using it either; this is why LITHIUM is not on either list; furthermore, my primary reason for mot including it on the positive list is due to its ANTI-NOOTROPIC effects, since COGNITIVE ENHANCEMENT is a primary goal of the majority of individuals within this forum

However, that is not to say that for some individuals, who are not concerned about its ANTI-NOOTROPIC effects, should not take LITHIUM to benefit from its MOOD STABILIZATION effects

With regards to what other items I recommend for MOOD STABILIZATION, that would include (but is not limited to) the following (in no particular order) :

4) PIRACETAM

6) RHODIOLA ROSEA


As such substances should be considered individually with respect to their own merit irrespective of whether they are technically classified as 'natural' or 'synthetic'

Yes i agree with you on the natural-unnatural statement, its just more of a matter of finding a cheaper alternative to pharmaceuticals thats all, i dont have any problem with synethticly produced substances, piracetam can exacerbate mania in some individuals so i dont know if its good for mood stabilization despite the anti anxiety properties it may have. rhodiola is an maoi so it too can cause a distance from mood stabilization. Lithium seems like the only true mood stabilizer that can be found easily otc.

lithium seems to be really effective if taken at night, especially for sleep and cognitive benefits.
perhaps its more suitable for that time since its sedative anti-nootropic properties make it more of a sleep aid?

[manic_racetam]

Fish oil is a mood stabilizator for me.

However, FISH OIL (EPA / DHA) causes and/or exacerbates DEPRESSION and/or ANXIETY for many individuals...

Seriously? How so? I don't doubt it because there are so many things hyped up and over-used that have negative consequences opposite to purported benefits... but you got a study/article?

[ScienceGuy]

Fish oil is a mood stabilizator for me.

However, FISH OIL (EPA / DHA) causes and/or exacerbates DEPRESSION and/or ANXIETY for many individuals...

Seriously? How so? I don't doubt it because there are so many things hyped up and over-used that have negative consequences opposite to purported benefits... but you got a study/article?

With regards to a study/article would the PRESCRIBING documentation for PHYSICIANS suffice?

It specifically states that FISH OIL can exacerbate ANXIETY DISORDERS and DEPRESSION, including BIPOLAR DISORDER.

This is further substantiated by clinical practice as well as many, many anecdotal user reports. Just GOOGLE: "fish oil causes anxiety" and "fish oil causes depression"

FISH OIL is not a 'one-shoe-fits-all' supplement, in that there are specifically two camps, namely POSITIVE RESPONDERS and NEGATIVE RESPONDERS. The POSITIVE RESPONDERS experience IMPROVED ANXIETY and/or DEPRESSION, whereas the NEGATIVE RESPONDERS experience SIDE EFFECTS which can include WORSENED ANXIETY and/or DEPRESSION

A primary factor which can influence whether someone is a POSITIVE RESPONDER or NEGATIVE RESPONDER is what is their existing levels of EPA and/or DHA. The rational behind FISH OIL supplementation stems from the fact that in general most individuals consume a disproportionate amount of OMEGA-6 fats within their diet versus OMEGA-3; as such, most individuals will benefit from supplementing with additional OMEGA-3 (= FISH OIL) because this NORMALIZES their pre-existing IMBALANCED FATTY ACID PROFILE; and since symptoms of TOO LITTLE EPA and/or DHA includes ANXIETY and DEPRESSION, for this segment of the population supplementing with FISH OIL will IMPROVE ANXIETY and/or DEPRESSION. However, for those individuals whose EPA and DHA levels are OK, supplementing with additional via taking FISH OIL can induce an IMBALANCED FATTY ACID PROFILE in the other direction, namely TOO MUCH EPA and/or DHA; and since since symptoms of TOO MUCH EPA and/or DHA also includes ANXIETY and DEPRESSION (i.e. there is a U-SHAPED CURVE), for this segment of the population supplementing with FISH OIL will in fact WORSEN ANXIETY and/or DEPRESSION

It is for these reasons that FISH OIL is not on the list

Edited by ScienceGuy, 16 February 2012 - 05:50 PM.

[manic_racetam]

Fish oil is a mood stabilizator for me.

However, FISH OIL (EPA / DHA) causes and/or exacerbates DEPRESSION and/or ANXIETY for many individuals...

Seriously? How so? I don't doubt it because there are so many things hyped up and over-used that have negative consequences opposite to purported benefits... but you got a study/article?

With regards to a study/article would the PRESCRIBING documentation for PHYSICIANS suffice?

It specifically states that FISH OIL can exacerbate ANXIETY DISORDERS and DEPRESSION, including BIPOLAR DISORDER.

This is further substantiated by clinical practice as well as many, many anecdotal user reports. Just GOOGLE: "fish oil causes anxiety" and "fish oil causes depression"

FISH OIL is not a 'one-shoe-fits-all' supplement, in that there are specifically two camps, namely POSITIVE RESPONDERS and NEGATIVE RESPONDERS. The POSITIVE RESPONDERS experience IMPROVED ANXIETY and/or DEPRESSION, whereas the NEGATIVE RESPONDERS experience SIDE EFFECTS which can include WORSENED ANXIETY and/or DEPRESSION

A primary factor which can influence whether someone is a POSITIVE RESPONDER or NEGATIVE RESPONDER is what is their existing levels of EPA and/or DHA. The rational behind FISH OIL supplementation stems from the fact that in general most individuals consume a disproportionate amount of OMEGA-6 fats within their diet versus OMEGA-3; as such, most individuals will benefit from supplementing with additional OMEGA-3 (= FISH OIL) because this NORMALIZES their pre-existing IMBALANCED FATTY ACID PROFILE; and since symptoms of TOO LITTLE EPA and/or DHA includes ANXIETY and DEPRESSION, for this segment of the population supplementing with FISH OIL will IMPROVE ANXIETY and/or DEPRESSION. However, for those individuals whose EPA and DHA levels are OK, supplementing with additional via taking FISH OIL can induce an IMBALANCED FATTY ACID PROFILE in the other direction, namely TOO MUCH EPA and/or DHA; and since since symptoms of TOO MUCH EPA and/or DHA also includes ANXIETY and DEPRESSION (i.e. there is a U-SHAPED CURVE), for this segment of the population supplementing with FISH OIL will in fact WORSEN ANXIETY and/or DEPRESSION

It is for these reasons that FISH OIL is not on the list

Thanks for an explanation. A study would be cool too, but if you won't deliver it on a platter I suppose I could search for it myself... LOL

[ScienceGuy]

Yes i agree with you on the natural-unnatural statement, its just more of a matter of finding a cheaper alternative to pharmaceuticals thats all, i dont have any problem with synethticly produced substances, piracetam can exacerbate mania in some individuals so i dont know if its good for mood stabilization despite the anti anxiety properties it may have. rhodiola is an maoi so it too can cause a distance from mood stabilization. Lithium seems like the only true mood stabilizer that can be found easily otc.

lithium seems to be really effective if taken at night, especially for sleep and cognitive benefits.
perhaps its more suitable for that time since its sedative anti-nootropic properties make it more of a sleep aid?

If you are not worried about the ANTI-NOOTROPIC effects of LITHIUM and it works well for you, without SIDE EFFECTS, then I recommend you keep taking it

However, a good alternative that you might consider trying is a combination of both LOW DOSE NALTREXONE (LDN) at a dosage of 1mg OD (taken at bedtime >9pm) and GARUM ARMORICUM EXTRACT (3 capsules OD taken upon waking), which will provide MOOD STABILIZATION through elevating levels of ENDORPHINS and ENCEPHALINS

Edited by ScienceGuy, 16 February 2012 - 06:01 PM.

[Ampa-omega]

Thanks, ill look into it.

[Ark]

An investigation into the efficacy of Scutellaria lateriflora in healthy volunteers.

Wolfson P, Hoffmann DL.

Source

Phytos Inc., San Anselmo, Calif., USA.

Abstract

Scutellaria lateriflora is an herbal medicine with long-standing traditional use as a relaxing nervine. There has been controversy in the literature with regards to its efficacy, and this study was designed to clarify its effectiveness in reducing anxiety, one of the phytotherapeutic indications. A double blind, placebo-controlled study of healthy subjects demonstrated noteworthy anxiolytic effects.

http://www.ncbi.nlm....pubmed/12652886



This stuff is amazing, I look foreword to hearing some back some feedback from others?!

http://www.longecity...oligopeptidase/

[ScienceGuy]

Scutellaria lateriflora...

This stuff is amazing, I look foreword to hearing some back some feedback from others?!

SKULLCAP (Scutellaria lateriflora)

SKULLCAP is akin to BENZODIAZEPINES, in that it is a GABA RECEPTOR AGONIST, in fact binding to the BENZODIAZEPINE RECEPTORS at the GABAA RECEPTOR.

Therefore prolonged usage for the medium to long-term is ill advised since this will induce down-regulation of the GABA RECEPTORS; and hence usage should be restricted exclusively to short-term use and/or CYCLING ON/OFF with the OFF period being sufficiently long such that status is allowed to fully return to basline

I should stress that it is perfectly safe to take SKULLCAP as long as usage is restricted exclusively to short-term use and/or CYCLING ON/OFF

See the following:

Phytomedicine. 2003 Nov;10(8):640-9.

Phytochemical and biological analysis of skullcap (Scutellaria lateriflora L.): a medicinal plant with anxiolytic properties.

Awad R, Arnason JT, Trudeau V, Bergeron C, Budzinski JW, Foster BC, Merali Z.

Source
Ottawa-Carleton Institute of Biology, University of Ottawa, Ottawa, Canada.

Abstract
The phytochemistry and biological activity of Scutellaria lateriflora L. (American skullcap) which has been traditionally used as a sedative and to treat various nervous disorders such as anxiety was studied. In vivo animal behaviour trials were performed to test anxiolytic effects in rats orally administered S. laterifolia extracts. Significant increases in the number of entries into the center of an "open-field arena"; number of unprotected head dips, number of entries and the length of time spent on the open arms of the Elevated Plus-Maze were found. The identification and quantification of the flavonoid, baicalin in a 50% EtOH extract (40 mg/g) and its aglycone baicalein in a 95% EtOH extract (33 mg/g), as well as the amino acids GABA in H2O and EtOH extracts (approximately 1.6 mg/g) and glutamine in a H2O extract (31 mg/g), was performed using HPLC. These compounds may play a role in anxiolytic activity since baicalin and baicalein are known to bind to the benzodiazepine site of the GABAA receptor and since GABA is the main inhibitory neurotransmitter.

PMID: 14692724

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British Journal of Wel. 2010 Jun;1(4):25-30

American skullcap (Scutellaria lateriflora): an ancient remedy for today’s anxiety?

Brock C., Whitehouse J., Tewfik I., Towell T.

Source

School of Life Sciences, University of Westminster, United Kingdom.

Extract from Full Text

Many orthodox anxiolytic treatments can have unwanted side effects. Benzodiazepines, for example, have been linked to muscle weakness, amnesia, headaches, vertigo, urinary retention, slurred speech and gastrointestinal disturbances. They may lead to tolerance and physical and psychological dependence, and are considered to be dangerous to use long–term (BNF, 2008)…

American skullcap (Scutellaria laterifl ora) (Figure 1) is one of the most commonly used herbs by western medical herbalists, particularly for anxiety and related conditions (Bergner, 2002–2003)…

Due to its potential sedative action (Greenfi eld and Davis, 2004), it may be advisable to refrain from using S. lateriflora in combination with other sedatives, such as alcohol and benzodiazepines. It is not possible to comment on the safety of its use in pregnancy…

Benzodiazepines are allosteric ligands for the GABAA receptor, a chloride channel that is gated by GABA. They bind to the benzodiazepine site of the GABAA receptor, thus increasing the affinity of the inhibitory neurotransmitter GABA for the GABA site of the GABAA receptor. This decreases the likelihood of action potentials by excitatory neurotransmitters (Rabow et al, 1995). One important study (Liao et al, 1998) indicated oroxylin A, baicalein and wogonin, which are flavonoids found in S. lateriflora, had weak affinities for the benzodiazepine site of GABAA receptors in mouse cerebral cortex in vitro. In another study Hui et al (2000) tested the capacity of baicalin, baicalein, scutellarein and wogonin to bind to the benzodiazepine site of the GABAA receptor in homogenised rat brain. Affinity to the benzodiazepine site for scutellarein was moderate and weak for baicalin. Contrary to results of the earlier study (Liao et al, 1998), the binding affinities of wogonin and baicalein [to the benzodiazepine receptors] were strong. The authors suggested the discrepancy may be due to differences in species and assay models used (Hui et al, 2000). The ability of the skullcap flavonoids to bind to the benzodiazepine site of the GABAA receptor suggests an anxiolytic effect for S. lateriflora…

Edited by ScienceGuy, 18 February 2012 - 10:20 AM.

[Raptor87]

I am evaluating Methylcobalamin right now.... This is what I have experienced.

5000mcg= (anxiolytic)
10000mcg=(anxiogenic)

And for fishoil. There´s some evidence that shows that fishoil affects receptors in prefrontal cortex. As we all know, affecting those regions in the brain can give various results depending on the individual. So be careful!

[ScienceGuy]

And for fishoil. There´s some evidence that shows that fishoil... can give various results depending on the individual. So be careful!

SECONDED

[ScienceGuy]

I am evaluating Methylcobalamin right now.... This is what I have experienced.

5000mcg= (anxiolytic)
10000mcg=(anxiogenic)

Thank you for sharing!

Though please note that the THRESHOLD regarding METHYLCOBALAMIN B12 supplmentation between ANXIOLYTIC and ANXIOLGENIC effects will vary significantly from person to person.

For some individuals (e.g. OVERMETHYLATED) even doses just above the RDA will trigger ANXIOLGENIC effects, however for others (e.g. UNDERMETHYLATED) it will be much higher doses, like yourself.

Also, for the record I am not an advocate of taking MEGA-DOSES / OVER-DOSES of VITAMINS, since there is mounting evidence regards the LONG-TERM effects being in fact very UNHELPFUL

[nupi]

Rhodiola is a MAOI (and my short term test makes me quite like it). How strongly it acts as one is subject to discussion bu I would definitely not mix it with Serotonergics

[MrSpud]

What about Niacinamide and Atarax. Which list would you put them into? Also, for someone who was using low doses of GABA agonists who wanted to start tapering down even more and/or wanted to avoid/lessen tolerance would cycling between GABA-A agonists and GABA-B agonsits be of any benefit?

[Nootr]

In Russia there is also a new anxiety drug “Normoxan” which includes the following ingredients:

L-Theanine (200 mg)
Baikal Skullcap (extract 4:1) 150 mg
Valeriana officinalis (standard extract) 150 mg
Passiflora incarnata (extract 6:1) 100 mg
5-Hydroxytryptophan (5-HTP) (99%) 30 mg

It is reported to be more effective than Afobazol and Tenoten by many patients. At the same time it is claimed to be truly harmless - no tolerance, withdrawal or negative side effects.

Recommendations on application by the adult to accept on 1 capsule 2 times a day or 2 capsules 2-3 times a day

[ScienceGuy]

In Russia there is also a new anxiety drug “Normoxan” which includes the following ingredients:

L-Theanine (200 mg)
Baikal Skullcap (extract 4:1) 150 mg
Valeriana officinalis (standard extract) 150 mg
Passiflora incarnata (extract 6:1) 100 mg
5-Hydroxytryptophan (5-HTP) (99%) 30 mg

It is reported to be more effective than Afobazol and Tenoten by many patients. At the same time it is claimed to be truly harmless - no tolerance, withdrawal or negative side effects.

Recommendations on application by the adult to accept on 1 capsule 2 times a day or 2 capsules 2-3 times a day

Please kindly note the following regarding “Normoxan”:

1) Based on its ingredient composition “Normoxan” is not in fact a DRUG, it is a SUPPLEMENT

2) There are very good reasons to avoid taking 4 out of 5 of its ingredients for prolonged periods (and with regards to 5-HTP at all). Therefore, this product is in fact NOT recommended for TREATING ANXIETY SAFELY & EFFECTIVELY. For details please kindly read this THREAD's initial post

[Nootr]

2) There are very good reasons to avoid taking 4 out of 5 of its ingredients for prolonged periods (and with regards to 5-HTP at all). Therefore, this product is in fact NOT recommended for TREATING ANXIETY SAFELY & EFFECTIVELY. For details please kindly read this THREAD's initial post

I know but can't they balance each other when taken all together like people take adderal and memantine to balance their negative sides and fight against tolerance?

[ScienceGuy]

2) There are very good reasons to avoid taking 4 out of 5 of its ingredients for prolonged periods (and with regards to 5-HTP at all). Therefore, this product is in fact NOT recommended for TREATING ANXIETY SAFELY & EFFECTIVELY. For details please kindly read this THREAD's initial post

can't they balance each other when taken all together like people take adderal and memantine to balance their negative sides and fight against tolerance?

In short, NO

Furthermore, you need to bear in mind that prolonged administration of L-5HTP, which is contained within that supplement, is not recommended due to INCREASING RISK OF CARDIOVASCULAR DISEASE

L-5HTP increases risk of CARDIOVASCULAR DISEASE via two mechanisms; firstly, by significantly increasing PLASMA RENIN ACTIVITY; and secondly, by significantly elevating levels of SYSTEMIC SEROTONIN.

See the following:

Pharmacol Biochem Behav. 1981 Jun;14(6):895-900.

Effects of serotonin and L-5-hydroxytryptophan on plasma renin activity in rats.

Barney CC, Threatte RM, Kikta DC, Fregly MJ.

Abstract
The effects of dipsogenic doses of l-5-hydroxytryptophan (5-HTP) and serotonin on plasma renin activity (PRA), blood pressure, and body temperature were determined in unanesthetized female rats. Both serotonin (2 mg/kg, s.c.) and 5-HTP (25 mg/kg, s.c.) induced six-fold increases in PRA measured 1 hr after drug administration. The central and peripheral decarboxylase inhibitor, benserazide (30 mg/kg, s.c.), as well as the peripheral decarboxylase inhibitor, carbidopa (6.5 mg/kg s.c.), prevented the increase in PRA associated with administration of 5-HTP. This suggests that 5-HTP must be converted to serotonin peripherally to increase PRA. At the doses used, serotonin decreased mean blood pressure and colonic temperature of unanesthetized rats while 5-HTP was without effect. The increase in PRA induced by 5-HTP does not appear, therefore, to be a response to either hypotension or a decrease in colonic temperature. Since 5-HTP must be converted to serotonin to initiate both a drinking response and an increase in PRA, the results suggest that the decrease in blood pressure and colonic temperature following administration of serotonin may not be important in induction of the drinking response and the increase in PRA. The mechanism by which activation of the renin-angiotensin system occurs following peripheral administration of either 5-HTP or serotonin remains for further study.

PMID: 7019933
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Am J Cardiol. 2011 Jul 15;108(2):246-51. Epub 2011 May 3.

Prognostic value of plasma renin activity in heart failure.

Vergaro G, Emdin M, Iervasi A, Zyw L, Gabutti A, Poletti R, Mammini C, Giannoni A, Fontana M, Passino C.

Source
Division of Cardiovascular Medicine, Fondazione Toscana G. Monasterio, Pisa, Italy.

Abstract
The prognostic role of specific biomarkers of the renin-angiotensin-aldosterone system and sympathetic activation pathways in heart failure has never been investigated in populations with current evidence-weighted treatment. To establish whether the plasma renin activity (PRA), among several neurohormonal biomarkers, is able to predict cardiac events in a population of patients with heart failure on up-to-date treatment, we selected 996 consecutive patients with systolic left ventricular dysfunction (ejection fraction <50%, mean age 65 ± 13 years), who underwent a complete clinical and humoral characterization and were then followed up (median 36 months, range 0 to 72) for cardiac death and appropriate implantable cardioverter device shock. We recorded 170 cardiac deaths and 27 shocks. On Cox multivariate analysis, only ejection fraction (hazard ratio 0.962, 95% confidence interval 0.938 to 0.986), N-terminal pro-brain natriuretic peptide (NT-proBNP; hazard ratio 1.729, 95% confidence interval 1.383 to 2.161) and PRA (hazard ratio 1.201, 95% confidence interval 1.024 to 1.408) were independent predictors of cardiac death. Receiver operating characteristic curve analysis identified a cutoff value for PRA of 2.30 ng/ml/hour that best predicted cardiac mortality. Independent predictors of PRA were ejection fraction, functional class, sodium, potassium, NT-proBNP, norepinephrine, aldosterone, C-reactive protein, and medical therapy. The association of high NT-proBNP and high PRA identified a subgroup (22% of the study population) with the greatest risk of cardiac death. In conclusion, PRA resulted an independent prognostic marker in patients with systolic heart failure additive to NT-proBNP level and ejection fraction. PRA might help to select those patients needing an enhanced therapeutic effort, possibly targeting incomplete renin-angiotensin-aldosterone system blockade.
-------------------------------------------------------------------------------------------------------------------------------

Circulation. 2005 Mar 29;111(12):1517-22. Epub 2005 Mar 21.

Long-term [systemic] serotonin administration induces heart valve disease in rats.

Gustafsson BI, Tømmerås K, Nordrum I, Loennechen JP, Brunsvik A, Solligård E, Fossmark R, Bakke I, Syversen U, Waldum H.
Source

Department of Internal Medicine, St Olavs Hospital HF, Trondheim University Hospital, Trondheim, Norway. bjorn.gustafsson@medisin.ntnu.no
Abstract

BACKGROUND:

The purpose of this study was to investigate whether rats dosed with serotonin develop changes similar to those seen in human carcinoid heart disease.
METHODS AND RESULTS:

Ten Sprague-Dawley rats were given serotonin injections subcutaneously once daily for 3 months; controls were given saline. A long-lasting hyperserotoninemia with a >10-fold increase in both platelet-poor plasma and dialysate from the femoral muscles appeared. The animals developed clinical signs such as flushing and loose stools. After 3 months, 6 of 10 rats given serotonin had pathological echocardiographs. Two animals had a combination of aortic and pulmonary valve insufficiency, 1 had isolated aortic valve insufficiency, and 3 had isolated pulmonary valve insufficiency. Histopathological examination revealed shortened and thickened aortic cusps and carcinoidlike plaques characterized by a collection of myofibroblasts within an extracellular matrix of collagen ground substance. Immunostaining for Ki-67 demonstrated an increased number of proliferating subendocardial cells. In the control group, no pathological changes were seen. With the use of reverse-transcription polymerase chain reaction, normal rat aortic cusps were shown to express mRNA for serotonin receptors 5-HT1A, 5-HT2A, and 5-HT2B and the serotonin transporter 5-HTT.
CONCLUSIONS:

For the first time, long-term [systemic] serotonin administration was performed in rats. Morphological and echocardiographic changes similar to those seen in human carcinoid heart disease developed. This study demonstrates that [systemic] serotonin most likely is involved in the pathogenesis of carcinoid heart disease.

PMID: 15781732

Edited by ScienceGuy, 21 February 2012 - 08:41 AM.

[Raptor87]

I am evaluating Methylcobalamin right now.... This is what I have experienced.

5000mcg= (anxiolytic)
10000mcg=(anxiogenic)

Thank you for sharing!

Though please note that the THRESHOLD regarding METHYLCOBALAMIN B12 supplmentation between ANXIOLYTIC and ANXIOLGENIC effects will vary significantly from person to person.

For some individuals (e.g. OVERMETHYLATED) even doses just above the RDA will trigger ANXIOLGENIC effects, however for others (e.g. UNDERMETHYLATED) it will be much higher doses, like yourself.

Also, for the record I am not an advocate of taking MEGA-DOSES / OVER-DOSES of VITAMINS, since there is mounting evidence regards the LONG-TERM effects being in fact very UNHELPFUL

I haven´t seen any evidence that suggest´s that M-B12 would be dangerous in higher dosages. That doesn´t mean that it isn´t dangerous. But I am thinking of keeping the mega dose on my long term stack because I have sensed some improvement. I hope that this doesn´t come and bite me in the ass though.

What I am more concerned about is my use of Modafinil, the drug has both anxiolytic and anxiogenic effects and evidence suggest´s that the drug affects both (gaba a) (gaba b) levels. But that´s another question and really doesnt fit the profile of this topic. Modafinil isn´t used as a anxiety treatment.

Thank you for making such a good post

[hooter]

I haven´t seen any evidence that suggest´s that M-B12 would be dangerous in higher dosages. That doesn´t mean that it isn´t dangerous. But I am thinking of keeping the mega dose on my long term stack because I have sensed some improvement. I hope that this doesn´t come and bite me in the ass though.

Excessive doses taken over long periods of time can cause nerve damage, numbness and dysfunctions in motor control. I'm not certain of the upper limits, but this would be a good topic of research. Be careful.

Edited by hooter, 21 February 2012 - 12:16 PM.

[ScienceGuy]

What I am more concerned about is my use of Modafinil, the drug has both anxiolytic and anxiogenic effects and evidence suggest´s that the drug affects both (gaba a) (gaba b) levels. But that´s another question and really doesnt fit the profile of this topic. Modafinil isn´t used as a anxiety treatment.

You're right we are going slight OFF-TOPIC here... but as an alternative to MODAFINIL, I recommend to look into AMPAKINES, such as the RACETAMS, and if you're seeking a some stimulation type alertness effect, I can specifically recommend PHENYLPIRACETAM

Thank you for making such a good post

You're welcome. I really hope it proves to be of use and helps to improve peoples' lives

[ScienceGuy]

I haven´t seen any evidence that suggest´s that M-B12 would be dangerous in higher dosages. That doesn´t mean that it isn´t dangerous. But I am thinking of keeping the mega dose on my long term stack because I have sensed some improvement. I hope that this doesn´t come and bite me in the ass though.

Excessive doses taken over long periods of time can cause nerve damage, numbness and dysfunctions in motor control... Be careful.

WHAT HE SAID

[Hebbeh]

I haven´t seen any evidence that suggest´s that M-B12 would be dangerous in higher dosages. That doesn´t mean that it isn´t dangerous. But I am thinking of keeping the mega dose on my long term stack because I have sensed some improvement. I hope that this doesn´t come and bite me in the ass though.

Excessive doses taken over long periods of time can cause nerve damage, numbness and dysfunctions in motor control... Be careful.

WHAT HE SAID

You must have B-12 confused with B-6. Totally different.

[hooter]

You must have B-12 confused with B-6. Totally different.

Ah, you're right! I was thinking B-Complex in general.

I've heard B12 can cause optic nerve damage or excess blood clots and has some other hematological effects. But the dose range for this is extremely high, much higher than B6 overdose.

Edited by hooter, 21 February 2012 - 06:56 PM.

[ScienceGuy]

I haven´t seen any evidence that suggest´s that M-B12 would be dangerous in higher dosages. That doesn´t mean that it isn´t dangerous. But I am thinking of keeping the mega dose on my long term stack because I have sensed some improvement. I hope that this doesn´t come and bite me in the ass though.

Excessive doses taken over long periods of time can cause nerve damage, numbness and dysfunctions in motor control... Be careful.

WHAT HE SAID

You must have B-12 confused with B-6. Totally different.

Not so

Excessive and/or long-term doses of VITAMIN B12 can cause the following SIDE EFFECTS:

HEADACHE, DIZZINESS, INSOMNIA, AGITATION, ANXIETY, PANIC ATTACKS, RESTLESSNESS, CARDIAC ARRHYTHMIA, ANGINA, TINGLING and NUMBNESS.

The SIDE EFFECTS profile for VITAMIN B12 is a U-SHAPED CURVE in that both TOO LITTLE and TOO MUCH induce similar SIDE EFFECTS

Furthermore, there is ever increasing substantiation that EXCESS VITAMIN B12 is CARCINOGENIC (i.e. CAUSES CANCER). For example, see the following:

Sem Hop. 1970 Jul 10;46(31):2170-4.

[Hazards of administering vitamin B12 to cancer patients].
[Article in French]

Chauvergne J, Hoerni B, Hugues A, Lagarde C, Le Treut A, Marée D, Touchard J.

PMID: 4318351

This study demonstrated that excessive B12 consumption encourages cell division in general and certain tumor cells in particular

------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

JAMA. 2009 Nov 18;302(19):2119-26.

Cancer incidence and mortality after treatment with folic acid and vitamin B12.

Ebbing M, Bønaa KH, Nygård O, Arnesen E, Ueland PM, Nordrehaug JE, Rasmussen K, Njølstad I, Refsum H, Nilsen DW, Tverdal A, Meyer K, Vollset SE.

Source
Department of Heart Disease, Haukeland University Hospital, Jonas Liesvei 65, Bergen, Norway 5021. marta.ebbing@helse-bergen.no

Abstract

CONTEXT:
Recently, concern has been raised about the safety of folic acid, particularly in relation to cancer risk.

OBJECTIVE:
To evaluate effects of treatment with B vitamins on cancer outcomes and all-cause mortality in 2 randomized controlled trials.

DESIGN, SETTING, AND PARTICIPANTS:
Combined analysis and extended follow-up of participants from 2 randomized, double-blind, placebo-controlled clinical trials (Norwegian Vitamin Trial and Western Norway B Vitamin Intervention Trial). A total of 6837 patients with ischemic heart disease were treated with B vitamins or placebo between 1998 and 2005, and were followed up through December 31, 2007.

INTERVENTIONS:
Oral treatment with folic acid (0.8 mg/d) plus vitamin B(12) (0.4 mg/d) and vitamin B(6) (40 mg/d) (n = 1708); folic acid (0.8 mg/d) plus vitamin B(12) (0.4 mg/d) (n = 1703); vitamin B(6) alone (40 mg/d) (n = 1705); or placebo (n = 1721).

MAIN OUTCOME MEASURES:
Cancer incidence, cancer mortality, and all-cause mortality.

RESULTS:
During study treatment, median serum folate concentration increased more than 6-fold among participants given folic acid. After a median 39 months of treatment and an additional 38 months of posttrial observational follow-up, 341 participants (10.0%) who received folic acid plus vitamin B(12) vs 288 participants (8.4%) who did not receive such treatment were diagnosed with cancer (hazard ratio  , 1.21; 95% confidence interval [CI], 1.03-1.41; P = .02). A total of 136 (4.0%) who received folic acid plus vitamin B(12) vs 100 (2.9%) who did not receive such treatment died from cancer (HR, 1.38; 95% CI, 1.07-1.79; P = .01). A total of 548 patients (16.1%) who received folic acid plus vitamin B(12) vs 473 (13.8%) who did not receive such treatment died from any cause (HR, 1.18; 95% CI, 1.04-1.33; P = .01). Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B(12). Vitamin B(6) treatment was not associated with any significant effects.

CONCLUSION:
Treatment with folic acid plus vitamin B(12) was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease in Norway, where there is no folic acid fortification of foods.

---------------------------------------------------------------------------------------------------------------------------------------------------------

Cancer Epidemiol Biomarkers Prev. 2010 Jun;19(6):1632-42. Epub 2010 May 25.

Circulating folate, vitamin B12, homocysteine, vitamin B12 transport proteins, and risk of prostate cancer: a case-control study, systematic review, and meta-analysis.

Collin SM, Metcalfe C, Refsum H, Lewis SJ, Zuccolo L, Smith GD, Chen L, Harris R, Davis M, Marsden G, Johnston C, Lane JA, Ebbing M, Bønaa KH, Nygård O, Ueland PM, Grau MV, Baron JA, Donovan JL, Neal DE, Hamdy FC, Smith AD, Martin RM.

Source
Department of Social Medicine, University of Bristol, Bristol, United Kingdom. simon.collin@bristol.ac.uk

Abstract

BACKGROUND:

Disturbed folate metabolism is associated with an increased risk of some cancers. Our objective was to determine whether blood levels of folate, vitamin B(12), and related metabolites were associated with prostate cancer risk.

METHODS:

Matched case-control study nested within the U.K. population-based Prostate testing for cancer and Treatment (ProtecT) study of prostate-specific antigen-detected prostate cancer in men ages 50 to 69 years. Plasma concentrations of folate, B(12) (cobalamin), holo-haptocorrin, holo-transcobalamin total transcobalamin, and total homocysteine (tHcy) were measured in 1,461 cases and 1,507 controls. ProtecT study estimates for associations of folate, B(12), and tHcy with prostate cancer risk were included in a meta-analysis, based on a systematic review.

RESULTS:

In the ProtecT study, increased B(12) and holo-haptocorrin concentrations showed positive associations with prostate cancer risk [highest versus lowest quartile of B(12) odds ratio (OR) = 1.17 (95% confidence interval, 0.95-1.43); P(trend) = 0.06; highest versus lowest quartile of holo-haptocorrin OR = 1.27 (1.04-1.56); P(trend) = 0.01]; folate, holo-transcobalamin, and tHcy were not associated with prostate cancer risk. In the meta-analysis, circulating B(12) levels were associated with an increased prostate cancer risk [pooled OR = 1.10 (1.01-1.19) per 100 pmol/L increase in B(12); P = 0.002]; the pooled OR for the association of folate with prostate cancer was positive [OR = 1.11 (0.96-1.28) per 10 nmol/L; P = 0.2) and conventionally statistically significant if ProtecT (the only case-control study) was excluded [OR = 1.18 (1.00-1.40) per 10 nmol/L; P = 0.02].

CONCLUSION:

Vitamin B(12) and (in cohort studies) folate were associated with increased prostate cancer risk.

---------------------------------------------------------------------------------------------------------------------------------------------------------

I should add that supplementation with excessive amounts of VITAMIN B6 is equally ill advised

Edited by ScienceGuy, 21 February 2012 - 07:44 PM.

[Hebbeh]

I haven´t seen any evidence that suggest´s that M-B12 would be dangerous in higher dosages. That doesn´t mean that it isn´t dangerous. But I am thinking of keeping the mega dose on my long term stack because I have sensed some improvement. I hope that this doesn´t come and bite me in the ass though.

Excessive doses taken over long periods of time can cause nerve damage, numbness and dysfunctions in motor control... Be careful.

WHAT HE SAID

You must have B-12 confused with B-6. Totally different.

Not so

Excessive and/or long-term doses of VITAMIN B12 can cause the following SIDE EFFECTS:

HEADACHE, DIZZINESS, INSOMNIA, AGITATION, ANXIETY, PANIC ATTACKS, RESTLESSNESS, CARDIAC ARRHYTHMIA, ANGINA, TINGLING and NUMBNESS.

The SIDE EFFECTS profile for VITAMIN B12 is a U-SHAPED CURVE in that both TOO LITTLE and TOO MUCH induce similar SIDE EFFECTS

Furthermore, there is ever increasing substantiation that EXCESS VITAMIN B12 is CARCINOGENIC (i.e. CAUSES CANCER). For example, see the following:

Sem Hop. 1970 Jul 10;46(31):2170-4.

[Hazards of administering vitamin B12 to cancer patients].
[Article in French]

Chauvergne J, Hoerni B, Hugues A, Lagarde C, Le Treut A, Marée D, Touchard J.

PMID: 4318351

This study demonstrated that excessive B12 consumption encourages cell division in general and certain tumor cells in particular

------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

JAMA. 2009 Nov 18;302(19):2119-26.

Cancer incidence and mortality after treatment with folic acid and vitamin B12.

Ebbing M, Bønaa KH, Nygård O, Arnesen E, Ueland PM, Nordrehaug JE, Rasmussen K, Njølstad I, Refsum H, Nilsen DW, Tverdal A, Meyer K, Vollset SE.

Source
Department of Heart Disease, Haukeland University Hospital, Jonas Liesvei 65, Bergen, Norway 5021. marta.ebbing@helse-bergen.no

Abstract

CONTEXT:
Recently, concern has been raised about the safety of folic acid, particularly in relation to cancer risk.

OBJECTIVE:
To evaluate effects of treatment with B vitamins on cancer outcomes and all-cause mortality in 2 randomized controlled trials.

DESIGN, SETTING, AND PARTICIPANTS:
Combined analysis and extended follow-up of participants from 2 randomized, double-blind, placebo-controlled clinical trials (Norwegian Vitamin Trial and Western Norway B Vitamin Intervention Trial). A total of 6837 patients with ischemic heart disease were treated with B vitamins or placebo between 1998 and 2005, and were followed up through December 31, 2007.

INTERVENTIONS:
Oral treatment with folic acid (0.8 mg/d) plus vitamin B(12) (0.4 mg/d) and vitamin B(6) (40 mg/d) (n = 1708); folic acid (0.8 mg/d) plus vitamin B(12) (0.4 mg/d) (n = 1703); vitamin B(6) alone (40 mg/d) (n = 1705); or placebo (n = 1721).

MAIN OUTCOME MEASURES:
Cancer incidence, cancer mortality, and all-cause mortality.

RESULTS:
During study treatment, median serum folate concentration increased more than 6-fold among participants given folic acid. After a median 39 months of treatment and an additional 38 months of posttrial observational follow-up, 341 participants (10.0%) who received folic acid plus vitamin B(12) vs 288 participants (8.4%) who did not receive such treatment were diagnosed with cancer (hazard ratio  , 1.21; 95% confidence interval [CI], 1.03-1.41; P = .02). A total of 136 (4.0%) who received folic acid plus vitamin B(12) vs 100 (2.9%) who did not receive such treatment died from cancer (HR, 1.38; 95% CI, 1.07-1.79; P = .01). A total of 548 patients (16.1%) who received folic acid plus vitamin B(12) vs 473 (13.8%) who did not receive such treatment died from any cause (HR, 1.18; 95% CI, 1.04-1.33; P = .01). Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B(12). Vitamin B(6) treatment was not associated with any significant effects.

CONCLUSION:
Treatment with folic acid plus vitamin B(12) was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease in Norway, where there is no folic acid fortification of foods.

---------------------------------------------------------------------------------------------------------------------------------------------------------

Cancer Epidemiol Biomarkers Prev. 2010 Jun;19(6):1632-42. Epub 2010 May 25.

Circulating folate, vitamin B12, homocysteine, vitamin B12 transport proteins, and risk of prostate cancer: a case-control study, systematic review, and meta-analysis.

Collin SM, Metcalfe C, Refsum H, Lewis SJ, Zuccolo L, Smith GD, Chen L, Harris R, Davis M, Marsden G, Johnston C, Lane JA, Ebbing M, Bønaa KH, Nygård O, Ueland PM, Grau MV, Baron JA, Donovan JL, Neal DE, Hamdy FC, Smith AD, Martin RM.

Source
Department of Social Medicine, University of Bristol, Bristol, United Kingdom. simon.collin@bristol.ac.uk

Abstract

BACKGROUND:

Disturbed folate metabolism is associated with an increased risk of some cancers. Our objective was to determine whether blood levels of folate, vitamin B(12), and related metabolites were associated with prostate cancer risk.

METHODS:

Matched case-control study nested within the U.K. population-based Prostate testing for cancer and Treatment (ProtecT) study of prostate-specific antigen-detected prostate cancer in men ages 50 to 69 years. Plasma concentrations of folate, B(12) (cobalamin), holo-haptocorrin, holo-transcobalamin total transcobalamin, and total homocysteine (tHcy) were measured in 1,461 cases and 1,507 controls. ProtecT study estimates for associations of folate, B(12), and tHcy with prostate cancer risk were included in a meta-analysis, based on a systematic review.

RESULTS:

In the ProtecT study, increased B(12) and holo-haptocorrin concentrations showed positive associations with prostate cancer risk [highest versus lowest quartile of B(12) odds ratio (OR) = 1.17 (95% confidence interval, 0.95-1.43); P(trend) = 0.06; highest versus lowest quartile of holo-haptocorrin OR = 1.27 (1.04-1.56); P(trend) = 0.01]; folate, holo-transcobalamin, and tHcy were not associated with prostate cancer risk. In the meta-analysis, circulating B(12) levels were associated with an increased prostate cancer risk [pooled OR = 1.10 (1.01-1.19) per 100 pmol/L increase in B(12); P = 0.002]; the pooled OR for the association of folate with prostate cancer was positive [OR = 1.11 (0.96-1.28) per 10 nmol/L; P = 0.2) and conventionally statistically significant if ProtecT (the only case-control study) was excluded [OR = 1.18 (1.00-1.40) per 10 nmol/L; P = 0.02].

CONCLUSION:

Vitamin B(12) and (in cohort studies) folate were associated with increased prostate cancer risk.

---------------------------------------------------------------------------------------------------------------------------------------------------------

I should add that supplementation with excessive amounts of VITAMIN B6 is equally ill advised

No where in your grasping for always thinking you have to be right....which you aren't...do I see any references to the claim at hand of:

Excessive doses taken over long periods of time can cause nerve damage, numbness and dysfunctions in motor control... Be careful.

You would also have a little more credibility if you ditch the annoying bold, red, and caps. I have to assume you either have no education, as a professor would have pitched you out of school if attempting to write papers in this manner...or you aren't old enough to be in school yet...or that you are prepping for a career in composing spam of the type we all so love to delete. Personally, I'm putting my money on not mature enough to be in school yet:

http://www.empowerin...nated-child.php#

[ScienceGuy]

No where in your grasping for always thinking you have to be right....which you aren't...do I see any references to the claim at hand of:

Excessive doses taken over long periods of time can cause nerve damage, numbness and dysfunctions in motor control... Be careful.

You would also have a little more credibility if you ditch the annoying bold, red, and caps. I have to assume you either have no education, as a professor would have pitched you out of school if attempting to write papers in this manner...or you aren't old enough to be in school yet...or that you are prepping for a career in composing spam of the type we all so love to delete. Personally, I'm putting my money on not mature enough to be in school yet:

http://www.empowerin...nated-child.php#

Hebbeh,

Firstly, please can we ditch the unwarranted antagonistic condescending tone and petty puerile jibes, since we are both adults and hopefully friends who are engaging in intelligent debate. Let's try to keep our posts to a professional academic nature and in line with the spirit of this forum shall we? OK?

Secondly, it is abundantly clear that something I have said has highly irritated you, so I would like to apologise if I have in any way caused you offense. Though I am reading back what I have posted and I cannot understand what this might be; so perhaps you might kindly enlighten me such that I can avoid repetition?

RE: "You would also have a little more credibility if you ditch the annoying bold, red, and caps" - Please kindly note that I specifically format my posts in the manner that I do to facilitate easy reading via highlighting of salient points and presenting facts in a concise and well organised way. It is my understanding that the majority of individuals in fact find this HELPFUL as opposed to ANNOYING I am very happy to change this process if I feel that the majority of individuals would wish me to do so, however the positive feedback that I have received to date outweighs any negative feedback. However, I will most certainly adjust my postings accordingly should the situation reverse itself.

RE: "always thinking you have to be right" - With the utmost respect, I am by no means perfect, and readily admit when I make mistakes. If you dig around on this forum you will find at least one instance where I have got something wrong due to suffering a brain fart

Furthermore, in this particular instance I do not believe there is a RIGHT and WRONG; in that, you hare quite correct that VITAMIN B6 induces the symptoms to which HOOTER was referring. However, please kindly note that VITAMIN B12 when administered at excessive dosages and/or for prolonged periods does indeed have the potential to cause the SIDE EFFECTS that I have listed. My posting was in no way 'me trying to be a clever clogs'. I contribute to this forum with a singular purpose, namely to help improve other peoples' quality of life. I would have hoped that the considerable amount of time that I have invested in this particular thread would be clearly indicative of this fact.

Taking OVERDOSES / MEGADOSES of VITAMINS is ill advised. There is an ever growing amount of scientific substantiation to support this fact. However, please kindly note that you do not have to take my advice if you don't want to. OK?

And finally, please kindly note that we are in fact venturing distinctly OFF TOPIC, since the title of this thread is not "HAZARDS OF HIGH DOSE VITAMIN B12"

[Hebbeh]

Hebbeh,

Firstly, please can we ditch the unwarranted antagonistic condescending tone and petty puerile jibes, since we are both adults and hopefully friends who are engaging in intelligent debate. Let's try to keep our posts to a professional academic nature and in line with the spirit of this forum shall we? OK?

Secondly, it is abundantly clear that something I have said has highly irritated you, so I would like to apologise if I have in any way caused you offense. Though I am reading back what I have posted and I cannot understand what this might be; so perhaps you might kindly enlighten me such that I can avoid repetition?

RE: "You would also have a little more credibility if you ditch the annoying bold, red, and caps" - Please kindly note that I specifically format my posts in the manner that I do to facilitate easy reading via highlighting of salient points and presenting facts in a concise and well organised way. It is my understanding that the majority of individuals in fact find this HELPFUL as opposed to ANNOYING I am very happy to change this process if I feel that the majority of individuals would wish me to do so, however the positive feedback that I have received to date outweighs any negative feedback. However, I will most certainly adjust my postings accordingly should the situation reverse itself.

RE: "always thinking you have to be right" - With the utmost respect, I am by no means perfect, and readily admit when I make mistakes. If you dig around on this forum you will find at least one instance where I have got something wrong due to suffering a brain fart

Furthermore, in this particular instance I do not believe there is a RIGHT and WRONG; in that, you hare quite correct that VITAMIN B6 induces the symptoms to which HOOTER was referring. However, please kindly note that VITAMIN B12 when administered at excessive dosages and/or for prolonged periods does indeed have the potential to cause the SIDE EFFECTS that I have listed. My posting was in no way 'me trying to be a clever clogs'. I contribute to this forum with a singular purpose, namely to help improve other peoples' quality of life. I would have hoped that the considerable amount of time that I have invested in this particular thread would be clearly indicative of this fact.

Taking OVERDOSES / MEGADOSES of VITAMINS is ill advised. There is an ever growing amount of scientific substantiation to support this fact. However, please kindly note that you do not have to take my advice if you don't want to. OK?

And finally, please kindly note that we are in fact venturing distinctly OFF TOPIC, since the title of this thread is not "HAZARDS OF HIGH DOSE VITAMIN B12"

It's interesting you use the term "condescending" as that seems to be your standard MO should anybody question or disagree with your opinions. You've been very condescending to a number of highly intelligent and educated individuals on the forum and I'm not the only one to have noticed that. A friendly bit of advice would be to take a good hard look at yourself before accusing others of being condescending.

[ScienceGuy]

No where in your grasping for always thinking you have to be right....which you aren't...

You would also have a little more credibility if you ditch the annoying bold, red, and caps.
I have to assume you either have no education, as a professor would have pitched you out of school if attempting to write papers in this manner...or you aren't old enough to be in school yet...or that you are prepping for a career in composing spam of the type we all so love to delete. Personally, I'm putting my money on not mature enough to be in school yet:

http://www.empowerin...nated-child.php#

Hebbeh,

Firstly, please can we ditch the unwarranted antagonistic condescending tone and petty puerile jibes, since we are both adults and hopefully friends who are engaging in intelligent debate. Let's try to keep our posts to a professional academic nature and in line with the spirit of this forum shall we? OK?

Secondly, it is abundantly clear that something I have said has highly irritated you, so I would like to apologise if I have in any way caused you offense...

It's interesting you use the term "condescending" as that seems to be your standard MO should anybody question or disagree with your opinions.
You've been very condescending to a number of highly intelligent and educated individuals on the forum and I'm not the only one to have noticed that.
A friendly bit of advice would be to take a good hard look at yourself before accusing others of being condescending.

OK, it's transparent that you are a very angry person.

With the utmost respect, I have done nothing whatsoever to warrant you verbally attacking me. Haven't you anything better to do than to come onto internet forums and try to pick fights with complete strangers? We have never even conversed before and yet you launch this wholly unwarranted barrage of attacks at me, when it is very clear to all that I am solely interesting in HELPING PEOPLE. What else do you do for kicks... visit hospitals and beat up cancer patients and old ladies for fun?

I am not going to fight with you. Furthermore, there is no need for me to defend myself when everything that you are saying is untrue.

I do not in any regard deserve this sort of verbal abuse, nor does anyone else who works within the medical industry who is devoting their entire life to HELPING PEOPLE; wherein individuals like you who persist in attacking the staff are nicely escorted off of the premises.

Please kindly note that I am in no regards angry with you, I have dealt with many people like your kind self who for one reason or another are currently ABUSIVE and AGGRESSIVE. In almost all case such people like you are not deep-down BAD PEOPLE; they simply currently have a DEMON that is causing them to act in said manner, such as ALCOHOLISM, DRUG ADDICTION or an ABUSIVE PARENT / SPOUSE. I have worked for many years within clinical practice and have treated many such individuals; some, I have managed to help beat their respective DEMON; but in other cases I have been unable to do so because said individual is not willing to help themselves or sometimes even acknowledge that they have a problem.

I will repeat the fact that I am by no means perfect. I make mistakes just like the next guy, and readily acknowledge as such when I do.

Furthermore, it is very easy to misconstrue my correcting factual inaccuracy as being somewhat condescending; however, this is an unfortunate hazard of the written word; it is easily misinterpreted. Believe me, if I was speaking with you in person you would have no doubt WHATSOEVER that my intentions are genuine and kind-hearted, and entirely devoid of condescension.

You can hurl all the verbal abuse you like at me, you will never get a rise out me, and so you will only be wasting your time. Please feel free to PM me and call me all the names you like. I would only ask that you cease contaminating this forum with your negativity which goes against the whole spirit of this forum.

Edited by ScienceGuy, 22 February 2012 - 11:06 AM.