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Production of gaba (γ – Aminobutyric acid) by microorganisms: a review.

Dhakal RBajpai VKBaek KH.

Source

School of Biotechnology, Yeungnam University, Gyeongsan , Gyeongbuk 712-749 , Republic of Korea.

Abstract

GABA (γ-aminobutyric acid) is a four carbon non-protein amino acid that is widely distributed in plants, animals and microorganisms. As a metabolic product of plants and microorganisms produced by the decarboxylation of glutamic acid, GABA functions as an inhibitory neurotransmitter in the brain that directly affects the personality and the stress management. A wide range of traditional foods produced by microbial fermentation contain GABA, in which GABA is safe and eco-friendly, and also has the possibility of providing new health-benefited products enriched with GABA. Synthesis of GABA is catalyzed by glutamate decarboxylase, therefore, the optimal fermentation condition is mainly based on the biochemical properties of the enzyme. Major GABA producing microorganisms are lactic acid bacteria (LAB), which make food spoilage pathogens unable to grow and act as probiotics in the gastrointestinal tract. The major factors affecting the production of GABA by microbial fermentation are temperature, pH, fermentation time and different media additives, therefore, these factors are summarized to provide the most up-dated information for effective GABA synthesis. There has been a huge accumulation of knowledge on GABA application for human health accompanying with a demand on natural GABA supply. Only the GABA production by microorganisms can fulfill the demand with GABA-enriched health beneficial food
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Influence of Light on the Free Amino Acid Content and γ-Aminobutyric Acid Synthesis in Brassica juncea Seedlings. ( Mustard Seed)

Li XKim YBUddin MRLee SKim SJPark SU.

Source

Department of Crop Science and ‡Department of Bio-Environmental Chemistry, Chungnam National University , 99 Daehak-ro, Yuseong-gu, Daejeon 305-764, Republic of Korea.

Abstract

Glutamate decarboxylase (GAD; EC 4.1.1.15) is an important enzyme in γ-aminobutyric acid (GABA) biosynthesis. Here we report the influence of light on amino acid accumulation and investigate the molecular mechanism by which light influences GABA biosynthesis at the seedling stage of two mustard ( Brassica juncea ) cultivars (green-leaf and purple-leaf). Gene expression profiles of four GAD-encoding genes (GAD1, GAD2, GAD4a, and GAD4b) and their impact on GABA biosynthesis were analyzed. Light exerted an obvious influence on amino acid accumulation in mustard seedlings. GAD gene expression was also significantly regulated by light/dark or dark treatment, which differentially regulated GABA biosynthesis in B. juncea seedlings. High-performance liquid chromatography (HPLC) revealed that the seeds of purple cultivars contain a higher amount of free amino acids and GABA than do the seeds of green cultivars. After seed germination, however, the accumulation of free amino acids peaked in dark-treated seedlings on day 9 in both cultivars, whereas GABA synthesis peaked at 9 days under light conditions. This study may provide a foundation for understanding the effect of light on amino acids, particularly GABA biosynthesis in Brassica plants.
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GABAA receptor modulation by piperine and a non-TRPV1 activating derivative. ( Black Pepper)

Khom SStrommer BSchöffmann AHintersteiner JBaburin IErker TSchwarz TSchwarzer CZaugg JHamburger MHering S.

Source

Department of Pharmacology and Toxicology, University of Vienna, Althanstraße 14, A-1090 Wien, Austria.

Abstract

The action of piperine (the pungent component of pepper) and its derivative SCT-66 ((2E,4E)-5-(1,3-benzodioxol-5-yl))-N,N-diisobutyl-2,4-pentadienamide) on different gamma-aminobutyric acid (GABA) type A (GABA(A)) receptors, transient-receptor-potential-vanilloid-1 (TRPV1) receptors and behavioural effects were investigated. GABA(A) receptor subtypes and TRPV1 receptors were expressed in Xenopus laevis oocytes. Modulation of GABA-induced chloride currents (I(GABA)) by piperine and SCT-66 and activation of TRPV1 was studied using the two-microelectrode-voltage-clamp technique and fast perfusion. Their effects on explorative behaviour, thermoregulation and seizure threshold were analysed in mice. Piperine acted with similar potency on all GABA(A) receptor subtypes (EC₅₀ range: 42.8±7.6 μM (α₂β₂)-59.6±12.3 μM (α₃β₂). I(GABA) modulation by piperine did not require the presence of a γ(2S)-subunit, suggesting a binding site involving only α and β subunits. I(GABA) activation was slightly more efficacious on receptors formed from β(2/3) subunits (maximal I(GABA) stimulation through α₁β₃ receptors: 332±64% and α₁β₂: 271±36% vs. α₁β₁: 171±22%, p<0.05) and α₃-subunits (α₃β₂: 375±51% vs. α₅β₂:136±22%, p<0.05). Replacing the piperidine ring by a N,N-diisobutyl residue (SCT-66) prevents interactions with TRPV1 and simultaneously increases the potency and efficiency of GABA(A) receptor modulation. SCT-66 displayed greater efficacy on GABA(A) receptors than piperine, with different subunit-dependence. Both compounds induced anxiolytic, anticonvulsant effects and reduced locomotor activity; however, SCT-66 induced stronger anxiolysis without decreasing body temperature and without the proconvulsive effects of TRPV1 activation and thus may serve as a scaffold for the development of novel GABA(A) receptor modulators.
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Plant-based medicines for anxiety disorders, Part 1: a review of preclinical studies.

Sarris JMcIntyre ECamfield DA.

Source

Department of Psychiatry, Faculty of Medicine, University of Melbourne, 2 Salisbury Street, Richmond, VIC, 3121, Australia. [email protected]

Abstract

Research in the area of herbal psychopharmacology has revealed a variety of promising medicines that may provide benefit in the treatment of general anxiety and specific anxiety disorders. However, a comprehensive review of plant-based anxiolytics has been absent to date. This article (part 1) reviews herbal medicines for which only preclinical investigations for anxiolytic activity have been performed. In part 2, we review herbal medicines for which there have been clinical investigations for anxiolytic activity. An open-ended, language-restricted (English) search of MEDLINE (PubMed), CINAHL, Scopus and the Cochrane Library databases was conducted (up to 28 October 2012) using specific search criteria to identify herbal medicines that have been investigated for anxiolytic activity. This search of the literature revealed 1,525 papers, from which 53 herbal medicines were included in the full review (having at least one study using the whole plant extract). Of these plants, 21 had human clinical trial evidence (reviewed in part 2), with another 32 having solely preclinical studies (reviewed here in part 1). Preclinical evidence of anxiolytic activity (without human clinical trials) was found for Albizia julibrissin ( SILK TREE ), Sonchus oleraceus ( SOW THISTLE), Uncaria rhynchophylla ( GOUTENG), Stachys lavandulifolia( LAVENDER), Cecropia glazioui (EMBAUBA), Magnolia spp., Eschscholzia californica ( CALIFORNIA POPPY  SEED), Erythrina spp ( CORAL TREE )., Annona spp., Rubus brasiliensis (BRAZILLIAN RASPBERRY), Apocynum venetum ( DOGBANE ), Nauclea latifolia (ENGLISH PIN CUSHION TREE-AFRICAN PEACH), Equisetum arvense ( HORSETAIL ), Tilia spp.( LINDEN FLOWER), Securidaca longepedunculata, Achillea millefolium ( YARROW ), Leea indica (BANDICOOT BERRY), Juncus effuses (SOFT RUSH), Coriandrum sativum ( CORIANDER), Eurycoma longifolia ( TONGAT ALI ), Turnera diffusa (DAMIANA), Euphorbia hirta (ASTHMAPLANT), Justicia spp., Crocus sativus ( SAFFRON), Aloysia polystachya, Albies pindrow, Casimiroa edulis, Davilla rugosa, Gastrodia elata, Sphaerathus indicus, Zizyphus jujube ( JUJUBE OR CHINESE DATE) and Panax ginseng ( GINSENG). Common mechanisms of action for the majority of botanicals reviewed primarily involve GABA, either via direct receptor binding or ionic channel or cell membrane modulation; GABA transaminase or glutamic acid decarboxylase inhibition; a range of monoaminergic effects; and potential cannabinoid receptor modulation. Future research should focus on conducting human clinical trials on the plants reviewed with promising anxiolytic activity.
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Citrus aurantium L. essential oil exhibits anxiolytic-like activity mediated by 5-HT(1A)-receptors and reduces cholesterol after repeated oral treatment.

Costa CACury TCCassettari BOTakahira RKFlório JCCosta M.

Source

Department of Pharmacology, Institute of Biosciences, Unesp – Univ Estadual Paulista, P.O. Box 51018618-970, Botucatu, São Paulo, Brazil.

Abstract

BACKGROUND:

The current treatments for anxiety disorders and depression have multiple adverse effects in addition to a delayed onset of action, which has prompted efforts to find new substances with potential activity in these disorders. Citrus aurantium was chosen based on ethnopharmacological data because traditional medicine refers to the Citrus genus as useful in diminishing the symptoms of anxiety or insomnia, and C. aurantium has more recently been proposed as an adjuvant for antidepressants. In the present work, we investigated the biological activity underlying the anxiolytic and antidepressant effects of C. aurantium essential oil (EO), the putative mechanism of the anxiolytic-like effect, and the neurochemical changes in specific brain structures of mice after acute treatment. We also monitored the mice for possible signs of toxicity after a 14-day treatment.

METHODS:

The anxiolytic-like activity of the EO was investigated in a light/dark box, and the antidepressant activity was investigated in a forced swim test. Flumazenil, a competitive antagonist of benzodiazepine binding, and the selective 5-HT(1A) receptor antagonist WAY100635 were used in the experimental procedures to determine the mechanism of action of the EO. To exclude false positive results due to motor impairment, the mice were submitted to the rotarod test.

RESULTS:

The data suggest that the anxiolytic-like activity observed in the light/dark box procedure after acute (5 mg/kg) or 14-day repeated (1 mg/kg/day) dosing was mediated by the serotonergic system (5-HT(1A) receptors). Acute treatment with the EO showed no activity in the forced swim test, which is sensitive to antidepressants. A neurochemical evaluation showed no alterations in neurotransmitter levels in the cortex, the striatum, the pons, and the hypothalamus. Furthermore, no locomotor impairment or signs of toxicity or biochemical changes, except a reduction in cholesterol levels, were observed after treatment with the EO.

CONCLUSION:

This work contributes to a better understanding of the biological activity of C. aurantium EO by characterizing the mechanism of action underlying its anxiolytic-like activity.
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Modulation of the γ-aminobutyric acid (GABA) system by Passiflora incarnata L.

Appel KRose TFiebich BKammler THoffmann CWeiss G.

Source

VivaCell Biotechnology GmbH, Denzlingen, Germany.

Abstract

Passiflora incarnata L. (Passifloraceae) is important in herbal medicine for treating anxiety or nervousness, Generalized Anxiety Disorder (GAD), symptoms of opiate withdrawal, insomnia, neuralgia, convulsion, spasmodic asthma, ADHD, palpitations, cardiac rhythm abnormalities, hypertension, sexual dysfunction and menopause. However, the mechanism of action is still under discussion. Despite gaps in our understanding of neurophysiological processes, it is increasingly being recognized that dysfunction of the GABA system is implicated in many neuropsychiatric conditions, including anxiety and depressive disorders. Therefore, the in vitro effects of a dry extract of Passiflora incarnata (sole active ingredient in Pascoflair® 425 mg) on the GABA system were investigated. The extract inhibited [(3) H]-GABA uptake into rat cortical synaptosomes but had no effect on GABA release and GABA transaminase activity. Passiflora incarnata inhibited concentration dependently the binding of [(3) H]- SR95531 to GABA(A) -receptors and of [(3) H]-CGP 54626 to GABA(B) -receptors. Using the [(35) S]-GTPγS binding assay Passiflora could be classified as an antagonist of the GABA(B) receptor. In contrast, the ethanol- and the benzodiazepine-site of the GABA(A) -receptor were not affected by this extract. In conclusion, the first evidence was shown that numerous pharmacological effects of Passiflora incarnata are mediated via modulation of the GABA system including affinity to GABA(A) and GABA(B) receptors, and effects on GABA uptake.
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These Substances may Alleviate or Treat Depression
Alkaloids
Galanthamine may exert a mild anti-depressant effect and may therefore be useful as an adjunct for the treatment of Depression (this occurs from Galanthamine preserving Acetylcholine levels in the Brain).  references
Amino Acids
5-Hydroxytryptophan (5-HTP) [300 – 600 mg per day] may alleviate various forms of Depression (including Endogenous Depression and Reactive Depression).  references
Acetyl-L-Carnitine (ALC) (500 – 3,000 mg per day) may alleviate Depression (especially in elderly people).  references
Glutamine (250 – 1,000 mg per day) may improve Mood in Depression patients.  references
Methionine may alleviate Depression where the Depression is caused by excess Histamine (due to the ability of Methionine to detoxify excessive Histamine).  references
Phenylalanine (usually L-Phenylalanine but some studies have shown benefit using DL-Phenylalanine or D-Phenylalanine) may alleviate Depression when Depression is caused by Norepinephrine or Phenylethylamine deficiency (by functioning as a precursor for the production of Norepinephrine and Phenylethylamine).  references
Proline may bring a sense of relief/happiness to many short-term Depression cases:  [more info]
S-Adenosylmethionine (SAMe) may alleviate (all forms of) Depression:  references
Many studies have confirmed that SAMe may be significantly (approximately 15%) more effective in the treatment of Depression than traditional Pharmaceutical Anti-Depressants for the treatment of Depression.
Taurine may alleviate some cases of Depression.  [more info]
Threonine (2,000 mg per day) may alleviate some cases of Depression.  references
Tryptophan may alleviate some types of Depression – the types of Depression that can be alleviated by Tryptophan are characterized by intense cravings for Carbohydrates and include the Depression associated with Menopause.  references
Tyrosine may alleviate many cases of Depression (due to its role as a precursor for the production of Norepinephrine).  references
Coenzymes
Supplemental, exogenous NADH (5 mg per day) may alleviate Depression (by boosting Brain Dopamine and Norepinephrine levels).  references
Enzymes
Optimal levels/activity of Tyrosine Hydroxylase are required for the prevention of Depression (due to Tyrosine Hydroxylase’s rate-
limiting role as a precursor for Catecholamine Neurotransmitters known to play a role in the prevention of Depression).  references
Glycosides – Saponins
Glycyrrhizin (a component of Licorice) may alleviate Depression.  [more info]
Hormones
Androstenedione may alleviate Depression
Dehydroepiandrosterone (DHEA) (30 – 90 mg per day) may alleviate Depression.  references
Melatonin may be useful for the treatment of some types of Depression.
Pregnenolone may help to alleviate Depression (where Depression is caused by excessive Cortisol).  references
Progesterone (i.e. Natural Progesterone and not synthetic Progestins) may alleviate Depression and may help to prevent Depression.  references
Depression may occur as a result of insufficient endogenous Testosterone levels (especially in men) and Testosterone replacement therapy may alleviate Depression.  references
Insufficient endogenous production of Triiodothyronine (T3) may cause Depression and administration of supplemental, exogenous T3 (20 – 50 mcg per day) may cause significant improvement in the Depression scores of otherwise difficult-to-treat cases of Depression.  references
Lipids
Optimal Cholesterol levels may help to prevent Depression (low Cholesterol (under 160 mg/dl) is associated with an increased risk of Depression).
Phosphatidylserine (300 – 400 mg per day for 30 – 60 days) may alleviate Depression – especially in elderly subjects.  references
Prostaglandin E1 (PGE1) may induce a sense of well being in Depression patients and Depression patients are often found to have sub
optimal levels of Prostaglandin E1.
An excessive ratio of Polyunsaturated Fatty Acids to Superunsaturated Fatty Acids may be a risk factor for Depression:  references
Depression may occur as a result of Docosahexaenoic Acid (DHA) deficiency.  references
Depression may occur as a result of Eicosapentaenoic Acid (EPA) deficiency.
Minerals
Depression may occur as a result of Bromine deficiency
Post-menopausal women afflicted with Depression are often deficient in Calcium and supplemental Calcium may alleviate Depression in post-menopausal women and elderly patients.  references
Chromium may alleviate Depression.
Magnesium deficiency is speculated to be an underlying cause of Depression:
Many Depression patients are found to be deficient in Magnesium, while those who achieve remission usually exhibit normal Magnesium levels
Manganese may alleviate some forms of Depression.
Depression may occur as a result of Potassium deficiency.
Depression may occur as a result of Selenium deficiency.
Depression may occur as a result of Zinc deficiency.
 
Neurotransmitters
Depression may occur as a result of Acetylcholine insufficiency.
Depression may occur as a result of Histamine insufficiency.
Norepinephrine insufficiency is a major cause of Depression.  references
Optimal Phenylethylamine (PEA) levels may help to prevent Depression.  references
Insufficient production of Serotonin or excessive destruction of Serotonin can cause Depression.  references
Nucleic Compounds
Cytidine may alleviate Depression.
Uridine may alleviate Depression.
Organic Acids
Anacardic Acid may possess antidepressant properties.  [more info]
Pigments
Hypericin may contribute to the ability of Saint John’s Wort to alleviate Depression (Hypericin inhibits the Monoamine Oxidase (MAO) enzyme that when activated excessively can cause Depression).
Polyphenols
Amentoflavone is speculated alleviate Depression (it is known that Amentoflavone binds to Benzodiazepine Receptors on GABAa Receptors via a similar mechanism to that of Pharmaceutical Benzodiazepines).  references
Smart Drugs
Adrafinil may alleviate some cases of Depression.
Bromocriptine may alleviate some cases of Depression (especially where Depression is attributable to Hyperprolactinemia – excessive production/secretion of Prolactin).  [more info]Deprenyl may alleviate many forms of Depression (including Major Depression):  references
Deprenyl is ideally administered in conjunction with Phenylalanine (1,000 – 6,000 mg per day) to alleviate Depression (including Major Depression).
The dosage of Deprenyl for the treatment of Depression can be further reduced by the addition of Vitamin B6 (100 mg per day) to the previous formula.  In one human study,  5 mg Deprenyl + 1-6 grams Phenylalanine + 100 mg Vitamin B6 caus77ed total alleviation of Depression symptoms in 60% of patients in 2-3 days.
Dimethylaminoethanol (DMAE) may reduce Apathy and may increase Motivation in Depression patients.  references
Gerovital (GH3) may alleviate Depression (especially in elderly people) (one of the mechanisms for this effect is Gerovital’s ability to mildly and reversibly inhibit Monoamine Oxidase enzymes that degrade Neurotransmitters such as Dopamine, Norepinephrine and Serotonin).  references
Minaprine may alleviate Depression:
When compared to the Tricyclic Antidepressant, Imipramine, Minaprine was found to be superior for the treatment of Depression in that it is faster acting and produces no side effects.
Nimodipine may alleviate Depression.
Oxiracetam may alleviate Depression in elderly Depression patients.
Picamilon may alleviate Depression.
Exogenous Vasopressin has produced positive results in some patients with histories of severe Depression (most Depression patients are found to have sub-optimal levels of endogenous Vasopressin).
Vincamine may alleviate Depression.
Vinpocetine (10 mg per day) may alleviate Depression in 74% of cases (especially where the underlying cause of Depression is Dementia or Cerebral Insufficiency).  references
Vitamins
Depression may occur as a result of Biotin deficiency.
Cytidine Diphosphate Choline (CDP-Choline) may alleviate severe Depression by increasing the utilization of Oxygen within the Brain.  references
Depression may occur as a result of Folic Acid deficiency (15% – 38% of Depression patients are found to have low Folic Acid levels).  references
“Happy” people are often found to have high Folic Acid levels.
Folic Acid (500 mcg per day or more) may increase the effectiveness of Selective Serotonin Reuptake Inhibitors (SSRIs) such as Prozac for the treatment of Depresssion.
Inositol (5 – 12 grams per day) may be effective for the treatment of Depression (due to it enhancing the ability of Vitamin B3 to bind to the Benzodiazepine Receptors in the Brain):  references
Depression patients often have decreased levels of Inositol in their Cerebrospinal Fluid.
The Nicotinic Acid form of Vitamin B3 binds to the Benzodiazepine Receptors in the Brain (and may therefore be useful for the treatment of Depression).  references
Para Aminobenzoic Acid (PABA) deficiency may cause Depression.  [more info]
Depression may occur as a result of Vitamin B1 deficiency.  references
Depression may occur as a result of Vitamin B2 deficiency.
Depression may occur as a result of Vitamin B5 deficiency.
Vitamin B6 may alleviate some types of Depression:
Vitamin B6 functions as a catalyst for the formation of the inhibitory Neurotransmitter – Gamma Aminobutyric Acid (GABA) from Glutamic Acid).
-Vitamin B6 functions as a catalyst for the conversion of Tryptophan into Serotonin (which is sometimes deficient in Depression patients).
Depression may occur as a result of Vitamin B12 deficiency.  r
Vitamin C (1,000 – 3,000 mg per day for at least three weeks) may alleviate Depression and 32% of Depression patients are found to be deficient in Vitamin C.
Depression may occur as a result of Vitamin D deficiency.
Volatile Oils
Anacardiol may possess anti-depressant properties.  [more info]
These Foods/Herbs may Alleviate Depression
Fruits
Mango may alleviate Depression (due to its Anacardic Acid and Anacardiol content).  [more info]
Herbs
Ashwagandha (6,000 mg per day for at least two months) may alleviate (Endogenous and Reactive) Depression.  references
Brahmi may alleviate Depression.
Camu-Camu is claimed to alleviate Depression.
Cat’s Claw may alleviate Depression.  ]
Damiana is claimed to possess antidepressant properties when Depression stems from Sexual Factors
Ginkgo Biloba may alleviate some cases of Depression (by improving Blood Circulation to the Brain).
Golden Root is claimed to alleviate Depression.
Gotu Kola may alleviate Depression.
Korean Ginseng may alleviate Depression.
Magnolia may alleviate Depression.
Marapuama reputedly alleviates some cases of Depression (according to folklore
Noni may alleviate some cases of Depression (according to anecdotal reports).
Passion Flower may be of some use in the treatment of some cases of Depression (due to its ability to calm the Central Nervous System).
Saint John’s Wort (900 – 1,050 mg per day standardized to contain 0.2% – 0.3% Hypericin + 2% – 3% Hyperforin) may significantly alleviate Depression – the mechanism by which Saint John’s Wort may alleviate Depression involves several underlying mechanisms:  references
The Amentoflavone content of Saint John’s Wort influences Benzodiazepine Receptors on GABAa Receptors.  references
The Flavonols and Hypericin content of Saint John’s Wort inhibit Monoamine Oxidase (MAO).  references
Saint John’s Wort inhibits the excessive destruction of Catecholamine Neurotransmitters (such as Norepinephrine) by the enzyme Catechol-O-Methyltransferase (COMT) – due to the Flavonols content of Saint John’s Wort.  references
-Saint John’s Wort inhibits the reuptake of Serotonin by 5-Hydroxytryptamine Receptors (it thereby functions in a similar fashion to Selective Serotonin Reuptake Inhibitors (SSRIs) such as Prozac).
Recent research indicates that the Hyperforin content of Saint John’s Wort plays a major role in the anti-depressant effects of Saint John’s Wort
Schizandra may alleviate Depression.
Suma reputedly alleviates some cases of Depression (according to folklore).
Turmeric may be useful for the treatment of Depression (due to its ability to inhibit the activity of Monoamine Oxidase Type A (MAO-A) in the Brain.
Valerian may alleviate Depression.
Oils (dietary Oils)
Flax Seed Oil may treat some cases of Depression.  [more info]
Oils (non-dietary Oils)
Lavender (Oil applied topically to the temples;  or added to a bath) is claimed to alleviate Depression (via its aroma)
Neroli Oil (vapors inhaled via Aromatherapy) may alleviate Depression.
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How Soft Drinks Impact Health
 
 
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Toxicity of Sugar Data Toxic sugar?  Mouse data suggests added-sugar diet may impact lifespan and reproduction The research shows that when mice consumed a diet containing 25% extra sugar – an amount considered safe and relevant in human consumption equivalents – females died at twice the rate of rats fed a standard diet, while males were 25% less likely to hold territory and reproduce. Writing in Nature Communications, the research team  describe the findings from an animal model ‘toxicity test’ developed at the University of Utah, USA – which gave the mice the equivalent level of sugar gained by humans from the consumption of three cans of soda. Our results provide evidence that added sugar consumed at concentrations currently considered safe exerts dramatic adverse impacts on mammalian health, said the study authors – led by seniour author Professor Wayne Potts. This demonstrates the adverse effects of added sugars at human-relevant levels, explained Potts, who noted that previous studies using other tests fed mice large doses of sugar disproportionate to the amount people consume in sweetened beverages, baked goods and candy. The new research, however, suggests that a 25% ‘added-sugar’ diet (12.5 percent dextrose and 12.5 percent fructose) may be just as harmful to the health of mice as being the inbred offspring of first cousins, said the researchers. Dr James Ruff, first author of the study, noted that while the mice did not become obese and showed few metabolic symptoms, the Utah study did show that mice fed the diet died more often and tended to have fewer babies. We have shown that levels of sugar that people typically consume – and that are considered safe by regulatory agencies – impair the health of mice, said Ruff. Human implications Commenting on the research, Catherine Collins, principal dietitian at St George’s Hospital NHS Trust, UK, noted that while the researchers state that this diet mimicked the high sugar diet (25% added sugar) commonly taken by some people in the US, a recent UK survey indicated an average sugar intake of around 11% of total calories – far less than half the amount fed to the mice in this study. So what can we take from this? Certainly, for swaggeringly territorial wild mice, a high sugar diet made them weaker at defending their homestead, and influenced fertility, said Collins. Unfortunately the study doesn’t address whether this was due to micronutrient deficiencies, or that well-sugared mice didn’t feel in the mood to recreate. Alison Boyd, director of Sugar Nutrition UK added: This is very early research in animals which cannot be translated into humans. The scientific evidence on sugar has been reviewed on numerous occasions by independent expert committees including the World Health Organization and European Food Safety Authority. They have concluded that moderate levels of sugar consumption are not implicated in any of the major lifestyle diseases, she commented. Like all sources of calories, sugar can be consumed within a healthy, calorie-balanced diet and active lifestyle. Study details The Utah study placed groups of mice in room-sized pens nicknamed ‘mouse barns’ with multiple nest boxes – something the researchers suggest is a much more realistic environment than small cages and allows the mice to compete more naturally for This, Potts said, reveals any subtle effects on performance. This is a sensitive test for health and vigour declines,” he explained, noting that in a previous study he used the same test to show how inbreeding hurt the health of mice. The experimental diet in the study provided 25% of calories from added sugar – half fructose and half glucose – no matter how many calories the mice ate. This diet is equivalent to the diet of a person who drinks three cans daily of sweetened soda in a day plus a perfectly healthy, no-sugar-added diet, said Potts. He explained that the mice used in the trial, descended from wild house mice, are ‘highly competitive’ over food, nesting sites and territories. This competition demands high performance from their bodies, so if there is a defect in any physiological systems, they tend to do more poorly during high competition. The team created two colonies with 156 ‘founders’ that were weaned at four weeks, and then assigned either to the added-sugar diet or the control diet – with half the males and half the females on each diet. Mice remained in cages with siblings of the same sex (to prevent reproduction) for 26 weeks while they were fed these in Then the mice were placed in the mouse barns to live, compete with each other and breed for 32 more weeks. All mice received the same added-sugar diet while in the mouse barns, so the study only tested for differences caused by the mice eating different for the previous 26 weeks, said Potts. The team revealed their key findings After 32 weeks in mouse barns, 35% of the females fed extrasugar diedThis was twice the 17% death rate for female control mice. There was no difference in the 55% death among males who did and did not get added sugar. Males on the added-sugar diet acquired and held 26% fewer territories than males on the control diet: control males occupied 47% of the territories while sugar-added mice controlled less than 36%. Males on the added-sugar diet produced 25% fewer offspring than control males, as determined by genetic analysis of the offspring. Sugar-added females had higher reproduction rates than controls initially – likely because the sugar gave them extra energy to handle the burden of pregnancy – but then had lower reproductive rates as the study progressed, partly because they had higher death rates linked to sugar-Human-relevant levels of added sugar consumption increase female mortality and lower male fitness in mice Special Note – this would carry over to Humans—initially when young people consume sugar will burn it off provided there are no other things added to it like soy or canola which can also cause issue—when combining these things you wind up with less energy not more since the organs that are affected here are the pancreas-thyroid-heart-liver –brain which gets taxed and pushed and begins to wear out long before it is supposed to as a result the immune system breaks down prematurely—and issues can arise usually in the endocrine and digestive systemsAnd proceed to the respiratory and heart—most people today are dying of cancer-heart failure-respiratory an digestive issues—men and women today are having unnecessary surgical procedures done to there endocrine system—prostate-testicles-breast-uterus and ovaries—this would explain this—the food industry is selling foods that would appear to be the root of illness—and it would be to the interest of the consumer to know what to eat and what to avoid!!
 
 
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Show of the Month  November 9 2013
 
Ginger for the fight against Lung Cancer
Wisconsin Ginseng (Panax quinquefolius) to improve cancer-related fatigue
 
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Ginger for the fight against Lung Cancer
6-gingerdiols as the major metabolites of 6-gingerol in cancer cells and in mice and their cytotoxic effects on human cancer cells.
J Agric Food Chem. 2012 Nov 14;60(45):11372-7
Authors: Lv L, Chen H, Soroka D, Chen X, Leung T, Sang S
Abstract
6-Gingerol, a major pungent component of ginger (Zingiber officinale Roscoe, Zingiberaceae), has been reported to have antitumor activities. However, the metabolic fate of 6-gingerol and the contribution of its metabolites to the observed activities are still unclear. In the present study, we investigated the biotransformation of 6-gingerol in different cancer cells and in mice, purified and identified the major metabolites from human lung cancer cells, and determined the effects of the major metabolites on the proliferation of human cancer cells. Our results show that 6-gingerol is extensively metabolized in H-1299 human lung cancer cells, CL-13 mouse lung cancer cells, HCT-116 and HT-29 human colon cancer cells, and in mice. The two major metabolites in H-1299 cells were purified and identified as (3R,5S)-6-gingerdiol (M1) and (3S,5S)-6-gingerdiol (M2) based on the analysis of their 1D and 2D NMR data. Both metabolites induced cytotoxicity in cancer cells after 24 h, with M1 having a comparable effect to 6-gingerol in H-1299 cells.–PMID: 23066935 [PubMed – indexed for MEDLINE]—
Special Comment –it appears for those who have Lung Cancer this is another method of reducing or ridding the are of cancer—taking the ginger in either a tea or extract would be the strongest method—and applying it in the diet—adding black pepper with it would expedite the components to get it into the system more effectively and make it more potent
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Wisconsin Ginseng (Panax quinquefolius) to improve cancer-related fatigue- a randomized, double-blind trial, N07C2.
J Natl Cancer Inst. 2013 Aug 21;105(16):1230-8
Authors: Barton DL, Liu H, Dakhil SR, Linquist B, Sloan JA, Nichols CR, McGinn TW, Stella PJ, Seeger GR, Sood A, Loprinzi CL
Abstract
BACKGROUND: Safe, effective interventions to improve cancer-related fatigue (CRF) are needed because it remains a prevalent, distressing, and activity-limiting symptom. Based on pilot data, a phase III trial was developed to evaluate the efficacy of American ginseng on CRF.
METHODS: A multisite, double-blind trial randomized fatigued cancer survivors to 2000mg of American ginseng vs a placebo for 8 weeks. The primary endpoint was the general subscale of the Multidimensional Fatigue Symptom Inventory-Short Form (MFSI-SF) at 4 weeks. Changes from baseline at 4 and 8 weeks were evaluated between arms by a two-sided, two-sample t test. Toxicities were evaluated by self-report and the National Cancer Institute’s Common Terminology Criteria for Adverse Events (CTCAE) provider grading.
RESULTS: Three hundred sixty-four participants were enrolled from 40 institutions. Changes from baseline in the general subscale of the MFSI-SF were 14.4 (standard deviation [SD] = 27.1) in the ginseng arm vs 8.2 (SD = 24.8) in the placebo arm at 4 weeks (P = .07). A statistically significant difference was seen at 8 weeks with a change score of 20 (SD = 27) for the ginseng group and 10.3 (SD = 26.1) for the placebo group (P = .003). Greater benefit was reported in patients receiving active cancer treatment vs those who had completed treatment. Toxicities per self-report and CTCAE grading did not differ statistically significantly between arms.
CONCLUSIONS: Data support the benefit of American ginseng, 2000mg daily, on CRF over an 8-week period. There were no discernible toxicities associated with the treatment. Studies to increase knowledge to guide the role of ginseng to improve CRF are needed.—PMID: 23853057 [PubMed – indexed for MEDLINE]
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Gut microbial metabolism of polyphenols from black tea and red wine/grape juice is source-specific and colon-region dependent.
J Agric Food Chem. 2012 Nov 14;60(45):11331-42
Authors: van Dorsten FA, Peters S, Gross G, Gomez-Roldan V, Klinkenberg M, de Vos RC, Vaughan EE, van Duynhoven JP, Possemiers S, van de Wiele T, Jacobs DM
Abstract
The colonic microbial degradation of a polyphenol-rich black tea extract (BTE) and red wine/grape juice extract (RWGE) was compared in a five-stage in vitro gastrointestinal model (TWINSHIME). Microbial metabolism of BTE and RWGE polyphenols in the TWINSHIME was studied subsequently in single- and continuous-dose experiments. A combination of liquid or gas chromatography with mass spectrometry (LC-MS or GC-MS) and NMR-based metabolic profiling was used to measure selected parent polyphenols, their microbial degradation into phenolic acids, and the production of short-chain fatty acids (SCFAs) in different colon compartments. Acetate production was increased by continuous feeding of BTE but not RWGE. During RWGE feeding, gallic acid and 4-hydroxyphenylpropionic acid remained elevated throughout the colon, while during BTE feeding, they were consumed in the distal colon, while 3-phenylpropionic acid was strongly produced. Gut microbial production of phenolics and SCFAs is dependent on colon location and polyphenol source, which may influence potential health benefits.—PMID: 23072624 [PubMed – indexed for MEDLINE]
Recipe—you may want to take a black tea and fuse it in wine by blender extraction—this will allow the 2 to become fused and there components allowing for better usage and there properties would then be effectively transferred throughout the colon supporting the colon
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Hot Salt Packs

The Japanese frequently use salt in their traditional healing techniques to encourage vitality and circulation to problem areas.  Hot salt energises and strengthens the vital organs, tonifying the uterus, bladder and intestines.  Salt packs work well with period problems (although hot packs should not be used while menstruating as they encourage more bleeding), as well as bladder weakness, cystitis, constipation and digestive weakness.  Salt packs support the kidneys to eliminate the toxins after Lymphatic Enhancement Therapy.
Directions
Place three cups of rock salt (supermarket variety is fine) in a clean oven dish or tray in a preheated oven at 180 degrees for 20-30 minutes.  The salt must be roasted not heated in a microwave.  Place heated salt in an old pillowcase.  Cover abdomen or kidneys with a towel before placing the heated salt pack on top.  Cover with another towel to conserve the heat and lie down and enjoy the salt pack for 30-45 minutes.  It is good to drink a glass of water while you are relaxing to encourage flushing of the kidneys.
The same salt can be used up to eight times or until it is discoloured.
Caution: Salt can become very hot so be careful not to burn the sk
Just heat one pound of coarse salt in a heavy pan and then VERY carefully, funnel the salt into a clean heavy cotton sock or bag. Avoid adding too much salt, you don’t want to have it be too rigid, but rather more the consistency of a bean bag chair. Close the end of the bag or sock with a heavy-duty safety pin and sit back and enjoy the warming effect of the salt pack where ever you need soothing heat. It will stay warm for almost 30 minutes and will help bring relief because it increases circulation to the aching area.
 
 
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EPSOM SALTS PACKS

The Edgar Cayce readings recommended a variety of packs to relieve pain, improve eliminations, and produce relaxation in the body.  Epsom salts packs were often recommended for symptomatic relief of abdominal or lower back pain.  Here are some simple directions for making and using Epsom salts packs for lower back pain:
–Dissolve Epsom salts in hot water (two cups to a quart of water) in a small basin
or pot.

  • Soak a large piece of flannel or heavy towel in the Epsom salts solution.
  • Apply the pack over the affected area.
  • Place plastic over the pack and then a heating pad to maintain the heat until the Epsom salts have completely dried or have become caked in the pack.
  • Leave the pack on until it becomes hardened or dried.
  • Cleanse the area with water.

Massage the area with pure (cold-pressed) peanut oil using all the oil that the body will absorb.
 
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How Epsom Salts Work

  • The main ingredient in Epsom salt is magnesium, which is “the second-most abundant element in human cells and the fourth-most important positively charged ion in the body,” according to the Epsom Salt Council. Magnesium relaxes muscles, reduces swelling, improves heart and circulatory health, improves the body’s ability to use insulin, helps flush toxins, improves nerve function by regulating electrolytes, and reduces stress. You can take magnesium as a dietary supplement, but it also can be absorbed through the skin. An Epsom poultice draws magnesium in through the skin, delivering it directly to sore muscles rather than waiting for an oral pain reliever to travel through the bloodstream to the affected area.

Epsom Poultices

Poultice packs made with Epsom salts are easy to make to treat muscle sprains and strains. They can be messy though, so use this treatment in the bath or bathroom, or wherever you can easily clean up. Mix Epsom salts with enough water to make a paste that will cover the area you are treating. Prepare a damp, warm towel and set it aside. Apply the thick paste to the sore area and spread it in an even layer over the skin. Take the warm towel, wrap it around the area covered with Epsom salts and secure it. Let the poultice sit for at least 20 minutes and then wash off the paste. You can add some intermittent heat directly to the moist towel with a hairdryer, but be careful not to burn yourself.
Read more: http://www.ehow.com/way_5700174_homemade-epsom-salt-poultice.html#ixzz2k1VKoqRr
 
 
Personal Use—when applying this initially you may not feel the heat but as the material is being used and set in place the heat will intensify—I have utilized with this turpentine and with the 2 appears to be very effective in the penetration and will find when it penetrates you will taste the salt and pine taste—if there is a candida –may see it excreted in the urine—will find almost immediate relief in pain and may find that where there is a condition will penetrate and move through an area—Caution this can burn so be wise in the usage
 
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14 Things People Probably Do Not Want To Know About Their Favorite Foods

There are hundreds of food industry facts that are sheltered from consumers and only made public by food scientists if absolutely necessary. The following are 14 of the more well known industry insider secrets that have been exposed now for some time, but still not common knowledge to millions of consumers.
Many consumer watchdogs have found that food label claims such as ‘pure’, ‘fresh’, ‘non-artificial’, ‘natural’ and ‘real’ are largely unregulated and false when these claims are investigated. Moreover, the processing of most foods, ingredients used in manufacturing, their byproducts, waste management and other details are often kept hidden from the public until they’ve been exposed by those willing to publicize the information.

  1. The manufacturing of Greek yogurt produces millions of tons of toxic waste every year, and nobody knows what to do with it.

For every three or four ounces of milk, companies who manufacture greek yogurt can produce only one ounce of creamy Greek yogurt. The rest becomes acid whey. It’s a thin, runny waste product that can’t simply be dumped. Not only would that be illegal, but whey decomposition is toxic to the natural environment, robbing oxygen from streams and rivers. That could turn a waterway into what one expert calls a “dead sea,” destroying aquatic life over potentially large areas. Spills of cheese whey, a cousin of Greek yogurt whey, have killed tens of thousands of fish around the country in recent years.
The $2 billion Greek yogurt market and state government officials are scrambling not just to figure out uses for whey, but how to make a profit off of it. Source
2. All grocery retail orange juice that is “not from concentrate” is processed with “artificial flavor” to ensure that each bottle tastes exactly the same.
No matter what time of year and regardless of the origin of oranges, large juice manufacturers like Pepsico are consistently blending perfectly flavored orange juice specifically through carefully controlled processes and artificial flavor calibration. These mixtures are added to replace the natural flavors lost when the juice chemically separates oxygen ( “deaerates” ) to be able to maintain shelf life for more than one year without oxidizing.
Because the added flavor is technically derived from orange oil extract (although it is completely, artifically and a chemically manufactured derivative), it does not need to be specifically listed in the ingredients. Source
3. Vegetarian burgers are far more toxic than conventional beef patties.
More than 99% of vegetarian burgers at grocery retailers are made with soy protein isolate (aka textured vegetable protein, aka soy meal). These substances derived from defatted soy flour are mostly used in pet foods, but sweetened up with sugar and spices to help improve their taste. Soy oil is generally separated from flaked soybeans — leaving defatted meal that’s ground into flour — using a chemical called hexane, one of the volatile organic compounds that constitutes natural gas, crude oil and gasoline. Since more than 95% of soy is also genetically modified, you’re also getting a nice dose of transgenic DNA in your veggie burgers.
The Cornucopia Institute, a U.S.-based progressive farm policy outfit, had samples of soy oil, soy meal and soy grits tested, and both the soy meal and soy grits exceeded the hexane limit in food of 10 parts per million. A bigger question we might be asking ourselves is why there is a hexane limit in our foods in the first place??? Source
4. Conventional milk is made by high heating, homogenizing, pasteurizing, re-packing and combining the milk of hundreds of cows fed genetically modified grain and injected with hormones.
Old-time farmers will say they can tell where their cows have been grazing by the taste of the milk. By contrast, the milk we buy in supermarkets will be uniformly white. Its cream won’t rise. And a lactic perfume will be detectable only if the milk is ultra heated.
Cows are kept in herds of about 800 and fed not grass, but standardized mixes of genetically modified grains, old citrus, alfalfa and nut husks. Today, according to UC Davis estimates, about a third of the herds in California are treated with hormones to increase production. The milk will be standardized, fortified, pasteurized and homogenized. Translated, this means that it will be taken apart and put back together again, not always in the same proportions. Then it will be cooked and emulsified. At that point do you think it’s still milk? Source
5. Producers of maraschino cherries chemically bleach (through a preserved brine solution) and then marinate the cherries in huge vats of corn syrup and food coloring (FD&C Red 40) to make the cherries red again. Source1 Source2

  1. Many canned soups are flavored with MSG, even when they specify they are NOT.

The food additive “MSG” is a slow poison which hides behind dozens of names, such as natural flavouring and yeast extract. Currently, labeling standards do not require MSG to be listed in the ingredient list of thousands of foods.
Secretly, soup manufacturers admit that they have refered to MSG as “natural” (that is refined from vegetable protein and yeast) and establish it in the list of ingredients as ” yeast extract “or” hydrolyzed protein. “War of ads broke in 2008 because Campbell and Progresso were so worried that customers would not buy soup if they knew the amount of MSG containing. Source
7. Processed canned soups go through such violent processing that manufacturers must grow mutant sized vegetables so they don’t disintegrate in the soup.
The food you make at home isn’t reheated while being violently shaken. In order to destroy any pathogens, FDA requirements dictate that soup, once canned, be heated to 250 degrees; many manufacturers speed that process by agitating the can, thereby ensuring that the heat distributes itself more rapidly. This requirement changes the flavor of soup also changes the way the soup itself is actually made.
Soup companies shy away from ingredients that break down in the canning process so they grow special freakish mutant vegetables like carrots which look like tree limbs–they’re like baseball bats. But once they go through the cooking process, they come out looking like the small young ones that you’d put into your soup. Source
8. Most ice creams are thickened and stabilized with a slew of toxic ingredients.
These include a variety of emulsifiers which prevent the ice cream from destabilizing. They include polysorbate 80, potassium sorbate, sodium benzoate, carrageenan, xanthan gum, guar gum and soy lecithin. If your store brand or parlor ice cream melts rapidly, that’s a good sign as it likely has a low overrun and little fat destabilization, which means a lower percentage of toxic emulsifiers and stabilizers. Source
9. Hot dogs are filled with a sticky mixture of cuts of mechanically separated chicken, pork, fats and starch or “grain fillers.” The red or light brown dog varieties usually on sale everywhere contain very little real meat. Instead, they are made up of 64 percent mechanically-recovered chicken and 17 percent is pork. Mechanically-recovered meat is the slimy paste created when a carcass — stripped of all traditional cuts — is forced through a metal sieve or blasted with water. The process is banned for beef, but is permitted for pigs and poultry, and the meat produced is ten times cheaper than normal meat.
Most hot dogs typically contain, high fructose corn syrup, starch, milk protein, sodium nitrite, flavors, potassium and sodium triphosphates, polyphosphates (E452), sodium ascorbate and carmine. Source

Life Force Energy