Production of gaba (γ - Aminobutyric acid) by microorganisms: a review.
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 X, Kim YB, Uddin MR, Lee S, Kim SJ, Park 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 S, Strommer B, Schöffmann A, Hintersteiner J, Baburin I, Erker T, Schwarz T, Schwarzer C, Zaugg J, Hamburger M, Hering 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 J, McIntyre E, Camfield DA.
Source
Department of Psychiatry, Faculty of Medicine, University of Melbourne, 2 Salisbury Street, Richmond, VIC, 3121, Australia. jsarris@unimelb.edu.au
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 CA, Cury TC, Cassettari BO, Takahira RK, Flório JC, Costa 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 K, Rose T, Fiebich B, Kammler T, Hoffmann C, Weiss 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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Toxicity of Sugar DataToxic sugar? Mouse data suggests added-sugar diet may impact lifespan and reproductionThe research shows that when mice consumed a diet containing 25% extra sugar - an amount considered safe and relevant inhuman 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[F1]. Writing in Nature Communications, the research team describe the findingsfrom an animal model 'toxicity test' developed at the University of Utah, USA - which gave the mice the equivalent level ofsugar gained by humans from the consumption of three cans of soda. Our results provide evidence that added sugarconsumed at concentrations currently considered safe exerts dramatic adverse impacts on mammalian health, saidthe study authors - led by seniour author Professor Wayne Potts. This demonstrates the adverse effects of added sugarsat human-relevant levels, explained Potts, who noted that previous studies using other tests fed mice large doses of sugardisproportionate 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 harmfulto 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 fedthe 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 theresearch, Catherine Collins, principal dietitian at St George’s Hospital NHS Trust, UK, noted that while the researchers state that thisdiet mimicked the high sugar diet (25% added sugar) commonly taken by some people in the US, a recent UK survey indicated an averagesugar 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 researchin animals which cannot be translated into humans. The scientific evidence on sugar has been reviewed on numerous occasions byindependent expert committees including the World Health Organization and European Food Safety Authority. They have concludedthat moderate levels of sugar consumption are not implicated in any of the major lifestyle diseases, she commented. Like all sources ofcalories, sugar can be consumed within a healthy, calorie-balanced diet and active lifestyle. Study details The Utah study placed groupsof mice in room-sized pens nicknamed 'mouse barns' with multiple nest boxes – something the researchers suggest is a much more realisticenvironment 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 howinbreeding 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 sweetenedsoda in a day plus a perfectly healthy, no-sugar-added diet, said Potts. He explained that the mice used in the trial, descended fromwild 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 with156 'founders' that were weaned at four weeks, and then assigned either to the added-sugar diet or the control diet - with half the males andhalf the females on each diet. Mice remained in cages with siblings of the same sex (to prevent reproduction) for 26 weeks while they werefed 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 receivedthe same added-sugar diet while in the mouse barns, so the study only tested for differences caused by the mice eating different for theprevious 26 weeks, said Potts. The team revealed their key findings After 32 weeks in mouse barns, 35% of the females fed extrasugar died. This was twice the 17% death rate for female control mice. There was no difference in the 55% death among maleswho did and did not get added sugar. Males on the added-sugar diet acquired and held 26% fewer territories than males onthe control diet: control males occupied 47% of the territories while sugar-added mice controlled less than 36%[F2].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 theburden of pregnancy – but then had lower reproductive rates as the study progressed, partly because they had higher death rates linkedto sugar-Human-relevant levels of added sugar consumption increase female mortality and lower male fitness in micethings added to it like soy or canola which can also cause issue---when combining these things you wind up with less energy not more sincethe organs that are affected here are the pancreas-thyroid-heart-liver –brain which gets taxed and pushed and begins to wear out long beforeit 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 andwomen 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 theconsumer to know what to eat and what to avoid!!
[F1]Another Form of Sterilization—when food combining—this is a form of biochemistry that is not being understood or not revealed that when mixing foods or carcinogenic foods there impact can be felt thousands of times more then when consumed alone and when adding pollutants with these poisons then the impacts become more deadly leading to a quicker death pr a painful one
[F2]Less ambitious—not as driven-and less interested in life
