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"Two neurotransmitters, gamma-amino butyric acid (GABA) and dopamine are responsible for the loss of impulse control in those who consume alcohol. Dopamine causes an excitatory response at dopamine receptors in the frontal lobes). Alcohol increases the amount of dopamine acting on receptors and enhances the normal feeling of pleasure associated with the dopamine system. Alcohol may function like cigarette smoke to inhibit the action of enzyme monoamine oxidase, the enzyme responsible for breaking down dopamine in the synaptic cleft. Since dopamine is not broken down as efficiently when ethanol is present, it can act on the post-synaptic neuron for a longer period of time. The feeling of pleasure will be increased and the individual will want to keep drinking to maintain the sensation. Individuals want to continue to experience the feelings caused by dopamine, so they continue to consume alcohol. The response of ordering another drink when one is already visibly intoxicated can be explained by the pleasurable effect that an increased alcohol concentration has on the brain."

Elizabeth Powell, "Alcohol and Impulse Control." Serendip (April 14, 2004).

"Alcohol may be particularly damaging to key components of the 'brain reward system.' Alcohol sensitizes dopamine and serotonin neurons to toxic excessive excitation or 'excitotoxicity.' "If dopamine and serotonin neurons are damaged," said Fulton T. Crews, Director of the Center for Alcohol Studies, University of North Carolina, "this would disrupt reward processes in ways that could contribute to addiction."

Ivan Diamond and Harriet de Wit, "Alcoholism: Clinical and Experimental Research." Research Society on Alcoholism (2011).

"Alcohol also helps to increase the release of dopamine, by a process that is still poorly understood but that appears to involve curtailing the activity of the enzyme that breaks dopamine down."

"How Drugs Affect Neurotransmitters." Canadian Inst. of Health Research


"These findings suggest that aspartame has a relatively potent effect of decreasing evoked extracellular dopamine levels when administered systemically under the conditions specified."

BP Bergstrom, DR Cummings and TA Skaggs, "Aspartame decreases evoked extracellular dopamine levels in the rat brain: an in vivo voltammetry study." Neuropharmacology. 2007 Dec;53(8):967-74. Epub 2007 Sep 29. PMID: 17976663

"If an aspartame-containing beverage is consumed along with, for example, a carbohydrate-rich, protein-poor dessert food, its effects on brain phenylalanine are doubled. This is because the insulin secretion elicited by the carbohydrate selectively lowers plasma levels of the branched-chain amino acids (by facilitating their uptake into skeletal muscle), without having much of an effect on plasma phenylalanine; this increases the effect of the aspartame on the plasma phenylalanine ratio. A similar doubling may occur if the eater happens to be one of the perhaps 10 million Americans who are, without knowing it, heterozygous for the phenylketonuria (PKU) gene. Once within brain, neurons producing certain neurotransmitters, such as dopaminergic nigrostriatal cells, the excess phenylalanine can inhibit enzymes (like tyrosine hydroxylase) needed to synthesize the neurotransmitters."

Timothy J. Maher and Richard J. Wurtman, "Possible Neurologic Effects of Aspartame - a Widely Used Food Additive." DORway to Discovery

Yokogoshi, H., Roberts, C. H., Caballero, B., and Wurtman, R.J. Effects of aspartame and glucose administration on brain and plasma levels of large neutral amino acids and brain 5-hydroxyindoles. Am. J. Clin. Nutr. 40: 1-7 (1984).

Maher T. J., Glaeser, B. S., and Wurtman, R. J. Diurnal variations in plasma concentrations of basic and neutral amino acids and in red cell concentrations of aspartate and glutamate: Effects of dietary protein. Am. J. Clin. Nutr. 39: 722-729 (1984).

Levy, H. L., and Waisbren, S. E. Effects of untreated maternal phenylketonuria and hyperphenylalanemia on the fetus. N. Engl. J. Med. 309:1269-1274 (1983).

"Physiologically it is impossible that aspartame can aid in weight loss! The ingestion of aspartame creates increased levels of phenylalanine that suppress the formation of dopamine and seratonin. Dopamine is a neurotransmitter that helps us to identify satiety, while seratonin reports carbohydrate metabolism. When seratonin levels are suppressed by excess phenylalanine these levels are incapable of normal increases that occur due to eating carbohydrates leaving you to crave more and more food! As well, methyl alcohol has also been long time recognized in medicine for its ability to block metabolism. In fact, according to Dr. H.J. Roberts, people getting off aspartame lose an average of 15 pounds. Plain and simple...neurotoxins act in the brain to stimulate appetite and you do not stand a fighting chance!"

Joshua Rubin "Aspartame: A Silent Killer." Self Improvement Association (April 23, 2011).


"Caffeine increases dopamine levels in your system, acting in a way similar to amphetamines, which can make you feel good after taking it, but after it wears off you can feel 'low'. It can also lead to a physical dependence because of dopamine manipulation."

Elizabeth Scott, M.S. "Caffeine, Stress and Your Health: Is Caffeine Your Friend or Your Foe?" Guide (Nov. 01, 2007)

"Using in vivo microdialysis in freely moving rats, we demonstrate that systemic administration of behaviorally relevant doses of caffeine can preferentially increase extracellular levels of dopamine and glutamate in the shell of the NAc. These effects could be reproduced by the administration of a selective adenosine A1 receptor antagonist but not by a selective adenosine A2A receptor antagonist. This suggests that caffeine, because of its ability to block adenosine A1 receptors, shares neurochemical properties with other psychostimulants, which could contribute to the widespread consumption of caffeine-containing beverages."

M. Solinas, S. Ferre, ZB You, M. Karcz-Kubicha, P. Popoli and SR Goldberg, "Caffeine induces dopamine and glutamate release in the shell of the nucleus accumbens." J Neurosci 2002 Aug 1;22(15):6321-4

"As well as providing an immediate 'feel-good' sensation, caffeine encourages long-term addiction by depriving the consumer of a good night's sleep. Because adenosine reception is essential to deep sleep and it is blocked by caffeine, consumers wake up feeling irritable, and use caffeine to mentally 'awaken' themselves so that they can function 'properly' - as though they had had a good night's sleep. In this way, a positive feedback loop is created, and consumers cannot abstain from caffeine consumption without adverse effects."

"Caffeine: How Caffeine Becomes Addictive." BBC: The Guide to Life, The Universe and Everything. (Sep. 25, 2001).


"A significant increase in major serotonin and dopamine metabolite concentrations in the brain has been reported after one year on a gluten-free diet."

C. Hallert and G. Sedvall, "Improvement in central monoamine metabolism in adult coeliac patient starting a gluten-free diet." Psychol Med. 1983 May;13(2):267-71. PMID: 6192458

"Gluten contains a neuropeptide which enhances dopamine activity."

FJ Mycroft, ET Wei, JE Bernardin and DD Kasarda, "MIF-like sequences in milk and wheat proteins.." N Engl J Med. 1982 Sep 30;307(14):895. PMID: 6125889

"Since such manipulations of serotonin are difficult to regulate, and unlikely to have long-lasting effects (although some of the mystery of obesity may be revealed in this dynamic) a much more important dietary factor in depression may be the morphine-like substances which derive from the incomplete digests of proteins in cereal grains and dairy products. These were first reported by Christine Zioudrou et al. who dubbed such peptides "exorphins". Further elucidation of this issue has been provided through the extensive work of Fukudome and Yoshikawa, published over the last decade who have identified and characterized five distinct exorphins in the pepsin digests of gluten. Eight distinct exorphins have also been identified in the pepsin digests of milk. This work has given us a clearer sense of the morphine-like psychoactive nature of the peptides which result from the incomplete digests of these dietary proteins, as well as offering a possible explanation for some of the reported psychiatric reactions to these proteins including the sense of "brain fog" that often accompanies immune reactions to these foods."

Ron Hoggan M.A.and James Braly M.D., "Food Allergies and Depression: How Modern Eating Habits May Contribute to Depression." Depression (December 08, 2003)

Zioudrou C, Streaty RA, Klee WA, Opioid peptides derived from food proteins. The exorphins. J Biol Chem. 1979 Apr 10;254(7): 2446-9.

Fukudome S, Shimatsu A, Suganuma H, Yoshikawa M Effect of gluten exorphins A5 and B5 on the postprandial plasma insulin level in conscious rats. Life Sci. 1995;57(7):729-34.

Fukudome S, Yoshikawa M Opioid peptides derived from wheat gluten: their isolation and characterization. FEBS Lett. 1992 Jan 13;296(1):107-11.

Mycroft FJ, et al. MIF-like sequences in milk and wheat proteins. N Engl. J Med. 1982 Sep 30;307(14):895.

Dohan FC. Genetic hypothesis of idiopathic schizophrenia: its exorphin connection. Schizophr Bull. 1988;14(4):489-94.

Saelid G, Haug JO, Heiberg T, Reichelt KL Peptide-containing fractions in depression. Biol. Psychiatry. 1985 Mar;20(3):245-56.

Hoggan, R. Absolutism's Hidden Message for Medical Scientism. Interchange. 1997; 28(2/3): 183-189.


"One night without sleep increases the chemical dopamine in the brain, which may help explain how how the sleep-deprived stay alert, U.S. researchers said. Compared to when well-rested, participants when sleep deprived showed reduced binding of a radiolabeled compound that binds to dopamine receptors in certain parts of the brains. The researchers concluded that sleep deprivation increases dopamine - in the striatum part of the brain - involved in motivation and reward - and in the thalamus - involved in alertness. Following sleep deprivation, the rise in dopamine, the researchers say, may promote wakefulness to compensate for sleep loss."

"Lack of sleep increases dopamine." United Press International (Aug. 22, 2011).

"First, the researchers treated the mice with a chemical that stops the production of dopamine entirely. In fairly short order, the mice had used up their initial supply of dopamine and were running on empty. The mice became rigid, immobile, and unable to sleep or dream, displaying symptoms similar to those experienced by patients with Parkinson's disease, the researchers said."

"Dopamine Imbalances Cause Sleep Disorders In Animal Models Of Parkinson's Disease And Schizophrenia." Medical News Today (Oct 13, 2006).

"Lack of sleep causes your body's dopamine levels to nose-dive. In an attempt to reproduce this hormone's feel-good effect, the neurons in your brain seek out a sugar fix. So you eat or drink or crave sex or nicotine - all dopamine releasers - and that helps satisfy your brain cells' craving for dopamine. But that fix lasts only so long, so you'll crave that sugary stuff again and again on the day after inadequate sleep. Too little sleep means your body also produces less rejuvenating human growth hormone (HGH), which likely affects your mood and energy level. So when you wake up each morning, all you want to do is go back to bed. And to top it all off, low levels of HGH also trigger sugar cravings, as well as a desire for salty foods. Of course, all of these side effects are also signs of depression."

Michael Roizen, M.D. "How Does Lack of Sleep Affect Your Health?" iVillage (March 9, 2011).

monosodium glutamate (msg)

"Adult rats which have received monosodium-L-glutamate (MSG) (4 mg/g body weight) on alternate days for the first ten days of life acquire neurotoxic lesions of the retina and arcuate nucleus and manifest an endocrine deficiency syndrome characterized by stunted growth, obesity, hypothyroidism, hypogonadism and pituitary atrophy. From these findings several conclusions were drawn: 1) The MSG-induced endocrine deficiency syndrome appears to result from the destruction of ARC-ME dopaminergic and cholinergic tuberoinfundibular systems within the hypothalamus; 2) a normal concentration of serotonergic and noradrenergic neurons within the hypothalamus does not insure normal central neuroendocrine regulation; 3) no more than 50% of the dopaminergic terminals in the ME arise from ARC perikarya; 4) cell bodies within the ARC contribute very few, if any, nerve terminals containing releasing factors to the ME; 5) MSG destroys the primary optic tracts while sparing the retino-hypothalamic projection; 6) LHRH, somatostatin and TRH are not contained within cholinergic nerve terminals in the ME."

Charles B. Nemeroff, Richard J. Konkol, Garth Bissette, William Youngblood, Joseph B. Martin, Paul Brazeau, Michael S. Rone, Arthur J. Prange, Jr., George R. Breese and John S. Kizer, "Analysis of the Disruption in Hypothalamic-Pituitary Regulation in Rats Treated Neonatally with Monosodium L-Glutamate (MSG): Evidence for the Involvement of Tuberoinfundibular Cholinergic and Dopaminergic Systems in Neuroendocrine Regulation." Endocrinology Vol. 101, No. 2 613-622, (1977).

"Histochemical examination of the hypothalamic arcuate area revealed a marked loss of dopaminergic perikarya in MSG V, but not MSG I animals; other catecholamine systems appeared intact. This raises the possibility that damage to the tubero-infundibular dopamine system may contribute to endocrinological and other deficits observed after neonatal MSG treatment."

Charles B. Nemeroffa, Lester D. Granta, Garth Bissettea, Gregory N. Ervina, Lindy E. Harrella and Arthur J. Prange Jr. "Growth, endocrinological and behavioral deficits after monosodium l-glutamate in the neonatal rat: possible involvement of arcuate dopamine neuron damage." Psychoneuroendocrinology Volume 2, Issue 2 (1977). Pages 179-196, Elsevier Ltd. doi:10.1016/0306-4530(77)90023-3

"Dopamine levels were significantly reduced (P < 0.01) in the arcuate nucleus of MSG-treated rats."

Louis V. DePaolo and Andres Negro-Vilar, "Neonatal Monosodium Glutamate Treatment Alters the Response of Median Eminence Luteinizing Hormone-Releasing Hormone Nerve Terminals to Potassium and Prostaglandin E2*." Endocrinology Vol. 110, No. 3 835-841 (1982).

"Wallace and Dawsons (1990) cited that, monosodium glutamate altered neurotranmitter content in discrete brain regions of adult male rats. several lines of evidence indicate that treatment with monosodium glutamate induced decreased in the brain levels of Dopamine, NE, E and 5-HT and the primary metabolites of these monoamines in some brain regions (Yoshida et al., 2004)."

Abeer M. Waggas, "Neuroprotective Evaluation of Extract of Ginger (Zingiber officinale) Root in Monosodium Glutamate-Induced Toxicity in Different Brain Areas Male Albino Rats." Pakistan Journal of Biological Sciences 12 (3): 201-212, 2011 ISSN 1028-8880


"The results indicate that weanling animals have a greater jejunal sodium absorption than older animals, probably because of higher noradrenergic tonus. A challenge with a high-salt diet results in a decrease of the intestinal sodium absorption in weaning rats but not in adult rats; endogenous dopamine appears to play an important role in this regulation."

Y. Finkel, AC Eklof, L. Granquist, P. Soares-da-Silva and AM Bertorello, "Endogenous dopamine modulates jejunal sodium absorption during high-salt diet in young but not in adult rats." Gastroenterology. 1994 Sep;107(3):675-9. PMID: 8076754

"These results suggest that sodium restriction leads to activation of antinatriuretic antidiuretic systems in HF patients. However, renal ability to synthesize dopamine is increased in this condition, probably as a counter-regulatory mechanism."

Margarida Alvelosa, Antonio Ferreiraa, Paulo Bettencourta, Paula Serraoc, Manuel Pestanad, Mario Cerqueira-Gomesa and Patricio Soares-da-Silvac,"The effect of dietary sodium restriction on neurohumoral activity and renal dopaminergic response in patients with heart failure." European Journal of Heart Failure Volume 6, Issue 5, Pp. 593-599. (November 19, 2003).

"These results suggest that salt-sensitive hypertension is modulated by dopaminergic activity, which in turn is attenuated in SS patients. Decreased dopaminergic activity induced sodium retention both by a direct effect on the kidney as well as indirectly via relatively increased aldosterone secretion. Both mechanisms would help to increase intravascular volume and blood pressure in salt-sensitive hypertension."

Reiko Shikuma, Anabu Yoshimura, Seichi Kambara, Hideaki Yamazaki, Ryosaku Takashina, Hakuo Takahashi, Kazuo Takeda and Hamao Ijichi, "Dopaminergic modulation of salt sensitivity in patients with essential hypertension." Life Sciences Volume 38, Issue 10, 10 March 1986, Pages 915-921 doi:10.1016/0024-3205(86)90259-6


"After a few days, the rats were "hooked" - wanting to drink more each day. Their brains created more dopamine receptors. After a month of this schedule, when the sugar was removed, or the dopamine was chemically blocked using a drug, anxiety increased, to the point that the rats' teeth audibly chattered -- a sign of withdrawal, Hoebel said. What was especially interesting was that rats got a dopamine high even if they didn't actually digest the sugar. One set of rats had drains placed in their stomachs that made all the fluid secrete out. Even in that group, the rats craved sugar."

Joy Victory, "Studying the 'Sweet Tooth': Rats Given High Sugar Diet Show Strong Urge to Have More and More." ABC News (May 25, 2006). BG Hoebel, P. Rada and NM Avena, "Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake". Neuroscience and Biobehavioral Review 32: 20-39. PMID 17617461 (2011).

"Recent behavioral tests in rats further back the idea of an overlap between sweets and drugs. Drug addiction often includes three steps. A person will increase his intake of the drug, experience withdrawal symptoms when access to the drug is cut off and then face an urge to relapse back into drug use. Rats on sugar have similar experiences. Researchers withheld food for 12 hours and then gave rats food plus sugar water. This created a cycle of binging where the animals increased their daily sugar intake until it doubled. When researchers either stopped the diet or administered an opioid blocker the rats showed signs common to drug withdrawal, such as teeth-chattering and the shakes. Early findings also indicate signs of relapse. Rats weaned off sugar repeatedly pressed a lever that previously dispensed the sweet solution."

Leah Ariniello, "Sugar Addiction" Brain Briefings, Society for Neuroscience (October 2003).

"We made a fake bee and let it fly over the blue and yellow flowers" with variable amounts of sugar, Dr. Montague said. Each time a virtual bee landed on a flower, its dopamine neuron was alerted. As in most animals, the dopamine neuron at rest fires signals at a steady, base-line rate. When it is excited, it fires more rapidly. When it is depressed, it ceases firing. The virtual bee's neuron was designed to give three simple responses. If the amount of sugar was more than expected (based on what the bee knows about similar looking flowers), the neuron would fire vigorously. Lots of dopamine meant lots of reward and instant learning. If the amount of sugar was less than predicted, the neuron would stop firing. Sudden lack of dopamine, going to other parts of the brain, told the bee to avoid what had just happened. If the amount of sugar was the same, as predicted, the neuron would not increase or decrease its activity. The bee learned nothing new. This simple prediction model -- the dopamine neuron "knows" what has just happened and is waiting to see if the next reward is greater or smaller or the same - offers one explanation for how the bee behavior might arise, Dr. Sejnowski said. When the dopamine neuron encounters an empty flower, it throws the bee brain into an unhappy state. The bee, in fact, cannot stand hitting so many empties. It would rather play it safe and get more numerous, smaller rewards - or no rewards at all - by sticking to the yellow flowers."

Sandra Blakeslee, "How Brain May Weigh the World With Simple Dopamine System." New York Times (March 19, 1996).

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