Tryptophan, serotonin, mood, diet, and depression-Amer Journ Clin Nutrition
 

Back in 1975 RJ Wurtman, an expert on diet and serotonin levels explained that our diets can affect our mood and depression by raising tryptophan (an amino acid) levels. It was found decades earlier that in autopsies of suicide victims showed markedly low levels of serotonin. Thus all the Serotonin Reuptake Inhibitors on the market (Prozac, Celexa, Trazodone, Paxil, etc.) for treating depression. In this article protein is said to interfere with tryptophan levels. Pure carbohydrate is said to increase tryptophan levels.

Dr. Eades in PPLP used this to show that people become chemically addicted to the mood altering affects of carbohydrates, a conclusion that Wurtman himself came to in 1989 Jan. Scientific American , "Carbohydrates and Depression".

However, others have used this to show that low-carbing is bad for you because you get low levels of serotonin and depression. However, you can supplement with Tryptophan (an amino acid). Plus on another thread I show another AJCN article showing that Whey Protein can itself increase tryptophan levels. Add to this the fact that the other AJCN study shown in this post shows that obese people are more likely to be depressed, then I think we can fairly conclude that when we used to eat carbohydrates we weren't less depressed.

American Journal of Clinical Nutrition, Vol 28, 638-647,

REVIEW ARTICLES

Control of brain monoamine synthesis by diet and plasma amino acids
RJ Wurtman and JD Fernstrom


The rates at which monoaminergic neurons in rat brains synthesize their neurotransmitters depend on the availability of the amino acid precursors tryptophan (for serotonin) and tyrosine (for dopamine and norepinephrine). The administration of tryptophan, the injection of insulin, or the consumption of a single protein-free high-carbohydrate meal all elevate brain tryptophan levels and, soon thereafter, the levels of serotonin and its major metabolite 5-hydroxyindole acetic acid. The addition of protein to the meal suppresses the increases in brain tryptophan and serotonin, because protein contributes to plasma considerably larger amounts of the other neutral amino acids (e.g., leucine, phenylalanine) than of tryptophan, and these other amino acids compete with tryptophan for uptake into the brain. The elevation of brain tyrosine (by injection of the amino acid or consumption of a single 40% protein meal) accelerates brain catecholamine synthesis, as estimated by measuring brain dopa accumulation after decarboxylase inhibition, or brain catecholamine accumulation after inhibition of monoamine oxidase. These observations suggest that serotonin- and catecholamine-containing brain neurons are normally under specific dietary control.

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American Journal of Clinical Nutrition, Vol 44, 772-778,
ORIGINAL RESEARCH COMMUNICATIONS


Changes in mood after carbohydrate consumption among obese individuals
HR Lieberman, JJ Wurtman and B Chew


Two groups of obese individuals who consume excessive calories primarily as snack foods have been identified. Carbohydrate cravers consume most or all snacks as carbohydrate-rich foods despite the equal accessibility of protein-rich snacks. Noncarbohydrate cravers consume about equal amounts of protein- and carbohydrate-rich snack foods. Using standardized self-report questionnaires, we measured mood before and 2 h after consumption of a high-carbohydrate lunch (104 g CHO). Responses to the meal differed significantly: noncarbohydrate cravers reported feeling considerably less alert, more fatigued and sleepy, while carbohydrate cravers described little or no change in these aspects of mood. Moreover, noncarbohydrate cravers experienced an increase in depression, while carbohydrate cravers reported feeling less depressed. Findings suggest that snacking habits of obese individuals may be related to subsequent mood states.

American Journal of Clinical Nutrition, Vol 56, 863-867, 1992

ORIGINAL RESEARCH COMMUNICATIONS


Eating behavior and adherence to dietary prescriptions in obese adult subjects treated with 5-hydroxytryptophan

C Cangiano, F Ceci, A Cascino, M Del Ben, A Laviano, M Muscaritoli, F Antonucci and F Rossi-Fanelli
3rd Department of Internal Medicine, University of Rome, La Sapienza, Italy.

Previous observations have shown that oral administration of 5- hydroxytryptophan (5-HTP) without dietary prescriptions causes anorexia, decreased food intake, and weight loss in obese subjects. To confirm these data over a longer period of observation and to verify whether adherence to dietary restriction could be improved by 5-HTP, 20 obese patients were randomly assigned to receive either 5-HTP (900 mg/d) or a placebo. The study was double-blinded and was for two consecutive 6-wk periods. No diet was prescribed during the first period, a 5040-kJ/d diet was recommended for the second. Significant weight loss was observed in 5-HTP-treated patients during both periods. A reduction in carbohydrate intake and a consistent presence of early satiety were also found. These findings together with the good tolerance observed suggest that 5-HTP may be safely used to treat obesity.

Endocrine Reviews 20 (6): 805-875
Copyright © 1999 by The Endocrine Society

Current and Potential Drugs for Treatment of Obesity
George A. Bray and Frank L. Greenway

c. Amino acids. Administration of 5-hydroxy tryptophan to obese and diabetic subjects (152, 318) will decrease food intake probably by enhancing brain tryptophan, which is converted to serotonin, a neurotransmitter known to reduce food intake. Tryptophan is transported across the blood brain barrier by a transporter that also transports other large neutral amino acids. When these other amino acids are increased, tryptophan entry is reduced by competition for the transporter.

More on the Wurtman's
 

Thanks for posting the abstracts on 5-HTP. It may be that, since elevating serotonin levels helps correct obsessive behaviours that this is the reason for its effect on obese people. In other words, anorectics and bulimics are helped because it corrects their obsession with not eating food , and it helps obese people because it helps their obsession with eating food.

Also, the Wurtman's ideas about saturated fats causing depression by decreasing serotonin levels have never been demonstrated or proven. They are also at direct odds with research showing that depression can be helped with vitamin D, which is only found in animal fats which are highly saturated. Also, the healthy primitive peoples that Stefansson and Price studied decades ago were known for their cheery dispositions--on diets rich in animal fats.

Thanks Dr. Byrnes for a good explanation of why 5-HTP works for the obese and the anorexic.

I was thinking that Wurtman's comments about obese people having depression was the combination of fats and high-carbohydrate. (Otherwise they wouldn't be obese, would they?) Does Wurtman single out saturated fat?

The Wurtmans and SFAs
 

Its my understanding that they finger saturates for causing low serotonin as well as memory problems. At least this is how Deborah Kesten and Dean Ornish explained it in their horrible book "The Healing Secrets of Food."

Thanks for the info Dr. Byrnes. I'll have to do further research. In the meantime this abstract confirms your point about carbohydrates creating an addictive cycle.

Obes Res 1995 Nov;3 Suppl 4:477S-480S

Brain serotonin, carbohydrate-craving, obesity and depression.

Wurtman RJ, Wurtman JJ.

Department of Brain and Cognitive Sciences and Clinical Research Center, Massachusetts Institute of Technology, Cambridge 02139, USA.

Serotonin-releasing brain neurons are unique in that the amount of neurotransmitter they release is normally controlled by food intake: Carbohydrate consumption--acting via insulin secretion and the "plasma tryptophan ratio"--increases serotonin release; protein intake lacks this effect. This ability of neurons to couple neuronal signaling properties to food consumption is a link in the feedback mechanism that normally keeps carbohydrate and protein intakes more or less constant. However, serotonin release is also involved in such functions as sleep onset, pain sensitivity, blood pressure regulation, and control of the mood. Hence many patients learn to overeat carbohydrates (particularly snack foods, like potato chips or pastries, which are rich in carbohydrates and fats) to make themselves feel better. This tendency to use certain foods as though they were drugs is a frequent cause of weight gain, and can also be seen in patients who become fat when exposed to stress, or in women with premenstrual syndrome, or in patients with "winter depression," or in people who are attempting to give up smoking. (Nicotine, like dietary carbohydrates, increases brain serotonin secretion; nicotine withdrawal has the opposite effect.) It also occurs in patients with normal-weight bulimia. Dexfenfluramine constitutes a highly effective treatment for such patients. In addition to producing its general satiety-promoting effect, it specifically reduces their overconsumption of carbohydrate-rich (or carbohydrate-and fat-rich) foods.

Information on dosage and safety of 5-HTP:

For dosage information on 5-HTP:
http://www.thorne.com/altmedrev/.fulltext/3/4/271.html

"In addition, biochemical studies show 5-HTP is closely involved in depressive disorders.

"The first large clinical trial using 5-HTP in depression was conducted by Sano in 1972. Using an open trial design, a total of 107 patients with endogenous unipolar or bipolar depression were given daily oral dosages of 5-HTP from 50 to 300 mg . Significant improvement was observed in 74 of the patients (69%), and no significant side effects were reported. The response rate in most of these patients was quite rapid (less than two weeks).11

"The issue of speed of response was subsequently addressed in a study of 59 patients with eight different types of depression. 5-HTP was administered orally in dosages from 150 to 300 mg daily for a period of three weeks . Thirteen patients (22%) were markedly improved, and another 27 patients (45.8%) showed moderate improvement. Of these 40 patients who improved, 20 (50%) began to show improvement within three days , and 32 patients (80%) improved within two weeks of beginning treatment with 5-HTP. 15 In contrast to many conventional antidepressants which may take 4 weeks or longer to achieve therapeutic response in most patients, those taking 5-HTP appear to have a significantly more rapid response."

For safety, drug interaction and possible side-effects:

http://www.5-htp.net/Safety.asp

5-HTP is generally better tolerated than its SSRI counterparts, such as Prozac®. The following chart compares the rate of side effects between 5-HTP and SSRIs.