One such brain messenger is serotonin, which is known to affect mood, promoting a relaxed feeling that Julia Ross, MD, perhaps best describes as "lightness" to support deep sleep and melatonin production, and to affect appetite, especially for carbohydrates.
The amino acid "building block" to serotonin is tryptophan. It is important to appreciate that the ratio of tryptophan to large neutral amino acids (LNNA) determines tryptophan availability to the brain. These LNNA are tyrosine, phenyalanine, and the branched-chain amino acids (BCAAs), namely leucine, isoleucine and valine, all of which compete with tryptophan to cross the protective blood-brain barrier to enter the brain.1
Furthermore, it is important to be aware that insulin, which is released as the result of ingesting carbohydrate, is, as any serious body builder knows, anabolic, meaning growth-promoting. Insulin facilitates the removal of protein, specifically the aromatic and branched-chain amino acids, from the bloodstream, to be largely directed to muscle tissue. This function of insulin helps remove these competitors to tryptophan's crossing the blood-brain barrier.
A recent paper in the American Journal of Clinical Nutrition2 reported that both the plasma tryptophan concentrations and ratios of tryptophan to LNNA were low at all times during and after successful weight-loss programs that maintained lean body mass. The authors also noted that the obese participants were often insulin-resistant. Such diminished insulin activity may be an aggravating factor in continued low plasma ratios of LNNA to tryptophan levels. Plasma concentrations of tryptophan, as such, were also reported to be low in dieting patients before, during and after successful weight loss. According to the authors, Breum et al., these two observations and their potential concomitant effects on mood and appetite may be part of the reasons for relapse after diet-induced weight loss!
These data strongly support the notion that obese persons may do well by supplementing with tryptophan. As both low levels of tryptophan and its availability to the brain vis-?-vis tryptophan/LNAA ratios tend to lead to below-optimal serotonin levels, which is subsequently conductive to carbohydrate cravings, poor sleep, low self-esteem and mood, and impulsive behavior. Such a notion is not without logical argument.
Unfortunately, the FDA continues what many convincingly argue is its unjustified prohibition of tryptophan as a dietary supplement. Perhaps not unrelated is the soaring prescription of selective serotonin reuptake inhibitors (SSRIs), perhaps the most familiar being Prozac. Perhaps the lack of "natural" competition from tryptophan is part of this multibillion-dollar-per-year "success" story!
An alternative, and perhaps even superior, approach may be to utilize high-quality whey protein blends. Such whey protein blends have an unusually rich supply of tryptophan and a higher ratio of tryptophan to BCAAs compared to other proteins, such as soy or casein. The ingestion of as little of 10 grams of carbohydrate at any one time initiates the release of insulin, with its potential salubrious effect on tryptophan uptake by the brain and its neurophysiology.
As whey protein also affords high levels of complete, biologically available and complete amino acids, with minimal additional calories from carbohydrate and fat, it may be in itself one of the more ideal food choices to include in weight-loss and lean-body-mass maintenance nutrition strategies. Based on the above understandings, it may be best to ingest whey protein without competition from other protein sources, and to not slow down the assimilation of the amino acids with simultaneous ingestion of large amounts of fiber or fat, if our desire is to generate a more immediate effect on mood, sleep, behavior and appetite.
References
- 3Pearson D, Shaw S, Fat and happy? Tryptophan concentrations reduced in obesity. Life Extension News, February 2004;7(1).
- Breum L, Rasmussen MH, Hilstead J, et al. Twenty-four-plasma tryptophan concentrations and ratios are below normal in obese subjects and are not normalized by substantial weight reduction. Am J Clin Nutr May 2003;77:1112-8
John Maher, DC, ABAAHP
Del Mar, California
www.greensfirst.com
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