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The NFL offseason has seen a flurry of free agents switch new teams and a NFL Draft loaded with drama and it's time to look ahead to the historical 17 games season. We can look at all the home and away opponents every one of the 32 teams will face next season thanks to the NFL scheduling formula. The additional game won't alter the current scheduling formula though, as each team will play four games against a first-place team fromfour games against the second-place team, four games against the third-place team and four games against the fourth-place team -- keeping the schedule as balanced as possible.
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For the last 4 decades, the question of how to manipulate the serotonergic system with drugs has been an important area of research in biological psychiatry, and this research has led to advances in the treatment of depression. Research on the association between various polymorphisms and depression supports the idea that serotonin plays a role, not only in the treatment of depression but also in susceptibility to depression and suicide.
The research focus here has been on polymorphisms of the serotonin transporter, but other serotonin-related genes may also be involved. Much less attention has been given to how this information will be used for the benefit of individuals with a serotonin-related susceptibility to depression, and little evidence exists concerning strategies to prevent depression in those with such a susceptibility.
Various studies have looked at early intervention in those with prodromal symptoms as well as at population strategies for preventing depression. Clearly, pharmacologic approaches are not appropriate, and given the evidence for serotonin's role in the etiology and treatment of depression, nonpharmacologic methods of increasing serotonin are potential candidates to test for their ability to prevent depression.
Another reason for pursuing nonpharmacologic methods of increasing serotonin arises from the increasing recognition that happiness and well-being are important, both as factors protecting against mental and physical disorders and in their own right. For example, the negative mood hostility is a risk factor for many disorders.
For the sake of brevity, hostility is discussed here mainly in relation to one of the biggest sources of mortality, coronary heart disease CHD. A meta-analysis of 45 studies demonstrated that hostility is a risk factor for CHD and for all-cause mortality.
Hostility is associated not only with the development of CHD but also with poorer survival in coronary artery disease CAD patients. For example, the opposite of hostility, agreeableness, was a ificant protective factor against mortality in a sample of older, frail participants. In a classic study, those in the lowest quartile for positive emotions, rated from autobiographies written at a mean age of 22 years, died on average 10 years earlier than those in the highest quartile.
Positive emotions protected against these outcomes. A recent review including meta-analyses assessed cross-sectional, longitudinal and experimental studies and concluded that happiness is associated with and precedes numerous successful outcomes. Research confirms what might be intuitively expected, that positive emotions and agreeableness foster congenial relationships with others.
Several studies found an association between measures related to serotonin and mood in the normal range. Lower platelet serotonin 2 receptor function was associated with lower mood in one study, 30 whereas better mood was associated with higher blood serotonin levels in another. In otherwise healthy individuals, a low prolactin response to the serotonin-releasing drug fenfluramine was associated with the metabolic syndrome, a risk factor for heart disease, 35 suggesting that low serotonin may predispose healthy individuals to suboptimal physical as well as mental functioning.
Nonpharmacologic methods of raising brain serotonin may not only improve mood and social functioning of healthy people — a worthwhile objective even without additional considerations — but would also make it possible to test the idea that increases in brain serotonin may help protect against the onset of various mental and physical disorders.
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Four strategies that are worth further investigation are discussed below. The article by Perreau-Linck and colleagues 36 of this issue provides an initial lead about one possible strategy for raising brain serotonin. Using positron emission tomography, they obtained a measure of serotonin synthesis in the brains of healthy participants who underwent positive, negative and neutral mood inductions. Reported levels of happiness were positively correlated and reported levels of sadness were negatively correlated with serotonin synthesis in the right anterior cingulate cortex.
The idea that alterations in thought, either self-induced or due to psychotherapy, can alter brain metabolism is not new.
Numerous studies have demonstrated changes in blood flow in such circumstances. However, reports related to specific transmitters are much less common. In one recent study, meditation was reported to increase release of dopamine. This raises the possibility that the interaction between serotonin synthesis and mood may be 2-way, with serotonin influencing mood and mood influencing serotonin.
Obviously, more work is needed to answer questions in this area. For example, is the improvement in mood associated with psychotherapy accompanied by increases in serotonin synthesis? If more precise information is obtained about the mental states that increase serotonin synthesis, will this help to enhance therapy techniques? Exposure to bright light is a second possible approach to increasing serotonin without drugs.
Bright light is, of course, a standard treatment for seasonal depression, but a few studies also suggest that it is an effective treatment for nonseasonal depression 38 and also reduces depressed mood in women with premenstrual dysphoric disorder 39 and in pregnant women suffering from depression. In human postmortem brain, serotonin levels are higher in those who died in summer than in those who died in winter.
In rats, serotonin is highest during the light part of the light—dark cycle, and this state is driven by the photic cycle rather than the circadian rhythm.
The mood-lowering effect of acute tryptophan depletion in healthy women is completely blocked by carrying out the study in bright light lux instead of dim light. Relatively few generations ago, most of the world population was involved in agriculture and was outdoors for much of the day. This would have resulted in high levels of bright light exposure even in winter.
Even on a cloudy day, the light outside can be greater than lux, a level never normally achieved indoors. In this group, summer bright light exposure was probably considerably less than the winter exposure of our agricultural ancestors. We may be living in a bright light—deprived society.
A large literature that is beyond the scope of this editorial exists on the beneficial effect of bright light exposure in healthy individuals. Lamps deed for the treatment of seasonal affective disorder, which provide more lux than is ever achieved by normal indoor lighting, are readily available, although incorporating their use into a daily routine may be a challenge for some.
However, other strategies, both personal and institutional, exist. Working indoors does not have to be associated with suboptimal exposure to bright light. A third strategy that may raise brain serotonin is exercise. A comprehensive review of the relation between exercise and mood concluded that antidepressant and anxiolytic effects have been clearly demonstrated. Exercise improves mood in subclinical populations as well as in patients. The most consistent effect is seen when regular exercisers undertake aerobic exercise at a level with which they are familiar.
Several lines of research suggest that exercise increases brain serotonin function in the human brain. Post and colleagues 56 measured biogenic amine metabolites in cerebrospinal fluid CSF of patients with depression before and after they increased their physical activity to simulate mania. Nonetheless, this finding stimulated many animal studies on the effects of exercise.
For example, Chaouloff and colleagues 57 showed that exercise increased tryptophan and 5-HIAA in rat ventricles. More recent studies using intracerebral dialysis have shown that exercise increases extracellular serotonin and 5-HIAA in various brain areas, including the hippocampus and cortex for example, see 58— Two different mechanisms may be involved in this effect.
As reviewed by Jacobs and Fornal, 61 motor activity increases the firing rates of serotonin neurons, and this in increased release and synthesis of serotonin. The largest body of work in humans looking at the effect of exercise on tryptophan availability to the brain is concerned with the hypothesis that fatigue during exercise is associated with elevated brain tryptophan and serotonin synthesis. A large body of evidence supports the idea that exercise, including exercise to fatigue, is associated with an increase in plasma tryptophan and a decrease in the plasma level of the branched chain amino acids BCAAs leucine, isoleucine and valine see 6465 for reviews.
The BCAAs inhibit tryptophan transport into the brain. Tryptophan is an effective mild hypnotic, 67 a fact that stimulated the hypothesis that it may be involved in fatigue.
A full discussion of this topic is not within the scope of this editorial; however, it is notable that several clinical trials of BCAA investigated whether it was possible to counter fatigue by lowering brain tryptophan, with that provided little support for the hypothesis. Further, exercise in an increase in the plasma ratio of tryptophan to the BCAAs before the onset of fatigue.
Whether motor activity increases the firing rate of serotonin neurons in humans, as in animals, is not known. However, it is clear that aerobic exercise can improve mood.
As with exposure to bright light, there has been a large change in the level of vigorous physical exercise experienced since humans were hunter-gatherers or engaged primarily in agriculture. The effect of exercise on serotonin suggests that the exercise itself, not the rewards that stem from exercise, may be important. If trials of exercise to prevent depression are successful, then prevention of depression can be added to the numerous other benefits of exercise.
The fourth factor that could play a role in raising brain serotonin is diet. According to some evidence, tryptophan, which increases brain serotonin in humans as in experimental animals, 69 is an effective antidepressant in mild-to-moderate depression. In the United States, it is classified as a dietary component, but Canada and some European countries classify it as a drug. Treating tryptophan as a drug is reasonable because, first, there is normally no situation in which purified tryptophan is needed for dietary reasons, and second, purified tryptophan and foods containing tryptophan have different effects on brain serotonin.
Although purified tryptophan increases brain serotonin, foods containing tryptophan do not. There is competition between the various amino acids for the transport system, so after the ingestion of a meal containing protein, the rise in the plasma level of the other large neutral amino acids will prevent the rise in plasma tryptophan from increasing brain tryptophan. The idea, common in popular culture, that a high-protein food such as turkey will raise brain tryptophan and serotonin is, unfortunately, false.
Another popular myth that is widespread on the Internet is that bananas improve mood because of their serotonin content. Although it is true that bananas contain serotonin, it does not cross the blood—brain barrier.
However, increasing the tryptophan content of the diet relative to that of the other amino acids is something that possibly occurred in the past and could occur again in the future. Kerem and colleagues 74 studied the tryptophan content of both wild chickpeas and the domesticated chickpeas that were bred from them in the Near East in neolithic times.
The mean protein content per mg dry seed was similar for 73 cultivars and 15 wild varieties. In the cultivated group, however, the tryptophan content was almost twice that of the wild seeds.
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Interestingly, the greater part of the increase was due to an increase in the free tryptophan content i. In cultivated chickpeas, almost two-thirds of the tryptophan was in the free form. Kerem and colleagues 74 argue that there was probably selection for seeds with a higher tryptophan content. This is plausible, given another example of an early strategy to increase the available tryptophan content of an important food source. Pellagra is a disorder caused by niacin deficiency, usually owing to poverty and a diet relying heavily on corn maizewhich has a low level of niacin and its precursor tryptophan.
Cultures in the Americas that relied greatly on corn used alkali during its processing e. This enhanced the nutritional quality of the corn by increasing the bioavailability of both niacin and tryptophan, a practice that prevented pellagra.
Breeding corn with a higher tryptophan content was shown in the s to prevent pellagra 76 ; presumably, it also raised brain serotonin. In a recent issue of Nature BiotechnologyMorris and Sands 77 argue that plant breeders should be focusing more on nutrition than on yield. Nonetheless, the possibility that the mental health of a population could be improved by increasing the dietary intake of tryptophan relative to the dietary intake of other amino acids remains an interesting idea that should be explored.
The primary purpose of this editorial is to point out that pharmacologic strategies are not the only ones worthy of study when devising strategies to increase brain serotonin function. The effect of nonpharmacologic interventions on brain serotonin and the implications of increased serotonin for mood and behaviour need to be studied more.
How to increase serotonin in the human brain without drugs
The amount of money and effort put into research on drugs that alter serotonin is very much greater than that put into non-pharmacologic methods. The magnitude of the discrepancy is probably neither in tune with the wishes of the public nor optimal for progress in the prevention and treatment of mental disorders. Competing interests: None declared.