For years, it has been known that multivitamins can induce anxiety. Anxiogenesis connected to multivitamins have been reported in laboratory rats after the administration of a drug that has a dose higher than 20mg/kg (Godinho et al., 2002). It is likely that anxiogensis related to multivitamins may be because of antagonism of adenosine receptors in rats. Studies have explored how certain ingredients in multivitamins could affect the rats’ aggression and anxiety. While anxious rat will significantly startle in response to noise, aggressive rats depict defensive response such as chasing, bite attacks and boxing.
Studies have used rats to assess the impact of vitamins on anxiety. Dopheide and Morgan (2008) examine rats in an open filed to determine their degree of anxiety. The result of the study demonstrates no significant change in anxiety level after chronic administration of vitamin A. de Oliveira and Young (2010) believe that pharmacological administration of vitamin A can trigger anxiety-like behaviors in rats. According to Oliveira and Young, (2010) administration of Vitamin A in rats depicts high anxiety which is portrayed by the refusal of rats entering the light compartment in the light-dark task. Hughes et al (2011) have demonstrated the rats to have a low level of anxiety exhibited through the open field task and acoustic startled when administering a combination of C vitamin and water. Besides, Kolosoca et al (2006) have demonstrated that causes high anxiety in Wistar rats but not impacting the degree of anxiety in OXYS rats. Studies have also examined the impact of minerals on rats’ anxiety. Godinho et al (2002) found no significant level of anxiety change in rats that were maintained for three days in water containing 1% calcium gluconate. Cope et al (2011) have depicted that deficiency of zinc decrease anxiety-like traits which were demonstrated by a reduce time in the open arms of the increased plus maze.
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Studies have also explored the impact of a multivitamin on aggression in rats. Trent et al. (2009) administered vitamin A to rats with the aim of minimizing aggression like behavior such as bite attach in the context of resident-intruder. The result of the study depicted a significant decrease in aggression level among those in the treatment group after two weeks of treatment and the aggression was lower than the control. Trent et al. (2009) concluded that the deficiency of prenatal zinc can trigger aggression in rats. Possibly, the supplementing the diet with zinc decreased aggression level. After long duration ingestion of copper salt, Bataineh et al (1998) discovered that male rats showed a reduced level of aggression portrayed by low aggressive activities such as fighting. These findings demonstrate the beneficial role of multivitamins in reducing aggression.
The development of brain pathways is lifelong from conception through adulthood, linking developmental events to the cognitive and behavioural changes later in life. The neural regulation of food intake and energy balance is controlled not only by a central processor (i.e., hypothalamus) but also by a more complex neural network that includes corticolimbic structures such as the hippocampus ( Andersen, 2003). Therefore, it is important to understand how the brain develops to identify the critical windows during which the brain is highly sensitive to environmental insults. The onset of development of brain pathways is time sensitive. In the majority of species, most of the pathways that control food intake are developed in utero. In rats, the most vulnerable time for the central nervous system formation is between GD 11-13, equivalent to GD 20-55 in humans. The hypothalamic neuropeptide structures are the best characterized in rodents. The hypothalamus in rats develops from GD 12-19 and continues to develop during the first two weeks after birth ( Andersen, 2003) . For instance, neuropeptide Y (NPY) mRNA expression in the arcuate nucleus (ARC) and dorsolateral hypothalamic area increases from birth, peaks at postnatal days (PND) 15-16 and starts declining to adult levels by PND 30. NPY neurons fully develop by postnatal week 3. On the other hand, pro-opiomelanocortin (POMC) neurons in the ARC are detected earlier at GD 12, but do not reach maturity until weaning.
The mesolimbic dopaminergic system, which involves emotion-based behaviour including reward, starts developing after GD 12 in rats. This system arises from dopaminergic cells in the ventral tegmental area (VTA) that develops from GD 13-16. The cells in the VTA innervate mainly to the nucleus accumbens (NAc, formed GD 12-22), olfactory tubercle (formed GD 12-19) but also projects to the septum (formed GD 13-17), amygdala (formed GD 12-19) and the hippocampus ( Andersen, 2003) . The hippocampus is one of the first regions of the brain to integrate with other brain areas during development. In rats, it develops from GD 15 until GD 20. Most of hippocampal dopamine neurons are derived between GD 11 and GD 14. However, some dopaminergic genes expressed by these neurons only at fetal brain development are absent in the adult brain. This transient expression of dopaminergic genes during early postnatal life and before adolescence shows that the adult’s brain neurotransmitter system remains plastic.
Experimental studies in rats have shown that a high multivitamin intake during pregnancy programs the male offspring for the development of components of the metabolic syndrome: impaired glucose regulation, increased food intake and body weight, and insulin resistance Methyl vitamins, especially folate, have been shown to be involved in mediating these changes. Although mechanisms underlying these metabolic outcomes remain poorly understood, these studies have identified a worrisome phenotype. The hippocampus, a brain structure involved in learning and memory function, has recently been linked with food intake control. For instance, hippocampal lesions in rats enhanced their response to sucrose reward. In humans, a strong hippocampal response to food rewards was detected using functional magnetic resonance imaging. KDP and RARs are expressed in the hippocampus. Gas6, a VKDP, has been associated to cell signalling actions, e.g., cell growth and myelination ( Andersen, 2003) . RARs have been widely identified in the hippocampus. Vitamin A signalling participates in the regulation of hippocampal functions including learning and memory. Therefore, due to RARs pleiotropic effects, it may be hypothesized that vitamin A could possibly affect less recognised hippocampal functions including food intake regulation. Different brain regions and mediators play an important role in the formation of feeding pathways. Homeostatic and non-homeostatic systems are regulated by physiological and molecular mechanisms.
In conclusion, animal models are often used to predict human response to drugs and other chemicals. An understanding of the underlying mechanisms of actions of multivitamins by using an animal model of high translational relevance is essential to explaining the effect of a multivitamin on anxiety. Clearly, minerals and vitamins have various impact on anxiety with some having increased anxiety while other having decreased anxiety levels. There is need to consider the benefits of using multivitamins in treating aggression. As with the assessment of anxiety, the changes related to multivitamins can only be connected to the supplement as whole rather than any of the individual ingredients.
References
Cope, E. C., Morris, D. R., Scrimgeour, A. G., Van Landingham, J. W., & Levenson, C. W. (2011). Zinc supplementation provides behavioral resiliency in a rat model of traumatic brain injury. Physiology and Behavior, 104, 942-947.
Dopheide, M. M., & Morgan, R. E. (2008). Isotretinoin (13- cis -retinoic-acid) alters learning and memory, but not anxiety-like behavior, in the adult rat. Pharmacology, Biochemistry, and Behavior, 91, 243-251.
Godinho, A. F., Trombini, T. V., & Oliveira, E. C. (2002). Effects of elevated calcium on the motor and exploratory activities of rats. Brazilian Journal of Medical and Biological Research, 35, 451-457.
Hughes, R. N., Lowther, C. L., & van Nobelen, M. (2011). Prolonged treatment with vitamins C and E separately and together decrease anxiety-related open-field behavior and acoustic startle in hooded rats. Pharmacology, Biochemistry, and Behavior, 97, 494-499.
Kolosova, N. G., Trofimova, N. A., & Fursova, A. Zh. (2006). Opposite effects of antioxidants on anxiety in Wistar and OXYS rats. Bulletin of Experimental Biology and Medicine, 141 (6), 734-737.
Olivier, B., & Young, L. J. (2002). Animal models of aggression. In K. L. Davis, D. Charney, J. T. Coyle, & C. Nemeroff (Eds.), Neuropsychopharmacology: the fifth generation of progress (5th ed., pp. 1699-1708). TN, USA: American College of Neuropsychopharmacology.
Trent, S., Drew, C. J. G., Mitchell, P. J., & Bailey, S. J. (2009). Chronic treatment with 13- cis -retinoic acid changes aggressive behaviors in the resident-intruder paradigm in rats. European Neuropsychopharmacology, 19, 876-886.
