The Psychological Effects Of Dietary Zinc Deficiency In Humans

All antidepressants work in a similar way, though there are various types of antidepressants—often called “families”—that each work a bit differently. They all, however, increase the brain’s concentration of various neurotransmitters. Antidepressants are psychiatric medications given to patients with depressive disorders to alleviate symptoms. They correct chemical imbalances of neurotransmitters in the brain which probably cause changes in mood and behavior. Antidepressants may be used for a wide range of psychiatric conditions, including social anxiety disorder, anxiety disorders. Antidepressants were initially developed in the 1950s. Their use has become progressively more common over the last twenty years. Generally speaking, anti­psychotic

Zinc: My intake value of zinc was 5.59 mg, while the DRI value 8.00 mg. This result should be concerned because Zinc acts as cofactors to protect from oxidative damage (Hammond, 2016f). Also, the symptoms of lacking Zinc includes diarrhea, slow wound healing, damaged digestive system and so on (Hammond, 2016h). Therefore, it is important to maintain a normal intake level of Zinc.

Zinc is needed because it helps produce insulin and enzymes. The dose needed is 11-12 milligrams. Food sources in which zinc can be found are red meats, poultry, beans, nuts, whole grains, fortified cereals, oysters and dairy products.

Drugs that are depressants include Zyprexa, Seroquel and Haldol, are known as major tranquilizers or antipsychotics, they reduce the symptoms of mental illness. Some other depressants, such as Amytal, Numbutal and Seconal, are classed as barbiturate, which are used as sedatives and sleeping pills. Depressants have the effect of feelings of well-being, lowered inhibition, slowed thinking, slowed muscular activity,a distorted view of the world, or hallucinations Depressants act on the brain by affecting the neurotransmitter GABA. By increasing GABA and inhibit brain activity,they produce a drowsy or calming effect beneficial to those suffering from anxiety or sleep

When antidepressant medication is advertised, benefits and negative side effects are provided, but what is not informed to the consumer is how it actually works. The truth behind antidepressant pills is that they don’t kick in right away and may take four to six weeks before they reach their full therapeutic effect. Many also find that it takes several trials before finding the one that works (Smith). This process can be long, strenuous, and costly. Additionally, a large portion of those who try pills in the end find that they are treatment-resistant to the medication, meaning all their efforts were a waste. There exists another form of resistance as well considered “depressive breakthrough” which is defined as the return of depressive symptoms

The body of an adult human contains almost 2-3 g of zinc. However, only 0,1% of it is found in the serum. As for other transition metals, circulating zinc is not free, but is complexed to proteins that maintain it in a non-reactive form in order to prevent their toxicity: almost 80% is bound to albumin and the remaining 20% is bound to α2-macroglobulin (Kambe et al., 2015). As zinc is required for many functions in living organisms, its transport across biological membranes is mediated by several proteins that can be classified in two major families of transporters: the SLC39 (Zrt-Irt-related Proteins, ZIPs) family, with 13 members identified, and the SLC30 (Zn-transporters, ZnTs) family, with 10 members (Fukada et al., 2011; Kambe et al.,

Selective Serotonin Reuptake Inhibitors (SSRIs) are currently one of the most controversial groups of medicines, with fluoxetine, more commonly known by its brand name Prozac, at the head of the controversy. Opponents of the use of SSRI medications as a successful and safe method for treating depression and related disorders assert that the actions of the drug are an unnatural and a dangerous form of tampering with our neurochemistry. Not only are these medications incredibly safe in almost all cases, they are actually an unnatural method of modifying an already disordered, natural sequence of chemicals in the brain, and therefore are not a form of tampering, but are a method for fixing

The linkage of serotonin to depression has been known for the past five years. From numerous studies, the most concrete evidence of this connection is the decreased concentration of serotonin metabolites like 5-HIAA (5-hydroxyindole acetic acid) in the cerebrospinal fluid and brain tissues of depressed people. If depression, as suggested, is a result of decreased levels of serotonin in the brain, pharmaceutical agents that can reverse this effect should be helpful in treating depressed patients. Therefore, the primary targets of various antidepressant medications are serotonin transports of the brain. Since serotonin is activated when released by neurons into the synapse, antidepressants function at the synapse to enhance serotonin activity. Normally, serotonin's actions in the synapse are terminated by its being taken back into the neuron then releases it at which point "it is either recycled for reuse as a transmitter or broken down into its metabolic by products and transported out of the brain." As a result, antidepressants work to increase serotonin levels at the synapse by blocking serotonin reuptake (2).

(3) While successful drug therapies which act on neurotransmitters in the brain imply that depression is a neurobiological condition (4), the fact that such medications do not help about 20 percent of depression-sufferers seems to show that not all depression is due to such imbalances. Rather, depression is not caused by one single factor; it is most often caused by many different things. Genetics, biochemical factors, medicines and alcohol, developmental and other external factors, and relationships, marriage and children all have effect on the development of clinical depression. (5) The strongest hypotheses on the pathways to depression are in decreases in the activity of specific neurotransmitters, or the overactivity of certain hormonal systems. (3)

The association between folate deficiency and depression has been reported by countless studies dating back to the mid-20th century. In 1962, Herbert V first reported the cognitive symptoms related to inadequate folate intake.32 By placing himself on a folate free diet for 4.5 months he experienced irritability, insomnia and forgetfulness, the cardinal symptoms of depression.32 He goes on to note that all his ailments disappeared within 2 days of starting folate supplementation. 32 Subsequently, in 1970, Reynolds et al. report subnormal serum folate (less than 2.5ng/ml) and vitamin B12 (less than 150pg/ml) levels in 101 patients with depressive illness.33 Folate deficiency was nearly twice as common as vitamin B12 among depressed

Kovich, H., & Delong, A. (2015, July 15). Common questions about the pharmacologic management of depression in adults.American Family Physician, 92(2), 94-100. Retrieved on 13th April 2017 from from http://www.aafp.org/afp/2015/0715/p94.html

Depression is a serious and potentially deadly illness that is one of America 's leading causes of disability. While it requires treatment, many patients have found that they are incompatible with mainstream treatment protocols, and reports of serious side-effects from selective serotonin re-uptake inhibitors (SSRIs) like Zoloft and Prozac are exceedingly common. I have personally tried literally every SSRI on the market--as well as a slew of other antidepressants-- and they have all, unanimously, worsened my depression. After spending my entire childhood, adolescence, and early adult hood undergoing seventeen painstaking years of conventional treatment, I arrived at the conclusion that the natural, do-it-yourself route is more beneficial

After 15 days of daily reserpine injection a significant decrease in the motor activity was recorded as assessed by the open field test (OFT). Together with the hunch back appearance that was observed after 15 days, these behavioral changes indicate the development of rat model of depression which was maintained by daily i.p. injection for another 15 days.

Moreover it suggests that both tricyclic and SSRI antidepressant drugs may be useful in the reversed of the behavioral changes induced by ZnD.

Nutritional deficiency of Zn in humans is associated with major disease conditions like growth retardation, cell-mediated immune dysfunction, cognitive impairment and increased susceptibility to infection. Zn modulates various aspects of the immune system. Many in vivo studies have shown the impact of Zn deficiency and supplementation on the normal development and key functions of immune cells. Dietary Zn deficiency is known to influence the onset of autoimmune diseases and also prolongs disease severity 35. A study showed that Zn suppresses Th17 mediated rheumatoid arthritis by inhibiting Th17 cell development 36. Furthermore, Zn supplementation therapy partially restores these immune deficiencies. Higher Zn intake is associated with improved resistance to infection and reduced duration of illness and improvements in specific lymphocyte subpopulation numbers for example T regs, Th1 and Th2 cells 37. In this study we show that zinc supplementation induced a tolerogenic phenotype in DCs both in vitro and in vivo and promoted the development of regulatory T cells and affected the Treg-Th17 balance favourably to induce tolerance.