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MALNUTRITION

 The concept of m. it has been further investigated and re-examined in the context of an extensive meaning that includes all the functional, anatomical-pathological, weight, and auxological biochemical alterations induced by quantitatively and qualitatively incongruous food intakes or by morbid conditions that hinder the normal use of nutritional factors.

According to a very widespread (albeit schematic and moreover not univocally understood) etiological classification, forms of m are distinguished. primitive (either by default: undernutrition or undernutrition; or by excess: hyper nutrition or supernutrition ), directly connected to the quantity and quality of food intake, and forms of msecondary (which can also be by default or, more rarely, by excess), symptomatic of many morbid pictures (or in any case consequential to these).

The m. secondary can coexist with the primary one: for example, a subject already undernourished due to inadequate food intake can be affected by diseases that are in themselves the cause of malnutrition.

The existence of another possibility is sometimes taken into consideration, that of "m. due to imbalance", connected to a marked disharmony of distribution in the food ration, despite the fact that the overall energy intake (provided by carbohydrates, fats, proteins, possibly alcohol) is normal or even excessive. The unbalanced distribution of energy factors (e.g. adequate protein ration with excess fat and low carbohydrate intake) almost always implies a deficiency condition (absolute or more often relative, usually without apparent clinical manifestations), even when the conditions' general characteristics of the subject are apparently prosperous or even marked by obesity. In the latter case, there is, therefore, both an m. caloric excess, as much as an m. by default,

Understood in its broadest sense, the m. is responsible for multiple conditions of organic suffering, which can manifest themselves with overt symptoms (detectable with clinical, anthropometric, laboratory, and possibly radiological findings) or which, much more often, run asymptomatically for a long time ( occult or subclinical disease ), however, impairing the psychophysical efficiency or increasing the morbidity towards certain pathologies, especially degenerative ones.

Examined in its various aspects, the problem of m. primitive transcends its clinical (and moral) implications to also have an extreme economic interest, above all in consideration of the negative repercussions on working capacity, morbidity, and mortality, and therefore on the social costs of these phenomena.

Malnutrition by default

- With the exception of those simple foods which, within certain limits, can be interchanged with others (e.g., for energy purposes, fats can be replaced, within certain limits, with isocaloric quantities of carbohydrates), the deficient supply or the insufficient use of a nutritional factor involves a progressive depletion of its possible reserves in the tissues; therefore a cellular impoverishment, with compromise of some osmotic, enzymatic, and more generally metabolic processes; finally, the onset of cellular and tissue degenerative lesions, some reversible, others irreparable.

While in the initial or occult forms, the diagnosis is possible only through laboratory tests (dosing of the blood contents, and sometimes cellular ones, of vitamins, minerals, proteins, etc.; determination of the nitrogen balance, or other), in the overt forms the diagnosis from the simple collection of clinical and anthropometric data (weight ratio, plyometric values, etc.), even if it needs to be deepened by laboratory research.

Among the many causes in the world that contribute to the persistence of m. primitive by default, those of a socio-economic nature predominate (underdevelopment, hence poverty and subculture, therefore the poor flow of nutritional and health information) and of a geological and ecological nature (this is the case of the endemic goiter due to iodine deficiency, which affects many mountain populations of all the continents). Other significant causes are in relation to contingent or recurring events (such as famines and other natural disasters, long-lasting war events, and the like) or unfavorable cultural influences (restrictive precepts of a religious or philosophical nature; superstitions, prejudices, and food cravings; irrational diets; repeated fasts in protest) or to inadequacies in eating behavior, for various reasons (personal tastes, repulsions or unconscious refusals).

Forms of m. secondary by default are observed in multiple defending pathological conditions: in some endocrine diseases (such as Simmonds's disease and Basedow's disease), psychic, tumoral, metabolic, infectious, and toxic. The latter include iatrogenic avitaminosis from antibiotics (deficiency of vitamins B 2, PP, etc.). In such cases, dietary therapy (oral, tube, or parenteral) plays an adjuvant or non-prominent role, with the exception of various metabolic diseases (see metabolismcongenital diseases of, in this App.; replacement , diseases del, in this App.; dietetics, in this App.), for post-operative conditions (which mainly make use of parenteral nutrition), for dyspeptic syndromes and for intestinal malabsorption (sprue syndromes; enteropathies due to intolerance to gluten, mono- and disaccharides; malabsorption methionine, tryptophan, vitamin B12, folic acid; abetalipoproteinemia, etc.).

Malnutrition by excess

- The primitive form is widespread in countries with high economic development (see below) and among the privileged classes of depressed countries. It has many metabolic aspects, which will be mentioned later.

The secondary form can be pathological or iatrogenic in nature. In the first case, it usually takes the form of endocrine obesity (from hyperadrenalism, hypothyroidism, diencephalic lesions, etc.) in which, due to the compromised efficiency of some homeostatic mechanisms, a slowing down of the metabolism is determined, among other things. energy, a marked accentuation of anabolic processes, and, therefore, an abnormal hoarding of fat.

Physiological components

Physiological components

    While emotional behavior is largely regulated by relatively ancient and deeper brain structures, the frontal lobe of the cortex is involved in human anxiety. It is no coincidence that destructive surgery of parts of it reduces anxiety in patients suffering from these disorders. The most important 'building blocks' of the brain are the neurons or nerve cells. Connected in highly complex networks, they transmit information through chemical substances that act as messengers: neurotransmitters (v.). At least fifty types have been identified, which differ considerably depending on the location: some of them are linked to a particular anatomical structure, and others are scattered throughout the brain. When we talk about anxiety, the three most important neurotransmitters are norepinephrine (also called 'norepinephrine'), serotonin, and GABA. The latter is an inhibitory neurotransmitter that reduces the likelihood of activating nerve cells; unlike norepinephrine and serotonin, it is located throughout the brain. The strongest evidence of a GABA connection to anxiety comes from pharmacological studies, especially those of benzodiazepines, anti-anxiety drugs that enhance the effects of GABA by causing reduced anxiety, relaxation of muscles, and drowsiness; they also exert an anti-convulsant action. Norepinephrine is used by so-called adrenergic neurons; it forms in both the central and peripheral nervous systems. The strongest evidence of a GABA connection to anxiety comes from pharmacological studies, especially those of benzodiazepines, anti-anxiety drugs that enhance the effects of GABA by causing reduced anxiety, relaxation of muscles, and drowsiness; they also exert an anti-convulsant action. Norepinephrine is used by so-called adrenergic neurons; it forms in both the central and peripheral nervous systems. anti-convulsant action. Norepinephrine is used by so-called adrenergic neurons; it forms in both the central and peripheral nervous systems. anti-convulsant action. Norepinephrine is used by so-called adrenergic neurons; it forms in both the central and peripheral nervous systems.

    As for the norepinephrine of the brain, 70% of it is found in a small blue area (locus coeruleus) located in an ancient and deep part of the brain that has evolved over time. There are also relatively few adrenergic cells in the locus coeruleus, but each of them then spreads widely by making contact with at least 100,000 other neurons. Since noradrenergic pathways cover large areas of the brain, it is not surprising that norepinephrine is implicated in so many activities, such as sleep and wakefulness, attention, learning, arousal, mood, and anxiety. Electrical stimulation of the locus coeruleus produces fear-like reactions in animals, while pharmacological stimulation of the same area, e.g. through high doses of yohimbine, creates subjective anxiety in men. A little higher than the locus coeruleus are the raphe nuclei, where we find the neurotransmitter serotonin. Like norepinephrine, it spreads to many other areas of the brain and the spine.

    Low serotonin levels have long been thought to be associated with low mood and depression, but more recent pharmacological research indicates that how serotonin works may be important in understanding anxiety and its disorders. Drugs that increase the availability of serotonin not only improve mood but also reduce the incidence and intensity of panic attacks, are effective in the treatment of aggression, while, as a side effect, they cause a lowering of libido. This suggests that serotonin has something to do with the organization of instinctual behavior, whether it is expressed in the form of aggression directed towards others, or instead manifested in the form of aggression towards oneself, such as, for example, in the case of depression, sudden and intense anxiety, the urge to overeat and sexual urges. Serotonin and norepinephrine certainly interact, but the mechanisms of the interaction are not fully known. Physiological changes in states of anxiety are not limited to the brain. The brain and spinal cord, which make up the central nervous system, are connected to all other organs through the autonomic nervous system. This, in turn, is divided into the sympathetic nervous system and the parasympathetic nervous system. The sympathetic nervous system has adrenaline and norepinephrine as transmitters. Once the brain activates the sympathetic parts of the autonomic nervous system, (nor)adrenaline is released into the blood resulting in an increased heart rate, with the dilation of the pupils, the inhibition of the lacrimal glands, and the opening of the respiratory tract. All of these responses, mediated by (nor)adrenaline, constitute that 'emergency reaction' of a physiological type that we experience as fear. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response. inhibition of the lacrimal glands, the opening of the respiratory tract. All of these responses, mediated by (nor)adrenaline, constitute that 'emergency reaction' of a physiological type that we experience as fear. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood, and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response. inhibition of the lacrimal glands, the opening of the respiratory tract. All of these responses, mediated by (nor)adrenaline, constitute that 'emergency reaction' of a physiological type that we experience as fear. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. 

If this system is activated, the neurotransmitter acetylcholine is released into the blood, and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood, and decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response.

    The emergency reaction prepares the organism perfectly to respond to danger. As soon as the danger subsides, the parasympathetic nervous system takes over and mounts a relaxation response such as for example, a slowing heart rate and a lowering of blood pressure.

    The biological implant is highly adaptive in the sense that it allows us to react appropriately to danger, but the neural pathways implicated in anxiety often activate in the absence of real danger (false alarms) and this can be disabling for the individual. False alarms generally occur in the event that the emergency system is hypersensitive (e.g. the locus coeruleus can, through hyperactive and noradrenergic activity, expand even in the presence of very slight voltages), or in the case in which, through learning processes, subjects associate harmless stimuli with some catastrophe. Even if the origin of false alarms is psychological, this does not mean that the process excludes physiological factors. As we have seen, the association of events is done in cortical areas. The subject's memory may contain a misrepresentation of which events are dangerous (eg, spiders), but this is not a brain problem; conversely, if the individual is constantly anxious due to the relative unavailability of GABA, this in fact represents a real brain problem.

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