Pregnancy for any woman – happiness, the greatest gift that nature could give. However, the expectation of the child imposes certain responsibilities, and one of them – the birth of a healthy and strong baby. To do this, not so much – to comply with proper nutrition during pregnancy

As we know obesity causes many human health problems, and excess weight during pregnancy threatens the emergence of complications is not only a future mother, but also for the crumbs that will only come to light. In order that the child receives all the necessary vitamins and felt comfortable in moms tummy, there must be a diet for pregnant women.

Diet during pregnancy does not involve any harmful organism for fasting or harsh restrictions. Most likely, on the contrary – the diet during pregnancy requires a 4-5 times a day, however, in small portions. Used food should be varied, ideally, a table must consist of three courses. Preference is given to the various fruits, vegetables and herbs, and foods containing large amounts of protein.

Daily diet of pregnant should include:
100-120g protein, 70-90g of animal origin (lean meat, fish, eggs, yogurt, cottage cheese, fermented baked milk, etc.);
80-100g of fat, of which 20g of vegetable origin;
carbohydrates – 300-400g (first half of pregnancy), 300gr recent months;
1-1.5 liters of water (pure);
daily dose of multivitamin preparations.

Diet for pregnant recommends the following distribution of food (caloric): 30% of breakfast, lunch – 40%, dinner – 10%. Additional techniques: lunch – 10%, snack – 10%. Supper should be 2-3 hours before bedtime digestible foods (cheese, yogurt, kefir). Breakfast – no less than an hour after awakening.

Proper nutrition during pregnancy involves eating boiled, steamed and baked dishes. Salt diet for pregnant women does not like – the consumption of this product should be limited to 5 6gr per day.

Diet during pregnancy allows the use the following products:
pastry and bread (up to 150 grams per day), but freshly, as well as products made of puff pastry and, with the cream cakes, pies, cakes, etc.;
meat and poultry (up to 200 g per day), all lean – a rabbit, beef, turkey, chicken;
fish (up to 150 grams) – cod, saffron cod, ice fish, pike and TE;
dairy products (up to 200g) – low-fat yogurt, cottage cheese, buttermilk, yogurt, whole milk, etc.;
raw vegetables – cucumbers, squash, zucchini, tomatoes, all varieties of cabbage, carrots, peas, radishes, etc.;
oil, cereals and pasta used only as a complex product in small quantities (soups, cereals).

Diet for pregnant women not completely rule out such products as alcohol, fast foods, strong spices and seasonings, mushrooms, salt and savory snacks, strong coffee, tea and chocolate.

Finally it is worth saying that proper nutrition during pregnancy also involves moderation in eating, that is, make a move to when there is still a slight feeling of hunger.

Afferent nerves need voltage-gated sodium channels for action potential conduction
from the nerve terminals to the central nervous system. Lignocaine and bupivicaine
are local anesthetics by virtue of their sodium channel blocking activity, and
block the cough response when delivered to the upper and lower airways by aerosol
(Hansson et al. 1994). These agents also dampen upper-airway protective reflexes,
and may occasionally induce bronchoconstriction, and therefore need to be used
with care. Lignocaine inhalation inhibits cough at doses that do not affect reflex
bronchoconstriction (Choudry et al. 1990). Lignocaine aerosol was also shown to
be quickly effective in 62 patients with COPD (Chong et al. 2005); however, nebulized
terbutaline was equally effective. Their duration of action is only of the order
of 30 min or less. At present, these are usually reserved for the severest persistent
coughers (Howard et al. 1977).
There has been some work in identifying specific sites of action of local anesthetics
and of novel anesthetic-like molecules with antitussive activity (Carr 2006).
Mexilitine, which has been shown to inhibit capsaicin cough response modestly
in human (Fujimura et al. 2000), specifically inhibits action potential formation in
guinea-pig tracheal mechanosensitive fibers which are cough receptors at concentrations
that do not block action potential conduction along the sensory nerve axon
(Carr 2006). This suggests that cough receptor nerve terminals express Na+ channels
that have properties that are different from those of their axons. In addition,
there is evidence that myelinated cough afferents may have nonmyelinated terminals
(Coleridge and Coleridge 1986), which may also explain these observations.
The quartenary ammonium compound RSD931, which inhibits spontaneous and
histamine-evoked discharges from airway RARs but activates pulmonary C-fibers,
reduces citric acid induced and capsaicin-induced cough in guinea pigs and rabbits
(Adcock et al. 2003). However, this profile of effect was dissimilar to that of
lignocaine, which was more generally inhibitory.
Other subtypes of Na+ channels such as the tetrodotoxin (TTX)-resistant Na+
channels are also expressed by airway afferent nerves. Capsaicin-sensitive neurones
are sensitized by inflammatory mediators, such as PGE2, an effect partly mediated
by an increase in TTX-resistant Na+ currents (Kwong and Lee 2005). These
neurones are inactivated in the normal airways, but are recruited in inflamed airways
to contribute to cough sensitization (Mazzone et al. 2005). Therefore, selective inhibitors
of TTX-resistant Na+ channels may be useful as cough suppressants in
chronic cough.

Isotonic solutions of low chloride concentrations can stimulate action potential discharge
of a subpopulation of Aδ-fibers and C-fibers in guinea pigs (Fox et al. 1995),
and activate afferent fibers in the dog (Sant’Ambrogio et al. 1993). Low-chloride
solutions induce cough in human, and the diuretic frusemide inhibits cough induced
by low-chloride solutions but not by capsaicin (Ventresca et al. 1990). Frusemide
inhibits to some extent airway afferent action potential discharge, and sensitizes
slowly adapting receptors and desensitizes RARs in rat airways (Sudo et al. 2000).
The mechanism by which frusemide works is unknown (Bolser et al. 2006b), but
it may inhibit a neuronally expressed chloride transporter in the airways (Mazzone
and McGovern 2006).
Frusemide-sensitive Na+/K+/2Cl− cotransporter (NKCC1) is expressed by the
majority of neurones in the vagal sensory ganglia and by the peripheral terminals
of low-threshold mechanosensors (cough receptors) in the guinea-pig trachea
(Mazzone and McGovern 2006) The cotransporter allows the accumulation of intracellular
chloride ions above the electrochemical equilibrium and opening of membrane
chloride channels results in a depolarizing chloride current that contributes
to the activation of sensory fibers. Lee et al. (Lee et al. 2005) have shown that
bradykinin-induced depolarization of airway afferent nerves is inhibited by niflumic
acid, a selective inhibitor of calcium-activated chloride channels, which reduces citric
acid induced cough in anaesthetized guinea pigs (Mazzone and McGovern 2006).

Tachykinins are present in capsaicin-sensitive primary afferent nerves and act
through tachykinin receptor subtypes, NK1R, NK2R, NK3R (Geppetti et al. 1999).
In rodents, capsaicin and other irritants can cause the release of tachykinins from
peripheral nerve endings in the lungs via a local axon reflex. Tachykinins are
potent bronchoconstrictors and increase microvascular permeability, and have various
proinflammatory effects. These, together with a direct effect on myelinated Aδ-
fibers, contribute to stimulation of cough. Tachykinins may enhance the responses
of rapidly adapting receptors (RARs) and have also been implicated in the central
“sensitization” of cough (Mutoh et al. 2000).
In the guinea pig, an NK2 receptor antagonist, SR48968, inhibited citric acid
induced cough, while an NK1 receptor antagonist was ineffective (Advenier et al.
1992; Girard et al. 1995). A study in asthmatic subjects found no effect of CP-99,994
against bronchoconstriction and cough induced by hypertonic saline (Fahy et al.
1995). A non-peptide NK3 receptor antagonist (SB235375), with low penetrance
into the central nervous system, inhibited citric acid induced cough and airways’
hyperreactivity in the guinea pig (Hay et al. 2002; Daoui et al. 1998) but its development
has been suspended.

Nociceptin/orphanin is the endogenous peptide ligand for the orphan “opioid-like”
NOP1, which is a G-protein-coupled seven-transmembrane receptor. Nociceptin
does not stimulate opioid receptors. NOP1 receptors are widely distributed in the
central nervous system and are also present in airway nerves in the guinea pig
(Fischer et al. 1998), where nociceptin has been found to inhibit nonadrenergic,
noncholinergic responses (Shah et al. 1998). Capsaicin-induced bronchoconstriction
is attenuated by nociceptin (Corboz et al. 2000), an action possibly due to inhibition
of tachykinin release from sensory C-fibers. Nociceptin administered intravenously
or via the intracerebroventricular route suppresses capsaicin-induced and mechanically
induced cough (McLeod et al. 2001; Bolser et al. 2001), effects blocked by
an NOP1 antagonist, J113397, but not by an opioid receptor antagonist. This NOP
antagonist does not appear to penetrate the blood–brain barrier in the guinea pig
when administered orally and remains effective as an inhibitor of capsaicin-induced
cough, indicating that it also acts peripherally (McLeod et al. 2004).
Nociceptin inhibits the airway microvascular leakage induced in guinea-pig airways
by intraesophageal hydrochloric acid infusion, acting probably at the prejunctional
level by inhibiting tachykinin release (Rouget et al. 2004). Furthermore, the
ability of nociceptin to block capsaicin-induced tachykinin release and bronchoconstriction
has been traced to the activation of an inward-rectifier potassium channel
(Jia et al. 2002). In the conscious guinea pig, nociceptin inhibited acid-induced
cough; this effect was shown to result from a direct inhibitory effect of nociceptin
on peripheral C-fibers caused by selective inhibition of acid-induced transient receptor
potential vanniloid-1 (TRPV-1) activation (Lee et al. 2006). Many nociceptin
agonists have been described (Chiou et al. 2007). A selective non-peptide
nociceptin agonist is Ro-64–619, for which preclinical data have been summarized
(Shoblock 2007). No data pertaining to humans have been published so far.

Opioid receptor agonists are classified by their activities at the opioid receptors μ,κ,
and δ. The current compounds, morphine and codeine, are mostly μ-receptor agonists
and may possess central as well as peripheral actions. BW443C, a μ-opioid
receptor agonist and a pentapeptide polar agonist, as an aerosol acts on μ receptors
on sensory receptors in the lung and has peripheral antitussive activity in the
lungs (Adcock et al. 1988), but this has not been demonstrated in humans (Choudry
et al. 1991).
Opioids may also act on κ-opioid receptors for their antitussive effects (Kamei
et al. 1990). A δ-selective receptor agonist (SB221122) was shown to inhibit citric
acid induced cough in the guinea pig (Kotzer et al. 2000), an effect prevented by
a δ-receptor antagonist (SB244525). However, an orally selective δ-opioid receptor
antagonist, TRK-851, with 100–250 times greater potency in inhibiting cough in rat
and guinea pig than codeine, has been considered as a potential antitussive (Ueno
et al. 2001).
Levodropropizine, a non-opioid antitussive and derivative of phenylpiperazinopropane,
inhibits vagally conducted cough in the guinea pig by activating a reflex
mediated by capsaicin-sensitive afferents, and not by a central mechanism of action
(Lavezzo et al. 1992). It inhibits C-fiber activity induced by chemical stimuli
(Shams et al. 1996). It has been compared with dextromethorphan in patients with
nonproductive cough and has been shown to have a more favorable benefit–risk
profile (Catena and Daffonchio 1997).

Research into the neuroanatomical and neurophysiological mechanisms of sensory
cough pathways has led to the identification of specific airway afferent nerve subtypes
and of receptors and channels involved and therefore to potential cough targets.
Importantly, this research is coupled with an understanding of the potential
abnormalities and dysfunction of these pathways in the hypertussive state, so that
these can be reversed or normalized. Most of the potential antitussives arising from
this research have yet to be tried in cough patients. While this list of potential novel
classes of nonspecific antitussives (Table 3) appears to focus on their effects at the
periphery, it should be remembered that they may also have central effects, which
remain more difficult to study. There have been recent reviews of the pharmacology
of the sensory neural pathway of cough and of potential targets (Chung 2005; Bolser
et al. 2006b; Dicpinigaitis 2006; Kollarik and Undem 2006).

The basis for using these agents as antitussives lies in the possibility that altering
the volume of secretions or their composition will lead to suppression of the
cough reflex. Mucolytic agents such as acetylcysteine, carbocisteine, bromhexine,
and methylcysteine are often used to facilitate expectoration by reducing sputum
viscosity in patients with chronic bronchitis. A small reduction in the exacerbation
of bronchitis has been reported with orally administered acetylcysteine, accompanied
by small improvement in cough, a decrease in volume of sputum, and some
ease of expectoration (Aylward et al. 1980); however, other studies have failed to
show beneficial effects on mucus clearance (Hautmeyers et al. 1999).
Aromatic agents such as eucalyptus and menthol have decongestant effects
in the nose and can be useful in short-term relief of cough. Menthol inhibits
capsaicin-induced cough in normal volunteers (Morice et al. 1994), and acts on a
cold-sensitive nervous sensor. Demulcents also form an important component of
many proprietary cough preparations and may be useful because the thick sugary
preparation may act as a protective layer on the mucosal surface. The beneficial effects
of honey in improving cough of the common cold in children (Paul et al. 2007)
may result from such a demulcent effect.

A range of centrally acting drugs have been reported to control cough in a group
of patients in whom other measures have been unsuccessful. In five patients with
cancer complaining of intractable cough not responding to codeine or morphine
and of pruritius, paroxetine, a serotonin-reuptake inhibitor used for treatment of depression,
was particularly effective (Zylicz and Krajnik 2004). There are positive
reports of the effects of the tricyclic antidepressant amitriptyline in 12 patients and
of gabapentin and carbamazepine, which are antiepileptic drugs, in two patients and
one patient, respectively (Bastian et al. 2006; Mintz and Lee 2006; Jacome 1985). A
randomized but open controlled study of amitriptyline (10 mg at nighttime) versus a
combination of codeine/guaifenesin in patients with chronic cough “resulting from
postviral vagal neuropathy,” an entity that is recognized by otolaryngologists as triggered
by an upper respiratory tract illness with injury to various branches of the vagus
nerves, showed significant suppression of cough with amitriptyline (Jeyakumar
et al. 2006). It is perhaps time that a double-blind controlled trial of amitriptyline in
chronic cough be undertaken.
The need for further studies in the antitussive effects of these agents such as
amitryptiline, gabapentin, and carbamezepine is supported by their use in the treatment
of neuropathic pain, and there are similar processing peripheral and central
mechanisms for chronic cough and chronic pain that could be controlled by these
drugs (Gracely et al. 2007). In addition, it is also possible that similar processing
mechanisms pertain to the sensation of dyspnoea, such that if cough and dyspnea
were associated together as in COPD or in advanced lung cancer, a potential symptomatic
antitussive might also improve dyspnoea (and pain). Capsaicin and voluntary
coughs activate supramedullary pathways (Mazzone et al. 2007; Simonyan
et al. 2007) and agents such as amitriptyline, gabapentin, and carbamezepine may
have antitussive effects through inhibition of these pathways.

There have been very few studies of these antitussives in patients with chronic
cough or chronic idiopathic cough. In fact, most of these studies have been performed
in patients with chronic bronchitis and are at least 20 years old (Table 2).
Codeine and dextromethorphan were previously shown to have an inhibitory effect
on chronic cough of bronchitis or COPD (Matthys et al. 1983; Aylward et al. 1984;
Sevelius and Colmore 1966; Sevelius et al. 1971). In studies involving larger groups
of patients, both levodropropizine and moguisteine were reported to be effective
in reducing cough frequency in chronic cough of bronchitis and COPD (Aversa
et al. 1993; Allegra and Bossi 1988). However, in a recent well-conducted study of
cough in COPD patients where cough scores, visual analogue scales, cough frequency
using an ambulatory cough recorder, and capsaicin cough sensitivity were
measured, a high dose of codeine (60mg) was not effective in reducing cough
(Smith et al. 2006). This casts some doubt on the results of some of the earlier
smaller studies that reported beneficial effects on cough. More controlled trials of
these antitussives in patients with chronic cough are needed.
Moguisteine, a peripherally acting antitussive, was not more effective than a
placebo, apart from reduction of cough in a subgroup of participants with severer
cough at night (Adams et al. 1993). It is to be noted that no efficacy of
dextromethorphan or codeine on cough in children has been demonstrated. In a
rare placebo-controlled study of children with acute nocturnal cough, neither dextromethorphan
nor codeine was significantly more effective than the placebo in reducing
the cough (Taylor et al. 1993).
The main issue with the opioids such as morphine, diamorphine, and codeine is
that any potentially effective dose is usually associated with physical dependence,
respiratory depression, and gastrointestinal colic. The use of morphine and diamorphine
has been restricted to the severe distressing cough (usually associated with
pain and distress) that often occurs in advanced lung cancer and with doses that
cause sedation, respiratory depression, and constipation. In a randomized doubleblind
crossover study in 27 patients with severe chronic cough, slow-release morphine
tablets (5 mg twice daily for 4 weeks) compared with a placebo (Morice
et al. 2007) attenuated cough scores significantly by approximately 40% with an improvement
in quality-of-life cough questionnaire scores, although citric acid cough
response remained unchanged. Patients tolerated the treatment well despite 40%
of them complaining of constipation and 25% of them complaining of drowsiness.
This study dispels the notion that morphine would not be tolerable in chronic cough
patients. This approach nevertheless should be used only in patients with the most
distressing cough.