Flight experience with the use of anti-anxiety medications like benzodiazepines or other relaxant/depressant drugs varies from person to person. Medication decreases the person's reflective function. Though this may reduce anxiety caused by inner conflict, reduced reflective function can cause the anxious flier to believe what they are afraid will happen is actually happening.

A double-blind clinical study at the Stanford University School of Medicine suggests that anti-anxiety medication can keep a person from becoming accustomed to flight. In the research, two flights were conducted. In the first flight, though patients given alprazolam (Xanax) reported less anxiety than those receiving a placebo, their measurable stress increased. The heart rate in the alprazolam group was 114 versus 105 beats per minute in the placebo group. Those who received alprazolam also had increased respiration rates (22.7 vs 18.3 breaths/min).

On the second flight, no medication was given. Seventy-one percent of those who received alprazolam on the first flight experienced panic as compared with only 29% of those who received a placebo on the first flight. This suggests that the participants who were not medicated on the first flight benefited from the experience via some degree of desensitization.

Typical pharmacologic therapy is 0.5 or 1.0 mg of alprazolam about an hour before every flight, with an additional 0.5-1.0 mg if anxiety remains high during the flight. The alternative is to advise patients not to take medication, but encourage them to fly without it, instructing them in the principles of self-exposure.

In some cases, education can considerably diminish concern about physical safety. Learning how aircraft fly, how airliners are flown in practice, and other aspects of aviation can reduce anxiety. Many people have dealt with the problem by learning to fly or skydive, effectively removing their fear of the unknown. Some educate themselves; others attend courses offered by pilots or airlines.

Though education plays an important role, the knowledge that turbulence will not destroy the aircraft does not stop the amygdala - the part of the brain responsible for generating most emotional responses, and via the Hypothalamic–pituitary–adrenal axis, the release of stress hormones - from reacting. In turbulence, repeated downward movements of the plane trigger one release of stress hormones after another. A build-up of stress hormones can cause a person to be terrified despite having every reason to know logically that the plane is not in danger. In such cases, therapy — in addition to education — is needed to prevent the release of stress hormones so that the anxious flier may gain relief.

Behavioral therapies such as systematic desensitization developed by Joseph Wolpe and cognitive behavior therapy developed by Aaron Beck rest on the theory that an initial sensitizing event (ISE) has created the phobia. The gradually increased exposure needed for systematic desensitization is difficult to produce in actual flight. Desensitization using virtual flight has been disappointing. Clients report that simulated flight using computer-generated images does not desensitize them to risk because throughout the virtual flight they were aware they were in an office. Research shows Virtual Reality Exposure Therapy (VRET) to be no more effective than sitting on a parked airplane. As a practical substitute for systematic desensitization, the amygdala can be taught to regard a stimulus as benign by linking it to an experience already regarded by the amygdala as benign. This alternative has been termed systematic inhibition of the amygdala.

Hypnotherapy generally involves regression to the ISE, uncovering the event, the emotions around the event, and helping the client understand the source of their fear. It is sometimes the case that the ISE has nothing to do with flying at all.

Neurological research by Allan Schore and others using EEG-fMRI neuroimaging suggests that though it may first be manifest following a turbulent flight, fear of flying is not the result of a sensitizing event. The underlying problem is inadequate development of ability to regulate emotion when facing uncertainty, except through feeling in control or able to escape. According to Schore, the ability to adequately regulate emotion fails to develop when relationship with caregivers is not characterized by attunement and empathy. "Because these mothers are unable to regulate their own distress, they cannot regulate their infant's distress." Chronic stress and emotional dysregulation during the first two years of life inhibits development of the right prefrontal orbito cortex, and hinders the integration of the emotional control system. This renders the right prefrontal orbito cortex incapable of carrying out its executive role in the regulation of emotion. Some who disagree with the importance of early experience regard this view point as contentious. However, Harvard University and the National Scientific Council on the Developing Child state, "Genes provide the basic blueprint, but experiences influence how or whether genes are expressed. Together, they shape the quality of brain architecture and establish either a sturdy or a fragile foundation for all of the learning, health, and behavior that follow."

When it senses anything unfamiliar or unexpected, the amygdala releases stress hormones. In humans, stress hormones activate both the sympathetic nervous system and executive function. The sympathetic nervous system produces an urge to mobilize. Initially, to assess the situation, executive function overrides the urge to mobilize. If assessment reveals no threat, executive function dismisses the matter, and signals the amygdala to end stress hormone release. If risk is apparent, executive function considers what can be done to deal with the risk. Upon commitment to a plan, either of action or of inaction, executive function signals the amygdala to end stress hormone release.

In a non-phobic person, the arousal caused by the release of stress hormones results in a sense of curiosity, not a sense of emergency. Phobic response is significantly different. The phobic person equates arousal with fear, and fear as proof that there is danger. Upon arousal, the person's executive function is called upon not merely to assess the situation, but - if stress hormones are to be regulated - to prove no danger exists. If danger cannot be ruled out, executive function can no longer inhibit the urge to mobilize. Though phobics regard control as the antidote to fear, it is commitment to a plan - not control alone that ends the release of stress hormones. If a person has control but cannot commit to a plan, fear persists. It is interesting to note that commitment to any action - even unwise action - provides relief, and signals the amygdala to terminate stress hormone release.

If a phobic flier were able to fly in the cockpit, the pilot's facial response to an unexpected noise or motion would adequately prove the absence of danger. But with information in the cabin limited, it is impossible to prove no danger exists. Stress hormones continue to be released. As levels rise, anxiety increases and the urge to escape becomes paramount. Since physical escape is impossible, panic may result unless the person can escape psychologically through denial, dissociation, or distraction.

In the cognitive approach, the passenger learns to separate arousal from fear, and fear from danger. Cognitive therapy is most useful when there is no history of panic. But since in-flight panic develops rapidly, often through processes which the person has no awareness of, conscious measures may neither connect with - nor match the speed of - the unconscious processes that cause panic.

In another approach, emotion is regulated by what neuroscientist Stephen Porges calls neuroception. In social situations, arousal is powerfully regulated by signals people unconsciously send, receive, and process. For example, when encountering a stranger, stress hormone release increases the heart rate. But if the stranger's signals indicate trustworthiness, these signals override the effect of stress hormones, slow the heart, calm the person, and allow social interaction to take place. Because neuroception can completely override the effect of stress hormones, can be controlled by linking the noises and motions of flight to neuroceptive signals that calm the person.

Lastly, frequent flyer experts at Flightfox suggest that fear of flying is a reaction caused by the panic and tension of so many travellers in close quarters - once one person is uneasy the rest soon feel uncomfortable as well. Their solution, odd as it may seem, is to fly in premium class to experience flying in a comfortable and relaxed setting, so as to avoid the tension and anxiety of coach.

Inclusion of NTDs into initiatives for malaria, HIV/AIDS, and tuberculosis, as well as integration of NTD treatment programs, may have advantages given the strong link between these diseases and NTDs. Some neglected tropical diseases share common vectors (sandflies, black flies, and mosquitos). Both medicinal and vector control efforts may be combined.

A four-drug rapid-impact package has been proposed for widespread proliferation. Administration may be made more efficient by targeting multiple diseases at once, rather than separating treatment and adding work to community workers. This package is estimated to cost US$0.40 per patient. When compared to stand-alone treatment, the savings are estimated to be 26–47%. While more research must be done in order to understand how NTDs and other diseases interact in both the vector and the human stages, safety assessments have so far produced positive results.

Many neglected tropical diseases and other prevalent diseases share common vectors, creating another opportunity for treatment and control integration. One such example of this is malaria and lymphatic filariasis. Both diseases are transmitted by the same or related mosquito vectors. Vector control, through the distribution of insecticide treated nets, reduces the human contact with a wide variety of disease vectors. Integrated vector control may also alleviate pressure on mass drug administration, especially with respect to rapidly evolving drug resistance. Combining vector control and mass drug administration deemphasizes both, making each less susceptible to resistance evolution.

WHO published in 2012 the NTD "roadmap" which contains milestones for 2015 and 2020 and which specifies targets for eradication, elimination, and intensified control of the different NTDs. For example:

- NTDs planned to be eradicated: dracunculiasis (by the year 2015), endemic treponematoses (yaws) (by 2020)

- NTDs planned to be eliminated globally by 2020: blinding trachoma, leprosy, human African trypanosomiasis, lymphatic filariasis

- NTDs planned to be eliminated in certain regions: rabies (by 2015 in Latin America, by 2020 in Southeast Asia and western Pacific regions), chagas disease (transmission through blood transfusion by 2015, intra-domiciliary transmission by 2020 in the region of the Americas), visceral leishmaniasis (by 2020 in the Indian subcontinent), oncocerciasis (by 2015 in Latin America), schistosomiasis (by 2015 in eastern Mediterranean region, Caribbean, Indonesia and the Mekong River basin, by 2020 in the region of the Americas and western Pacific region)

- NTDs planned to be eliminated in certain countries: human African trypanosomiasis (by 2015 in 80 percent of areas in which it occurs), oncocerciasis (by 2015 in Yemen, by 2020 in selected countries in Africa), schistosomiasis (by 2020 in selected countries in Africa)

- Intensified control with specific targets for the years 2015 and 2020 are provided for these NTDs: dengue, buruli ulcer, cutaneous leishmaniasis, taeniasis/cysticercosis and echinococcosis/hydatidosis, foodborne tremadode infections, soil-transmitted helmintheases