SDG2 recognizes that dealing with hunger is not only based on increasing food production but also on proper markets, access to land and technology and increased and efficient incomes for farmers.A report by the International Food Policy Research Institute (IFPRI) of 2013 argued that the emphasis of the SDGs should be on eliminating hunger and under-nutrition, rather than on poverty, and that attempts should be made to do so by 2025 rather than 2030. The argument is based on an analysis of experiences in China, Vietnam, Brazil, and Thailand and the fact that people suffering from severe hunger face extra impediments to improving their lives, whether it be by education or work. Three pathways to achieve this were identified: 1) agriculture-led; 2) social protection- and nutrition- intervention-led; or 3) a combination of both of these approaches. Regional
Much of the worlds regional alliances are located in Africa. For example, the Alliance for Food Sovereignty in Africa or the Alliance for a Green Revolution in Africa.The Food and Agriculture Organization of the UN has created a partnership that will act through the African Unions CAADP framework aiming to end hunger in Africa by 2025. It includes different interventions including support for improved food production, a strengthening of social protection and integration of the right to food into national legislation. National
Examples of hunger relief organisations that operate on the national level include The Trussell Trust in the United Kingdom, the Nalabothu Foundation in India, and Feeding America in the United States.
Cutis laxa may also be seen in association with inherited connective tissue disorders such as Ehlers–Danlos syndromes. Another syndrome associated with cutis laxa is Lenz-Majewski syndrome which is due to a mutation in the phosphatidylserine synthase 1 (PTDSS1) gene.In contrast, acquired cutis laxa often has a triggering event such as urticaria, drugs (such as penicillin) or neoplasms. Acquired cutis laxa may also be immunologically mediated, as it can involve dermal deposit of immunoglobulins and it can occur with autoimmune diseases. Acquired cutis laxa has been associated with granular immunoglobulin A deposits as well as abundant neutrophils. One hypothesis for the cause is excessive elastase release from neutrophils and macrophages. It has also been considered that mutations in elastin (ELN) and fibulin-5 (FBLN5) genes can increase susceptibility of elastic fibres to inflammatory degradation in acquired cutis laxa.Acquired cutis laxa has also been seen in conjunction with a number of conditions including: rheumatoid arthritis, systemic lupus erythematosus, celiac disease, and monoclonal gammopathies. It can also occur as a postinflammatory response after urticaria. Urticarial skin fibroblasts have shown a 2- to 3- fold increase in elastase activity in a patient with acquired cutis laxa. Diagnosis
Treatment
As of 2019, there is no treatment for cutis laxa. Procedures aimed at mitigating symptoms and identifying subsequent conditions are often advised. No pharmacological  agent has been able to stop the progression of the disease. However, cosmetic surgeries are potentially an option as cutis laxa does not generally involve vascular fragility. See also
Occipital horn syndrome
List of cutaneous conditions

References
Further reading
External links

Medscape entry on Cutis Laxa