<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Diabetic neuropathy and explain in detail? [/INST] Diabetic neuropathy refers to various types of nerve damage associated with diabetes mellitus. Symptoms depend on the site of nerve damage and can include motor changes such as weakness; sensory symptoms such as numbness, tingling, or pain; or autonomic changes such as urinary symptoms. These changes are thought to result from microvascular injury involving small blood vessels that supply nerves (vasa nervorum). Relatively common conditions which may be associated with diabetic neuropathy include distal symmetric polyneuropathy; third, fourth, or sixth cranial nerve palsy; mononeuropathy; mononeuropathy multiplex; diabetic amyotrophy; and autonomic neuropathy.

Signs and symptoms
Diabetic neuropathy can affect any peripheral nerves including sensory neurons, motor neurons, and the autonomic nervous system. Therefore, diabetic neuropathy has the potential to affect essentially any organ system and can cause a range of symptoms. There are several distinct syndromes based on the organ systems affected.

Sensorimotor polyneuropathy
Longer nerve fibers are affected to a greater degree than shorter ones because nerve conduction velocity is slowed in proportion to a nerves length. In this syndrome, decreased sensation and loss of reflexes occurs first in the toes on each foot, then extends upward. It is usually described as a glove-stocking distribution of numbness, sensory loss, dysesthesia and night time pain. The pain can feel like burning, pricking sensation, achy or dull. A pins and needles sensation is common. Loss of proprioception, the sense of where a limb is in space, is affected early. These patients cannot feel when they are stepping on a foreign body, like a splinter, or when they are developing a callus from an ill-fitting shoe. Consequently, they are at risk of developing ulcers and infections on the feet and legs, which can lead to amputation. Similarly, these patients can get multiple fractures of the knee, ankle or foot, and develop a Charcot joint. Loss of motor function results in dorsiflexion, contractures of the toes, loss of the interosseous muscle function that leads to contraction of the digits, so-called hammer toes. These contractures occur not only in the foot but also in the hand where the loss of the musculature makes the hand appear gaunt and skeletal. The loss of muscular function is progressive.

Autonomic neuropathy
The autonomic nervous system is composed of nerves serving the heart, lungs, blood vessels, bone, adipose tissue, sweat glands, gastrointestinal system and genitourinary system. Autonomic neuropathy can affect any of these organ systems. One commonly recognized autonomic dysfunction in diabetics is orthostatic hypotension, or becoming dizzy and possibly fainting when standing up due to a sudden drop in blood pressure. In the case of diabetic autonomic neuropathy, it is due to the failure of the heart and arteries to appropriately adjust heart rate and vascular tone to keep blood continually and fully flowing to the brain. This symptom is usually accompanied by a loss of respiratory sinus arrhythmia – the usual change in heart rate seen with normal breathing. These two findings suggest autonomic neuropathy.Gastrointestinal manifestations include gastroparesis, nausea, bloating, and diarrhea. Because many diabetics take oral medication for their diabetes, absorption of these medicines is greatly affected by the delayed gastric emptying. This can lead to hypoglycemia when an oral diabetic agent is taken before a meal and does not get absorbed until hours, or sometimes days later when there is normal or low blood sugar already. Sluggish movement of the small intestine can cause bacterial overgrowth, made worse by the presence of hyperglycemia. This leads to bloating, gas and diarrhea.Urinary symptoms include urinary frequency, urgency, incontinence and retention. Again, because of the retention of urine, urinary tract infections are frequent. Urinary retention can lead to bladder diverticula, kidney stones, and reflux nephropathy.

Cranial neuropathy
When cranial nerves are affected, neuropathies of the oculomotor nerve (cranial nerve #3 or CNIII) are most common. The oculomotor nerve controls all the muscles that move the eye except for the lateral rectus and superior oblique muscles. It also serves to constrict the pupil and open the eyelid. The onset of a diabetic third nerve palsy is usually abrupt, beginning with frontal or pain around the eye and then double vision. All the oculomotor muscles innervated by the third nerve may be affected, but those that control pupil size are usually well-preserved early on. This is because the parasympathetic nerve fibers within CNIII that influence pupillary size are found on the periphery of the nerve (in terms of a cross-sectional view), which makes them less susceptible to ischemic damage (as they are closer to the vascular supply). The sixth nerve, the abducens nerve, which innervates the lateral rectus muscle of the eye (moves the eye laterally), is also commonly affected but fourth nerve, the trochlear nerve,  (innervates the superior oblique muscle, which moves the eye downward) involvement is unusual. Damage to a specific nerve of the thoracic or lumbar spinal nerves can occur and may lead to painful syndromes that mimic a heart attack, gallbladder inflammation, or appendicitis. Diabetics have a higher incidence of entrapment neuropathies, such as carpal tunnel syndrome.

Pathogenesis
The following processes are thought to be involved in the development of diabetic neuropathy:

Microvascular disease
Vascular and neural diseases are closely related. Blood vessels depend on normal nerve function, and nerves depend on adequate blood flow. The first pathological change in the small blood vessels is narrowing of the blood vessels. As the disease progresses, neuronal dysfunction correlates closely with the development of blood vessel abnormalities, such as capillary basement membrane thickening and endothelial hyperplasia, which contribute to diminished oxygen tension and hypoxia. Neuronal ischemia is a well-established characteristic of diabetic neuropathy. Blood vessel opening agents (e.g., ACE inhibitors, α1-antagonists) can lead to substantial improvements in neuronal blood flow, with corresponding improvements in nerve conduction velocities. Thus, small blood vessel dysfunction occurs early in diabetes, parallels the progression of neural dysfunction, and may be sufficient to support the severity of structural, functional, and clinical changes observed in diabetic neuropathy.

Advanced glycated end products
Elevated levels of glucose within cells cause a non-enzymatic covalent bonding with proteins, which alters their structure and inhibits their function. Some of these glycated proteins have been implicated in the pathology of diabetic neuropathy and other long-term complications of diabetes.

Polyol pathway
Also called the sorbitol/aldose reductase pathway, the polyol pathway appears to be implicated in diabetic complications, especially in microvascular damage to the retina, kidney, and nerves.

Diagnosis
Diabetic peripheral neuropathy can be diagnosed with a history and physical examination. The diagnosis is considered in people who develop pain or numbness in a leg or foot with a history of diabetes. Muscle weakness, pain, balance loss, and lower limb dysfunction are the most common clinical manifestations. Physical exam findings may include changes in appearance of the feet, presence of ulceration, and diminished ankle reflexes. The most useful physical examination finding for large fiber neuropathy is an abnormally decreased vibration perception to a 128-Hz tuning fork (likelihood ratio (LR) range, 16–35) or pressure sensation with a 5.07 Semmes-Weinstein monofilament (LR range, 11–16). Normal results on vibration testing (LR range, 0.33–0.51) or monofilament (LR range, 0.09–0.54) make large fiber peripheral neuropathy from diabetes less likely.  Nerve conduction tests may show reduced functioning of the peripheral nerves, but seldom correlate with the severity of diabetic peripheral neuropathy and are not appropriate as routine tests for the condition. Small fiber neuropathy measured by QST and Sudomotor function tests, through electrochemical skin conductance, is more and more indicated to assess early signs of diabetic neuropathy and autonomic neuropathy.

Classification
Diabetic neuropathy encompasses a series of different neuropathic syndromes which can be categorized as follows:
Focal and multifocal neuropathies:
Mononeuropathy which affects one nerve
Amyotrophy or radiculopathy such as proximal diabetic neuropathy, affecting a specific pattern of nerves
Multiple lesions, affecting nerves that dont follow a specific pattern, also called "mononeuritis multiplex"
Nerve damage from entrapment (e.g. median, ulnar, peroneal)
Symmetrical neuropathies:
Sensory
Autonomic
Distal symmetrical polyneuropathy (DSPN), the diabetic type of which is also known as diabetic peripheral neuropathy (DPN) (most common presentation)

Prevention
Diabetic neuropathy can be largely prevented by maintaining blood glucose levels and lifestyle modifications. Enhanced glucose control methods include more frequent subcutaneous insulin administration, continuous insulin infusion, oral antidiabetic agents, while lifestyle modifications may include exercise alone, or in combination with dietary modifications. Enhanced glucose control prevents the development of clinical neuropathy and reduces nerve abnormalities in type 1 diabetes, and delays the onset of neuropathy in both types of diabetes. However, such methods may increase the likelihood of experiencing a hypoglycemic event, and many of these more aggressive methods require more frequent insulin use which has been associated with excessive risk of falls.

Treatment
Blood glucose management
Treatment of early manifestations of sensorimotor polyneuropathy involves improving glycemic control. Tight control of blood glucose can reverse the changes of diabetic neuropathy if the neuropathy and diabetes are recent in onset. This is the primary treatment of diabetic neuropathy that may change the course of the condition as the other treatments focus on reducing pain and other symptoms.

Topical agents
Capsaicin applied to the skin in a 0.075% concentration has not been found to be more effective than placebo for treating pain associated with diabetic neuropathy. There is insufficient evidence to draw conclusions for more concentrated forms of capsaicin, clonidine, or lidocaine applied to the skin. About 10% of people who use capsaicin cream have a large benefit.

Medications
Medication options for pain control include antiepileptic drugs (AEDs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and tricyclic antidepressants (TCAs).A systematic review concluded that "tricyclic antidepressants and traditional anticonvulsants are better for short term pain relief than newer generation anticonvulsants."  A further analysis of previous studies showed that the agents carbamazepine, venlafaxine, duloxetine, and amitriptyline were more effective than placebo, but that comparative effectiveness between each agent is unclear.The only three medications approved by the United States Food and Drug Administration for diabetic peripheral neuropathy (DPN) are the antidepressant duloxetine, the anticonvulsant pregabalin, and the long-acting opioid tapentadol ER (extended release). Before trying a systemic medication, some doctors recommend treating localized diabetic peripheral neuropathy with lidocaine patches.

Antiepileptic drugs
Multiple guidelines from medical organizations such as the American Association of Clinical Endocrinologists, American Academy of Neurology, European Federation of Neurological Societies, and the National Institute of Clinical Excellence recommend AEDs, such as pregabalin, as first-line treatment for painful diabetic neuropathy. Pregabalin is supported by low-quality evidence as more effective than placebo for reducing diabetic neuropathic pain but its effect is small. Studies have reached differing conclusions about whether gabapentin relieves pain more effectively than placebo. Available evidence is insufficient to determine if zonisamide or carbamazepine are effective for diabetic neuropathy. The first metabolite of carbamazepine, known as oxcarbazepine, appears to have a small beneficial effect on pain. A 2014 systematic review and network meta-analysis concluded topiramate, valproic acid, lacosamide, and lamotrigine are ineffective for pain from diabetic peripheral neuropathy. The most common side effects associated with AED use include sleepiness, dizziness, and nausea.

Serotonin-norepinephrine reuptake inhibitors
As above, the serotonin-norepinephrine reuptake inhibitors (SNRIs) duloxetine and venlafaxine are recommended in multiple medical guidelines as first or second-line therapy for DPN. A 2017 systematic review and meta-analysis of randomized controlled trials concluded there is moderate quality evidence that  duloxetine and venlafaxine each provide a large benefit in reducing diabetic neuropathic pain. Common side effects include dizziness, nausea, and sleepiness.

Tricyclic antidepressants
TCAs include imipramine, amitriptyline, desipramine, and nortriptyline. They are generally regarded as first or second-line treatment for DPN. Of the TCAs, imipramine has been the best studied. These medications are effective at decreasing painful symptoms but lead to multiple side effects that are dose-dependent. One notable side effect is cardiac toxicity, which can lead to fatal abnormal heart rhythms. Additional common side effects include dry mouth, difficulty sleeping, and sedation. At low dosages used for neuropathy, toxicity is rare, but if symptoms warrant higher doses, complications are more common. Among the TCAs, amitriptyline is most widely used for this condition, but desipramine and nortriptyline have fewer side effects.

Opioids
Typical opioid medications, such as oxycodone, appear to be no more effective than placebo. In contrast, low-quality evidence supports a moderate benefit from the use of atypical opioids (e.g., tramadol and tapentadol), which also have SNRI properties. Opioid medications are recommended as second or third-line treatment for DPN.

Medical devices
Monochromatic infrared photo energy treatment (MIRE) has been shown to be an effective therapy in reducing and often eliminating pain associated with diabetic neuropathy. The studied wavelength of 890 nm is able to penetrate into the subcutaneous tissue where it acts upon a specialized part of the cell called the cytochrome C. The infrared light energy prompts the cytochrome C to release nitric oxide into the cells. The nitric oxide in turn promotes vasodilation which results in increased blood flow that helps nourish damaged nerve cells. Once the nutrient rich blood is able to reach the affected areas (typically the feet, lower legs and hands) it promotes the regeneration of nerve tissues and helps reduce inflammation thereby reducing and/or eliminating pain in the area.
Transcutaneous electrical nerve stimulation (TENS) and interferential current (IFC) use a painless electric current and the physiological effects from low frequency electrical stimulation to relieve stiffness, improve mobility, relieve neuropathic pain, reduce oedema, and heal resistant foot ulcers.

Physical therapy
Physical therapy may help reduce dependency on pain relieving drug therapies.  Certain physiotherapy techniques can help alleviate symptoms brought on from diabetic neuropathy such as deep pain in the feet and legs, tingling or burning sensation in extremities, muscle cramps, muscle weakness, sexual dysfunction, and diabetic foot.Gait training, posture training, and teaching these patients the basic principles of off-loading can help prevent and/or stabilize foot complications such as foot ulcers.  Off-loading techniques can include the use of mobility aids (e.g. crutches) or foot splints.  Gait re-training would also be beneficial for individuals who have lost limbs, due to diabetic neuropathy, and now wear a prosthesis.Exercise programs, along with manual therapy, will help to prevent muscle contractures, spasms and atrophy.  These programs may include general muscle stretching to maintain muscle length and a persons range of motion. General muscle strengthening exercises will help to maintain muscle strength and reduce muscle wasting. Aerobic exercise such as swimming and using a stationary bicycle can help peripheral neuropathy, but activities that place excessive pressure on the feet (e.g. walking long distances, running) may be contraindicated. Exercise therapy has been shown to increase the blood flow to the peripheral nerves, can improve gait function.Heat, therapeutic ultrasound, hot wax are also useful for treating diabetic neuropathy. Pelvic floor muscle exercises can improve sexual dysfunction caused by neuropathy </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Necrotizing enterocolitis and explain in detail? [/INST] Necrotizing enterocolitis (NEC) is a devastating intestinal disease that affects premature or very low birth weight infants. Symptoms may include poor feeding, bloating, decreased activity, blood in the stool, vomiting of bile, bowel death, multiorgan failure, and even death.The exact cause is unclear. However, several risk factors have been identified. Consistently described risk factors include formula feeding, intestinal dysbiosis, low birth weight, and prematurity. Maternal factors such as chorioamnionitis, cocaine abuse, in utero growth restriction, intrahepatic cholestasis during pregnancy, increased body mass index, lack of prenatal steroids, mode of delivery, placental abruption, preeclampsia, and smoking have not been consistently implicated with the development of NEC. Other risk factors potentially implicated include congenital heart disease, birth asphyxia, exchange transfusion, and prelabor rupture of membranes. The underlying mechanism is believed to involve a combination of poor blood flow and infection of the intestines. Diagnosis is based on symptoms and confirmed with medical imaging.Prevention includes the use of breast milk and probiotics. Treatment includes bowel rest, orogastric tube, intravenous fluids, and intravenous antibiotics. Surgery is required in those who have free air in the abdomen. A number of other supportive measures may also be required. Complications may include short-gut syndrome, intestinal strictures, or developmental delay.About 7% of those who are born prematurely develop NEC; however the odds of an infant developing this illness is directly related to the intensive care unit they are placed in. Onset is typically in the first four weeks of life. Among those affected, about 25% die. The sexes are affected with equal frequency. The condition was first described between 1888 and 1891.

Signs and symptoms
The condition is typically seen in premature infants, and the timing of its onset is generally inversely proportional to the gestational age of the baby at birth (i.e., the earlier a baby is born, the later signs of NEC are typically seen).Initial symptoms include feeding intolerance and failure to thrive, increased gastric residuals, abdominal distension, and bloody stools. Symptoms may progress rapidly to abdominal discoloration with intestinal perforation and peritonitis and systemic hypotension requiring intensive medical support.

Cause
The exact cause is unclear. Several risk factors have been implicated:

Maternal factors
Acid-suppressing medications
Chorioamnionitis
Cocaine abuse
In utero growth restriction
Increased body mass index
Intrahepatic cholestasis during pregnancy
Lack of prenatal steroids
Mode of delivery
Placental abruption
Pre-eclampsia
Smoking

Main risk factors
Low birth weight
Prematurity
Formula feeding (bovine based)
Intestinal dysbiosis

Other risk factors
Acute hypoxia
Antibiotic exposure
Blood transfusions
Cardiac anomalies
Neonatal anemia
Poor intestinal perfusion
Prolonged use of indomethacin for patent  ductus arteriosus closure

Diagnosis
Diagnosis is usually suspected clinically, but often requires the aid of diagnostic imaging, most commonly radiography, which can show the intestines and may show areas with death tissue or a bowel perforation. Specific radiographic signs of NEC are associated with specific Bells stages of the disease:
Bells stage 1 (suspected disease):
Mild systemic disease (apnea, lethargy, slowed heart rate, temperature instability)
Mild intestinal signs (abdominal distention, increased gastric residuals, bloody stools)
Nonspecific or normal radiological signs
Bells stage 2 (definite disease):
Mild to moderate systemic signs
Additional intestinal signs (absent bowel sounds, abdominal tenderness)
Specific radiologic signs (pneumatosis intestinalis or portal venous gas)
Laboratory changes (metabolic acidosis, too few platelets in the bloodstream)
Bells stage 3 (advanced disease):
Severe systemic illness (low blood pressure)
Additional intestinal signs (striking abdominal distention, peritonitis)
Severe radiologic signs (pneumoperitoneum)
Additional laboratory changes (metabolic and respiratory acidosis, disseminated intravascular coagulation)Ultrasonography has proven to be useful, as it may detect signs and complications of NEC before they are evident on radiographs, specifically in cases that involve a paucity of bowel gas, a gasless abdomen, or a sentinel loop. Diagnosis is ultimately made in 5–10% of very-low-birth-weight infants (<1,500g).

Diagnosis of NEC is more challenging in premature infants, due to inexplicit symptoms and radiographic signs. The most preterm infant is at highest risk of developing NEC.

Prevention
Prevention includes the use of breast milk and probiotics. A 2012 policy by the American Academy of Pediatrics recommended feeding preterm infants human milk, finding "significant short- and long-term beneficial effects," including reducing the rate of NEC by a factor of one-half to three-quarters.Small amounts of oral feeds of human milk starting as soon as possible, while the infant is being primarily fed intravenously, primes the immature gut to mature and become ready to receive greater intake by mouth. Human milk from a milk bank or donor can be used if mothers milk is unavailable. The gut mucosal cells do not get enough nourishment from arterial blood supply to stay healthy, especially in very premature infants, where the blood supply is limited due to immature development of the capillaries, so nutrients from the lumen of the gut are needed.Towards understanding intervention with human milk, experts have noted cows and human milk differ in their immunoglobular and glycan compositions. Due to their relative ease of production, human milk oligosaccharides (HMO) are a subject of particular interest in supplementation and intervention.A Cochrane review in 2020 found low- to moderate-quality evidence that supplementation of probiotics enterally "prevents severe NEC, as well as all-cause mortality in preterm infants" and that further high-quality trials are needed to inform policy and practice.Advancing enteral feed volumes at lower rates does not appear to reduce the risk of NEC or death in very preterm infants and seems to increase the risk of invasive infection.  Not beginning feeding an infant by mouth for more than 4 days does not appear to have protective benefits.

Treatment
If a baby is diagnosed with NEC, treatment should begin immediately. Treatment consists primarily of supportive care, including providing bowel rest by stopping enteral feeds, gastric decompression with intermittent suction, fluid repletion to correct electrolyte abnormalities and third-space losses, support for blood pressure, parenteral nutrition, and prompt antibiotic therapy.
Monitoring is clinical, although serial supine and left lateral decubitus abdominal X-rays should be performed every six hours.As an infant recovers from NEC, feeds are gradually introduced. "Trophic feeds" or low-volume feeds (<20 ml/kg/day) are usually initiated first. How and what to feed are determined by the extent of bowel involved, the need for surgical intervention, and the infants clinical appearance.Where the disease is not halted through medical treatment alone, or when the bowel perforates, immediate emergency surgery to resect the dead bowel is generally required, although abdominal drains may be placed in very unstable infants as a temporizing measure. Surgery may require a colostomy, which may be able to be reversed at a later time </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Strain (injury) and explain in detail? [/INST] A strain is an acute or chronic soft tissue injury that occurs to a muscle, tendon, or both. The equivalent injury to a ligament is a sprain. Generally, the muscle or tendon overstretches and partially tears, under more physical stress than it can withstand, often from a sudden increase in duration, intensity, or frequency of an activity. Strains most commonly occur in the foot, leg, or back. Immediate treatment typically includes five steps abbreviated as P.R.I.C.E.: protection, rest, ice, compression, elevation.

Signs and symptoms
Typical signs and symptoms of a strain include pain, functional loss of the involved structure, muscle weakness, contusion, and localized inflammation. A strain can range from mild overstretching to severe  tears, depending on the extent of injury.

Cause
A strain can occur as a result of improper body mechanics with any activity (e.g., contact sports, lifting heavy objects) that can induce mechanical trauma or injury. Generally, the muscle or tendon overstretches and is placed under more physical stress than it can withstand. Strains commonly result in a partial or complete tear of a tendon or muscle, or they can be severe in the form of a complete tendon rupture </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hunger and explain in detail? [/INST] In politics, humanitarian aid, and the social sciences, hunger is defined as a condition in which a person does not have the physical or financial capability to eat sufficient food to meet basic nutritional needs for a sustained period. In the field of hunger relief, the term hunger is used in a sense that goes beyond the common desire for food that all humans experience, also known as an appetite. The most extreme form of hunger, when malnutrition is widespread, and when people have started dying of starvation through lack of access to sufficient, nutritious food, leads to a declaration of famine.

Throughout history, portions of the worlds population have often suffered sustained periods of hunger. In many cases, hunger resulted from food supply disruptions caused by war, plagues, or adverse weather. In the decades following World War II, technological progress and enhanced political cooperation suggested it might be possible to substantially reduce the number of people suffering from hunger. While progress was uneven, by 2014, the threat of extreme hunger had receded for a large portion of the worlds population. According to the FAOs 2021 The State of Food Security and Nutrition in the World (SOFI) report, the number of people suffering from chronic hunger began to rise gradually between 2014 and 2019. In 2020, there was a significant increase, resulting in 768 million people suffering from malnutrition.While most of the worlds people continue to live in Asia, much of the increase in hunger since 2015 occurred in Africa and South America. The FAOs 2017 report discussed three principal reasons for the recent increase in hunger: climate, conflict, and economic slowdowns. The 2018 edition focused on extreme weather as a primary driver of the increase in hunger, finding rising rates to be especially severe in countries where agricultural systems were most sensitive to extreme weather variations. The 2019 SOFI report found a strong correlation between increases in hunger and countries that had suffered an economic slowdown. The 2020 edition instead looked at the prospects of achieving the hunger related Sustainable Development Goal (SDG). It warned that if nothing is done to counter the adverse trends of the past six years, the number of people suffering from chronic hunger is on track to rise by over 150 million by 2030. The 2021 report reported a sharp jump in hunger caused by the COVID-19 pandemic.
Many thousands of organizations are engaged in the field of hunger relief, operating at local, national, regional, or international levels. Some of these organizations are dedicated to hunger relief, while others may work in several different fields. The organizations range from multilateral institutions to national governments, to small local initiatives such as independent soup kitchens. Many participate in umbrella networks that connect thousands of different hunger relief organizations. At the global level, much of the worlds hunger relief efforts are coordinated by the UN and geared towards achieving SDG 2 of Zero Hunger by 2030.

Definition and related terms
There is one globally recognized approach for defining and measuring hunger generally used by those studying or working to relieve hunger as a social problem. This is the United Nations FAO measurement, which is typically referred to as chronic undernourishment (or in older publications, as food deprivation, chronic hunger, or just plain hunger.) For the FAO:

Hunger or chronic undernourishment exists when "caloric intake is below the minimum dietary energy requirement (MDER). The MDER is the amount of energy needed to perform light activity and to maintain a minimum acceptable weight for attained height." The FAO use different MDER thresholds for different countries, due to variations in climate and cultural factors. Typically a yearly "balance sheet" approach is used, with the minimum dietary energy requirement tallied against the estimated total calories consumed over the year. The FAO definitions differentiate hunger from malnutrition and food insecurity:
Malnutrition results from  "deficiencies, excesses or imbalances in the consumption of macro- and/or micro-nutrients." In the FAO definition, all hungry people suffer from malnutrition, but people who are malnourished may not be hungry. They may get sufficient raw calories to avoid hunger but lack essential micronutrients, or they may even consume an excess of raw calories and hence suffer from obesity.
Food insecurity occurs when people are at risk, or worried about, not being able to meet their preferences for food, including in terms of raw calories and nutritional value. In the FAO definition, all hungry people are food insecure, but not all food-insecure people are hungry (though there is a very strong overlap between hunger and severe food insecurity.). The FAO have reported that food insecurity quite often results in simultaneous stunted growth for children, and obesity for adults. For hunger relief actors operating at the global or regional level, an increasingly commonly used metric for food insecurity is the IPC scale.
Acute hunger is typically used to denote famine like hunger, though the phrase lacks a widely accepted formal definition. In the context of hunger relief, people experiencing acute huger may also suffer from chronic hunger. In contrast to the way the word acute is often used elsewhere, the word is used mainly to denote severity, not a lack of long term duration.Not all of the organizations in the hunger relief field use the FAO definition of hunger. Some use a broader definition that overlaps more fully with malnutrition. The alternative definitions do however tend to go beyond the commonly understood meaning of hunger as a painful or uncomfortable motivational condition; the desire for food is something that all humans frequently experience, even the most affluent, and is not in itself a social problem.Very low food supply can be described as "food insecure with hunger." A change in description was made in 2006 at the recommendation of the Committee on National Statistics (National Research Council, 2006) in order to distinguish the physiological state of hunger from indicators of food availability. Food insecure is when food intake of one or more household members was reduced and their eating patterns were disrupted at times during the year because the household lacked money and other resources for food. Food security statistics is measured by using survey data, based on household responses to items about whether the household was able to obtain enough food to meet their needs.

World statistics
The United Nations publish an annual report on the state of food security and nutrition across the world. Led by the FAO, the 2020 report was joint authored by four other UN agencies: the WFP, IFAD, WHO and UNICEF. Compared to older reports, the 2020 version revised down the numbers of people suffering from severe hunger, though this applied to figures for each year going back to 2000, so the trend for hunger to have increased since 2014 was still evident. The FAOs yearly report provides a statistical overview on the prevalence of hunger around the world, and is widely considered the main global reference for tracking hunger. No simple set of statistics can ever fully capture the multi dimensional nature of hunger however. Reasons include that the FAOs key metric for hunger, "undernourishment", is defined solely in terms of dietary energy availability – disregarding micro-nutrients such as vitamins or minerals. Second, the FAO uses the energy requirements for minimum activity levels as a benchmark; many people would not count as hungry by the FAOs measure yet still be eating too little to undertake hard manual labour, which might be the only sort of work available to them. Thirdly, the FAO statistics do not always reflect short-term undernourishment.
An alternative measure of hunger across the world is the Global Hunger Index (GHI). Unlike the FAOs measure, the GHI defines hunger in a way that goes beyond raw calorie intake, to include for example ingestion of micronutrients. GDI is a multidimensional statistical tool used to describe the state of countries’ hunger situation. The GHI measures progress and failures in the global fight against hunger. The GHI is updated once a year. The data from the 2015 report showed that Hunger levels have dropped 27% since 2000. Fifty two countries remained at serious or alarming levels. The 2019 GHI report expresses concern about the increase in hunger since 2015. In addition to the latest statistics on Hunger and Food Security, the GHI also features different special topics each year. The 2019 report includes an essay on hunger and climate change, with evidence suggesting that areas most vulnerable to climate change have suffered much of the recent increases in hunger.

The fight against hunger
Pre World War II
Throughout history, the need to aid those suffering from hunger has been commonly, though not universally, recognized. The philosopher Simone Weil wrote that feeding the hungry when you have resources to do so is the most obvious of all human obligations. She says that as far back as Ancient Egypt, many believed that people had to show they had helped the hungry in order to justify themselves in the afterlife. Weil writes that Social progress is commonly held to be first of all, "...a transition to a state of human society in which people will not suffer from hunger."
Social historian Karl Polanyi wrote that before markets became the worlds dominant form of economic organization in the 19th century, most human societies would either starve all together or not at all, because communities would invariably share their food.While some of the principles for avoiding famines had been laid out in the first book of the Bible, they were not always understood. Historical hunger relief efforts were often largely left to religious organizations and individual kindness. Even up to early modern times, political leaders often reacted to famine with bewilderment and confusion. From the first age of globalization, which began in the 19th century, it became more common for the elite to consider problems like hunger in global terms. However, as early globalization largely coincided with the high peak of influence for classical liberalism, there was relatively little call for politicians to address world hunger.In the late nineteenth and early twentieth century, the view that politicians ought not to intervene against hunger was increasingly challenged by campaigning journalists. There were also more frequent calls for large scale intervention against world hunger from academics and politicians, such as U.S. President Woodrow Wilson. Funded both by the government and private donations, the U.S. was able to dispatch millions of tons of food aid to European countries during and in the years immediately after WWI, organized by agencies such as the American Relief Administration. Hunger as an academic and social topic came to further prominence in the U.S. thanks to mass media coverage of the issue as a domestic problem during the Great Depression.

Efforts after World War II
While there had been increasing attention to hunger relief from the late 19th century, Dr David Grigg has summarised that prior to the end of World War II, world hunger still received relatively little academic or political attention; whereas after 1945 there was an explosion of interest in the topic.After World War II, a new international politico-economic order came into being, which was later described as Embedded liberalism. For at least the first decade after the war, the United States, then by far the periods most dominant national actor, was strongly supportive of efforts to tackle world hunger and to promote international development. It heavily funded the United Nations development programmes, and later the efforts of other multilateral organizations like the International Monetary Fund (IMF) and the World Bank (WB).The newly established United Nations became a leading player in co-ordinating the global fight against hunger. The UN has three agencies that work to promote food security and agricultural development: the Food and Agriculture Organization (FAO), the World Food Programme (WFP) and the International Fund for Agricultural Development (IFAD). FAO is the worlds agricultural knowledge agency, providing policy and technical assistance to developing countries to promote food security, nutrition and sustainable agricultural production, particularly in rural areas. WFPs key mission is to deliver food into the hands of the hungry poor. The agency steps in during emergencies and uses food to aid recovery after emergencies. Its longer term approaches to hunger helps the transition from recovery to development. IFAD, with its knowledge of rural poverty and exclusive focus on poor rural people, designs and implements programmes to help those people access the assets, services and opportunities they need to overcome poverty.Following successful post WWII reconstruction of Germany and Japan, the IMF and WB began to turn their attention to the developing world. A great many civil society actors were also active in trying to combat hunger, especially after the late 1970s when global media began to bring the plight of starving people in places like Ethiopia to wider attention.  Most significant of all, especially in the late 1960s and 70s, the Green revolution helped improved agricultural technology propagate throughout the world.The United States began to change its approach to the problem of world hunger from about the mid 1950s. Influential members of the administration became less enthusiastic about methods they saw as promoting an over reliance on the state, as they feared that might assist the spread of communism. By the 1980s, the previous consensus in favour of moderate government intervention had been displaced across the western world. The IMF and World Bank in particular began to promote market-based solutions. In cases where countries became dependent on the IMF, they sometimes forced national governments to prioritize debt repayments and sharply cut public services. This sometimes had a negative effect on efforts to combat hunger.

Organizations such as Food First raised the issue of food sovereignty and claimed that every country on earth (with the possible minor exceptions of some city-states) has sufficient agricultural capacity to feed its own people, but that the "free trade" economic order, which from the late 1970s to about 2008 had been associated with such institutions as the IMF and World Bank, had prevented this from happening. The World Bank itself claimed it was part of the solution to hunger, asserting that the best way for countries to break the cycle of poverty and hunger was to build export-led economies that provide the financial means to buy foodstuffs on the world market. However, in the early 21st century the World Bank and IMF became less dogmatic about promoting free market reforms. They increasingly returned to the view that government intervention does have a role to play, and that it can be advisable for governments to support food security with policies favourable to domestic agriculture, even for countries that do not have a Comparative advantage in that area. As of 2012, the World Bank remains active in helping governments to intervene against hunger.Until at least the 1980s—and, to an extent, the 1990s—the dominant academic view concerning world hunger was that it was a problem of demand exceeding supply. Proposed solutions often focused on boosting food production, and sometimes on birth control. There were exceptions to this, even as early as the 1940s, Lord Boyd-Orr, the first head of the UNs FAO, had perceived hunger as largely a problem of distribution, and drew up comprehensive plans to correct this. Few agreed with him at the time, however, and he resigned after failing to secure support for his plans from the US and Great Britain. In 1998, Amartya Sen won a Nobel Prize in part for demonstrating that hunger in modern times is not typically the product of a lack of food. Rather, hunger usually arises from food distribution problems, or from governmental policies in the developed and developing world. It has since been broadly accepted that world hunger results from issues with the distribution as well as the production of food.  Sens 1981 essay Poverty and Famines: An Essay on Entitlement and Deprivation played a prominent part in forging the new consensus.In 2007 and 2008, rapidly increasing food prices caused a global food crisis. Food riots erupted in several dozen countries; in at least two cases, Haiti and Madagascar, this led to the toppling of governments. A second global food crisis unfolded due to the spike in food prices of late 2010 and early 2011. Fewer food riots occurred, due in part to greater availability of food stock piles for relief. However, several analysts argue the food crisis was one of the causes of the Arab Spring.

Efforts since the global 2008 crisis
In the early 21st century, the attention paid to the problem of hunger by the leaders of advanced nations such as those that form the G8 had somewhat subsided. Prior to 2009, large scale efforts to fight hunger were mainly undertaken by governments of the worst affected countries, by civil society actors, and by multilateral and regional organizations. In 2009, Pope Benedict published his third encyclical, Caritas in Veritate, which emphasised the importance of fighting against hunger. The encyclical was intentionally published immediately before the July 2009 G8 Summit to maximise its influence on that event. At the Summit, which took place at LAquila in central Italy, the LAquila Food Security Initiative was launched, with a total of US$22 billion committed to combat hunger.Food prices fell sharply in 2009 and early 2010, though analysts credit this much more to farmers increasing production in response to the 2008 spike in prices, than to the fruits of enhanced government action. However, since the 2009 G8 summit, the fight against hunger became a high-profile issue among the leaders of the worlds major nations and was a prominent part of the agenda for the 2012 G-20 summit.In April 2012, the Food Assistance Convention was signed, the worlds first legally binding international agreement on food aid. The May 2012 Copenhagen Consensus recommended that efforts to combat hunger and malnutrition should be the first priority for politicians and private sector philanthropists looking to maximize the effectiveness of aid spending. They put this ahead of other priorities, like the fight against malaria and AIDS. Also in May 2012, U.S. President Barack Obama launched a "new alliance for food security and nutrition"—a broad partnership between private sector, governmental and civil society actors—that aimed to "...achieve sustained and inclusive agricultural growth and raise 50 million people out of poverty over the next 10 years." The UKs prime minister David Cameron held a hunger summit on 12 August, the last day of the 2012 Summer Olympics.The fight against hunger has also been joined by an increased number of regular people. While folk throughout the world had long contributed to efforts to alleviate hunger in the developing world, there has recently been a rapid increase in the numbers involved in tackling domestic hunger even within the economically advanced nations of the Global North. This had happened much earlier in North America than it did in Europe. In the US, the Reagan administration scaled back welfare the early 1980s, leading to a vast increase of charity sector efforts to help Americans unable to buy enough to eat. According to a 1992 survey of 1000 randomly selected US voters, 77% of Americans had contributed to efforts to feed the hungry, either by volunteering for various hunger relief agencies such as food banks and soup kitchens, or by donating cash or food.
Europe, with its more generous welfare system, had little awareness of domestic hunger until the food price inflation that began in late 2006, and especially as austerity-imposed welfare cuts began to take effect in 2010. Various surveys reported that upwards of 10% of Europes population had begun to suffer from food insecurity. Especially since 2011, there has been a substantial increase in grass roots efforts to help the hungry by means of food banks, within both the UK and continental Europe.

By July 2012, the 2012 US drought had already caused a rapid increase in the price of grain and soy, with a knock on effect on the price of meat. As well as affecting hungry people in the US, this caused prices to rise on the global markets; the US is the worlds biggest exporter of food. This led to much talk of a possible third 21st century global food crisis. The Financial Times reported that the BRICS may not be as badly affected as they were in the earlier crises of 2008 and 2011. However, smaller developing countries that must import a substantial portion of their food could be hard hit. The UN and G20 has begun contingency planning so as to be ready to intervene if a third global crisis breaks out.
By August 2013 however, concerns had been allayed, with above average grain harvests expected from major exporters, including Brazil, Ukraine and the U.S. 2014 also saw a good worldwide harvest, leading to speculation that grain prices could soon begin to fall.In an April 2013 summit held in Dublin concerning Hunger, Nutrition, Climate Justice, and the post 2015 MDG framework for global justice, Irelands President Higgins said that only 10% of deaths from hunger are due to armed conflict and natural disasters, with ongoing hunger being both the "greatest ethical failure of the current global system" and the "greatest ethical challenge facing the global community."
$4.15 billion of new commitments were made to tackle hunger at a June 2013 Hunger Summit held in London, hosted by the governments of Britain and Brazil, together with The Childrens Investment Fund Foundation.Despite the hardship caused by the 2007–2009 financial crisis and global increases in food prices that occurred around the same time, the UNs global statistics show it was followed by close to year on year reductions in the numbers suffering from hunger around the world. By 2019 however, evidence had mounted that this progress seemed to have gone into reverse over the last four years. The numbers suffering from hunger had risen both in absolute terms and very slightly even as a percentage of the worlds population.In 2019, FAO its annual edition of The State of Food and Agriculture which asserted that food loss and waste has potential effects on food security and nutrition through changes in the four dimensions of food security: food availability, access, utilization and stability. However, the links between food loss and waste reduction and food security are complex, and positive outcomes are not always certain. Reaching acceptable levels of food security and nutrition inevitably implies certain levels of food loss and waste. Maintaining buffers to ensure food stability requires a certain amount of food to be lost or wasted. At the same time, ensuring food safety involves discarding unsafe food, which then is counted as lost or wasted, while higher-quality diets tend to include more highly perishable foods. How the impacts on the different dimensions of food security play out and affect the food security of different population groups depends on where in the food supply chain the reduction in losses or waste takes place as well as on where nutritionally vulnerable and food-insecure people are located geographically.In April and May 2020, concerns were expressed that the COVID-19 pandemic could result in a doubling in global hunger unless world leaders acted to prevent this. Agencies such as the WFP have warned that this could include the number of people facing acute hunger rising from 135 million to about 265 million by the end of 2020. Indications of extreme hunger have been seen in various cities, such as fatal stampedes when word spread that emergency food aid was being handed out. Letters calling for co-ordinated action to offset the effects of the COVID-19 pandemic have been written to the G20 and G7, by various actors including NGOs, UN staff, corporations, academics and former national leaders.
Following the 2022 invasion of Ukraine, concerns have been raised over hunger resulting from rising food prices. This is forecast to risk civil unrest even in many middle income countries, where government capability to protect their populations was largely exhausted by the Covid pandemic, and has not yet recovered.

Hunger relief organisations
Many thousands of hunger relief organisations exist across the world. Some but not all are entirely dedicated to fighting hunger. They range from independent soup kitchens that serve only one locality,  to global organisations. Organisations working at the global and regional level will often focus much of their efforts on helping hungry communities to better feed themselves, for example by sharing agricultural technology. With some exceptions, organisations that work just on the local level tend to focus more on providing food directly to hungry people.  Many of the entities are connected by a web of national, regional and global alliances that help them share resources, knowledge, and coordinate efforts.

Global
The United Nations is central to global efforts to relieve hunger, most especially through the FAO, and also via other agencies: such as WFP, IFAD, WHO and UNICEF.  After the Millennium Development Goals expired in 2015, the Sustainable Development Goals (SDGs) became key objectives to shape the worlds response to development challenges such as hunger. In particular Goal 2: Zero Hunger sets globally agreed targets to end hunger, achieve food security and improved nutrition and promote sustainable agriculture.Aside from the UN agencies themselves,  hundreds of other actors address the problem of hunger on the global level, often involving participation in large umbrella organisations. These include national governments, religious groups, international charities and in some cases international corporations. Though except perhaps in the cases of dedicated charities, the priority these organisations assign to hunger relief may vary from year to year.  In many cases the organisations partner with the UN agencies, though often they pursue independent goals. For example, as consensus began to form  for the SDG zero hunger goal to aim to end hunger by 2030, a number of organizations formed initiatives with the more ambitious target to achieve this outcome early, by 2025:

In 2013 Caritas International started a Caritas-wide initiative aimed at ending systemic hunger by 2025. The One human family, food for all campaign focuses on awareness raising, improving the impact of Caritas programs and advocating the implementation of the right to food.
The partnership Compact2025, led by IFPRI with the involvement of UN organisations, NGOs and private foundations develops and disseminates evidence-based advice to politicians and other decision-makers aimed at ending hunger and undernutrition in the coming 10 years, by 2025.  It bases its claim that hunger can be ended by 2025 on a report by Shenggen Fan and Paul Polman that analyzed the experiences from China, Vietnam, Brazil and Thailand and concludes that eliminating hunger and undernutrition was possible by 2025.
In June 2015, the European Union and the Bill & Melinda Gates Foundation have launched a partnership to combat undernutrition especially in children. The program will initially be implemented in Bangladesh, Burundi, Ethiopia, Kenya, Laos and Niger and will help these countries to improve information and analysis about nutrition so they can develop effective national nutrition policies.

Sustainable Development Goal 2 (SDG 2 or Goal 2)
The objective of SDG 2 is to "end hunger, achieve food security and improved nutrition and promote sustainable agriculture" by 2030. 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.

Local
Food bank
A food bank (or foodbank) is a non-profit, charitable organization that aids in the distribution of food to those who have difficulty purchasing enough to avoid hunger. Food banks tend to run on different operating models depending on where they are located. In the U.S., Australia, and to some extent in Canada, foodbanks tend to perform a warehouse type function, storing and delivering food to front line food orgs, but not giving it directly to hungry peoples themselves. In much of Europe and elsewhere, food banks operate on the front line model, where they hand out parcels of uncooked food direct to the hungry, typically giving them enough for several meals which they can eat in their homes. In the U.S and Australia, establishments that hand out uncooked food to individual people are instead called food pantries, food shelves or food closets.
In Less Developed Countries, there are charity-run food banks that operate on a semi-commercial system that differs from both the more common "warehouse" and "frontline" models. In some rural LDCs such as Malawi, food is often relatively cheap and plentiful for the first few months after the harvest, but then becomes more and more expensive. Food banks in those areas can buy large amounts of food shortly after the harvest, and then as food prices start to rise, they sell it back to local people throughout the year at well below market prices. Such food banks will sometimes also act as centers to provide small holders and subsistence farmers with various forms of support.

Soup kitchen
A soup kitchen, meal center, or food kitchen is a place where food is offered to the hungry for free or at a below market price. Frequently located in lower-income neighborhoods, they are often staffed by volunteer organizations, such as church or community groups. Soup kitchens sometimes obtain food from a food bank for free or at a low price, because they are considered a charity, which makes it easier for them to feed the many people who require their services.

Others
Local establishments calling themselves "food banks" or "soup kitchens" are often run either by Christian churches or less frequently by secular civil society groups.  Other religions carry out similar hunger relief efforts, though sometimes with slightly different methods. For example, in the Sikh tradition of Langar, food is served to the hungry direct from Sikh temples. There are exceptions to this, for example in the UK Sikhs run some of the food banks, as well as giving out food direct from their Gurdwaras.

Hunger and gender
In both developing and advanced countries, parents sometimes go without food so they can feed their children. Women, however, seem more likely to make this sacrifice than men. World Bank studies consistently find that about 60% of those who are hungry are female. The apparent explanation for this imbalance is that, compared to men, women often forgo meals in order to feed their children. Older sources sometimes claim this phenomenon is unique to developing countries, due to greater sexual inequality. More recent findings suggested that mothers often miss meals in advanced economies too. For example, a 2012 study undertaken by Netmums in the UK found that one in five mothers sometimes misses out on food to save their children from hunger.In several periods and regions, gender has also been an important factor determining whether or not victims of hunger would make suitable examples for generating enthusiasm for hunger relief efforts. James Vernon, in his Hunger: A Modern History, wrote that in Britain before the 20th century, it was generally only women and children suffering from hunger who could arouse compassion. Men who failed to provide for themselves and their families were often regarded with contempt.This changed after World War I, where thousands of men who had proved their manliness in combat found themselves unable to secure employment. Similarly, female gender could be advantageous for those wishing to advocate for hunger relief, with Vernon writing that being a woman helped Emily Hobhouse draw the plight of hungry people to wider attention during the Second Boer War.

Hunger and age
The elderly are among some of the most vulnerable populations; increasing their risk of going hungry as well as significantly increasing the negative effects of hunger.  The number of seniors experiencing hunger rose 88% between the years of 2001 and 2011.  Researchers predict that if this upwards trend continues, the amount of food insecure seniors will increase by 50% by 2025.This age group suffers the most from chronic conditions, including heart disease, diabetes, and respiratory diseases.  Eighty percent of this group has a minimum of one chronic condition, and almost 70% have two or more. These illnesses are exacerbated and are more likely to develop under the addition of hunger.  A report from 2017 shows that seniors facing this issue are 60% more likely to experience depression than seniors who are not hungry, and 40% are more likely to develop congestive heart failure.  The added stress of inconsistent and inadequate feedings make these conditions much more dangerous.Fixed incomes often limit the elderly’s ability to freely purchase food necessities.  Medical costs and housing may take priority over quality foods.  Limited mobility makes it difficult for these individuals to physically leave their homes, especially in areas lacking public transportation or transportation catering to a disabled body.  The COVID-19 pandemic has made things even more difficult, as this group is extremely vulnerable to contracting variants.  They are high-risk, and are faced with the threat of this disease, more so than other age groups, when they leave their homes.  This continues to limit their food access.
The Supplemental Nutrition Assistance Program (SNAP) provides aid to low-income seniors in relation to food security.  This is an opportunity for seniors who receive benefits to allocate money in their budgets for other needs, such as medical or housing bills </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Acute-phase protein and explain in detail? [/INST] Acute-phase proteins (APPs) are a class of proteins whose concentrations in blood plasma either increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction (also called acute-phase response). The acute-phase reaction characteristically involves fever, acceleration of peripheral leukocytes, circulating neutrophils and their precursors. The terms acute-phase protein and acute-phase reactant (APR) are often used synonymously, although some APRs are (strictly speaking) polypeptides rather than proteins.
In response to injury, local inflammatory cells (neutrophil granulocytes and macrophages) secrete a number of cytokines into the bloodstream, most notable of which are the interleukins IL1, and IL6, and TNF-α.  The liver responds by producing many acute-phase reactants. At the same time, the production of a number of other proteins is reduced; these proteins are, therefore, referred to as "negative" acute-phase reactants. Increased acute-phase proteins from the liver may also contribute to the promotion of sepsis.

Regulation of synthesis
TNF-α, IL-1β and IFN-γ are important for the expression of inflammatory mediators such as prostaglandins and leukotrienes, and they also cause the production of platelet-activating factor and IL-6. After stimulation with proinflammatory cytokines, Kupffer cells produce IL-6 in the liver and present it to the hepatocytes. IL-6 is the major mediator for the hepatocytic secretion of APPs. Synthesis of APP can also be regulated indirectly by cortisol. Cortisol can enhance expression of IL-6 receptors in liver cells and induce IL-6-mediated production of APPs.

Positive
Positive acute-phase proteins serve (as part of the innate immune system) different physiological functions within the immune system. Some act to destroy or inhibit growth of microbes, e.g., C-reactive protein, mannose-binding protein, complement factors, ferritin, ceruloplasmin, serum amyloid A and haptoglobin. Others give negative feedback on the inflammatory response, e.g. serpins. Alpha 2-macroglobulin and coagulation factors affect coagulation, mainly stimulating it. This pro-coagulant effect may limit infection by trapping pathogens in local blood clots </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Nitrovasodilator and explain in detail? [/INST] A nitrovasodilator is a pharmaceutical agent that causes vasodilation (widening of blood vessels) by donation of nitric oxide (NO), and is mostly used for the treatment and prevention of angina pectoris.
This group of drugs includes nitrates (esters of nitric acid), which are reduced to NO in the body, as well as some other substances.

Examples
Here is a list of examples of the nitrate type (in alphabetical order):

Nitrovasodilators which arent nitrates include molsidomine and its active metabolite linsidomine, as well as sodium nitroprusside. These substances do not need to be reduced to donate NO.

Medical uses
The nitrates are used for the treatment and prevention of angina and acute myocardial infarction, while molsidomine acts too slowly to be useful for the treatment of acute angina. For quick action in the treatment of angina, glyceryl trinitrate is used in form of a sublingual spray (nitro spray) or as soft capsules to be crunched.Nitroprusside is used intravenously for the treatment of hypertensive crises, heart failure, and lowering of blood pressure during surgery.

Contraindications
Nitrovasodilators are contraindicated under circumstances where lowering of blood pressure can be dangerous. This includes, with some variation between the individual substances, severe hypotension (low blood pressure), shock including cardiogenic shock, and anaemia. Whether a specific drug is useful or harmful under heart failure and myocardial infarction depends on its speed of action: Fast acting substances such as glyceryl trinitrate and nitroprusside can be helpful for controlling blood pressure and consequently the amount of blood the heart has to pump, if the application is monitored continuously. Slow acting substances would hold the danger of ischaemia due to an uncontrollably low blood pressure and are therefore contraindicated. Depending on the circumstances, even fast acting substances can be contraindicated – for example, glyceryl trinitrate in patients with obstructive heart failure.These drugs are also contraindicated in patients that have recently taken PDE5 inhibitors such as sildenafil (Viagra).

Adverse effects
Most side effects are direct consequences of the vasodilation and the following low blood pressure. They include headache ("nitrate headache") resulting from the widening of blood vessels in the brain, reflex tachycardia (fast heart rate), flush, dizziness, nausea and vomiting. These effects usually subside after a few days if the treatment is continued.Occasionally, severe hypotension occurs shortly after beginning of treatment, possibly resulting in intensified angina symptoms or syncope, sometimes with bradycardia (slow heart rate).

Interactions
A number of drugs add to the low blood pressure caused by nitrovasodilators: for example, other vasodilators, antihypertensive drugs, tricyclic antidepressantss, antipsychotics, general anaesthetics, as well as ethanol. Combination with PDE5 inhibitors, including sildenafil (Viagra), is contraindicated because potentially life-threatening hypotension may occur.Nitrates increase the bioavailability of dihydroergotamine (DHE). High DHE levels may result in coronary spasms in patients with coronary disease. This interaction is not described for non-nitrate nitrovasodilators.

Mechanism of action
Nitrovasodilators are prodrugs that donate NO by various mechanisms. Nitrates undergo chemical reduction, likely mediated by enzymes. Molsidomine and nitroprusside already contain nitrogen in the right oxidation state (+2) and liberate NO without the aid of enzymes.NO stimulates the soluble form of the enzyme guanylate cyclase in the smooth muscle cells of blood vessels. Guanylate cyclase produces cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). cGMP in turn activates cyclic nucleotide-dependent protein kinase G, which phosphorylates various proteins that play a role in decreasing intracellular calcium levels, leading to relaxation of the muscle cells and thus to dilation of blood vessels.The most important effect in angina is the widening of veins, which increases their capacity to hold blood ("venous pooling") and reduces the pressure of the blood returning to the heart (the preload). Widening of the large arteries also reduces the pressure against which the heart has to pump, the afterload </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Muscle atrophy and explain in detail? [/INST] Muscle atrophy is the loss of skeletal muscle mass. It can be caused by immobility, aging, malnutrition, medications, or a wide range of injuries or diseases that impact the musculoskeletal or nervous system. Muscle atrophy leads to muscle weakness and causes disability.
Disuse causes rapid muscle atrophy and often occurs during injury or illness that requires immobilization of a limb or bed rest. Depending on the duration of disuse and the health of the individual, this may be fully reversed with activity. Malnutrition first causes fat loss but may progress to muscle atrophy in prolonged starvation and can be reversed with nutritional therapy. In contrast, cachexia is a wasting syndrome caused by an underlying disease such as cancer that causes dramatic muscle atrophy and cannot be completely reversed with nutritional therapy. Sarcopenia is age-related muscle atrophy and can be slowed by exercise. Finally, diseases of the muscles such as muscular dystrophy or myopathies can cause atrophy, as well as damage to the nervous system such as in spinal cord injury or stroke. Thus, muscle atrophy is usually a finding (sign or symptom) in a disease rather than being a disease by itself. However, some syndromes of muscular atrophy are classified as disease spectrums or disease entities rather than as clinical syndromes alone, such as the various spinal muscular atrophies.
Muscle atrophy results from an imbalance between protein synthesis and protein degradation, although the mechanisms are incompletely understood and are variable depending on the cause. Muscle loss can be quantified with advanced imaging studies but this is not frequently pursued. Treatment depends on the underlying cause but will often include exercise and adequate nutrition. Anabolic agents may have some efficacy but are not often used due to side effects. There are multiple treatments and supplements under investigation but there are currently limited treatment options in clinical practice. Given the implications of muscle atrophy and limited treatment options, minimizing immobility is critical in injury or illness.

Signs and symptoms
The hallmark sign of muscle atrophy is loss of lean muscle mass. This change may be difficult to detect due to obesity, changes in fat mass or edema. Changes in weight, limb or waist circumference are not reliable indicators of muscle mass changes.The predominant symptom is increased weakness which may result in difficulty or inability in performing physical tasks depending on what muscles are affected. Atrophy of the core or leg muscles may cause difficulty standing from a seated position, walking or climbing stairs and can cause increased falls. Atrophy of the throat muscles may cause difficulty swallowing and diaphragm atrophy can cause difficulty breathing. Muscle atrophy can be asymptomatic and may go undetected until a significant amount of muscle is lost.

Causes
Skeletal muscle serves as a storage site for amino acids that can be used for energy production when demands are high or supplies are low. If metabolic demands remain greater than protein synthesis, muscle mass is lost. Many diseases and conditions can lead to this imbalance, either through the disease itself or disease associated appetite-changes. Causes of muscle atrophy, include immobility, aging, malnutrition, certain systemic diseases (cancer, congestive heart failure; chronic obstructive pulmonary disease; AIDS, liver disease, etc.), deinnervation, intrinsic muscle disease or medications (such as glucocorticoids).

Immobility
Disuse is a common cause of muscle atrophy and can be local (due to injury or casting) or general (bed-rest). The rate of muscle atrophy from disuse (10-42 days) is  approximately 0.5–0.6% of total muscle mass per day although there is considerable variation between people. The elderly are the most vulnerable to dramatic muscle loss with immobility. Much of the established research has investigated prolonged disuse (>10 days), in which the muscle is compromised primarily by declines in muscle protein synthesis rates rather than changes in muscle protein breakdown. There is evidence to suggest that there may be more active protein breakdown during short term immobility (<10 days).

Cachexia
Certain diseases can cause a complex muscle wasting syndrome known as cachexia. It is commonly seen in cancer, congestive heart failure, chronic obstructive pulmonary disease, chronic kidney disease and AIDS although it is associated with many disease processes, usually with a significant inflammatory component. Cachexia causes ongoing muscle loss that is not entirely reversed with nutritional therapy. The pathophysiology is incompletely understood but inflammatory cytokines are considered to play a central role. In contrast to weight loss from inadequate caloric intake, cachexia causes predominantly muscle loss instead of fat loss and it is not as responsive to nutritional intervention. Cachexia can significantly compromise quality of life and functional status and is associated with poor outcomes.

Sarcopenia
Sarcopenia is the degenerative loss of skeletal muscle mass, quality, and strength associated with aging. This involves muscle atrophy, reduction in number of muscle fibers and a shift towards "slow twitch" or type I skeletal muscle fibers over "fast twitch" or type II fibers. The rate of muscle loss is dependent on exercise level, co-morbidities, nutrition and other factors. There are many proposed mechanisms of sarcopenia and is considered to be the result of changes in muscle synthesis signalling pathways and gradual failure in the satellite cells which help to regenerate skeletal muscle fibers, but is incompletely understood.Sarcopenia can lead to reduction in functional status and cause significant disability but is a distinct condition from cachexia although they may co-exist. In 2016 an ICD code for sarcopenia was released, contributing to its acceptance as a disease entity.

Intrinsic muscle diseases
Muscle diseases, such as muscular dystrophy, amyotrophic lateral sclerosis (ALS), or myositis such as inclusion body myositis can cause muscle atrophy.

Central nervous system damage
Damage to neurons in the brain or spinal cord can cause prominent muscle atrophy. This can be localized muscle atrophy and weakness or paralysis such as in stroke or spinal cord injury. More widespread damage such as in traumatic brain injury or cerebral palsy can cause generalized muscle atrophy.

Peripheral nervous system damage
Injuries or diseases of peripheral nerves supplying specific muscles can also cause muscle atrophy. This is seen in nerve injury due to trauma or surgical complication, nerve entrapment, or inherited diseases such as Charcot-Marie-Tooth disease.

Medications
Some medications are known to cause muscle atrophy, usually due to direct effect on muscles. This includes glucocorticoids causing glucocorticoid myopathy or medications toxic to muscle such as doxorubicin.

Endocrinopathies
Disorders of the endocrine system such as Cushings disease or hypothyroidism are known to cause muscle atrophy.

Pathophysiology
Muscle atrophy occurs due to an imbalance between the normal balance between protein synthesis and protein degradation. This involves complex cell signalling that is incompletely understood and muscle atrophy is likely the result of multiple contributing mechanisms.Mitochondrial function is crucial to skeletal muscle health and detrimental changes at the level of the mitochondria may contribute to muscle atrophy. A decline in mitochondrial density as well as quality is consistently seen in muscle atrophy due to disuse.The ATP-dependent ubiquitin/proteasome pathway is one mechanism by which proteins are degraded in muscle. This involves specific proteins being tagged for destruction by a small peptide called ubiquitin which allows recognition by the proteasome to degrade the protein.

Diagnosis
Screening for muscle atrophy is limited by a lack of established diagnostic criteria, although many have been proposed. Diagnostic criteria for other conditions such as sarcopenia or cachexia can be used. These syndromes can also be identified with screening questionnaires.Muscle mass and changes can be quantified on imaging studies such as CT scans or Magnetic resonance imaging (MRI). Biomarkers such as urine urea can be used to roughly estimate muscle loss during circumstances of rapid muscle loss. Other biomarkers are currently under investigation but are not used in clinical practice.

Treatment
Muscle atrophy can be delayed, prevented and sometimes reversed with treatment. Treatment approaches include impacting the signaling pathways that induce muscle hypertrophy or slow muscle breakdown as well as optimizing nutritional status.Physical activity provides a significant anabolic muscle stimulus and is a crucial component to slowing or reversing muscle atrophy. It is still unknown regarding the ideal exercise "dosing." Resistance exercise has been shown to be beneficial in reducing muscle atrophy in older adults. In patients who cannot exercise due to physical limitations such as paraplegia, functional electrical stimulation can be used to externally stimulate the muscles.Adequate calories and protein is crucial to prevent muscle atrophy. Protein needs may vary dramatically depending on metabolic factors and disease state, so high-protein supplementation may be beneficial. Supplementation of protein or branched-chain amino acids, especially leucine, can provide a stimulus for muscle synthesis and inhibit protein breakdown and has been studied for muscle atrophy for sarcopenia and cachexia. β-Hydroxy β-methylbutyrate (HMB), a metabolite of leucine which is sold as a dietary supplement, has demonstrated efficacy in preventing the loss of muscle mass in several muscle wasting conditions in humans, particularly sarcopenia. Based upon a meta-analysis of seven randomized controlled trials that was published in 2015, HMB supplementation has efficacy as a treatment for preserving lean muscle mass in older adults. More research is needed to determine the precise effects of HMB on muscle strength and function in various populations.In severe cases of muscular atrophy, the use of an anabolic steroid such as methandrostenolone may be administered to patients as a potential treatment although use is limited by side effects. A novel class of drugs, called selective androgen receptor modulators, is being investigated with promising results. They would have fewer side effects, while still promoting muscle and bone tissue growth and regeneration. These effects have yet to be confirmed in larger clinical trials.

Outcomes
Outcomes of muscle atrophy depend on the underlying cause and the health of the patient. Immobility or bed rest in populations predisposed to muscle atrophy, such as the elderly or those with disease states that commonly cause cachexia, can cause dramatic muscle atrophy and impact on functional outcomes. In the elderly, this often leads to decreased biological reserve and increased vulnerability to stressors known as the "frailty syndrome." Loss of lean body mass is also associated with increased risk of infection, decreased immunity, and poor wound healing. The weakness that accompanies muscle atrophy leads to higher risk of falls, fractures, physical disability, need for institutional care, reduced quality of life, increased mortality, and increased healthcare costs.

Other animals
Inactivity and starvation in mammals lead to atrophy of skeletal muscle, accompanied by a smaller number and size of the muscle cells as well as lower protein content </s>