Effect of chronic pain in the workplace
In the workplace, chronic pain conditions are a significant problem for both the person with the condition and the organization; a problem only expected to increase in many countries due to an aging workforce. In light of this, it may be helpful for organizations to consider the social environment of their workplace, and how it may be working to ease or worsen chronic pain issues for employees. As an example of how the social environment can affect chronic pain, some research has found that high levels of socially prescribed perfectionism (perfectionism induced by external pressure from others, such as a supervisor) can interact with the guilt felt by a person with chronic pain, thereby increasing job tension, and decreasing job satisfaction. Mobility and road safety impacts
A 2022 systematic review found that chronic pain could increase crash risk among drivers. Chronic pain drivers report experiencing difficulties with safety maneuvers, such as shoulder checking for blind spots, merging with traffic, turning corners, and reversing the vehicle. See also
Childhood chronic pain
Neuroinflammation
Neurodegeneration
Dopaminergic pathways

References
Further reading
External links
Chronic Pain Syndromes at Curlie
 Media related to pain at Wikimedia Commons
International Association for the Study of Pain Archived 2021-05-01 at the Wayback Machine
These sweeteners are not common in formulas used today. Symptoms such as vomiting, nausea, restlessness, pallor, sweating, trembling and lethargy can also first present in infants when they are introduced to fruits and vegetables. These can progress to apathy, coma and convulsions if the source is not recognized early.When patients are diagnosed with HFI, a dietary history will often reveal an aversion to fruit and other foods that contain large amounts of fructose. Most adult patients do not have any dental caries. Fructose metabolism
After ingestion, fructose is converted to fructose-1-phosphate in the liver by fructokinase. Deficiencies of fructokinase cause essential fructosuria, a clinically benign condition characterized by the excretion of unmetabolized fructose in the urine. Fructose-1-phosphate is metabolized by aldolase B into dihydroxyacetone phosphate and glyceraldehyde. HFI is caused by a deficiency of aldolase B.A deficiency of aldolase B results in an accumulation of fructose-1-phosphate, and trapping of phosphate (fructokinase requires adenosine triphosphate (ATP)). The downstream effects of this enzyme block are the inhibition of glucose production and reduced regeneration of ATP. Diagnosis
Because of the ease of therapy (dietary exclusion of fructose), HFI can be effectively managed if properly diagnosed. In HFI, the diagnosis of homozygotes is difficult, requiring a genomic DNA screening with allele-specific probes or an enzyme assay from a liver biopsy.