Assessing social anhedonia
There are several self-report psychometric measures of schizotypy which each contain subscales related to social anhedonia:

Revised Social Anhedonia Scale—Chapman Psychosis Proneness Scales
No Close Friends Subscale – Schizotypal Personality Questionnaire
Introverted Anhedonia Subscale—Oxford–Liverpool Inventory of Feelings and Experiences

Genetic components
L.J. and J.P. Chapman were the first to discuss the possibility that social anhedonia may stem from a genetic vulnerability. The disrupted in schizophrenia 1 (DISC1) gene has been consistently associated with risk for, and cause of, schizophrenia-spectrum disorders and other mental illnesses. More recently, DISC1 has been associated with social anhedonia within the general population. Tomppo identified a specific DISC1 allele that is associated with an increase in characteristics of social anhedonia. They also identified a DISC1 allele associated with decreased characteristics of social anhedonia, that was found to be preferentially expressed in women. More research needs to be conducted, but social anhedonia may be an important intermediate phenotype (endophenotype) between genes associated with risk for schizophrenia and phenotype of the disorder. Neurobiological correlates
Researchers studying the neurobiology of social anhedonia posit that this trait may be linked to dysfunction of reward-related systems in the brain. This circuitry is critical for the sensation of pleasure, the computation of reward benefits and costs, determination of the effort required to obtain a pleasant stimulus, deciding to obtain that stimulus, and increasing motivation to obtain the stimulus.
Facial eczema is a mycotoxic disease that affects the liver of several animals, mainly sheep and cattle, but can also infect other ungulates. It is caused by ingesting sporidesmins released by the fungus Pithomyces chartarum. Its visible symptoms are characterized by red skin that turns black and crusty before peeling off, as well as inflammation that can cause swelling of the udder, teats, ears and face. The disease is not always visible. Other symptoms include weight loss, weakness and death. P. chartarum
It grows mostly in New Zealand but also occurs in Australia, France, South Africa, and South America. The fungus grows on dead plants, especially on perennial ryegrass near the ground (25mm height). It most commonly grows between January and May, as it requires warm, humid conditions, as well as moisture at ground level. Areas of spore growth can include urine patches and areas sheltered by hedges. The fungus grows in clusters and is normally invisible to human eye. It produces millions of spores with the toxic substance sporidesmin. Fresh spores are particularly toxic. Contaminated pasture loses its toxicity after 2 weeks. Pathophysiology
The incubation period is 7-20 days after poison intake. Sporidesmin is hepatotoxic and leads to hepatogenous photosensitization and phylloerythrin accumulation in the bloodstream. It damages the bile ducts and then the liver. The worst case is liver necrosis. This causes – as a secondary effect – photosensitization, this means the inflammation of unpigmented areas and exposed skin (ears, teat, face) and photodynamic dermatitis. Only 5% of affected animals show the respective clinical signs.