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Research in mice suggests that a history of obesity is linked to a higher risk of age-related macular degeneration. Image credit: Dylan Pahl/EyeEm/Getty Images.
  • Researchers investigated how obesity affects the risk for age-related macular degeneration (AMD) in mouse models.
  • They found that a history of obesity increases AMD risk — even if mice have lost weight and are no longer obese.
  • Further research is needed to see whether these findings translate over to humans.

Age-related macular degeneration (AMD) is a neuroinflammatory condition and the leading cause of blindness globally. Experts believe it arises due to genetic and environmental risk factors.

After smoking, obesity is the most important genetic risk factor for late AMD. Studies show that stressors such as obesity or pathogens like bacteria and viruses cause inflammation in the eye.

While there is abundant research on genetic risk factors for AMD, there is little research on how environmental and lifestyle influence risk for the condition.

Further research into how lifestyle and environmental factors affect AMD could explain why some people with AMD-related genes do not develop the condition. It could also inform treatment and prevention strategies.

Recently, researchers investigated how changes in body fat affected AMD risk in mice.

“The study suggests that diet-induced obesity earlier in life changes the immune system […] which may then [increase risk for] AMD,” Dr. Radwan Ajlan, an ophthalmologist at the University of Kansas Health System, not involved in the study, told Medical News Today.

The study appears in the journal Science.

For the study, the researchers fed male mice a high-fat diet for 11 weeks to induce obesity. Next, they placed the mice on a regular diet for 9 weeks to reduce their weight. Control mice received a regular diet over the same 20-week period.

The researchers noted that after 11 weeks, the mice on high-fat diets gained three times more weight than those on the regular diet. However, after 6 weeks on the regular diet, their weight decreased to match that of control mice.

They noted that metabolic measures such as insulin and glucose tolerance also matched those of control mice by the end of the 20-week study period.

After the 20-week dietary study period, the researchers induced choroidal neovascularization (CNV) in mice. CNV describes the growth of new blood vessels in the eye, and is a major cause of vision loss. It is also present in over 80% of cases of AMD.

After 2 weeks, the researchers then measured the rate of CNV in both groups of mice.

They found that mice fed a high-fat diet followed by a regular diet had 40% more CNV than those fed a regular diet exclusively.

The researchers next conducted some tests on the fat tissue in mice. Although metabolic measures among formerly obese mice matched those of mice without a history of obesity, they found that their fat tissue retained properties that increase AMD risk.

“This study suggests that increase in body fat causes hormonal and cell signaling changes throughout the rest of the body,” Dr. Benjamin Bert, an ophthalmologist at MemorialCare Orange Coast Medical Center in Fountain Valley, CA, not involved in the study, told MNT.

“In particular, the researchers hypothesize that an increase in waist size, meaning more abdominal fatty tissue, increases these effects. In this study, they hypothesize that an increase in fatty tissue leads to permanent changes in the way that the fatty tissue sends signals to other parts of the body, even after weight loss,” he explained.

When asked whether obesity may be linked to AMD via other mechanisms than those in the study, Dr. Howard R. Krauss, surgical neuro-ophthalmologist and director of Pacific Neuroscience Institute’s Eye, Ear & Skull Base Center at Providence Saint John’s Health Center in Santa Monica, CA, told MNT:

“There may be associated dietary factors in [those with obesity], with consequent excesses of toxic substances or deficiency of necessary nutrients, which have a direct effect on the retina independent of immune-mediated pathways. It is well known that nutrition can affect macular degeneration.”

“The Age-Related Eye Disease Study (AREDS) taught us that nutrient supplementation, which can now be found in over-the-counter AREDS 2 vitamin formulations, can slow the progression of [a common type] of macular degeneration,” Dr. Bert added.

“Since obesity can be diet-related, it is possible that these patients are not consuming the necessary nutrients to help lessen the progression of macular degeneration. Obesity can also be related to other metabolic conditions like diabetes and high blood pressure, which can also increase the risk of other retinal diseases,” he noted.

Dr. Bert noted that as the study was conducted on a mouse model, it remains to be seen if the findings translate over to humans. He also noted that the mice studied did not have AMD.

“These mice had laser applied to their retina to induce a similar type of damage to that caused by macular degeneration. However, laser damage […] is a different kind of trauma to the retina and may not behave exactly the same as macular degeneration,” he explained.

To conclude, animal studies with more precise models of AMD alongside human studies are needed to know how far these findings apply to people.