Restricting Calorie Intake Could Delay or Prevent EndometriosisMar 22, 2018
Reducing calorie intake without cutting out any specific nutrients could stop the development of endometriosis in mice.
- Reducing calorie intake without cutting out any specific nutrients could stop the development of endometriosis.
- These findings may stimulate more research on how lifestyle changes could delay or prevent endometriosis.
- The endometrial lesions of mice that were fed a restricted diet before the induction of endometriosis were 88.5 percent lighter than those of the animals that ate at will.
- The weight of the endometrial lesions was even lower when the caloric restriction was implemented after endometriosis was induced (93 percent less than mice that ate at will)
- Caloric restriction increased autophagy both when it was implemented before or after the induction of endometriosis.
- Proliferation, angiogenesis, steroidogenesis, and fibrosis, all events associated with endometriosis, were reduced in the lesions of animals whose calorie intake was restricted compared to those who could eat as much as they wanted.
- Caloric restriction likely suppresses the development of endometriosis by reducing PI3K/AKT/mTOR signaling and increasing SIRT1, and AMPK signaling, which all promote autophagy and reduce local estrogen production cellular proliferation, angiogenesis, and fibrogenesis.
Limitations of the study:
The experiments were conducted in mice and more research is needed to confirm these findings in a clinical setting.
Reducing the intake of calories could stop the development of endometriosis according to research conducted in mice. This could be the case even after the lesions are established, i.e. endometriosis has started. Dietary supplements or drug candidates that mimic the beneficial effects of restricting calories may have the same effect.
Many studies have shown that reducing calorie intake by 30 to 40 percent without causing deficiencies of any specific nutrients, can prolong lifespan, reduce tumor growth and spread, and delay the onset and progression of age-related diseases in different animal species.
However, the effect of reducing calorie intake on endometriosis has not been studied before. In the present study researchers from China conducted two experiments in mice to see whether restricting calorie intake can delay or prevent endometriosis.
In the first experiment, they used 20 mice, which they divided into two groups. They allowed the animals in the first group to eat as much as they wanted, whereas they cut down the intake of calories of the animals in the second group by 30 percent compared to the first group. Two weeks after this regime, they induced endometriosis in all the animals. Two weeks after this, they analyzed the endometrial lesions of the animals.
In the second experiment, the researchers induced endometriosis in another 20 mice but only restricted their calorie intake two weeks after the induction of endometriosis. Four weeks after this, they also analyzed the endometrial lesions of the animals.
They found that when calorie intake of the animals was restricted before the induction of endometriosis, the weight of the lesions was reduced by 88,5 percent. When the restriction of calorie intake was done after endometriosis was initiated, the weight of the lesions was reduced by 93 percent.
The researchers also found that restriction calorie intake increased autophagy, a process by which the body cleans out various debris. Conversely, it reduced cell division, the formation of new blood vessels, angiogenesis, the production of steroids, and fibrosis or scaring in lesions, all events associated with endometriosis.
“…[caloric restriction] instituted either before or after the induction of endometriosis, dramatically curbs the growth of endometriotic lesions and fibrogenesis through multiple mechanisms,” the researchers wrote. “Given the scarcity in research on how lifestyle can impact on the development of endometriosis, our study should hopefully stimulate more research in this area,” they concluded.
The results were published in the peer-reviewed scientific journal Reproductive Sciences.
Research Source: https://www.ncbi.nlm.nih.gov/pubmed/29439622
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