We have gone through the evolutionary path, the historical turn of events, and the metabolic shifts that our women ancestors went through to create a body that serves an exceptional function: survival. PCOS’s genetic predisposition has not changed in the last 50,000 years. In fact, the only modifications that we have been through are technological, nutritional, and environmental transitions that we have been exposed to in the last centuries.
Nevertheless, the same hormonal changes used to protect us and our offspring in a dangerous and stressful setting is now the effects that we characterized as dysfunction. This raises the question, are we still living in a dangerous and stressful setting? Are hormonal changes trying to protect us from something? Or, is our environment a trigger for this condition? Maybe it is the same question with a different set of words.
Continuing with the protective effects that insulin resistance (IR) used to preserve lean body mass in starvation. Another hypothesis is that IR or the insulin response on certain cells would provide glucose for inflammatory responses. In fact, this would protect the body from disease and trauma when exposed to starvation. Also, it would allow growth during pregnancy and puberty and prepare for migration/hibernation. Anthropologists and archeologists hypothesized that the metabolic disorders started to appear once the transition from hunter-gatherer to sedentary-agricultural lifestyle took place.
- Stressors changed, from starvation and migration to social and ecological problems.
- In a settlement setting and food abundance, the IR played a different role and became a feature of PCOS.
The shift on gonadotropins.
The follicular stimulating hormone receptor (FSHR) and its functions are closely linked to the PCOS’s pathogenic factors. Furthermore, studies reported that variants in FSHR and FSHB could be considered as candidate genes for PCOS, and it is strongly associated with disrupted levels of LH, affecting LH/FSH ratios. Another important variant was found in the GATA4 region. It was found that GATA4, when deleted, could disrupt the gonadotropin responsiveness.
In PCOS, FSH is dysfunctional. This negatively affects ovarian folliculogenesis. Besides, LH regulates theca cell testosterone synthesis, also found in PCOS. Variants in LHCGR and FSHR, both related to gonadotropin action, may have contributed to ovarian follicles not growing as much as a dominant follicle. Besides, the variants in FSHB related to gonadotropin secretion are associated with increased LH levels, leading to hyperandrogenemia.
The changes in gonadotropin functions are related, in an evolutionary matter, to adaptations in the form of protective contraception and decreased ovulation. In fact, looking back, we could see this adaptation associated with the lack of food-related to the hunter-gatherer lifestyle. Also, the adapted contraception is linked to the fact that carrying fewer infants could be beneficial for survival in migration settings. In fact, Natufian women (semisedentary, 12,500-9,500 BC) had fewer offspring and lived longer than men. Further, the decreased number of pregnancies related to the protective presence of PCOS ensured a smaller family size, which meant more food for every member and reduced mortality in children.
Fast forward to the Neolithic revolution. Family size slowly began to increase as a consequence of the growing agricultural setting. The bigger the family, the more hands to sow and collect food. Nevertheless, lifestyle change affected women and men differently. In fact, the increase in the number of births in women without PCOS raised female mortality. Therefore, meaning that women presenting PCOS traits were the ones who survive, and those are the same genes studied and carried through generations. Also, we have to consider that obesity was not as common today, meaning that women with PCOS could still bear children.
To know is to directly treat the problem. We have been treating PCOS with great clinical guidelines, diagnosed with clinical symptoms, and hormone testing. Nevertheless, technology can provide excellent help by determining our gene predisposition, which leads to personalized treatment.
Adipose tissue variation is related to the seasonality of food acquisition on the hunter-gatherer lifestyle. The hypothesis about how evolution affected women’s developmental stages has stated that a prolonged juvenile period and extended gestation time are related to the food supply in early times. In fact, this deficient food supply could lead to fat tissue insufficiency, leading to decreased hormonal synthesis and leptin. Besides, the role of leptin in pregnancy and the pubertal role has proven to be important. The reduced leptin levels on our ancestors would increase insulin resistance, and this IR would protect the body from protein loss. Besides, IR and leptin reduction would prevent ovulation due to the interfered dynamics of gonadotropins.
In the modern age, fast living and fast food, this genetic predisposition would lead to IR, leptin insufficiency, and finally to an accelerated overgrowth of adipose cells. Following, the increased body fat would reflect on a low-grade inflammation setting, carrying more IR, reflecting on hyperandrogenemia.
It is estimated that the shift from hunter-gatherer to a more sedentary lifestyle was made 350 generations ago. Followed by the industrial revolution, 7 generations ago, and consequently our last major change; 2 generations. This present generation is considered the exact opposite of the hunters we used to be.
|No need for physical activity.|
|A large amount of food intake.|
The impact of increased caloric intake and the “almost immobile” lifestyle that we carry nowadays provide the perfect environment for metabolic disease. Therefore, the features that were supposed to help us survive and reproduce (on a logical rate) affect women’s fertility and quality of life.
Reducing inflammation through food
What we eat can influence with great severity our histone codification and therefore affect our gene expression. Remember, we can carry a gene variation and show no signs of a specific condition or disease. Once this gene interacts with the environment and activates, the risk of developing a disease can increase.
Let’s prevent this from happening through a varied food plan. Fruits and vegetables provide a wide array of nutrients and fiber, they also help with donating methyl groups.-Ana Paola Rodríguez Arciniega. Master in Clinical Nutrition.
RED AND ORANGE: bell peppers, blood oranges, cranberries, cherries, grapefruit (pink), goji berries, grapes, onions, plums, pomegranate, radicchio, radishes, raspberries, strawberries, sweet red peppers, rhubarb, rooibos tea, tomato (including sun-dried tomatoes), watermelon, apricots, pumpkin, mango, sweet potato, turmeric, tangerines, apples, and beets.
GREEN: artichokes, asparagus, avocados, bean sprouts, bell peppers, bitter melon, bok choy, broccoli, broccoli sprouts, Brussels sprouts, cabbage, celery, cucumbers, edamame, green beans, green peas, greens (arugula, beet, chard, collard, dandelion, escarole, spinach and kale)
PURPLE, BLUE, AND BLACK: berries, cabbage, carrots, and eggplant.
Ünlütürk, Uğur, Efe Sezgin, and Bulent Okan Yildiz. “Evolutionary determinants of polycystic ovary syndrome: part 1.” Fertility and sterility 106.1 (2016): 33-41.
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