15_-_Evolution_of_Sex_and_Reproduction

Lecture Notes:

• Goal: Find a mate and reproduce

• Adaptations: Things that increase reproductive fitness

Asexual reproduction:

• Cloning

• Fast

• Bad mutations are stuck in the gene pool → genetic load

• “Mueller’s Ratchet” → Once a bad gene is introduced in a sexually reproducing population, it gets stuck in it.

Why did sexual reproduction evolve?

• Increased variation due to recombination

• Reduces genetic load (bad genes)

How did sexual reproduction evolve? → Isogamy (same gametes) to Anisogamy (different gametes) via DISRUPTIVE SELECTION

• Isogamy → Anisogamy due to disruptive selection (A+C vs. B+B)

• A (sperm) + C (eggs) are favored over B+B

• C are limited relative to A so females are more selective than males

Reproductive differences between males and females

• Potential (higher in males than in females), males can impregnate multiple women, females can only get pregnant from one male at a time

• Investment (higher in females than males), females are pregnant, breastfeed. Males can ejaculate and go.

• Certainty (higher in females than males), males can never know whether his kids are theirs, females know 100%.

How males make sperm → SPERMATOGENESIS

Starts at a certain testosterone threshold. Hypothalamus releases GNRH → GNRH goes to pituitary → anterior pituitary produces gonadotropins (LH and FSH) → LH tells leydig cells to start making testosterone → FSH help bind testosterone to testis to keep it there.

1. Primordial Germ Cell: The process starts with primordial germ cells, which are formed during the early embryonic development of the organism.

2. Migration: These primordial germ cells migrate to the developing gonads (testes in males).

3. PCG → Spermatogonial stem cells: PGCs differentiate into diploid spermatogonial stem cells, which reside in the seminiferous tubules of the testes.

4. Spermatogonial stem cells → Spermatogonia: Stem cells multiply into spermatogonia.

5. Spermatogonia → 1° Spermatocyte via Mitosis: Spermatogonia undergo mitotic divisions to ensure a continuous supply of stem cells and produce primary spermatocytes.

6. 1° Spermatocyte → 2° Spermatocyte via Meiosis I: Each primary spermatocyte, which is diploid, undergoes meiosis I, resulting in two haploid secondary spermatocytes. A cytoplasmic bridge remains between teh two cells which allows for the same genetic expression becuase they have the same proteins

7. 2° Spermatocyte → Early spermatids via Meiosis II: Each secondary spermatocyte undergoes meiosis II to yield a total of four haploid spermatids per primary spermatocyte.

8. Early spermatids → Mature sperm via differentiation: Spermatids undergo spermiogenesis, where they transform into mature sperm cells through morphological changes, including the development of a flagellum, dumping of cytoplasm via exocytosis, condense the nucleus, cytoplasmic bridge gets cut, golgi moves to the front and becomes the acrosome which helps the sperm penetrate the egg.

9. Mature Sperm: The final result is a streamlined, motile mature sperm ready for fertilization.

• Meiotic drive: X vs Y chromosomes are directly in competition with each other. X is selected for so the X lineage will kill the Y lineage to ensure more females in the next generation.

How females make eggs → OOGENESIS

1. Primordial Germ Cells: The process of oogenesis begins with primordial germ cells that are formed during early embryonic development of the organism.

2. Migration: These primordial germ cells migrate to the developing gonads (ovaries in females).

3. PGC → Oogonia (not stem cells like in males) via mitosis: Primordial germ cells divide into diploid oogonia, which are the initial cells that will eventually develop into eggs.

4. Oogonia → 1° Oocytes via Mitosis: Oogonia undergo mitotic divisions to ensure a continuous supply of germ cells, producing primary oocytes. Each primary oocyte is diploid and enters prophase I of meiosis, where they remain arrested until puberty. They are stored in a follicle. This can cause birth defects (down syndrome; trisomy 21) if they are arrested for too long. This is why older women are prone to birth defects.

5. 1° Oocyte → 2° Oocyte via Meiosis I: At puberty, hormonal changes stimulate the primary oocyte to complete meiosis I, yielding one haploid secondary oocyte and a smaller polar body that eventually degenerates.

6. 2° Oocyte → Ovum via Meiosis II: The secondary oocyte starts meiosis II but is arrested at metaphase II. It will only complete meiosis II if fertilization occurs, resulting in a mature ovum (egg) and another polar body that also degenerates. If fertilization does not occur, it will degenerate and the corpus luteum will shed out (menstruation).

7. Ovulation: The mature ovum is released from the ovary during ovulation, where it can be fertilized by sperm.

8. Polar Bodies: Throughout the process, polar bodies are formed as a result of unequal cytokinesis meant to discard excess genetic material, allowing the ovum to retain the majority of the cytoplasm and organelles necessary for early development after fertilization.

• Meiotic drive: Meiosis creates variaiton and therefore selection. Or competition between what genes get into the egg. Some genes will get into the egg by more than 50% because they control where corssign over happens during meiosis.

Preventing polyspermy: 1. FAST BLOCK 2. SLOW BLOCK. Triggered by the acrosome in sperm.

1. Fast-block (oviparous organims):

• Egg dumps out chloride ions, pulls in sodium ions, releases internally calcium ions. Makes the egg very positively charged.

• The egg goes from negative → positive which repels the sperm.

2. Slow-block (all organisms have it):

• Cortical granules release calcium, proteins, peroxidases, and GAD when the sperm contacts the egg (cortical reaction)

• This stuff gets dumped into the space between the outside and inside of the cell, forming a process.

  • This removes the sperm receptors,

  • Causes the fertilization envelope to harden

  • GAD pulls in water, causing the egg to expand.

FSH and LH in females: Menstruation

• Hypothalamus releases GNRH → GNRH goes to pituitary → anterior pituitary produces gonadotropins (LH and FSH)

1. Follicular Phase: Begins with the first day of menstruation. The hypothalamus releases GnRH, stimulating the anterior pituitary to produce FSH and LH. FSH promotes the growth of ovarian follicles, leading to the maturation of primary oocytes into secondary oocytes. The follicles secrete estrogen, thickening the uterine lining.

2. Ovulation: Around day 14, a surge in LH, triggered by increased estrogen from the mature follicle, leads to the release of the mature ovum from the ovary. This marks the peak of estrogen levels and the transition to the luteal phase.

3. Luteal Phase: The ruptured follicle transforms into the corpus luteum, which secretes progesterone and some estrogen. Progesterone maintains the endometrial lining for potential implantation of a fertilized egg. If fertilization does not occur, the corpus luteum degenerates, leading to decreased hormone levels.

4. Menstruation: If the egg is not fertilized, the levels of progesterone and estrogen drop, causing the uterine lining to shed, resulting in menstrual bleeding. This marks the end of the cycle and the beginning of a new one.

BUG questions

What is genetic load?

• Accumulated bad mutations that are locked into the gene pool of asexually reproducing organisms.

• Genetic load is the burden of deleterious mutations within a population.

• It measures the reduction in fitness compared to a theoretical population free of mutations.

• Accumulation of mutations leads to genetic load, potentially reducing survival and reproductive success.

What is Muller’s ratchet? How can this eventually spell doom for asexually reproducing organisms?

• Muller’s ratchet is a theoretical concept in evolutionary biology that explains how asexually reproducing populations accumulate deleterious mutations over generations.

• In such populations, the best genomes are not frequently rejuvenated through recombination, leading to a gradual increase in the mutation load.

• Once a population has lost the best genotype, it cannot revert to it, resulting in a decline in overall fitness.

• This accumulation of harmful mutations can eventually lead to the extinction of asexually reproducing organisms, as they become less viable over time due to increased genetic load.

What is the two fold cost of sexual reproduction?

• Only half of a population (females) can produce offspring, while males do not directly contribute to new offspring.

• Males consume resources and space that could otherwise support reproducing females.

• Sexual reproduction can lead to a slower rate of population growth compared to asexual reproduction because it takes more time and energy to find and compete for mates, along with the need for two individuals to combine their genetic material to produce progeny.

Why are males not truly a cost to reproduction?

• Only half of a population (females) can produce offspring.

• Males do not directly contribute to new offspring.

• Leads to a slower rate of population growth compared to asexual reproduction.

• Males can make sperm their entire lives, females cannot produce offspring their entire lives.

• Takes more time and energy to find and compete for mates.

• Requires two individuals to combine their genetic material to produce progeny.

What are the two evolutionary benefits of sexual reproduction?

• Increased genetic diversity, which enhances adaptability and survival of the population by providing a greater pool of traits that may be beneficial in changing environments.

• The ability to eliminate harmful mutations through recombination and natural selection, which helps maintain overall population fitness over generations. It decreases genetic load and therefore accumulation of bad mutations.

What is hidden variation? How can it improve response to selection if not interfacing with selection?

• Hidden variation → genetic diversity within a population that is not immediately expressed in phenotype but may affect fitness under certain conditions. Often exists in the form of recessive alleles or traits that are not selected for until environmental changes create new challenges.

• This variation can improve response to selection by providing a reservoir of potential adaptations that may be beneficial if environmental conditions change.

• Even when not interfacing with selection directly, hidden variation can persist in a population, ensuring that there is genetic potential available for future generations to adapt to new or altered environments.

What is Muller’s rachet? Why is this not an issue with sexual reproduction?

• Muller’s ratchet explains how asexually reproducing populations accumulate harmful mutations over generations.

• In asexual populations, the best genomes are not rejuvenated through recombination, leading to increased mutation load.

• Once the best genotype is lost, the population cannot revert, resulting in decreased overall fitness.

• This is less of an issue in sexual reproduction because:

  • Sexual populations undergo recombination, which shuffles genetic material.

  • Recombination allows for the removal of deleterious mutations and the restoration of healthier genotypes.

  • This process helps maintain overall fitness in sexual populations over generations.

What is at the foundation of sexual selection?

• Disruptive selection → traits evolve not just for survival, but also for reproductive success. These can be visual, behavioural, cognitive.

• Focused on getting a mate, not survival.

• Differential reproductive success based on individual attributes.

• Traits influencing mating success enhance attractiveness or competitive abilities.

• Favorable traits are passed on to future generations.

• Leads to the development of secondary sexual characteristics and behaviors.

• These characteristics may not directly correlate with survival but improve reproductive success.

What is sexual conflict?

Sexual conflict refers to the differences in reproductive interests and strategies between males and females, which can lead to conflicting behaviors. This can occur when:

• Males and females have different optimal mating strategies—males may maximize mating frequency, while females may prioritize mate quality.

• Females may evolve mechanisms to resist unwanted mating attempts by males.

• Males may develop traits or behaviors to coerce or manipulate female choice.

• This ongoing arms race can drive sexual selection, influencing the evolution of both male and female traits.

• Ex: Males prioritize quantity over quality. Females are the opposite, this can lead to conflict.

What is anisogamy? Considering the original condition was isogamy, why was anisogamy favored? what type of natural selection is this (stabilizing, disruptive, directional)?

• Anisogamy: Sexual reproduction with two different types of gametes (large eggs and small sperm).

• Contrast with Isogamy: Isogamy involves gametes of similar size.

• Advantages of Anisogamy:

  • Increased specialization of gametes:

  • Eggs optimized for nurturing and development.

  • Sperm optimized for mobility and fertilization efficiency.

  • Enhances reproductive success and genetic variation.

• Type of Natural Selection: Disruptive selection, promoting the evolution of distinct gamete types instead of a single intermediate form, maximizing the fitness of each type.

Why do developing sperm maintain cytoplasmic bridges?

• Because they don’t undergo cytokinesis

• Facilitate the sharing of resources and nutrients among developing germ cells.

• Ensure synchrony in the development of sperm cells, promoting uniformity in the maturation process.

• Allow for the exchange of genetic information, potentially enhancing genetic diversity and stability.

• Aid in the overall efficiency of spermatogenesis, as multiple sperm can develop in tandem from a single precursor cell.

What are four ways that mature sperm differ phenotypically from spermatids?

1. Size: Mature sperm are typically smaller than spermatids, as mature sperm have shed excess cytoplasm and are streamlined for mobility.

2. Shape: Mature sperm have a distinct head, midpiece, and tail structure, while spermatids have a more rounded shape without the specialized structures of mature sperm.

3. Presence of Flagellum

4. Realses cytoplasm to get smaller

5. Condensed DNA nucleus

6. Acrosome forms from Golgi to hold and store enzymes.

7. Motility: Mature sperm possess a flagellum that allows for swimming, enabling them to reach and fertilize the egg. Spermatids lack the developed tail necessary for motility.

8. Capsacitation: Mature sperm undergo biochemical changes (capacitation) after being deposited in the female reproductive tract, which are critical for fertilization; spermatids do not undergo this process as they are still in the earlier stages of development.

Why does getting kicked in the testicles hurt?

• High density of nerve endings in the testicles increases sensitivity to pain.

• Testicles are sensitive organs that are susceptible to trauma.

• Fluid in testes gets pushed into areas that aren’t compressed when kicked, this is why it hurts.

• Impact results in intense pain that can radiate to other areas, such as the abdomen.

• Located outside the body in the scrotum, making them less protected from injury.

• Innervated by nerves that quickly transmit pain signals to the brain upon impact.

What are the two blocks to polyspermy? How do they work?

1. Fast Temporary Block to Polyspermy:

   • Immediate electrical response after fertilization. Goes from positive to negative to temporarily block sperm.

   • When a sperm fuses with the egg, it causes a change in the egg's membrane potential, which prevents other sperm from fusing with the egg.

2. Slow Permanant Block to Polyspermy (Cortical Reaction):

   • Slower chemical response that occurs shortly after fertilization.

   • The fusion of sperm activates the egg, leading to the release of cortical granules (Ca+) from the egg.

   • These granules modify the zona pellucida (the layer surrounding the egg), making it impenetrable to additional sperm. It also removes sperm receptors

   • This block effectively ensures that only one sperm can fertilize the egg, preventing polyspermy and ensuring proper embryo development.

Explain how the same gonadotropins drive different gametogenesis in the two sexes.

Hypothalamus releases GRH, which stimulates the reelase of gonadotrophins.

Gonadotropins, which include Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH), play critical roles in the gametogenesis of both sexes, but their functions differ significantly.

• In Males:

  • LH stimulates Leydig cells to produce testosterone, which is crucial for spermatogenesis and the maturation of sperm.

  • FSH promotes the function of Sertoli cells, supporting sperm development and providing necessary nutrients and hormones.

• In Females:

  • LH triggers ovulation and the formation of the corpus luteum, which produces progesterone essential for the regulation of the menstrual cycle.

  • FSH stimulates ovarian follicles' growth and maturation, leading to the production of estrogen in follicular phase, and eggs (ova). Make progesterone during luteal phase.

This differential response to the same gonadotropins ensures that males produce sperm continuously, while females have a cyclical process for egg production and ovulation.

What are the various effects of estradiol? Aside from these, how does it influence the production of LH at its various concentrations?

Estradiol has several effects:

• Development and maintenance of female reproductive organs

• Growth of endometrium

• Regulation of the menstrual cycle

• Contribution to secondary sexual characteristics such as breast development

• Supprts follical maturation in ovaries.

• Influence on bone density and reduction of osteoporosis risk

• Role in cardiovascular health by potentially improving vascular function

• Effects on mood and cognitive functions, contributing to emotional well-being.

Influence on LH Production:

• At low concentrations, estradiol tends to inhibit the production of Luteinizing Hormone (LH) through negative feedback on the pituitary gland.

• At moderate concentrations, estradiol supports the mid-cycle surge of LH necessary for ovulation, demonstrating a switch to positive feedback.

• High concentrations can maintain this positive feedback loop until ovulation occurs, leading to a peak in GNRH and LH secretion, which triggers ovulation.

Describe how estradiol and LH produce a positive feedback loop?

As estradiol levels rise, particularly as a follicle develops, estradiol acts on the pituitary gland to stimulate an increase in LH production. This surge in estradiol promotes additional LH release, further enhancing the production of estradiol.

• Initial Phase: Rising estradiol levels lead to increased LH secretion from the anterior pituitary gland.

• Surge Phase: At a certain threshold, high estradiol levels send a strong positive feedback signal to the pituitary, resulting in a rapid surge of LH.

• Ovulation Trigger: This LH surge is what triggers ovulation, signaling the ovarian follicle to release the matured egg.

The positive feedback loop thus continues until ovulation is achieved, at which point estradiol levels drop and the feedback shifts to negative control in the subsequent phases of the menstrual cycle, regulating LH and estradiol levels thereafter.

How does the function of the follicle change when it forms a corpus luteum?

• Hormone Production: The corpus luteum produces progesterone and some estrogen. Progesterone is crucial for preparing the endometrium for a potential implantation of a fertilized egg.

• Maintenance of the Endometrium: Progesterone ensures that the uterine lining remains thick and supportive, creating an optimal environment for embryo development.

• Inhibition of Further Follicle Development: The presence of progesterone and estrogen from the corpus luteum inhibits the release of Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) through negative feedback, preventing the maturation of new follicles during this phase.

• Lifecycle Trigger: If pregnancy does not occur, the corpus luteum degenerates into the corpus albicans, leading to a decrease in hormone production, which triggers menstruation.

Thus, the transition from a follicle to a corpus luteum marks a shift in focus from egg maturation to preparing the body for possible pregnancy.

A professional male athlete was suspended for taking fertility drugs. He claims it was to have a family. How can you argue against his excuse?

Fertility drugs are often associated with enhancing testosterone levels, which can improve athletic performance. The argument can be made that his usage of these drugs was more about gaining a competitive edge.

What are the two effects of progesterone?

1. Prepares the endometrium for potential implantation of a fertilized egg, ensuring that the uterine lining is thick and supportive for embryo development.

2. Inhibits the release of Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) through negative feedback, preventing the maturation of new follicles during the luteal phase of the menstrual cycle.

How do birth control pills influence the hormones that drive the ovarian cycle to stop the maturation of eggs?

• Birth control pills contain synthetic hormones, primarily estrogen and progestin.

• These hormones work to prevent the natural hormonal fluctuations of the menstrual cycle.

• They inhibit the release of Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH) from the pituitary gland.

• Lower levels of LH and FSH prevent the maturation of ovarian follicles and ovulation.

• The pills maintain a steady level of hormones in the bloodstream, reducing the likelihood of the hormonal peak needed for ovulation.

• It mimics the hormonal state as if you were already pregnant.

What is endometriosis? Which hormone should you try to regulate to ease the symptoms?

• Endometriosis is a painful condition characterized by tissue similar to the uterine lining (endometrium) growing outside the uterus.

• Symptoms may include severe menstrual cramps, chronic pelvic pain, pain during intercourse, and infertility.

• To alleviate symptoms, it is important to regulate estrogen levels, as high estrogen can worsen the growth of the endometrial-like tissue outside the uterus.

• You wouldn’t want to take progesterone because it maintains the endometrial lining.

What is a downside to estradiol? Why is this a modern issue for humans? What can women do to try to prevent it?

• A downside to estradiol is its potential to contribute to the development of certain reproductive cancers because it decreases cell divisions.

• This is a modern issue for humans because increased exposure to estradiol, often from environmental sources, less tendency for pregnancy, or hormonal therapies, may elevate risk factors for these cancers.

• Women can try to prevent these issues by maintaining a healthy lifestyle, reducing exposure to external estrogens.

Why is exercise so important for female health as far as reducing the rate of reproductive cancers and avoiding osteoporosis?

• Reducing the risk of reproductive cancers through improved hormonal balance, weight management, and enhanced immune function, which may lower the likelihood of cancer development.

• Helping maintain optimal body weight, as obesity is linked to higher risks for certain reproductive cancers.

• Decreasing estrogen levels, which can help mitigate factors that contribute to the growth of hormone-sensitive cancers.

• Strengthening bones and reducing the risk of osteoporosis by promoting bone density through weight-bearing exercises, which can enhance calcium absorption and retention. Regular physical activity helps stimulate bone formation and reduces bone loss as women age.

Essay question: “Explain what is meant by evolutionary mismatch. Then explain one of these mismatches. The essay should include a description of the system effected and its usual function, an explanation of the disease or dysfunction, and how it is product of—or exacerbated by—our modern environment. Also, include an explanation of how our environment has changed. Lastly, describe evidence in support of this disease or dysfunction as an evolutionary mismatch, and what we can do to try to alleviate this issue for future generations.“

• Define evolutionary mismatch, how it occurs, what it means. Traits that used to be beneficial, now are not.

• Give an example of an evolutionary mismatch. Obesity, myopia, anxiety, addiction to social media, type 2 diabetes

• Usual evolutionary function of the system, what purpose this adaptation used to serve during hunter gatherer times.

• Disease of dysfunction that results from this mismatch

• Compare and contrast the past and modern environment, what’s different and how does that contribute to the problem

• How we can ameliorate this in the future.

Ex (1): An evolutionary mismatch is when an adaptive trait in one environment becomes maladaptive in another. As humans, we have natural fat-cravings because of hunter-gatherers. They needed to consume fat in order to have energy to go out and hunt for more food. It was a continuous cycle of consumign fat and then burning it off. Obesity in our modern environment is the maladaptive form of the need for fat. High fat foods are readiliy accessible through drive thrus, there is no effort beign put in to get this food and burn fat in the process. So humans are now faced with the problem of too much food because it the modern environment had food readily accessible everywhere. To alleviate this issues for future generations, we can create educational prgrams around phycical activity, nutrition, and general wellness.

Ex (2): An evolutionary mismatch is a concept within the realm of evolutionary medicine in which characteristics that once served as adaptations in previous environments, typically that of hunter-gatherers, now prove to be disadvantageous and maladaptive in other environments, typically the modern environment. One of these mismatches is reflected in humans being prone to being obese, and the rising levels of obesity associated with human development. The effected system is metabolic capacity, and the body’s tendency to store and conserve nutrients. Hunter gatherers evolved to avoid negative energy balances by craving high-caloric foods and conserving fat as much as possible because it was during times when food was scarce. Obesity is the over consumption of calories leading to excess storage in the form of fat. Our modern environment increases the chance of becoming obese because high caloric foods like meat, and sugar are readily available in endless amounts. It also perpetuates a sedentary lifestyle, making it harder to exercise. The previous environment required considerable effort and a strong craving for a high-calorie food like meat. Now we get meat without the effort while the strong cravings for it remain from the hunter-gatherer days. It is now easier to maintain a positive energy balance and gain weight when it was almost possible before. Our accessibility to high calorie foods increased, but our craving for those foods did not go down, making it impossible to over eat. This is evidenced by increasing obesity rates in the human population, increases access to high-calorie foods, and an increased sedentary lifestyle. To alleviate this issue, regular exercise and healthy eating habits can help reduce obesity.

One example of human evolutionary mismatch is the prevalence of obesity in modern society, a condition primarily caused by the disconnection between our evolutionary adaptations and contemporary environments. Historically, humans evolved in environments where food scarcity necessitated efficient energy storage, leading to a preference for high-calorie foods. In today’s society, characterized by abundant, easily accessible food, particularly processed carbohydrates and fats, these once-advantageous traits now contribute to excessive weight gain and associated health issues like diabetes and heart disease. This mismatch is exacerbated by sedentary lifestyles prevalent in industrialized countries, where physical activity levels have significantly decreased compared to our ancestors. Evidence supporting this evolutionary mismatch includes rising obesity rates correlating with changes in lifestyle and food availability, indicating that to alleviate these issues, we might need to promote better dietary habits, increase physical activity, and foster environments that encourage healthier choices for future generations.

Another significant example of human evolutionary mismatch is the heightened stress response in modern society. Evolutionarily, humans developed a fight-or-flight response to deal with immediate threats, such as predators or natural disasters, allowing for quick decision-making and survival. However, contemporary society often subjects individuals to chronic stressors like financial issues, job security, and social pressures, which are not life-threatening but activate the same physiological responses. This constant activation of the stress response can lead to numerous health problems, including anxiety, depression, cardiovascular diseases, and weakened immune function. Evidence of this mismatch can be seen in the increasing rates of stress-related disorders, highlighting the need for better coping mechanisms and environments that reduce chronic stress in our daily lives to promote overall health and well-being.

Evolutionary mismatch refers to the disparity between traits that were adaptive in ancestral environments and their maladaptive consequences in modern contexts, exemplified by type 2 diabetes. This condition arises from a breakdown of the body's metabolic system, which traditionally regulated blood glucose levels through insulin secretion, optimized for a lifestyle of food scarcity and physical activity. In contrast, today's environment, characterized by an abundance of processed foods and sedentary behaviors, promotes excessive caloric intake and inadequate energy expenditure, leading to insulin resistance and type 2 diabetes. Evidence of this mismatch is reflected in the rising prevalence of obesity and diabetes in industrialized societies, strongly correlating with lifestyle changes and food availability. To address these challenges for future generations, we must promote healthier eating habits, increase physical activity awareness, and support public health initiatives aimed at improving access to nutritious foods.