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Egg Quality

Egg Quality: Biology, Evidence, and YOUR Power to Optimize IVF Outcomes

26 February 2026 · 27 min read min read

(A science-based guide to sperm factors, supplements, PGT-A, and donor egg decisions)

Disclaimer: This article is for informational and discussion purposes only and does not constitute medical advice. Its goal is not to push you to start endless treatments and supplements, but rather to raise awareness on all that is possible – or not – to hopefully improve egg and sperm quality. Always consult with your reproductive endocrinologist or fertility specialist before making treatment decisions, including on supplements to take or approaches to follow.

"It's your age" is the laziest diagnosis in fertility medicine … because there are things you can do to improve IVF egg quality, sperm quality, and (hopefully) obtain more euploids.

You just had your post-retrieval consult and were told:

“There’s nothing we can do about your egg quality” ………

"It's your age, you’re too old" ………

“Your eggs are poor quality, you should consider donor eggs instead” ……….

“At 40 years old, you have no chance without donor eggs” ………..

And suddenly, you felt like a death sentence verdict slammed you in the face.

If you’ve ever wondered whether your eggs are truly “worth nothing,” this article is for you.

Age matters. But the science is far more nuanced than most clinic conversations allow.

Quite sadly, "it's your age" is one of the most common things 35+ women hear in fertility clinics, sometimes after a single failed cycle, a batch of abnormal PGT-A results, or even (shockingly) before getting started with IVF. The leap from "you're 38+" to "your eggs are worthless" is not only scientifically lazy: it can be actively harmful.

Note: don't get me wrong, age is really our enemy when it comes to making babies. It is THE key biological factor we, women, have to fight against. But there are more nuances than a lot (most??) fertility doctors let on. You do not have to give up and move to donor eggs simply because you are 41, or because your first batch of embryos was poor.

Plain truth too few clinics will tell you: if you have poor embryo outcomes, there is almost no certainty whether it's because of egg quality, sperm quality, or both - or even a lab quality issue. Older age is correlated with higher rates of chromosomally abnormal embryos, yes. But correlation is not causation, and the sperm side of the equation is chronically under-investigated.

Clinics that immediately default to "it's your age, do donor eggs" may be taking the short road, whether due to lack of motivation to investigate, SART success score pressure[*], or other non-patient-centric reasons. That doesn't mean they're malicious, but it may mean they're not the right fit for complex cases. Donor egg cycles do have higher success rates, and those rates make clinics look good on paper. Some may default to simplified age-based counseling instead of helping patients optimize.

But … can egg quality be improved??

The reality? There are numerous evidence-based interventions to improve both egg and sperm quality. And before anyone jumps to donor gametes (= eggs and sperm), those options deserve a serious, dedicated consideration – and maybe a little effort.

1. The Oft Overlooked Half of the Story: Sperm Quality Matters More Than You Think

It may sometimes be a harder subject to tackle, but it is fairly widely known that if “male factors” exist (poor sperm quality, very limited or non-existent sperm), it can reduce the chances of fertilization.

And so, the one (and often, only) test that fertility clinics run on the male partner, is a simple sperm analysis looking at the volume and appearance of the sample, and the count, concentration, morphology and motility of the sperm.

Key drawback: those elements, as useful as they are for other diagnostic purposes, do not provide any insight as to the actual quality of the sperm, in terms of DNA integrity – which is key to making a healthy, genetically normal embryo.

a. Sperm DNA Fragmentation’s Role in IVF Outcomes

When a couple faces repeated IVF failure, or high aneuploid rates, the default clinical assumption is almost always the eggs - especially if the woman is over 35.

A growing body of research has however shown that something called “sperm DNA fragmentation” is a significant and independent contributor to poor embryo development, failed implantation, and miscarriage.[5]

One of the research pieces highlighted that standard semen analysis (the test most fertility clinics rely on – per above) does not assess DNA integrity at all. A man can indeed have perfectly normal motility and morphology numbers from a sperm analysis, while carrying significant DNA damage in his sperm.[5]

Simple fact: in many cases where a clinic says "your eggs are the problem", sperm DNA fragmentation has likely never even been tested. And when sperm DNA fragmentation has not been evaluated, attributing poor outcomes solely to egg quality may absolutely represent an incomplete assessment.

Additionally, it is worth noting that advanced paternal age has also been associated with increased DNA fragmentation, de novo mutations, and miscarriage risk. While the age effect is less dramatic in sperm than in eggs, it is not negligible, and absolutely should be part of the conversation.

b. What can be done for sperm quality?

Very fortunately, a number of things can be done to improve sperm quality via upstream biologic improvements.

Once in the lab, some techniques around sperm selection (downstream lab-level optimization) can also circumvent further MFI and sperm quality issue.

1. Upstream biologic improvements with supplements and lifestyle
  • Oxidative Stress Optimization: a number of supplements have been shown by research to of reduce sperm DNA fragmentation and improve motility. For instance, a 2019 Cochrane review found that antioxidant supplementation in subfertile males was associated with increased live birth and pregnancy rates. Evidence-backed components include:
  • Omega-3s (2-3 g EPA/DHA daily)
  • Vitamin E (200-400 IU)
  • Vitamin C (500-1000 mg)
  • Zinc (15-30 mg)
  • Selenium (100-200 mcg)
  • L-carnitine (1-2 g/day)
  • CoQ10 ubiquinol (200-400 mg daily)
  • “NAC” or N-acetylcysteine (600–1200 mg)
  • NAC, CoQ10 and L-Carnitine together tend to have the strongest signal for motility and DNA fragmentation improvement.
  • Sleep and metabolic health: sperm quality is extremely sensitive to systemic inflammation. Acting on the below factors can help:
  • Treat sleep apnea if present
  • Maintain fasting glucose < 95
  • Optimize triglycerides
  • Reduce visceral fat
  • Avoid heat exposure (sauna, hot tubs, laptops on lap, long hot baths, tight clothing)
  • Other lifestyle modifications are known to be key in improving sperm quality:
  • managing weight
  • eliminating tobacco
  • reducing or eliminating alcohol
  • Improving sleep and sleeping enough
  • Reducing environmental toxin exposure, such as toxins from plastics or cosmetics
  • If the “DNA Fragmentation Index” (DFI) is high: doing the below can contribute to lowering the score and improving outcomes:
  • Ejaculate every 1-2 days (reduces oxidative damage accumulation)
  • Short abstinence (12-24 hours) before retrieval
  • Consider using testicular sperm if DFI severe (more below)

Important note: for any upstream “optimization techniques” to have any effect on sperm quality, they will need to be implemented for at least 3+ months. See Section 3 “The 3-Month Rule” below for detailed explanation.

2. Upstream biologic improvements via medical/pharmacologic optimization
  • Check essential hormones for proper levels: sperm production is hormone-driven. If the hormonal signals from the brain to the testes are off, sperm quality can suffer, even if a basic semen analysis looks okay.
  • Total and free testosterone, and SHBG (Sex Hormone–Binding Globulin)
  • FSH, LH, estradiol, prolactin (yes, men do have some small amounts of those hormones too!)
  • Some drugs can be used to help certain aspects, if male hormone levels are abnormal; often, they work by increasing testosterone levels.
  • Clomid (Clomiphene Citrate, by blocking “estrogen feedback”, raises LH/FSH, which in turn increases endogenous testosterone. That can help men with low testosterone with normal/low FSH, secondary hypogonadism, or borderline sperm parameters with low testosterone
  • hCG, which mimics LH to stimulate “Leydig cells”, which increases testosterone. This can be used with low testosterone, secondary hypogonadism, prior exogenous testosterone suppression
  • hMG (such as Menopur): if FSH is low, adding FSH stimulation can directly improve spermatogenesis (= the growing of sperm).

A word on Testosterone replacement: intuitively, it may sound logical that, if a man’s sperm issue is due to low testosterone, supplementing testosterone would work. This should however never be tried, if trying to conceive: supplementing testosterone suppresses FSH and therefore kills sperm production.

3. Upstream biologic improvements via surgery
  • Varicocele: one of the most under-addressed male factors, this is when there is a “varicose vein” of the testicle. A varicocele increases testicular heat and oxidative stress, potentially harming sperm quality and increasing DNA fragmentation. It can be surgically repaired or improved, thereby improving sperm count, motility and/or DNA fragmentation
  • Testicular Sperm (via TESA, TESE or micro-TESE): with significant sperm DNA fragmentation, using testicular sperm instead of ejaculated sperm can lower fragmentation, improve blast formation, reduce miscarriage. Testicular sperm is collected surgically, directly from the testes (either with a needle in the testes, or making a small incision into the testicle), instead of being naturally evacuated via the epididymis – and possibly being damaged in the process.

4. Downstream lab-level optimization

Downstream lab-level optimization: for the first 2 decades of IVF, fertilization was only done by placing sperm in the same dish as the eggs and letting the natural fertilization process happen (now called “conventional fertilization”). Some fantastic tool then started emerging in the mid-1990’s, helping greatly with MFI:

  • ICSI: its goal is to first manually select a sperm that visually appears “better” as well as to bypass the need for sperm to penetrate the egg on its own, eliminating one obstacle of the process. After sperm washing, the embryologist manually selects a single sperm based on visual assessment of morphology and motility, then injects it directly into the egg using a microneedle. It has become the standard for male factor infertility, poor prior fertilization, or low sperm counts. The limitation is that selection is subjective and based on appearance alone, which tells you nothing about DNA integrity inside the sperm.
  • Calcium ionophore (assisted oocyte activation): its goal is to “give a push” to the fertilization process, by placing sperm + egg in a calcium ionophore bath, which helps trigger the cascade of events needed after sperm enters the egg. For cases of repeated fertilization failure or poor embryo development, this can artificially activate the egg. Some research demonstrated improved fertilization rates with calcium ionophore in cycles using surgically retrieved sperm. This addresses cases where the sperm may lack the oocyte-activating factor needed for normal fertilization.
  • ZyMōt microfluidic sperm selection: its goal is to reduce oxidative damage exposure for sperm. Unlike traditional sperm washing (centrifugation), ZyMōt uses a microfluidic chip that mimics the natural selection process of the female reproductive tract (via the cervix, cervical mucus and uterus). Sperm must swim through a porous membrane, selecting for motility and lower DNA fragmentation without the mechanical damage caused by centrifugation. Studies show ZyMōt-selected sperm have significantly lower DNA fragmentation rates (Yaghoobi et al., Lab Chip, 2024)[8].
  • PICSI (Physiological ICSI): its goal is to select more mature sperm. A physiological enhancement of ICSI; where sperm are selected based on their hyaluronic acid binding, which correlates with lower DNA fragmentation and chromosomal normality. It's a simple, low-cost add-on to ICSI.
  • A few other techniques do exist but are more at an experimental stage, and there is mixed evidence on their usefulness
  • MACS (Magnetic Activated Cell Sorting) removes apoptotic sperm. It can sometimes be helpful in high DNA fragmentation index cases.
  • IMSI (High-magnification sperm selection), another variation of ICSI, can be occasionally helpful in severe morphology issues.

2. Egg quality improvement: what works … and what doesn’t

a. What IS egg quality, exactly?

Before diving into supplements and protocols, we need to define what “egg quality” actually means. It is not a moral judgment. It is not a fixed destiny. And it is certainly not a single lab value. Egg quality is a composite of different key elements:

  • mitochondrial energy production,
  • chromosomal segregation accuracy during meiosis, and
  • the biochemical environment in which the oocyte matures. Some aspects are age-driven.

Some of those elements are biologically modifiable, while some remain outside our control. And so, the goal is not perfection – but optimization.

b. Egg quality optimization: challenging the fatalistic narrative

The narrative around egg quality is often presented as a one-way street: “you're born with all your eggs, they decline with age, and there's nothing you can do about it”. While the first part is true (women do not produce new eggs), the second part (that nothing can be done) is increasingly being challenged by research.

Egg "quality" is primarily about mitochondrial function, chromosomal integrity during meiosis, and the cellular environment surrounding the oocyte. And it turns out that several of these factors are modifiable (at least to a degree), as more and more emerging research suggests.

This is what is defended and discussed in an excellent book that many infertility patients come across at some point in their journey: It Starts with the Egg, by Rebecca Fett. She argues that egg quality is not fixed by age alone, but is heavily influenced by mitochondrial function, which is vulnerable to environmental toxins (BPA, phthalates), oxidative stress, and nutritional deficiencies.

The book's core thesis is that targeted supplements combined with reducing toxin exposure can measurably improve egg quality over a 3-4 months window. It references published research on mitochondrial function, oxidative stress, and environmental toxins, and translates it into actionable recommendations.

It became a bible in the fertility community for giving women actionable science instead of "there's nothing you can do". The book has shifted (and continues to shift) the narrative - and rightly so. But in fertility, hope can quickly turn into marketing, and science can become simplified into checklists.

The real question is not whether egg quality can be influenced at all. The real question is becoming “which interventions are supported by meaningful evidence, and which are extrapolated from theory?”

c. Evidence-based interventions for egg quality
  • Similar to what we discussed for MFI in section 2, there are a number of supplements and lifestyle improvements which research has shown can be effective upstream in improving egg quality.
  • Other medical, pharmacologic and non-medical approaches are also available in preparation for stims and egg retrieval, though their usefulness will vary on the case/patient.
  • Lastly, “clinic/lab side” downstream options, similar to what we covered in section 2 for male patients, also exist.

Important note: for any upstream “optimization techniques” to have any effect on egg quality, they will need to be implemented for at least 3+ months. See Section 3 below for detailed explanation.

1. Upstream biologic improvements through supplements

Upstream biologic improvements through supplements: not all fertility clinics recommend supplements to their patients, arguing that research has not proven their benefits sufficiently. But increasingly, clinics will actually recommend certain supplements based on actual recent research – some will even recommend certain types or brands and be very directive. Below are a number of certain supplements that clinics may recommend occasionally or routinely.

  • DHEA (Dehydroepiandrosterone): DHEA is a “precursor hormone” that converts to testosterone and estrogen in the ovaries. Several studies in women with DOR suggest that DHEA (commonly 75 mg/day) may improve ovarian response and possibly reduce aneuploidy. However, evidence regarding improvement in live birth rates remains mixed, and supplementation should be lab-guided. It's one of the most studied supplements in reproductive medicine for poor responders.
  • Coenzyme Q10 (CoQ10 Ubiquinol): CoQ10 is a critical component to the function of mitochondria. As women age, CoQ10 levels in oocytes decline, leading to reduced mitochondrial energy production - directly linked to errors during meiosis (chromosome division). A study showed that CoQ10 supplementation in aging mice restored oocyte quality and reversed age-related fertility decline.[2] While the strongest mechanistic data come from animal models, emerging human data suggest potential improvements in ovarian response and embryo parameters, though large randomized live-birth trials are still limited. Recommended dose: 400-600 mg/day of ubiquinol form (better absorbed than ubiquinone).
  • Vitamin D: vitamin D receptors are present in the ovaries, endometrium, and placenta. Deficiency is associated with lower AMH, poorer IVF outcomes, and higher miscarriage rates. Optimizing levels (40–60 ng/mL) is a low-cost, evidence-supported intervention.
  • Omega-3 fatty acids (DHA and EPA): essential for cell membrane integrity and anti-inflammatory signaling. DHA in particular is concentrated in follicular fluid and plays a role in oocyte maturation. Studies suggest supplementing (1,000-2,000 mg combined EPA + DHA daily) may improve egg and embryo quality, particularly in 35+ women.
  • Melatonin: a powerful antioxidant that is naturally present in high concentrations in follicular fluid. Studies have shown that melatonin supplementation (3 mg/night) reduces oxidative stress in the follicular environment and may improve oocyte quality and fertilization rates.
  • Myo- and D-chiro-inositol: often used for PCOS/insulin signaling, but research also looks at egg maturity and fertilization outcomes in ART settings. Recent meta-analyses suggest improvements in markers like MII oocytes (mature eggs) and fertilization in some groups (especially PCOS).
  • Resveratrol: an antioxidant found in red grapes that activates a protein involved in DNA repair and mitochondrial biogenesis. Animal studies show improved oocyte quality with supplementation; human data is emerging.
  • N-acetylcysteine (NAC): included in multiple fertility supplement reviews/meta-reviews, and it shows up as a potential antioxidant/anti-inflammatory adjunct in some ART contexts (not a guaranteed live-birth improver, but it’s on the “commonly tried” list).
  • L-carnitine: more commonly discussed in PCOS and metabolic contexts, but there’s also interest in egg/embryo quality and oxidative stress pathways; recent clinical literature continues to explore it.
  • Selenium, vitamins C/E, “antioxidant stacks”: a lot of “egg quality” supplementation is essentially antioxidant strategy; reviews exist, but results vary by population and study design (and more isn’t always better).
  • NAD+ precursors (NMN / NR): NAD boosters may benefit egg mitochondria. Strong mechanistic rationale exists from aging and mitochondrial biology research, and early fertility studies are underway. Human IVF outcome data remain limited at this time.

Important note: Supplement stacks should be targeted, evidence-informed, dose-aware, and periodically reassessed - not permanent monuments.

Anything hormonal (especially DHEA), but also other markers like Vitamin D, are very individualized, and can backfire unless it’s tightly lab-guided: ask your doctor for bloodwork before blindly start any supplementing.

For instance, a patient who has had high free/bioavailable testosterone historically, would not benefit at all from DHEA (and on the contrary). You don’t want anything you do to increase egg quality, to actually damage them.

“Antioxidant mega-dosing” can be counterproductive in some contexts: balance matters, as “oxidative” molecules are also needed in the body, as they play normal signaling roles in ovulation and follicular maturation.

There is emerging research in other fields (sports science, aging biology) showing that excessive antioxidant supplementation can dampen beneficial cellular adaptation processes.

2. Upstream biologic improvements through lifestyle

Upstream biologic improvements through lifestyle

  • Mediterranean-style diet pattern: while not a magic wand, this is one of the more consistent lifestyle signals in IVF outcomes literature (vs. any single “superfoods”).
  • It is a food diet rich in vegetables, fruits, legumes, whole grains, fish, olive oil, and lean protein.
  • Observational studies suggest that greater adherence to a Mediterranean-style diet has been associated in some cohorts with higher clinical pregnancy and live birth rates in IVF, as well as improved embryo yield. While evidence is not uniform, overall diet quality — including adequate protein intake and lower consumption of ultra-processed foods — appears more relevant than any single “superfood”.
  • In short: “Mediterranean + high protein + low ultra-processed foods”.
  • Reduce/avoid the big fertility “killers”, consistently associated in the literature with adverse fertility outcomes.
  • Smoking tobacco is linked to reduced ovarian reserve, increased oxidative stress in follicles, earlier menopause, and poorer IVF outcomes.
  • Consuming alcohol: heavy alcohol use is associated with reduced fecundability and increased miscarriage risk.
  • Using recreational drugs (including marijuana, cocaine, opioids, and amphetamines) can interfere with hormonal regulation, ovulation, implantation, and early embryonic development. While evidence strength varies by substance, avoidance is broadly recommended during fertility treatment. Data on occasional marijuana use are mixed and evolving, but given potential endocrine and implantation effects, caution is advised.
  • Consuming high caffeine quantities: high caffeine intake has been associated in some studies with reduced fertility or increased miscarriage risk, although findings are mixed; most reproductive societies recommend moderation.
  • Endocrine disruptors (see below) and air pollution have been associated in observational human studies with altered ovarian reserve markers, impaired follicular development, lower IVF success rates, and increased pregnancy loss. While causation is difficult to prove, exposure to certain environmental toxins correlates with oxidative stress and hormonal disruption, both of which are biologically relevant to oocyte development.
  • In short: eliminating or minimizing exposure to the above factors is considered a reasonable precautionary strategy given the plausibility and accumulating data.
  • Endocrine disruptor exposure (“EDC”) reduction: this is increasingly discussed because higher exposure to certain EDCs (e.g., BPA, phthalates, PFAS, PCBs, parabens) has been associated with adverse reproductive outcomes and poorer IVF parameters in reviews. In short:
  • use glass/stainless to cook and eat,
  • use less fragrance,
  • avoid air fresheners or plug-ins, scented candles and such,
  • use fewer (even zero) plastics (especially do not microwave plastics)
  • filter water for pollutants
  • read the tags of all your skin care, make-up, personal hygiene products (soaps, shampoos, etc.) to stop using those with known EDCs
  • Chronic psychological stress can influence hormonal regulation and ovulation. While it is rarely the sole cause of infertility (and “just relax” is not a treatment plan, nor is it easy to achieve when battling infertility!) supporting mental health may help optimize overall physiologic balance and make the fertility journey more sustainable.

Note: Dietary patterns and healthy lifestyle habits are associated with fertility signals, and all fertility patients should absolutely strive to maintain the healthiest lifestyle habit while TTC and pregnant.

Even if they do not in themselves guarantee improved egg quality or IVF success, they are one part of a broader optimization strategy, and they are surprisingly easy to implement.

3. Upstream biologic optimization: adjunct and non-pharmacologic approaches

Upstream biologic optimization: adjunct and non-pharmacologic approaches

  • Iron and ferritin optimization: adequate iron status supports oxygen delivery and mitochondrial function. Both iron deficiency and overload can affect reproductive outcomes. Checking ferritin levels and correcting deficiencies is a simple, evidence-supported optimization step.[6]
  • Red Light Therapy (photo-biomodulation):
  • The theory is straightforward: aging eggs struggle primarily because their mitochondria can't produce enough energy for proper chromosome division. If you can boost mitochondrial output, you may improve “meiotic fidelity” (= how well the egg prepares for becoming an embryo).
  • That is what low-level red and near-infrared (NIR) light therapy (wavelengths 600–1000 nm) are presumed to do, by targeting some molecules in mitochondria, boosting ATP production.
  • A 2022 pilot study showed improved egg quality markers following photo-biomodulation treatment.
  • While large-scale human trials are still underway, the mitochondrial mechanism is well-characterized in other tissues, and intervention appears low-risk when used appropriately – though fertility-specific data remain limited and standardized reproductive protocols are not yet established.
  • Protocols typically involve 10-20 minutes of red/NIR light applied to the lower abdomen, several times per week, for 8–12 weeks before retrieval.
  • Acupuncture: frequently used in fertility settings, acupuncture is proposed to improve pelvic blood flow, modulate stress pathways, and influence neuroendocrine signaling. Some studies suggest modest improvements in IVF pregnancy rates when used around embryo transfer, though results are mixed and highly protocol-dependent. While it does not “fix” egg quality directly, stress reduction and improved ovarian blood flow are plausible mechanisms. It is generally considered low risk when performed by a qualified practitioner.
  • Sleep optimization: sleep regulates circadian hormones that influence ovulation and metabolic function. Chronic sleep deprivation is associated with insulin resistance and inflammation, both relevant to follicular development. While direct egg-quality trials are lacking, consistent sleep timing and adequate duration are biologically supportive.

4. Upstream biologic improvements via medical/pharmacologic optimization

Upstream biologic improvements via medical/pharmacologic optimization

  • Human Growth Hormone (HGH): Growth hormone plays a role in folliculogenesis (= the egg’s development process) and egg maturation through its effects on “IGF-1 signaling” within the ovary.
  • Some research did not find a significant increase in live birth rates for poor responders, however several studies have shown that HGH co-treatment in poor responders can improve egg numbers and quality.[7]
  • Many reproductive endocrinologists continue to use HGH as an adjunct based on individual patient response. It is typically administered as daily subcutaneous injections in the weeks leading up to egg retrieval.
  • Insulin sensitivity optimization: even in non-PCOS patients, subtle insulin resistance can affect ovarian steroidogenesis and follicular environment. Addressing metabolic health through diet, exercise, and (when indicated) medications may support ovarian function indirectly.
  • Ovarian PRP (Platelet-Rich Plasma): a small amount of your blood is processed to concentrate platelets and growth factors, and the resulting “PRP” is then injected into your ovaries under ultrasound guidance.
  • Small observational studies and case series (patients’ reports) have reported increases in AMH and antral follicle count following intraovarian PRP. However, randomized controlled data are limited, and whether these changes consistently translate into improved live birth rates remains uncertain.[1]
  • Worth noting: because PRP is autologous (using your own blood), it is minimally invasive and carries low risk.
  • Rapamycin / mTOR modulation (fertility-aging trials):  a fairly new one in IVF territory because of recent research, thought to be helpful for premature ovarian insufficiency, diminished ovarian reserve and mitochondrial function modulation (to help egg quality). Not standard IVF practice, very experimental, and evidence is very limited (and mostly on animals). Also, it is an immunomodulating drug with real risks and should only be considered under a formal protocol.

5. Downstream protocol and lab-level optimization

Downstream protocol and lab-level optimization:

  • Clinical add-ons and “lab-side” tactics: these don’t change your DNA age, but they can improve the odds that the eggs cohort you get is handled optimally.
  • These are clinic-specific decisions, not suitable for everyone, to be discussed with your doctor; therefore, evidence varies by indication.
  • Protocol optimization: adjusting doses, trigger choice, priming approach, stimulation style, luteal stim/DuoStim in select cases, etc.. This is often the biggest “lever” compared with any single supplement.
  • Trigger strategy: hCG vs Lupron trigger vs “dual trigger” to support final oocyte maturation appropriately
  • Lab techniques - when indicated, such as ICSI (vs. conventional), calcium ionophore, etc.. Refer to Section 2 for detail on those.

d. Emerging and community-discussed add-ons and approaches
  • In fertility patient groups and online forums, a number of additional “tools” or “techniques” are frequently mentioned (and sometimes strongly endorsed by individual patients). While some may be relatively safe (though not necessarily effective), others may be costly, counterproductive, or even harmful.
  • In most cases, there is little to no high-quality evidence demonstrating that these approaches improve egg quality or live birth rates.
  • Some of those approaches include:
  • “Mitochondrial support” stacks beyond those mentioned above, such as Pyrroloquinoline Quinone (PQQ), Alpha-Lipoic Acid (ALA, etc.). These are often marketed for cellular energy support, but robust fertility-specific data are lacking.
  • IV “Fertility Cocktail” infusions, including NAD+, glutathione, high-dose vitamin C, iron, and various antioxidant blends. While some (such as NAD+) are theorized to enhance mitochondrial function, research is limited – particularly regarding IV administration. It is also important to note that ovaries are not passive “sponges” that directly absorb wellness infusions in a targeted way.
  • Sauna and cold plunge protocols: these are typically discussed in relation to stress reduction or inflammation rather than direct effects on egg quality. There is currently no evidence demonstrating improved fertility outcomes, though stress reduction itself may be beneficial.
  • Dietary eliminations or restrictive regimens, such as removing seed oils, adopting carnivore, ketogenic, or gluten-free diets. Responses are highly individual, evidence is inconsistent, and some patients report negative effects.
  • Air filtration / HEPA systems and “clean indoor air” strategies, especially around stimulation or retrieval cycles. While minimizing environmental toxins is a reasonable general health goal, fertility-specific outcome data are limited.
  • Ozone therapy: a fringe intervention marketed for “oxygenation” and mitochondrial support. It is not supported by reproductive medicine organizations and lacks credible fertility outcome data.
  • Stem cell / exosome IVs: ultra-experimental approaches often paired with “ovarian rejuvenation” marketing. There is extremely limited data regarding effectiveness or safety in fertility settings.

Important note: the above are listed for general awareness, not endorsement. These interventions are widely discussed in infertility communities, sometimes also boosted by targeted marketing campaigns. Evidence is often mixed, preliminary, or even absent. In some cases, enthusiasm may be driven more by anecdotal experience than by reproducible clinical data.

Before pursuing such experimental add-ons, you may wish to ensure that foundational factors (such as protocol optimization, lab quality, metabolic health, and evidence-based supplementation) have been addressed first.

Always do your research, do not decide to proceed with some “egg quality boosting technique” based solely on what other infertility patients report.

3. The 3-month rule: why timing matters

Here is a critical biological fact that (impatient) clinics often gloss over, or that patients simply are unaware of: both egg and sperm development take approximately 90 days.

  • Women are born with their lifetime supply of eggs. Each egg undergoes a recruitment and growth process lasting approximately 3-4 months before ovulation.
  • Sperm take approximately 74 days to develop, and another 12-21 days for final maturation.

This means that a 3-month optimization window is biologically meaningful, and any upstream intervention or quality optimization techniques should ideally be implemented for at least 3+ months to influence the gametes that will be used in a retrieval cycle.

So, starting supplements 2 weeks before retrieval is unlikely to influence the cohort of eggs being retrieved, as the eggs retrieved in your next cycle were already developing when you started the supplements.

Tip: a responsible fertility plan should include a dedicated 3+ month optimization period for both partners before the next retrieval. Then, after optimizing, do at least 1 other retrieval with (hopefully) “optimized” gametes before even discussing donor eggs.

4. PGT-A after optimization: a screening tool, its limits, and the reality

You have worked very hard for months to prepare for your ovarian stims and egg retrieval.

You were happy to have a solid number of blastocysts …

And they all came back from PGT-A as “non-euploid”.

What to make of this?? Was it all for naught?!

a. The harsh reality …

Regardless of age, regardless of your egg/sperm quality improvement efforts, it is always possible that most or all blastocysts from 1 cycle are genetically abnormal (whether you opt for genetic testing, or not). It is unfortunate, sad, frustrating, sometimes maddening, devastating … and it can feel very similar to losing a loved one or a piece of self.

However. The outcomes of one cycle do not forecast the outcomes of other future cycles.

I will repeat: it is not because most/all your embryos from one cycle were abnormal, that “you cannot produce normal embryos”.

Sometimes, it just happens, and that will be the case regardless of what you have done or not. And sometimes, most or all of your blastocysts will be genetically normal, even if you changed nothing to your protocol, supplements, preparation etc..

There is absolutely no certainty in IVF, and whether embryos will be normal or not, is one of the (truly maddening) variables.

Personal note: while it is absolutely gut-wrenching to have bad results, do not let the poor or bad outcomes of one cycle bring you down and make you give up altogether.

My very first IVF cycle returned 2 abnormal embryos. My second cycle, absolutely identical, yielded 2 normal embryos.

Many infertility patients have to handle poor, bad, suboptimal or unexpected outcomes from their IVF cycles, before finding success. Self-advocating and persistence are key.

So, is PGT-A even worth it? Wouldn’t it be better to not test, and not know?

b. PGT-A: is it worth it?

First and foremost: this is a very personal decision, that needs to be based in facts. I truly believe that there is no right or wrong when it comes to deciding whether to test – there are only varying circumstances making you lean one way or another at different points in time.

With that said, here is the (inconvenient) truth about genetic testing …. While it can absolutely be helpful and “life-saving” to some, PGT-A is not the gospel.

PGT-A is presented by most clinics as the gold standard for selecting "good" embryos, and it is especially pushed for older patients as “a necessity”, their age increasing the odds for abnormal embryos. Their pitch is simple: test your embryos, transfer only the chromosomally normal ones, avoid miscarriage, have a healthy baby. It all sounds irrefutable and so much easier.

While it is true that knowing whether embryos are genetically normal may help reduce miscarriages, it does not eliminate the risk altogether, just like the results of PGT-A do not provide a guarantee of the embryo transfer leading to a live birth – especially if you are in a RIF or RPL situation.

The science indeed tells a more complicated story.

Personal note: my first 3 embryo transfers were with PGT-A normal, or “euploid”, embryos. Because PGT-A was presented to us as the gold standard to avoid miscarriages, we were stunned beyond words that the first resulted in a miscarriage, and the second 2 in “chemical pregnancies”. We have since learned that our embryos’ euploidy did not matter in our case and won’t prevent loss, as I have multiple other factors making me an extraordinarily complex “RPL” patient.

See my other article “WTF - What did my Transfer Fail??” (to be published soon).

c. A test possibly flawed from the start

PGT-A works by biopsying a few cells (usually ~5) from the trophectoderm (the “TE”), the outer layer of the blastocyst that becomes the placenta - not the baby. The inner cell mass (ICM), which actually becomes the baby, is not tested.

Those few cells then undergo "whole genome amplification" as 5 cells are not enough material to complete the chromosomal analysis. During amplification, specialized enzymes copy the tiny DNA from those few cell samples millions of times, to generate enough material for chromosomal analysis. This process can introduce “artifacts”: research shows allele dropout (= missing parts of chromosomes) and loss of heterozygosity (= the chromosome no longer having 2 different alleles of a particular gene) in up to 25% of cases.

Whole genome amplification can introduce technical artifacts such as allele dropout (= missing parts of chromosomes) and loss of heterozygosity (= the chromosome no longer having 2 different alleles of a particular gene), which have been documented in certain testing contexts.

Compounding this, a significant proportion of human blastocysts are naturally mosaic: different cells within the same embryo can have different chromosomal makeups. As one study put it: "In the presence of mosaicism, biopsy of TE cells cannot provide accurate results regarding the chromosomal make-up of the inner cell mass."

Translation: a handful of placental cells (not baby cells) are amplified with a process that can introduce errors, from an embryo that may naturally contain mixed chromosomal populations – meaning, there is potential for error at each step of the PGT-A process.

Despite this, labs report accuracy thresholds typically north of 95%, and in the vast majority of cases, embryos tested as euploid do result in genetically normal babies - which is reassuring.

Now, this also means that, in some cases (rare, but still happening) embryos tested as “euploid” will result in a genetically abnormal baby … reinforcing the importance of genetic testing later on during pregnancy whether by bloodwork early on (NIPT / NIPS

Tests), Chorionic Villus Sampling (CVS (placental tissue testing), or by amniocentesis later on in the 2nd trimester.

And in some other cases, embryos reported as non-euploid (aneuploid, segmental, polyploid, mosaic etc.) will actually lead to a healthy, genetically normal baby.

d. Healthy babies from "abnormal" embryos

Before getting into this discussion, it is worth noting that the majority of clearly aneuploid embryos (such as full trisomies such as “+13” or monosomies such as “-16” on reports) do not result in viable pregnancies. The below discussion primarily applies to mosaic or certain very specific aneuploids (such as segmental, chaotic etc.), not universally to all abnormal classifications.

Some studies have suggested that a substantial proportion of embryos classified as "mosaic aneuploid" may ultimately demonstrate normal chromosomal outcomes in live births[3] - raising the question of how many viable embryos have been discarded based on PGT-A classification alone.

In recent years, both labs and clinics have adjusted protocols accordingly: mosaic embryos are now separated into "low level mosaic" (LLM) and "high level mosaic" (HLM) categories rather than being grouped with aneuploids, and many clinics now treat LLMs as transferable - should patients wish.

One study went further, calling for PGT-A to be restricted to research protocols only, arguing that "because of high embryo mosaicism at the blastocyst stage and the high false-positive rate" of current TE biopsy technology, routine PGT-A screening may be unreliable.[4]

In short: the message across these peer-reviewed papers is clear: PGT-A is a screening tool with significant limitations, not a definitive diagnostic tool. Some clinics will transfer aneuploid embryos at patients' request — and the evidence suggests that such a decision deserves serious, informed consideration rather than reflexive dismissal – or even just discarding such embryos.

For this reason, some clinics – albeit not a majority, will transfer all embryos, including aneuploid ones, should their patients wish to.

And as a matter of fact, and due to all the PGT-A limitations, some embryos labeled "abnormal" may be perfectly capable of producing healthy babies - and discarding them based on a screening test with documented false-positives and limitations, is a decision that deserves far more nuance than most clinics provide.

Anecdotal note: In recent years, there have been increasing reports (including in community groups and forums of IVF patients) of embryos initially categorized as aneuploid (including some described as segmental, complex, polyploid, or “insufficient data”) being transferred and resulting in healthy live births.

While most scientific data support prioritizing euploid embryos, patient-reported outcomes and emerging case reports suggest that embryo genetics may not always behave in absolute terms.

These cases remain uncommon, and significantly larger studies are needed before changing clinical standards. However, they do offer an important reminder: for patients who receive only aneuploid results, the story may not always be entirely closed.

Importantly, decisions around transferring such embryos should always be made in close consultation with a reproductive specialist and/or a geneticist, with a clear understanding of the potential risks and (limited) likelihood of success.

5. Red flags: when your clinic isn’t working for you

I also cover this possibility in section 3 of the article “Infertility 101: where to start?”, explaining that sometimes, things just don’t go as planned - and that’s okay.

You may indeed realize that the clinic you chose isn’t the right fit after all, for a whole variety of reasons – and that reason could very well be related to their response, when you inquire about boosting egg quality or PGT-A.

Below are a number of scenarios which may be the sign that changing clinic could possibly be a better choice for you:

  • They recommend donor eggs after a single failed cycle without thorough investigation.
  • They don't discuss or offer any egg/sperm quality optimization strategies.
  • They don't offer (or they decline) advanced sperm selection techniques (ZyMōt, ICSI) when male factor hasn't been ruled out.
  • When recommending some supplements or lifestyle chances, they don't recommend at least 3 months of optimization before a subsequent retrieval.
  • They dismiss supplements, lifestyle changes, or adjunct therapies as "unproven" without engaging with the actual evidence.
  • They never mention or test sperm DNA fragmentation after some disappointing results.
  • They present PGT-A results as absolute truth and/or with no discussion of mosaicism or false positives.
  • They push donor eggs in a way that feels like it's about their success rates rather than your best outcome.
  • They refuse to transfer mosaic embryos or aneuploid embryos, and as a “policy” they discard all such embryos without you having a say.

The examples above are not exhaustive, of course, but they provide good examples of situations which any IVF patient may be in, and which call for caution at the very least – and changing clinics if that is necessary.

The bottom line …

Even if you are experiencing difficulties in your IVF cycles, your eggs are not "worth nothing". Age is a factor, not a death sentence. The science of gamete quality improvement is real, growing, and far more nuanced than the black and white "your eggs aren’t good, no choice but using donor eggs", that too many clinics present.

Before accepting a donor egg recommendation, at a minimum:

  • Test sperm DNA fragmentation: not just a standard semen analysis.
  • Both partners commit to a 3+ month supplement and lifestyle optimization protocol.
  • Consider adjunct therapies: ovarian PRP, red light therapy, growth hormone (where appropriate).
  • Ensure the lab is using advanced sperm selection (ICSI, ZyMōt, PICSI) and assisted activation (calcium ionophore) where indicated.
  • Do at least 1 more retrieval with fully optimized gametes.
  • If PGT-A is used, understand its limitations: ask about mosaicism, false-positive rates, and whether "abnormal" embryos might still be viable or at least transferrable
  • Seek a second opinion from a clinic that specializes in complex cases, not one that treats every patient over 37 as a donor egg candidate.

Your eggs have been with you since before you were born. They deserve better than an unsubstantiated assumption or hasty dismissal.

And you absolutely deserve decisions made from full investigation, not from reflex conclusions.

… and one more thing.

On top of everything we just discussed, an important point must also be kept in mind: the laboratory quality and embryologist expertise matter way more than we (patients) realize Indeed, those significantly and directly influence fertilization, blastocyst development, and embryo survival.

This topic is not covered here in detail, but IVF success is not determined by biology alone (good or bad egg/sperm): laboratory performance varies between clinics and is (quite shockingly) rarely transparent to patients – at least in the US.

Lastly, it is important to distinguish between egg quality and embryo competence. Egg quality contributes significantly, but as we’ve exposed it, sperm quality and lab conditions matter and influence the final outcome – but so does your uterine environment, not enough talked about.

For more information on embryo competence, uterine environment and successful vs. failed embryo transfers, read our article “WTF - Why did my Transfer Fail??” (to be published soon).

Age is a factor, not a verdict. You deserve a clinic that fights for your biology before suggesting you replace it.

References

[1] Ahmadi F, Gharaei R, Shirali E, et al. "The impact of platelet-rich plasma (PRP) on ovarian function and oocyte quality: A comprehensive review." Journal of Reproductive Immunology. 2025;172:104649.

[2] Ben-Meir A, Burstein E, Borber-Haeri A, et al. "Coenzyme Q10 restores oocyte mitochondrial function and fertility during reproductive aging." Aging Cell. 2015;14(5):887-895.

[3] Cai L, Zeng Q, Gao C, et al. "Majority of transferred mosaic embryos developed healthy live births." Journal of Assisted Reproduction and Genetics. 2022;39(11):2483-2504.

[4] Casper RF. "PGT-A: Houston, we have a problem." Journal of Assisted Reproduction and Genetics. 2023;40(10):2325-2332.

[5] Dabiri M, et al. "Sperm DNA fragmentation and its influence on mammalian reproduction." Nature Reviews Urology. 2026.

[6] Lin PH, et al. "Investigating the role of ferroptosis-related genes in ovarian aging and the potential for nutritional intervention." Nutrients. 2023;15(11):2461.

[7] Norman RJ, et al. "Human growth hormone for poor responders: a randomized placebo-controlled trial." Reproductive BioMedicine Online. 2019;38(6):908-915.

[8] Yaghoobi M, et al. "Faster sperm selected by rheotaxis leads to superior early embryonic development in vitro." Lab on a Chip. 2024;24(2):210-223.

[*] SART = Society for Assisted Reproductive Technology — the organization that tracks and publishes IVF clinic success rates in the US.