When women come into my clinic today (many in their late 20s or early 30s), they’re increasingly worried about fertility. And they should be. Infertility rates are rising, miscarriage rates are rising, and more couples are needing medical help to conceive than ever before.
Talking with Dr. Natalie Crawford made one thing very clear: fertility isn’t just about getting pregnant. It’s a window into your whole-body health.
It reflects inflammation, metabolic flexibility, stress resilience, thyroid function, muscle health, sleep quality, and even your environment. Whether or not you want kids, understanding fertility gives you valuable insight into how your body is really doing.
Infertility Is Rising, and Both Men and Women Are Affected
Fifteen years ago, infertility affected about 1 in 8 couples. Today, it’s:
- 1 in 6 globally
- 1 in 5 couples in the U.S. trying for their first pregnancy
And it’s not just women. About half the time, the primary issue is male factor, and in many couples, both partners have something going on.
Sperm counts have dropped by more than 50% in the last 50 years. Women are being diagnosed with low ovarian reserve earlier. Egg quality challenges are appearing sooner. Miscarriage rates are higher.
Something in our modern environment—a combination of inflammation, stress, diet, toxins, and sleep disruption—is creating a perfect storm for reproductive dysfunction.
The Central Driver: Inflammation
When Natalie says inflammation is hijacking fertility, she’s not being dramatic. She’s describing one of the most consistent and overlooked patterns we see in women struggling to conceive. And this isn’t “wellness-speak.” Chronic inflammation changes how the reproductive system works at almost every level.
Research shows that long-standing inflammation interferes with the entire reproductive process , from egg development to implantation. It can disrupt hormonal signaling between the brain and ovaries, alter the way follicles mature, and even damage mitochondrial function inside the egg, which are the very machinery that fuels early embryo growth. When those mitochondria are compromised, the embryo has a much harder time dividing and developing normally.
In men, inflammation from sources like obesity, varicocele, infections, toxin exposure, or even chronic stress can damage Sertoli and Leydig cells , disrupt testosterone production, and trigger oxidative stress inside the testes. The result is DNA damage, abnormal sperm, reduced motility, and lower overall fertility potential.
You don’t need to “look unhealthy” to be inflamed. I see plenty of women who appear perfectly fit and still carry signs of chronic inflammatory stress like poor sleep, blood sugar swings, autoimmune tendencies, high training loads without enough recovery, environmental exposures, or years of cumulative stress. It all adds up.
The good news is that inflammation is one of the most modifiable factors we have. Diet plays a massive role here. Anti-inflammatory dietary patterns, like the Mediterranean diet, have consistently been associated with better menstrual regularity, improved sperm parameters, healthier ovulation, and even higher success rates with IVF and other assisted reproductive technologies.
So when we step back and look at the entire picture, the through-line is unmistakable:
Inflammation is the common denominator behind many of the fertility issues we’re seeing today, and lowering it often becomes the turning point in someone’s journey.
Can Egg Quality Improve? Yes — Through Metabolic Health
One of the biggest myths I hear from women is that egg quality is fixed. “You’re born with all your eggs,” the logic goes, “so there’s nothing you can do.”
But that’s not what the science actually shows.
Yes, age affects chromosome stability, and we can’t reverse that. But the metabolic quality of your eggs—their mitochondrial strength, their ability to mature properly, and their resilience during early embryo development—is highly modifiable.
Natalie and I both emphasize this: the health of the environment surrounding the egg matters just as much as the egg itself. And mitochondrial DNA inside eggs appears far less damaged by aging than once believed. That means your habits still have tremendous influence over:
- how your follicles develop
- how well your eggs mature
- how strong your luteal phase is
- how viable early embryos become
You’re not powerless here. You’re not stuck with whatever biology handed you at birth. But you are influenced by your daily metabolic environment.
If you look at the diagram below, you can see just how far oxidative stress reaches . Fallopian tubes, ovaries, eggs, and the uterus are all affected. These aren’t small disruptions. They’re the kinds of impairments that decide whether fertilization happens, whether implantation succeeds, and whether an embryo can continue developing.
A remarkable 2024 experimental trial from Singapore helps explain why the metabolic environment is so critical. Researchers created a chimeric follicle model and discovered that it wasn’t the age of the egg that determined its developmental potential, but the age of the follicular environment around the egg.
When young eggs were placed inside aged follicles, they behaved like aged eggs with poor maturation, impaired mitochondrial function, reduced developmental potential.
But when aged eggs were placed inside younger, healthier follicles, they improved. Their mitochondrial output looked better. Their maturation rate improved. Their capacity to support early development rebounded.
This challenges a long-held assumption that declining egg quality is solely due to intrinsic aging. Instead, the surrounding follicular cells and the metabolic signals they deliver play a central role.
That’s why lifestyle matters so profoundly. You are continually shaping the environment in which your eggs mature.
Egg quality is not a static, predetermined outcome. It’s a metabolic reflection of your internal environment. When you improve mitochondrial function, reduce inflammation, stabilize blood sugar, and support nutrient status, you tip the balance toward better ovulation, better embryo development, and better fertility outcomes.
Sleep: The Most Undervalued Fertility Lever
I’ll be honest, I was hoping Natalie wouldn’t say it, because no one likes hearing this.
But she said it anyway.
Sleep is the foundation of hormonal health. In many ways, it sits even underneath nutrition and training. When sleep starts to fray, every hormone involved in reproduction begins to drift out of balance.
Poor sleep disrupts:
- Insulin sensitivity
- Inflammation levels
- Progesterone production
- Testosterone in men
- Stress hormones like cortisol
- Deep-sleep pulses that regulate menstrual cycles
And it matters for men just as much as women. Men regenerate sperm every ~70 days. If he’s sleeping poorly, drinking, using cannabis, or under stress, sperm quality can change dramatically.
Natalie recommends 7–9 hours a night, ideally consistent, ideally starting before midnight so you don’t miss the early-morning hormonal pulses that regulate ovulation.
If you’re trying to conceive, sleep becomes non-negotiable because sleep deprivation isn’t neutral. It pushes your physiology toward a metabolic and inflammatory state that works directly against fertility.
Large datasets, like those from the UK Biobank, show that irregular sleepers have a 53% higher risk of all-cause mortality. And that same pattern of irregular, insufficient sleep also predicts reproductive problems, especially in women undergoing treatment.
A comprehensive review of 19 studies found that women with infertility report poorer sleep quality, more “evening chronotype” tendencies, and a significantly higher rate of sleep disorders. Among women going through fertility treatments, poor sleep is associated with:
- fewer retrieved oocytes
- lower-quality embryos
- reduced fertilization rates
Mechanistically, disrupted sleep interferes with:
- the CLOCK gene system that regulates reproductive timing
- melatonin production (critical for egg maturation)
- oxidative stress pathways
- immune and inflammatory regulation
When deep sleep breaks down, the reproductive axis loses its rhythm. Hormones stop arriving on schedule. Ovulation becomes less predictable. Implantation becomes less reliable.
Thyroid and Autoimmunity: The Hidden Infertility Drivers
One thing I appreciate about Natalie is her bluntness. She doesn’t tiptoe around thyroid health or autoimmune issues, because these are some of the most overlooked causes of infertility in women.
Your thyroid is not just a “metabolism gland.” It’s a reproductive-control center. Thyroid hormones influence ovulation timing, luteal phase stability, implantation, and early pregnancy development. When thyroid function is even slightly impaired, the entire reproductive system becomes less predictable and less resilient.
Hashimoto’s (autoimmune thyroid disease) is incredibly common in women and shockingly underdiagnosed. And you don’t need full-blown hypothyroidism to experience fertility effects. Subclinical dysfunction and low-grade autoimmunity can be enough to disrupt cycles, weaken ovulation, or increase risk of miscarriage.
This is why Natalie almost always screens her patients with:
- a full thyroid panel (TSH, Free T4, Free T3)
- thyroid antibodies (TPO and Tg antibodies)
- celiac screening
- broader autoimmune panels when infertility is “unexplained”
A lot of women diagnosed with “unexplained infertility” are not unexplained at all. They’re simply undiagnosed. What looks like bad luck is often unrecognized inflammation or subtle autoimmune activity affecting ovulation, ovarian reserve, or implantation.
Her rule of thumb is that unexplained infertility is undiagnosed inflammation until proven otherwise. And the earlier you catch it, the more reversible it often is.
Autoimmune conditions are tightly intertwined with fertility challenges. Systemic autoimmune diseases like lupus, rheumatoid arthritis, antiphospholipid syndrome, and celiac disease are all associated with higher rates of subfertility . Even medications used in severe autoimmune conditions (like cyclophosphamide) can cause premature ovarian failure.
But thyroid autoimmunity stands out.
Thyroid antibodies (TPOAb and TgAb) affect nearly 10% of women of reproductive age, and their impact reaches far beyond the thyroid itself. Research shows that women with thyroid autoimmunity, even with normal thyroid hormone levels, have:
- higher rates of infertility
- more irregular cycles
- increased risk of miscarriage
- higher prevalence of endometriosis and premature ovarian insufficiency
- more difficulty with implantation and early pregnancy stability
The mechanisms aren’t fully understood yet, but several theories suggest that antibodies may directly affect the ovaries or endometrium, autoimmunity may reduce immune tolerance needed for implantation, subtle thyroid hormone insufficiency may impair early embryo development, and autoimmune conditions often coexist, amplifying inflammation.
Interestingly, outcomes for women with thyroid antibodies undergoing IVF have improved in recent years, likely because modern techniques like ICSI bypass some of the earlier barriers.
One important takeaway from the research is that simply giving meds to antibody-positive women doesn’t reliably fix the problem. The issue isn’t only hormone levels, it’s immune dysregulation.
Which brings us back to the bigger theme: Inflammation isn’t a side character in fertility. It’s shaping the entire reproductive landscape. And thyroid autoimmunity is one of the clearest examples of that.
Supplements: What Helps, What Hurts, and What Actually Moves the Needle
By the time many women land in my clinic, they’re already taking an entire pharmacy of “hormone-supporting” supplements they found online. And Natalie was unequivocal about this: If you’re trying to conceive, anything that manipulates hormones without medical supervision can work against you.
For example, vitex has a long history of suppressing libido in monks, and glandulars often contain dried animal endocrine tissue, meaning unpredictable amounts of thyroid hormone, progesterone, estrogen, prolactin, even cortisol. Most “hormone-balancing” formulas are black boxes with no quality control.
You cannot “fix” a disrupted hormonal system by swallowing someone else’s gland in a capsule.
That doesn’t mean supplements are useless. It means the right ones matter, and the wrong ones can actively interfere with ovulation, implantation, and early embryo development. Natalie’s rule is simple: Avoid hormone-modulating herbs and glandulars. Support deficiencies. And use evidence-based nutrients with real clinical outcomes.
And thankfully, several supplements truly do make a meaningful difference.
Myo-Inositol (4 g/day): one of the most reliable fertility supplements we have
- A meta-analysis of nearly 1,000 IVF patients found a 45% increase in clinical pregnancy rates and a 74% reduction in miscarriage with myo-inositol.
- In a double-blind RCT , women taking inositol produced more eggs, more mature eggs, and had higher pregnancy and live birth rates than placebo (57% vs. 23% pregnancy; 27% vs. 10% live birth).
- Even in “poor responders,” inositol improved embryo quality, fertilization, and implantation.
Inositol works by improving insulin sensitivity, lowering inflammation, and supporting the metabolic function of the follicle, exactly the environment eggs need to develop properly.
CoQ10 (600 mg/day): a powerhouse for mitochondrial health, which is the foundation of egg quality.
- A meta-analysis of over 1,500 women with diminished ovarian reserve showed an 84% improvement in clinical pregnancy and a 62% reduction in miscarriage with CoQ10.
- In another meta-analysis of five RCTs, CoQ10 doubled pregnancy rates (28% vs. 14%) and increased live birth rates, especially in women with PCOS (7.5% → 31%).
- Higher CoQ10 levels in follicular fluid consistently correlate with better embryos and stronger implantation.
As women age, mitochondrial energy production in oocytes naturally declines. CoQ10 helps restore the TCA cycle and electron transport chain, supporting healthier eggs with better developmental potential.
Melatonin (3–8 mg at night): not just a sleep hormone, but one of the most powerful antioxidants inside the follicle.
- Women with higher follicular melatonin levels retrieve more oocytes and produce higher-quality embryos.
- Supplementation boosts antioxidant capacity in the follicle, protects oocytes from oxidative stress, and improves fertilization rates.
- A 2024 meta-analysis of 17 trials showed melatonin improved fertilization, follicle growth, and mature oocytes, with a trend toward a 22% increase in pregnancy rates.
- Another meta-analysis found a 43% increase in pregnancy and a 38% increase in live births with nightly melatonin.
N-Acetylcysteine (NAC, 1200–1800 mg/day): especially effective for women with PCOS
- A meta-analysis of 2,300 women found NAC boosted clinical pregnancy rates by 55% and increased live births threefold.
- In women with PCOS , NAC also improved insulin resistance, lowered testosterone, and outperformed metformin in reducing fasting insulin, glucose, and lipids.
For women whose fertility challenges stem from metabolic dysfunction, NAC is one of the most supportive and well-studied supplements available.
Environmental Toxicants: You Can Reduce Exposure Dramatically
Inositol works by improving insulin sensitivity, lowering inflammation, and supporting the metabolic function of the follicle, exactly the environment eggs need to develop properly.
This is the part of the conversation that tends to feel the most overwhelming. But it’s also the part where small changes make huge differences.
Endocrine-disrupting chemicals like BPA, phthalates, PFAS, pesticides, and plasticizers are everywhere. And they don’t just raise vague “toxin” concerns, they directly interfere with reproductive biology. These chemicals influence:
- Ovulation and menstrual regularity
- Ovarian reserve and follicle development
- Sperm count, motility, morphology, and DNA integrity
- Miscarriage risk and implantation
- Thyroid function
- Gut inflammation and immune signaling
You cannot eliminate all exposure. But you can cut your personal burden dramatically by focusing on the places where exposure happens every single day.
1. Water and Air
- Use an air filter.
- Use a water filter matched to your local water quality (EPA has lookup tools).
- Bottled water in plastic is not better, it’s often worse.
2. Kitchen and Cooking
- Replace nonstick cookware.
- Use glass or stainless steel for heating and storing food.
- Never microwave plastic.
- Transfer takeout from plastic containers immediately.
3. Personal Care
- Shampoo, lotion, laundry detergent, perfumes matter because you use them daily.
- Replace products as they run out instead of throwing everything away at once.
Small changes stack up.
Muscle: A Direct Link to Ovarian Reserve
This is where fertility medicine and muscle-centric medicine meet in the middle.
Natalie explained something most women have never been told: the ovary isn’t just a reproductive organ, it’s a metabolic sensor. It constantly monitors signals from the brain, liver, fat tissue, gut, and muscle to decide whether the body is in a position to support ovulation and pregnancy.
And when those signals are disrupted, ovarian function is one of the first systems to falter.
Insulin resistance damages the internal environment of the ovary, including the “vault” where follicles are stored and developed. Improving insulin sensitivity, therefore, directly improves ovarian function, and nothing improves insulin sensitivity more reliably than skeletal muscle.
Muscle helps by:
- Increasing insulin sensitivity without requiring insulin
- Reducing systemic inflammation
- Improving metabolic flexibility
- Supporting stable hormone production
- Lowering the stress burden on the hypothalamus and pituitary
More muscle means a better internal environment for follicles to develop in, and that translates into better ovarian reserve, more predictable ovulation, and healthier eggs.
If you’re trying to conceive, strength training isn’t a luxury. It’s protective.
Keep in mind, however, that the ovary reads energy availability with remarkable sensitivity. Too little energy, and signaling from the brain slows. Too much energy, and insulin begins to overwhelm the system.
In undernutrition — low-calorie diets, endurance training, fasting, or sustained stress — the brain downregulates reproductive signaling to conserve energy. This can lead to functional hypothalamic amenorrhea (FHA) where cycles may look “normal,” but ovulation is often impaired.
In a In a study tracking daily hormones:
- 30% of athletic women had luteal phase defects
- 20% were not ovulating at all, despite reporting normal 26–35 day cycles
- Almost all sedentary women ovulated normally
A regular period does not always mean a healthy cycle.
In overnutrition and obesity, the problem flips. High insulin levels act directly on the ovary , stimulating increased androgen production and impairing follicle selection. Daily ultrasound tracking shows:
- Fewer recruited follicles
- Fewer dominant follicles
- More luteal phase defects
- More “silent” ovulatory dysfunction, even when cycles appear normal
But the good news? After just six months of improved metabolic health, ovarian function often rebounds. Follicles mature more predictably, ovulation normalizes, and progesterone production rises, a clear sign that the ovary is responding.
The takeaway? A “normal” cycle length doesn’t always mean normal ovarian function, especially when energy expenditure outweighs intake.
How to Actually Time Sex (Simple, Not Stressful)
Most couples overcomplicate this part, or stress themselves into paralysis. You really don’t need to. Sperm can survive up to 5 days, and the egg lives about 24 hours after ovulation. That means your real goal is to have healthy sperm waiting when the egg arrives.
The biggest mistake couples make is “saving up” their sperm. Long periods of abstinence actually make sperm quality worse, not better.
Across multiple clinical trials and reviews
- Shorter abstinence consistently leads to higher pregnancy rates.
- Live birth rates are higher when men ejaculate more frequently.
- DNA fragmentation — one of the strongest predictors of failed fertilization — goes up with longer abstinence.
- Motility declines the longer sperm sit in the system.
Yes, semen volume and sperm count increase with abstinence… but they also carry more DNA damage and lower fertilization potential. It’s a net negative. In other words, more days without ejaculation does not produce better sperm. It produces older, less functional sperm.
So here’s the simple, low-stress timing plan. Have sex during:
- The 5 days before ovulation
- The day of ovulation
- And the day after a positive LH test
That’s it. You don’t need charts or spreadsheets.
Use any of these tools if you want more clarity
- Cervical mucus: Egg-white consistency = your peak fertile window.
- Ovulation predictor kits: A positive LH surge means ovulation is coming tomorrow; plan sex the day of and the day after.
- Wearables / temperature tracking: Helpful for confirming ovulation patterns but not required.
The goal isn’t perfection. The goal is exposure to fresh, healthy sperm during your fertile window. Keep it simple. Keep it consistent. And don’t save up, because that’s the one strategy that reliably works against you.
The Takeaway
If there’s one message running through this entire conversation, it’s that fertility is not fragile, but it is responsive.
Your ovaries and your partner’s sperm aren’t operating in isolation. They’re responding to everything the body is sensing… sleep, stress, inflammation, nutrition, metabolic health, environmental exposures, and yes, even how often you lift weights.
You don’t need perfection. You don’t need a 17-step protocol. You don’t need to do everything all at once. But you do need to understand that fertility is a full-body reflection of metabolic resilience.
- Reduce inflammation, and hormones signal better.
- Improve sleep, and ovulation stabilizes.
- Build muscle, and ovarian reserve improves.
- Lower environmental toxicants, and egg and sperm quality rise
- Support your thyroid and immune system, and cycles normalize.
None of this guarantees pregnancy. No single intervention ever will. But together, these levers meaningfully shift the environment where eggs mature, embryos develop, and pregnancies take hold.
That’s the real work. Not hacks. Not “hormone-balancing” herbs. Not fear-based fertility culture.
Just science, consistency, and the basics done well.
And you can start today.
Your Fertility Action Checklist
Use this as a simple starting point, not a rigid protocol.
1. Lower Inflammation
- Build a Mediterranean-style plate (olive oil, fish, legumes, colorful plants).
- Reduce ultra-processed foods and added sugars.
- Address blood sugar swings and insulin resistance early.
2. Protect Egg and Sperm Quality
- Prioritize sleep (7–9 hours, consistent bedtime, lights out before midnight).
- Strength train 3+ days per week.
- Limit alcohol and avoid cannabis entirely.
- Add proven supplements when appropriate (inositol, CoQ10, melatonin, NAC).
3. Optimize Thyroid and Autoimmune Health
- Request a full thyroid panel, not just TSH.
- Screen for thyroid antibodies, celiac markers, and autoimmune patterns — especially with “unexplained” infertility.
- Treat abnormalities early to protect ovulation and luteal phase quality.
4. Reduce Toxicant Exposure
- Filter drinking water and indoor air.
- Use glass or stainless steel for cooking and storage.
- Replace nonstick and plastic gradually.
- Swap daily personal-care products for lower-toxic alternatives.
5. Support Metabolic Resilience
- Eat 25–35% of calories from protein.
- Maintain a healthy body composition without extreme dieting.
- Avoid prolonged fasting if cycles are irregular.
- Prioritize muscle as a metabolic organ.
6. Time Sex Correctly
- Aim for sex in the 5 days before ovulation and the day of the LH surge.
- Don’t “save up” — ejaculation every 2–3 days supports healthier sperm.
- Use cervical mucus, OPKs, or wearables to simplify timing.
