Why Normal Labs Aren't Good Enough_ Mirthe Precision Health and Longevity
Why 'Normal' Lab Results Aren't Good Enough For Optimal Health, Longevity & Prevention.

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Why ‘Normal’ Labs Aren’t Good Enough

If you want to optimise health and longevity

You have been to your GP. You have had your bloods done. Or even a bigger private health panel. And you have been told: everything is fine. That’s great..? Or is it not?

.. But you don’t feel fine. You are tired in a way that sleep doesn’t fix. Maybe your hair is falling out, or your body composition doesn’t match the hard work you feel like you are putting into it. 

You feel maybe your hormones are off, but your GP tells you there is no point in testing them as they fluctuate throughout the day anyhow (and if you are a woman with a cycle, throughout the month too). 

Or perhaps you do feel fine, but are watching your parents age, starting to accumulate all sorts of meds (statins, blood pressure meds, etc etc, and the list is long), or run into a full blown health crisis like diabetes, Alzheimer’s, a stroke or heart attack, and think: I don’t want that. 

You pay attention to your health — and would like to be proactive, not reactive. You’d rather prevent and optimise for longevity. 

You have heard that ‘normal’ lab results don’t always mean optimal? So getting those labs back with the comment ‘they are fine’, makes you somewhat suspicious, because? 

You are onto something there. ‘Normal’ is often just not quite good enough if optimal health and longevity is your goal. If you want to thrive, rather than survive. – Let me explain.

Why standard lab reference ranges often aren’t good enough, if optimal health and longevity is your goal

Standard lab reference ranges are built on statistical averages of the general population — including people with undiagnosed disease, chronic fatigue, poor metabolic health, and early-stage conditions that haven’t yet declared themselves. These ranges tell you what’s common. They don’t tell you what’s ideal for thriving, now nor into your 70s, 80s, and beyond.

In my practice, I use a different set of ranges. Narrower. Evidence-based. Grounded in the research that links specific biomarker levels to prevention and optimisation, to energy, cognitive clarity, hormonal resilience, cardiovascular protection, and longevity. Many of those tests are simple, and you likely already had them done with your GP or annual health check. And if not, they are usually ‘easy’ to have added without having to go to any expensive specialty clinics. 

Below are some of the key biomarkers I look at with every client — and the optimal ranges the research actually supports.

1. Ferritin

Optimal: 60–100 µg/L     |  Standard labs: 15–300 µg/L

Ferritin is your iron storage protein. Most labs will only flag a problem if you fall below 15 µg/L — by which point you’re already profoundly deficient. The research tells a different story.

Why it matters: Iron is needed to create red blood cells and allow for them to transport oxygen to your cells. At levels below 60 µg/L, your cells are literally starving. Many people experience fatigue, hair loss, poor concentration, and impaired thyroid hormone conversion — all long before they’d be diagnosed with ‘iron deficiency anaemia’. 

At the other end, ferritin above 100 µg/L is not just iron overload — it’s also a marker of inflammation and oxidative stress, independently associated with increased cardiovascular disease, Alzheimer’s (R) and cancer risk.

The sweet spot is 60–100 µg/L. Low enough to avoid iron excess. High enough to support energy, immunity, and thyroid function.

Source:

https://academic.oup.com/metallomics/article/13/6/mfab030/6287580 

https://pubmed.ncbi.nlm.nih.gov/34469815/ 

2. Vitamin D

Optimal: 100–150 nmol/L  or 40-60 ng/ml   |  Standard lab: 50–250 nmol/L or 20-100 ng/ml

Vitamin D is not just a vitamin — it’s a precursor hormone, and many cells in your body have receptors for it. Yet most labs consider 50 nmol/L ‘sufficient’. The research says otherwise.

Why it matters: Studies consistently show that levels below 100 nmol/L are insufficient for cancer prevention, immune regulation, and neurological health. At 100–150 nmol/L, research shows 77% lower all-cancer incidence, significantly reduced autoimmune disease risk, and the strongest association with longevity markers.

Note: VDR and CYP2R1 genetic variants affect how you respond to Vitamin D supplementation and levels. Some people need higher doses to achieve the same circulating levels, and some people benefit from making sure they are in the very top of even that optimal range in order to get the benefits inside the cells. DNA testing can clarify this.

Sources:

3. Folate (Vitamin B9)

Optimal: 30–45 nmol/L or 13-20 ng/ml     |  Standard lab: 7–45 nmol/L or 3-20 ng/ml

Folate is essential for methylation — the biochemical process that controls DNA repair, neurotransmitter (like the happy molecule serotonin, and the focus molecule dopamine) production, and homocysteine metabolism (more on homocysteine in just a moment!). It is also crucial for healthy pregnancies and fetal development. Most labs consider anything above 7 nmol/L ‘normal’. That is far too low.

Why it matters: Low folate drives elevated homocysteine, increases depression and cognitive decline risk, impairs hormone detox pathways and the body’s capacity to decide which genes to ‘turn on’ or ‘off’. Other common symptoms are fatigue and restless legs. For those with MTHFR gene variants — extremely common in the general population — active methylfolate (5-MTHF) is required, not standard folic acid found in most cheaper supplements.

Source: Clinical consensus — see Morris et al., American Journal of Clinical Nutrition, 2010 

4. Vitamin B12

Optimal: >550 pmol/L (ideally approaching 1000 pmol/L for neurological health)  or >745 pg/ml   |  Standard labs: 148–740 pmol/L or 200- 1000 pg/ml

This one is often low in vegans, and not picked up on until overt issues present. The lab flags deficiency below 148 pmol/L. By that point, neurological damage may already be occurring.

Why it matters: B12 is critical for myelin production (that sheath around nerves), nerve function, DNA synthesis, and energy. Levels between 148–300 pmol/L are a grey zone where functional deficiency is common but often missed. For brain protection, optimal is above 550 pmol/L — and closer to 1000 pmol/L in older adults or those with neurological symptoms. Vitamin B12 is also needed for methylation and all its wonderful functions, as described just earlier in the folate section. Similar to folate deficiency, being below optimal here can contribute to fatigue, restless leg syndrome and tingling (ie ‘pins and needles’).

Note: Serum B12 can sometimes be high even though there is a deficiency at a cellular level, so if you wanted to go a step further you can work with an experienced practitioner to look at more in depth panels. 

Source:

5. TSH (Thyroid Stimulating Hormone)

Optimal: 0.5–2.5 mIU/L     |  Standard labs: 0.35–5.5 mIU/L

Your thyroid governs your metabolism, energy, mood, weight, cardiovascular function and fertility. Yet the standard reference range allows TSH up to 5.5 mIU/L (+/- depending on the lab) — a level at which research shows real metabolic consequences.

Why it matters: TSH above 2.5 mIU/L — still ‘normal’ by most lab standards — is independently associated with increased insulin resistance, metabolic syndrome, cardiovascular risk, and cortisol dysregulation. In rigorously screened healthy adults, over 95% have TSH below 2.5 mIU/L. That is where optimal thyroid function lives.

In adults over 70, the research supports a slightly higher optimal range of 1.9–2.5 mIU/L (R). 

Note: Similar to B12, TSH only gives us a glimpse into the window of thyroid function and health. For a more in depth thyroid panel, consider adding at least free T3, free T4 and thyroid antibodies.

Source:

6. HbA1c (Blood Sugar Control)

Optimal: 5.0–5.4% or 31-36 mmol/mol    |  Standard lab: <5.7% or <39 mmol/mol

HbA1c reflects your average blood sugar over the previous three months. Most GPs don’t flag anything until 39 mmol/mol (5.7%) or above. Some labs even consider 41 mmol/mol to be acceptable! The damage unfortunately begins long before that.

Why it matters: Research tracking over 14,000 non-diabetic adults for up to 12 years found that the lowest all-cause mortality was in those with HbA1c of 5.0–5.4%. Risk begins rising meaningfully above 5.5%. The dose-response curve for cardiovascular mortality is not flat — it rises progressively once you move out of the 5.0–5.4% zone.

Important caveat: HbA1c is an average and can mask dangerous post-meal glucose spikes (or dips!). I generally use continuous glucose monitoring (CGM) for 2 weeks alongside HbA1c for all my clients to get the full picture. 

For optimal health and longevity, blood sugar should ideally remain within 3.9–5.9 mmol/L for the majority of the time. 

Source:

7. hsCRP (High-Sensitivity C-Reactive Protein)

Optimal: <0.5 mg/L or <0.05 mg/dl     |  Standard labs: <3.0 mg/L or 0.3 mg/dL

hsCRP is your primary marker of systemic inflammation. Most labs don’t flag it until 3.0 mg/L. By that standard, you can have years of low-grade chronic inflammation going completely undetected. In my practice, I often don’t see this marker elevated even in individuals with chronic inflammatory conditions. When it has come to the point of being even just suboptimally high (ie above optimal, but still within the normal ranges), I generally consider that an alarm stage to really dig into what might be causing that inflammation. 

Why it matters: Chronic low-grade inflammation — even at levels of 0.5–1.0 mg/L — is a driver to anything from PCOS, autoimmune disease, anxiety and depression, endometriosis, to cardiovascular disease and high blood pressure, Alzheimer’s, accelerated cellular ageing, and cancer progression. Chronic inflammation is one of the 12 hallmarks of aging, which have been shown to contribute to almost all detrimental health outcomes.

And remember, there is always a why. Inflammation is an essential mechanism in the body, needed to fight off infections and heal wounds. When it lingers after its expiry date, ie in the case of chronic inflammation, we need to find out ‘why?’. Inflammation always has a reason. So instead of simply throwing in anti-inflamatory meds or supplements, tricks and tools (which can all be wonderful helpers), I always recommend to put on a detective hat and look for the underlying trigger. Some common ones include: chronic infections (such as viral, gut microbiome imbalances, SIBO or SIFO, mould, candida), hidden food intolerances, visceral adiposity and more. Head over to my blog post on inflammation to find out more on its triggers and what can be done about it – here. 

Source: Multiple cardiovascular and longevity studies consistently associate hsCRP >0.5 mg/L with elevated disease risk. American Heart Association guidelines. 

8. Uric Acid

Optimal: <300 µmol/L (<5.0 mg/dL)     |  Standard labs: <420 µmol/L (<7.0 mg/dL)

Uric acid is most commonly associated with gout. But the research shows it is in fact a much broader metabolic and cardiovascular risk marker, linked to many other ill health outcomes aside from gout.

Why it matters: Even at levels considered normal by labs, if suboptimal, uric acid is associated with elevated CRP, IL-6, and TNF-alpha (inflammatory markers). It has been shown to be an independent risk factor for hypertension, type 2 diabetes, and cardiovascular disease. Some research suggests <360 µmol/L identifies healthy subjects, with more conservative estimates supporting <300 µmol/L for optimal cardiovascular protection.

Sources:

9. GGT (Gamma-Glutamyltransferase)

Optimal: <15 U/L for men, <10 U/L for women    |  Standard labs: <55 U/L men / <38 U/L women

GGT is listed on most blood panels as a liver enzyme. That framing undersells it enormously. GGT is actually one of the most powerful predictive biomarkers for oxidative stress, metabolic dysfunction, and long-term mortality risk.

Why it matters: GGT catalyses the recycling of glutathione — your body’s master antioxidant. When GGT rises, it signals that your oxidative stress (=free radical) burden is outpacing your antioxidant capacity. GGT above optimal is associated with insulin resistance, cancer, cardiovascular disease, and an increase in ‘all-cause mortality’:

  • A large Austrian cohort of 163,944 adults followed for 17 years found optimal GGT cutoff values of 15.5 U/L for men and 10.5 U/L for women for predicting cardiovascular mortality. AHA Journals
  • A Vienna General Hospital study of 283,438 adults found GGT above ≥9 U/L in women and ≥14 U/L in men was significantly associated with all-cause, cancer, and vascular mortality. PubMed
  • A UK Biobank study of 293,667 participants confirmed that GGT ≥16 U/L in men and ≥9 U/L in women was associated with a 71% increased risk of heart failure. PubMed Central
  • A meta-analysis of 9 prospective studies covering 527,589 participants found a clear dose-response relationship — every 10 U/L increase in GGT increased cardiovascular mortality risk by 10%, applying to both men and women. PubMed Central

Sources: 

10. Homocysteine

Optimal: 8–10 µmol/L     |  Standard labs: <15 µmol/L

Homocysteine is a marker of methylation capacity (remember, that process we looked at in the folate section).

Why it matters: Elevated homocysteine (above 10 µmol/L) has been shown to be a risk factor for cardiovascular disease, Alzheimer’s, stroke, and bone fractures. But the relationship is U-shaped: very low homocysteine (<6 µmol/L, in some research <8) appears to also be problematic, associated with impaired methylation, cognitive decline, and poor bone matrix formation.

The optimal zone of 8–10 µmol/L supports adequate methylation capacity while maintaining cardiovascular protection. 

Elevated homocysteine can often as a first line be addressed simply by optimising B vitamin levels, in particular with methylfolate, methylcobalamin (B12), and B6, as they are needed to lower homocysteine via methylation, that process we looked at earlier in the folate section. If that doesn’t ‘do the trick’, a more in depth investigation might be required to look at why methylation is inadequate, and homocysteine elevated as a result. 

Some common contributing factors include: chronic viral infections, gut microbiome imbalances with bacterial infections and overgrowth, candida albicans, mould and heavy metal load. 

Sources:

11. Lipids (HDL & Triglycerides)

HDL Cholesterol

Optimal: >1.6 mmol/L (>60 mg/dL)     |  Standard labs: >1.0 mmol/L or >40 mg/dl in men / >1.2 mmol/L or >45 mg/dl in women 

HDL is your ‘protective’ cholesterol — but not all HDL is equal, and most labs only flag it as low if it drops below 1.0 mmol/L. Optimal cardiovascular protection requires significantly more.

Why it matters: HDL carries out reverse cholesterol transport, removing cholesterol from arterial walls. Levels above 1.6 mmol/L are associated with substantially lower cardiovascular risk. Below 1.0 mmol/L is a serious red flag that requires investigation into lifestyle, metabolic function, and inflammation. Note: HDL cholesterol is only a small piece of the cholesterol and lipids puzzle. To really know what is going on, you might want to run a bigger panel, including a lipoprotein profile, oxidized LDL, and more. 

Triglycerides

Optimal: <1.0 mmol/L (<88 mg/dL)     |  Standard labs: <1.7 mmol/L (<150 mg/dL)

Why it matters: Elevated triglycerides reflect excess carbohydrate, sugar or alcohol intake, insulin resistance, and metabolic dysfunction. The Triglyceride:HDL ratio is one of the strongest indirect markers of insulin resistance. An elevated level has been associated with increased fatty liver, cardiovascular, and metabolic disease risk.

12. Sex hormones

Last but not least, sex hormones. Better known as estrogen, progesterone and testosterone. And yes, women make and need testosterone, and men make and need estrogen. However, levels and their functions in the body differ, so they each merit different sections. 

When it comes to estrogen and progesterone in women, they change drastically from the years a woman has a cycle (ie the ‘reproductive years’, starting anywhere in the teenage years, and finalising somewhere in the mid 40ies to 50ies when the periods stop), and post-menopause, when the ovaries stop producing estrogen and progesterone, and other organs such as the adrenal glands (mostly responsible for stress biochemistry such as adrenaline and cortisol, and to a smaller extent sex hormones) take over and keep producing them, just to a much lesser amount. Most women benefit from Hormone Replacement Therapy (HRT) in the perimenopausal years (ie the ‘transition phase’) and throughout menopause, for their wonderful bone, brain, skin and many more benefits. More on the pros to HRT in a different post, click here for an in depth review. 

However, and this is where most go wrong: Everyone responds differently to HRT, and will require slightly different dosing to achieve the level that is both beneficial and safe! 

Here is what the research supports as optimal.

Estrogen (Oestradiol) — in Premenopausal Women (Luteal Phase/ Around Day 21)

First things first, what’s oestradiol, you may ask? Oestradiol, or estradiol as used in some countries, is the most potent form of estrogen, and as such used in this post interchangeably with estrogen. There are also 2 other forms of estrogen, but they are more important during pregnancy and post menopause and as such don’t play as much of a role here. If you ask a lab to run estrogen, they will generally test oestradiol. 

Ok, now that we got that out of the way, let’s confuse you even more. Estrogen levels and their optimal ranges during the reproductive years are somewhat less clearcut than progesterone, testosterone, and estrogen post menopause, hence I have decided to not include ‘optimal ranges’ here as contrary to the belief circulating in many Functional Medicine, naturopathic or longevity medicine communities, research currently does not support this, and this report sticks to science. (Note: This does not mean this cannot change, if at any point research comes out supporting a set narrow range for estrogen!). However, why I included this marker here regardless, is that it does play a role in relation to the other hormones – and is often misunderstood. So, let’s get into it:

Research suggests that a wide range appears to be fine, as long as it is adequately balanced by progesterone! Some research suggests that above a range of 1468 pmol/l (400 pg/ml) it might be indicative of issues, but still not on its own a reason for concern, if progesterone is above 31.8 nmol/l (R, R). 

It appears that it is estradiol without adequate progesterone opposition where problems arise. Think of oestradiol as the accelerator and progesterone as the brake. You need both, in the right balance.

The optimal mid-luteal Pg:E2 ratio (both in pg/mL) appears to be 100–500 — below 100 suggests relative oestrogen dominance, usually from insufficient progesterone rather than truly excess oestradiol. However, the accuracy of this is still under scientific debate. 

Luteal phase oestradiol alone is NOT independently associated with breast cancer risk when progesterone is adequate (>30 nmol/L). This is one of the most important and underappreciated facts in women’s health. Cancer risk only appears to increase when estradiol is elevated in combination WITH low progesterone, OR if estrogen is being broken down into toxic metabolites. When estrogen is being ‘detoxed’, ie broken down to be excreted, it can either be broken down into a protective ‘2-OH’ form, a more proliferative ‘16-OH’ linked to common ‘estrogenic symptoms’ such as fibroids, cysts, fibrocystic breasts and endometriosis,or worst case, into a very reactive ‘4-OH’ that if accumulating can cause damage to our DNA and thereby has been linked to the increased estrogen related cancer risk. 

What does this mean? Instead of looking at just estradiol levels in blood, make sure to measure progesterone, in addition with potentially running a more comprehensive panel on how the body is metabolizing estrogen (via urine testing, such as the DUTCH), which is where the majority of the issues associated with hormones arise. 

Luteal progesterone (>31.8 nmol/l) appears to be more important for fertility than total estrogen levels. 

In summary: 

  • In ovulatory, naturally cycling women with adequate progesterone (>31.8 nmol/L) and favorable estrogen metabolism (≥50% 2-OH pathway), serum estradiol levels across the entire physiological reference range (151–1,941 pmol/L / 41–529 pg/mL in the luteal phase) are safe and not independently associated with increased cancer, fibroid, or endometriosis risk.
  • However, when progesterone is insufficient, metabolism is skewed toward 16-OH or 4-OH pathways, or estradiol is chronically elevated (anovulation, obesity), then higher serum estradiol levels provide excess substrate for harmful metabolite production, and risk increases.

To complicate this matter even more, fibroid risk seems to be associated with the combination of high bioavailable E2 AND high testosterone, not estrogen alone, and no strict range has been clarified for what ‘high’ means (R). 

This leads to the most important point about estrogen: it cannot be assessed in isolation and as such I decided to not include one optimal range here. If you feel estrogen might be an issue for you, work with an experienced practitioner to look at the interplay of the different hormones, and ideally also invest in the DUTCH test to see how your body is breaking down it down.

Progesterone — Luteal Phase (approx. Day 21 of Cycle)

Optimal: >30 nmol/L  or >9.4 ng/ml   |  Standard labs: >10 nmol/L or 3.14 ng/ml

Why it matters: Progesterone might just be one of the most underappreciated hormones in women’s health. It is calming, sleep-promoting, neuroprotective, and critically — it counterbalances oestradiol’s proliferative effects on breast and uterine tissue.

As just elaborated on, estradiol alone does not appear to significantly increase breast cancer risk. The risk appears to rise when oestradiol is high AND progesterone is low (in particular if estrogen is broken down into its toxic metabolite 4-OH). A woman with optimal progesterone (>30 nmol/L) mid-luteal has a fundamentally different hormonal environment than a woman who is oestrogen-dominant with low progesterone. 

One study found that optimal luteal phase progesterone levels for fertility and health was approximately 30 nmol/L or higher, with levels below 20 nmol/L associated with luteal phase defect and reduced fertility (R). Others show that luteal phase progesterone below 30 nmol/L is associated with luteal phase defect, reduced endometrial thickness, and adverse pregnancy outcomes. 

Progesterone is further needed for sleep, to calm anxiety, support mood via GABA production in the brain, assists in lowering histamine and associated symptoms, and much more. 

 

Sources:

Oestradiol — Postmenopausal Women on Bioidentical HRT

Optimal: 220–400 pmol/L (60–109 pg/mL)     |  Standard labs: Variable

Why it matters: 

For optimal bone and brain health while minimizing risks, the target serum estradiol (E2) range on transdermal HRT should be:

  • Optimal range: 220–400 pmol/L (60–109 pg/mL)
  • Bone health threshold: ≥130 pmol/L (35 pg/mL) appears to prevent bone loss; ≥220 pmol/L (60 pg/mL) achieves maximal benefit. One study indicated no additional bone benefit above 90 pg/mL (330 pmol/L) (R)
  • Brain/cognitive benefit: ≥220 pmol/L (60 pg/mL); some data suggest 300–400 pmol/L may be optimal for symptom relief.
  • Women with pre-existing fibroids should be aware that levels above 400 pmol/L may stimulate growth (SWAN study) (R)
  • Avoid sustained levels of >400 pmol/l ideally, but at the very least >550 pmol/L (150 pg/mL) without clear clinical indication. 
  • Limited data suggest that up to 20% of women are “poor absorbers” of transdermal estradiol. failing to prescribe a dose sufficient to elevate serum estradiol levels into the therapeutic range is more likely to cause harm because women will continue to experience distressing symptoms, and they will not benefit from estrogen’s bone-, cardio-, neuro-, and breast- protective effects (R). 
 

Notes: 

When it comes to hormone replacement therapy, it is all about not only the blood levels, but also the manner of administration (oral or transdermal), the form (bioidentical or derived from horse urine), whether it is combined with progesterone, and the age or the amount of time passed since menopause at initiation. 

  • Risks appear lowest when initiated within 5 years of menopause, using estradiol transdermally (patches or gel) rather than orally estrogen, combined with oral or vaginal bioidentical progesterone rather than transdermal progesterone or the progestins (the synthetic version of progesterone). 
  • While transdermal Estradiol has lower risks vs. oral, risk still appears to increase with sustained high levels (>400–550 pmol/L). In women that have a uterus, it is imperative to combine estrogen with progesterone in order to prevent endometrial cancer development.  
  • Bioidentical micronised progesterone (Utrogestan) appears to be the only form that preserves the cardioprotective and neuroprotective benefits of oestradiol. Synthetic progestins (MPA) negate these benefits and are independently associated with increased cardiovascular and breast cancer risk. 
  • Emerging clinical and experimental evidence points to progestogens as the primary hormonal driver underlying seemingly estrogen-associated breast cancer risk — specifically synthetic progestins, not natural progesterone. Estrogen-alone HRT has little impact on breast cancer risk, whereas estrogen-plus-progestin HRT consistently shows increased risk (R). 
 

And one more note: Nurses’ Health Study II: Endogenous Estradiol >72.5 pg/mL was associated with 2.17-fold increased breast cancer risk (R). Endogenously elevated oestradiol is oestrogen produced by the body itself, often driven by excess body fat and aromatase activity — not to therapeutic transdermal oestradiol in women on HRT with adequate progesterone.

For more info on timings and forms of HRT, head over to a recent post I did where I compiled current research indications. Click here. 

Source:

Testosterone — Women

Optimal: >1.0 nmol/L     |  Standard labs: 0.3–2.8 nmol/L

Why it matters: Low testosterone in women is chronically under-recognised. It contributes to fatigue, low motivation, poor concentration, reduced libido, and loss of muscle mass — symptoms that are frequently attributed to ‘just getting older’ or ‘stress’. 

On blood testing, always assess testosterone alongside sex hormone binding globulin (SHBG), as it binds testosterone. High SHBG binds testosterone, reducing free levels and its active form, even when total testosterone looks adequate on blood testing.

Optimal total testosterone levels in premenopausal women range from 0.8-2.8 nmol/L, with some studies suggesting levels above an even narrower range of 1.0 nmol/L to be associated with better health outcomes including bone health and metabolic function (R). 

Postmenopausal women with testosterone levels above at least 0.7 nmol/L show better metabolic and bone health markers, though optimal ranges for postmenopausal women remain less clearly defined than for premenopausal women (R). 

Sources:

Testosterone — Men

Optimal: >17 nmol/L     |  Standard labs: 8–30 nmol/L

Why it matters: Testosterone in men governs muscle mass, cardiovascular health, energy, mood, cognitive function, bone density, metabolic health and more. Research shows that men with testosterone above 17 nmol/L have significantly better cardiovascular, metabolic, and longevity outcomes compared to those below 12 nmol/L. As with women, SHBG must be assessed alongside total testosterone to understand free hormone availability.

Source: https://pubmed.ncbi.nlm.nih.gov/15477348/

So What To Do With This?

First: If you have any symptoms, always make sure you go to your GP FIRST, to get them to investigate any sinister causes. If you get the ALL CLEAR by them, only then continue to step number 2:

 

Step 2: Ask your GP or go to a local self-referral lab which they are nowadays omnipresent, and make sure to get tested at the right time. If you are on HRT, the ideal time is around noon, 4-6 hours after the application of estrogel/ testogel. If you aren’t on HRT, the best time is the morning, to reflect the body’s natural rhythm (‘circadian rhythm’) of testosterone, but also in case you need to be fasted. Most tests don’t require you to be fasted, with the only two on our list being triglycerides and homocysteine, however if you opt for a bigger panel that includes more markers, you might need to be. Always make sure to ask the lab. 

 

Step 3: Get your results interpreted against optimal ranges, not just standard lab normals. A result in the ‘normal’ range can still be suboptimal — and that gap is often where symptoms live. Ideally with the help of an experienced Functional Medicine practitioner. If anything flags up as red or outside the ‘normal range’, go back to your GP to run this past them. But a good Functional Medicine practitioner will guide you to do so anyhow.

 

Step 4: Look for the Why. Every suboptimal result is a signal. Suboptimal ferritin might simply mean you aren’t eating enough red meat and thus iron, but could also signify poor absorption and gut microbiome imbalances. Elevated homocysteine might mean an MTHFR variant, not just a B12 deficiency. Elevated GGT might mean mould exposure, not just alcohol. The numbers are the starting point. The investigation and connecting the dots on a deeper root cause level is where precision health optimisation and longevity really begins.

There is always a why. The goal is to find (and address) the root cause — before it turns into a real problem. Turning you into the CEO of your health trajectory. 

 

If you are looking for help implementing what you have learned in this guide, reach out to my team at hello@mprecisionhealth.com to book an initial consultation with me, either via zoom worldwide, or in person in Kensington, London (UK). I look forward to assisting you become the best and healthiest version of yourself. 

In Health, 

Mirthe

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Mirthe

It is my goal to empower you to become the CEO of your health trajectory, preventing and optimising with precision and science backed strategies to live your best life & thrive.

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Mirthe Health & Longevity Optimisation London Public Speaking 9

HI, I'M MIRTHE

It is my goal to empower you to become the CEO of your health trajectory, preventing and optimising with precision and science backed strategies to live your best life & thrive.

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