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Why I Stopped Trusting BMI Alone (And What I Use Instead)

Why I Stopped Trusting BMI Alone (And What I Use Instead)

Metabolic Health

If you’ve ever stepped on the scale, checked your BMI, and been told you’re “normal” while your clothes don’t fit right, your energy is gone, and your labs are telling a different story, I want you to know that you’re not imagining it. BMI was never designed to tell the whole story, and in my clinical practice, I don’t let a single marker make that call.

I want to walk you through a tool I use with my clients that fills in a critical gap BMI leaves wide open: waist-to-height ratio.

 

The Problem With BMI Alone

BMI is a ratio of weight to height. It doesn’t know the difference between muscle and fat, and it has no way of telling you where your fat is actually stored. That second point matters more than most people realize, because fat location changes your risk profile substantially.

Research backs this up in a way that surprised even me. In a large national survey of British adults, 35% of men and 14% of women who fell within a “normal” BMI range were still carrying elevated central fat, the kind of fat distribution linked to real cardiometabolic risk. In other words, BMI alone would have completely missed their risk. That’s not a small blind spot. That’s a significant number of people walking around believing they’re metabolically fine when they aren’t.

 

What Waist-to-Height Ratio Actually Measures

Waist-to-height ratio (WHtR) is exactly what it sounds like: your waist circumference divided by your height, measured in the same units. To calculate it, measure your waist at the belly button, then divide by your height.

The target: keep that number under 0.5. In practical terms, that means your waist circumference should be less than half your height. No complex charts, no calculators required.

Why does this simple ratio outperform BMI in my clinical experience? Because it directly reflects central obesity, the fat stored around your abdomen, which is far more predictive of cardiovascular and metabolic risk than total body weight.

 

The Role of Visceral Fat

Here’s where this gets important. The fat that accumulates around your waist isn’t sitting there passively. Visceral fat surrounds your organs and behaves like an active endocrine tissue. It produces inflammatory compounds, disrupts hormone signaling, and interferes with insulin sensitivity.

This is different from subcutaneous fat, the fat just under the skin that pinches between your fingers. Subcutaneous fat isn’t nearly as metabolically disruptive. Visceral fat is the one driving the inflammation, the fatigue, the brain fog, and the hormone imbalance so many of my clients describe when they come to me feeling unheard by conventional medicine.

 

What a WHtR Above 0.5 Is Associated With

A waist-to-height ratio above 0.5 has been consistently linked to:

  1. Increased cardiovascular risk. Research from the University of Pittsburgh found that people with a BMI under 30, but a WHtR over 0.5, showed higher rates of coronary artery calcification, a marker of future cardiovascular disease, even without other classic risk factors present.
  2. Higher rates of type-2 diabetes and metabolic syndrome. In a study of over 7,000 adults at high cardiovascular risk, WHtR outperformed other anthropometric measurements in predicting type-2 diabetes, hyperglycemia, hypertension, and atherogenic dyslipidemia.
  3. Elevated triglycerides, cholesterol, and blood pressure. Adjusted analyses comparing people above and below the 0.5 threshold found meaningfully higher levels of triglycerides, LDL, HbA1c, fasting glucose, and both systolic and diastolic blood pressure in the higher WHtR group, independent of BMI.
  4. Increased mortality risk at higher levels. A 2025 cohort study found the relationship between WHtR and mortality is J-shaped, with risk climbing more steeply above 0.58. At that level, researchers found meaningfully elevated risk of death from cardiovascular disease, cerebrovascular disease, and diabetes.

 

Why This Matters More During Perimenopause and Postmenopause

I see this constantly in my practice. As estrogen shifts during perimenopause and postmenopause, fat storage patterns change too. Fat that once distributed more evenly, or settled in the hips and thighs, tends to migrate toward the abdomen. This means visceral fat can increase during this life stage even when total body weight barely moves. Your scale might say nothing has changed, while your metabolic risk quietly climbs.

This is exactly why I don’t rely on the scale, or on BMI alone, to assess what’s really going on with a client. A tape measure and a simple ratio tell me more.

 

What I Want You to Do With This

Grab a tape measure. Measure your waist at the belly button. Divide by your height. See where you land.

This single number won’t tell you everything, and I don’t want it to replace a full picture of your health. But alongside the other markers I look at with clients, blood sugar, inflammatory markers, hormone panels, it gives us a clearer, more honest starting point than BMI alone ever could.

If your ratio has you concerned, or if you’ve been told your labs and BMI look “fine” while you feel anything but, I’d love to help you dig into what’s really going on. Root-cause work starts with asking better questions and using better tools, and this is one of the simplest ones I know.

 

References

1     University of Pittsburgh School of Medicine, “Waist-to-Height Ratio Outperforms BMI in Predicting Heart Disease Risk.” medschool.pitt.edu

2     Ashwell, M., et al. “Waist-to-height ratio is a simple and effective obesity screening tool for cardiovascular risk factors: Analysis of data from the British National Diet and Nutrition Survey.” PMC. ncbi.nlm.nih.gov

3     Ashwell, M., et al. “Waist-to-height ratio as an indicator of ‘early health risk.'” PubMed. pubmed.ncbi.nlm.nih.gov

4     Frontiers in Nutrition, “Association of waist-to-height ratio with all-cause and obesity-related mortality in adults: a prospective cohort study.” frontiersin.org

5     PREDIMED study, “Waist-to-Height Ratio and Cardiovascular Risk Factors in Elderly Individuals at High Cardiovascular Risk.” PMC. ncbi.nlm.nih.gov

As of: July 19, 2026

Why Your Gut Doesn’t Respond Like Everyone Else’s

Why Your Gut Doesn’t Respond Like Everyone Else’s

Gut Health

By Brigitte Spurgeon | Board-Certified Functional Genomics Practitioner | Doctor of Orthomolecular Nutrigenomics

What your DNA is trying to tell you about your digestive health and gut health SNPs

You’ve cleaned up your diet. You’ve cut out gluten, dairy, maybe even coffee. The probiotics, the digestive enzymes, the elimination protocols. You’ve tried them all. And yet your gut still isn’t cooperating. The answer may lie in your gut health SNPs. The bloating returns, the brain fog lingers, the inflammation quietly persists.

I’m about to share a truth you can anchor to: your unresolved symptoms don’t mean your body is broken or that you have failed. Your body is speaking to you. And that in itself is reason for hope.

In my clinical experience, the women who struggle most with stubborn gut symptoms are often doing many things right. What’s missing isn’t effort. It’s the layer of information that explains why their body responds differently than someone else’s doing the exact same protocol. That layer is your genetics.

Your microbiome isn’t just shaped by what you eat. It’s shaped by what your genes allow your body to do with what you eat. And until we understand that, we’re guessing.

 

THE MISSING PIECE IN MOST GUT PROTOCOLS

Most gut health approaches treat the microbiome as though every body starts from the same place. Take a probiotic. Add fermented foods. Eat more fiber. These are reasonable starting points, but they don’t account for your genetics. You may carry single nucleotide polymorphisms, or SNPs (pronounced “snips”), that fundamentally alter how your body processes histamine, absorbs B vitamins, clears toxins, or feeds your beneficial bacteria.

A SNP is a variation in a single position in your DNA sequence. These variations are incredibly common. We all carry them. But certain combinations can quietly undermine gut healing at the cellular level. They don’t cause disease on their own. What they do is create vulnerabilities that, in the right conditions, become the root cause of the symptoms you can’t explain.

Here are six of the most clinically relevant gut health SNPs I assess, and what they mean for your healing process.

 

FUT2: ARE YOUR GUT BACTERIA GETTING FED?

FUT2 is one of the first SNPs I look at when a client tells me her probiotics “don’t seem to do anything.” This gene controls your secretor status: whether or not your gut lining produces the compounds that your beneficial bacteria, particularly Bifidobacterium, need to survive and thrive.

Roughly 20% of people are non-secretors, meaning they carry two non-functional copies of the FUT2 gene. In these women, the gut mucosa is less fucosylated. In plain terms, the environment that Bifidobacterium depends on simply isn’t there. You can take the most excellent probiotic on the market, and if FUT2 variants mean your gut can’t support colonization, the benefit will be minimal.

What this looks like clinically: poor Bifidobacterium colonization, reduced microbial diversity, a higher susceptibility to gut infections, and difficulty sustaining improvements from probiotic supplementation.

What actually helps: strain-specific probiotics chosen for non-secretors, prebiotic fibers that feed the strains most compatible with your terrain (resistant starch and inulin are particularly valuable here), and understanding that your microbial rebuilding phase needs more time and more targeted support than a general protocol would suggest.

There’s one more piece of the FUT2 picture that most practitioners miss entirely, and it matters deeply for the women I work with. FUT2 non-secretors have a well-documented association with impaired B12 absorption. The mechanism is direct: FUT2 influences the fucosylated glycans on the gut mucosa that are involved in binding and absorbing the intrinsic factor-B12 complex in the ileum. When that mucosal environment is compromised, B12 uptake at the intestinal level is reduced. This happens even when diet is adequate and intrinsic factor is functioning normally. This means a non-secretor can be eating plenty of B12-rich foods, taking an oral supplement, and still running low.

I see this pattern regularly in my perimenopausal clients who present with fatigue, brain fog, low mood, and cognitive sluggishness. These symptoms are easily attributed to hormonal changes. The real driver may be chronically suboptimal B12 that standard oral supplementation can’t fully correct. For these women, sublingual B12 is my preferred recommendation. It bypasses the ileal absorption mechanism altogether, absorbing directly through the oral mucosa and delivering reliably regardless of what FUT2 is or isn’t doing in the gut.

 

PEMT: THE FAT METABOLISM GENE THAT AFFECTS MORE THAN YOUR WAISTLINE

If you’ve been eating well, exercising consistently, and still struggling to shift body fat, PEMT may be part of your answer. This is one of the patterns I see most often in my perimenopausal clients, and it’s one of the least talked about in gut health conversations.

PEMT stands for phosphatidylethanolamine N-methyltransferase. It’s the gene responsible for your body’s ability to produce phosphatidylcholine (PC) internally. Phosphatidylcholine is not a supplement term worth skipping over. It’s a structural fat found in every cell membrane in your body. It also makes up a primary component of the mucus layer that lines and protects your gut wall. Bile production depends on it too. Bile is how your body emulsifies and absorbs dietary fats, fat-soluble vitamins, and hormones.

Here’s what makes PEMT particularly relevant for women in their 40s and 50s: estrogen upregulates PEMT expression. While estrogen levels are healthy, many women with PEMT variants compensate without knowing it. As estrogen declines through perimenopause, that compensation disappears. PEMT activity drops and phosphatidylcholine production falls. Suddenly a woman who managed fine for decades begins struggling with fat metabolism, sluggish bile flow, and a gut lining that’s losing structural integrity.

What this looks like clinically:

– Difficulty losing body fat despite doing the right things

– Bloating or discomfort after fatty meals

– Poor absorption of fat-soluble vitamins like A, D, E, and K

– A gut lining that’s more reactive and harder to repair than it should be

What actually helps: I address PEMT more simply than most protocols suggest. Eggs are my first recommendation. Egg yolks are one of the richest dietary sources of choline and phosphatidylcholine, and for women with PEMT variants, making eggs a daily staple is genuinely therapeutic. If you’ve been avoiding egg yolks out of outdated cholesterol concerns, this is your clinical permission to bring them back.

Beyond food, I supplement with phosphatidylcholine directly or with sunflower lecithin, which is a well-tolerated and effective PC source. The other nutrients commonly associated with this pathway are usually addressed through other SNPs in a comprehensive protocol, so there’s no need to overcomplicate it. Food first. Targeted supplementation second. That’s the PEMT approach that works in my clinic.

 

DAO AND HNMT: WHEN FERMENTED FOODS MAKE YOU FEEL WORSE

This is one of the most common clinical puzzles I encounter. A woman starts doing everything she’s been told is good for her gut: sauerkraut, kimchi, kefir, kombucha. Instead of feeling better, she feels worse. More anxious. More inflamed. Headaches. Heart palpitations. Flushing. Insomnia.

The instinct is to blame the food. The real answer is usually her histamine pathway genes: DAO and HNMT.

Histamine is a compound found naturally in fermented and aged foods, and it’s also produced by your own immune cells. Your body manages histamine through two main enzymes: DAO (diamine oxidase), which breaks down histamine from food in the gut, and HNMT (histamine N-methyltransferase), which clears histamine from your body’s tissues and brain. When either of these enzymes is genetically impaired, histamine accumulates, and the symptoms that follow look a lot like what my clients often mistake for hormone imbalance, anxiety, or autoimmune flares.

The SNPs in the AOC1 gene (which encodes the DAO enzyme) reduce enzyme activity, meaning histamine from food isn’t broken down efficiently in the gut. The HNMT Thr105Ile variant produces a less stable enzyme that degrades more quickly in cells, leaving histamine to accumulate in tissues, including the brain.

What this looks like clinically:

– Reactions to fermented foods, wine, aged cheese, and leftovers

– Histamine-driven anxiety and insomnia

– Skin flushing and gut motility issues

– Symptoms that look hormonal but don’t resolve with hormonal interventions

What actually helps: a low-histamine approach during the microbiome rebuilding phase, DAO enzyme support before meals, and methylation support: specifically B6 (as P5P), copper, and vitamin C, which are the cofactors DAO depends on to function. The fermented foods can come later, once the enzyme pathways are better supported.

 

MTHFR: THE METHYLATION GENE THAT TOUCHES EVERYTHING

If there’s one SNP my clients have heard of, it’s MTHFR. And while it has become something of a buzzword in integrative health circles, the clinical reality is more nuanced and more significant than most people realize.

MTHFR, methylenetetrahydrofolate reductase, is the gene that controls a critical step in your methylation cycle. Methylation is a biochemical process that happens over a billion times per second in your body. It’s involved in detoxification, DNA repair, neurotransmitter production, hormone regulation, and immune function. When MTHFR variants impair this process, the effects ripple through every system, including the gut.

In the context of gut health, here’s what matters: the MTHFR C677T and A1298C variants reduce the body’s ability to convert folate into its active form, methylfolate. This impairs the production of SAMe (S-adenosylmethionine), the body’s primary methyl donor. HNMT, the histamine-clearing enzyme we just discussed, depends on SAMe to function. So MTHFR variants can compound histamine issues and impair the gut lining’s ability to repair itself. They also significantly reduce detoxification capacity.

In my clinical work, I pay close attention to MTHFR status before any pathogen-clearing protocol. Women with compound heterozygous MTHFR variants often experience more intense detox reactions. Not because the protocol is wrong, but because their Phase 1 and Phase 2 liver detoxification pathways are under-resourced. Before we clear candida, heavy metals, or parasites, we make sure methylation is supported.

What actually helps: active, bioavailable forms of folate and B12 (not folic acid, not cyanocobalamin), alongside B6 as P5P, magnesium, and riboflavin. I want to be specific here: the right form of folate and B12 for you depends on your full SNP picture, not just MTHFR in isolation. Compound heterozygous patterns are worth understanding in full. A slow COMT alongside MTHFR, in particular, can mean that pushing methylation too hard creates its own set of problems: anxiety, irritability, sleep disruption. This is precisely why I don’t recommend a blanket supplement protocol for MTHFR. The support needs to match your specific variant combination, and that requires looking at the full map, not a single gene.

 

TNF-ALPHA AND IL-6: YOUR INFLAMMATORY THERMOSTAT

Some women have guts that inflame easily and calm down slowly. Others move through gut healing protocols with minimal reaction. A significant part of that difference comes down to cytokine gene variants, specifically TNF-alpha and IL-6. These two genes regulate how aggressively your immune system mounts an inflammatory response.

TNF-alpha (tumor necrosis factor alpha) and IL-6 (interleukin-6) are inflammatory signaling molecules. Certain SNPs in these genes create a tendency toward heightened immune activation, meaning the same gut insult that causes mild bloating in one woman can trigger significant systemic inflammation in another. In the context of gut healing, this matters enormously for two phases of your protocol:

– The initial gut barrier restoration phase, where inflammation needs to be reduced before rebuilding can begin

– The pathogen-clearing phase, where die-off reactions can be more severe and prolonged

What this looks like clinically:

– Heightened reactivity to foods, supplements, and protocols

– A gut that seems to stay inflamed even when dietary triggers are removed

– Difficulty tolerating the pathogen-clearing phase without significant fatigue or immune symptoms

What actually helps: curcumin, omega-3 fatty acids, and quercetin are among the most clinically meaningful anti-inflammatory supports for these variants. But the sequence matters. Inflammation has to come down before you can effectively rebuild or clear. This is one of the reasons I don’t rush clients through the early phases of a gut protocol, no matter how eager they are to get to the “detox” stage.

 

WHAT THIS MEANS FOR YOUR GUT HEALING JOURNEY

Here’s what I want you to take from this: your gut symptoms are not random, and they are not your fault. They are the downstream expression of genetic patterns working in the background your entire life. Stress, environmental exposures, hormonal shifts, and the cumulative burden that lands so heavily on women in their 40s and beyond all amplify those patterns.

The reason gut protocols fail so often is not that the protocols are wrong. It’s that they’re not built around the person following them. Two women can do everything identically and have completely different outcomes, because their FUT2 status is different, their DAO activity is different, their methylation capacity is different. The protocol that heals one woman can make another one worse.

This is why understanding your gut health SNPs is central to how I practice nutrigenomics. Not as an add-on to gut health. As the foundation of it. When I know your SNP profile, I can sequence your protocol correctly, choose the right strains and supplements for your specific terrain, modify the phases that need more support, and anticipate where your body will push back.

Your DNA is not your destiny. But it is your map. And working without it is like trying to navigate a new city without knowing which roads are closed.

If you’re ready to stop guessing and start working with the biology that is actually yours, a Nutrigenomics Report is where we begin. This is the work I do with my 1-on-1 clients. I run a thorough analysis of the SNPs most relevant to your symptoms, then translate that into a protocol that fits how your body actually works.

 

You can learn more and book a discovery call at brigittespurgeon.com.

 

 

*Brigitte Spurgeon, BCFGP, DON*

*Doctor of Orthomolecular Nutrigenomics*

*Board Certified Functional Genomics Practitioner*

Brigitte Spurgeon is not a medical doctor. This article is for educational purposes only and does not constitute medical advice. Nothing in this article is intended to diagnose or treat any medical condition.

 

Your Skin Is Aging From The Inside Out

Your Skin Is Aging From The Inside Out

Longevity

By Brigitte Spurgeon | Board-Certified Functional Genomics Practitioner | Doctor of Orthomolecular Nutrigenomics

There is a conversation I have been having more frequently with my clients, and it usually begins the same way.

A woman comes to me in her late forties or fifties. She eats well. She exercises. She takes her supplements. She does everything right. And yet something has shifted. Her skin has changed in ways that feel disproportionate to her age. There is a heaviness around her eyes that wasn’t there before. Fine lines that appeared almost overnight. A dullness to her complexion that no serum has been able to restore. She looks tired in a way that sleep does not fix. And she is frustrated, because she knows she is doing the work.

What she doesn’t know, and what most people have never been told, is that the visible changes on her face may be a reflection of something happening deep inside her cells. Something that the anti-aging industry has almost entirely ignored, and that the science of longevity is now identifying as one of the most significant drivers of biological aging we have ever discovered.

It is called cellular senescence. And understanding it may change everything about how you approach aging.

 

The Cells That Refuse to Die

Every cell in your body has a lifespan. When a cell is damaged beyond repair — by oxidative stress, UV exposure, telomere shortening, environmental toxins, or the cumulative wear of time, it is supposed to do something remarkably cooperative: it is supposed to self-destruct in an orderly process called apoptosis, clearing the way for new, healthy cells to take its place.

But some cells don’t cooperate. Instead of dying, they enter a state of permanent arrest. They stop dividing. They stop functioning. But they don’t leave. They linger in tissues, metabolically active and deeply disruptive, secreting a cocktail of inflammatory signaling molecules, proteases, and reactive oxygen species into the surrounding cellular environment. Scientists have given these persistent, dysfunctional cells a name that is both scientifically precise and somewhat unsettling: senescent cells. In the popular science literature, they are increasingly referred to as zombie cells — because they are, in a meaningful sense, the undead of cellular biology.

A small number of senescent cells is a normal feature of healthy biology. In youth, the immune system efficiently identifies and clears them. But as we age, two things happen simultaneously: the rate at which cells become senescent increases, and the efficiency of immune surveillance that clears them decreases. The result is a gradual but relentless accumulation of zombie cells in tissues throughout the body — the skin, the fat, the joints, the brain, the immune system itself.

The inflammatory molecules these cells release, a pattern researchers have named the SASP, or Senescence-Associated Secretory Phenotype, do not stay local. They diffuse into surrounding tissue, damaging neighboring healthy cells, promoting chronic low-grade inflammation, and disrupting the cellular signaling networks that govern everything from collagen production to hormone regulation to metabolic function. This is not a peripheral process. It is now understood to be a central mechanism in the development of many age-related chronic conditions, including cardiovascular disease, metabolic syndrome, cognitive decline, and the kind of whole-body inflammatory burden that makes people feel and look older than their years.

 

What This Has to Do With Your Face

The skin is not separate from this process. It is one of its most visible theaters.

Dermal fibroblasts, the cells responsible for producing collagen and elastin, are among the cell types most susceptible to senescence. As senescent fibroblasts accumulate in skin tissue, collagen production falls. The existing collagen matrix is degraded by the metalloproteinases that SASP secretion upregulates. Skin architecture loses its scaffolding. What was once firm and resilient becomes thinner, less elastic, more prone to lines and sagging. Melanocytes, the pigment-producing cells, also become senescent, contributing to the uneven skin tone and hyperpigmentation that characterize aging skin. The microvascular changes that accompany SASP signaling reduce blood flow to the dermis, contributing to the dullness and pallor that no highlighter quite covers.

This is not the whole story of skin aging. UV damage, oxidative stress, glycation, and hormonal changes all play significant roles. But cellular senescence is increasingly recognized as an upstream driver of all of them. The inflammatory environment that SASP creates amplifies the damage from every other aging mechanism simultaneously. It is, in biological terms, a force multiplier for everything else that goes wrong.

This is why topical approaches, as sophisticated as some have become, will always be working around the edges of the problem. You cannot resolve cellular senescence with a serum. The change has to happen from inside the cell.

 

Enter Epigenetics: Why Your Genes Are Not Your Destiny

Before I explain what can actually be done about senescent cells, I want to address something that I consider foundational, and that profoundly shapes how I approach aging with my clients.

Your genetic code is fixed. The sequence of base pairs in your DNA is the same today as it was the day you were born. But here is what most people have never been told: the expression of that genetic code is not fixed. The way your genes are read, which genes are switched on, which are silenced, which pathways are activated or suppressed, is governed by a layer of information above the DNA itself. This is epigenetics, from the Greek epi, meaning above or over.

Epigenetic regulation works through several mechanisms: the methylation of DNA at specific sites, the modification of the histone proteins around which DNA is wrapped, and the activity of non-coding RNA molecules that regulate gene expression. These mechanisms determine which parts of your genome are accessible to the cellular machinery that reads genes, and which are locked away. They are the volume controls on your genetic blueprint.

What is extraordinary, and what carries enormous implications for aging, is that these epigenetic marks are not permanent. They respond to your environment, to what you eat, to how you move, to chronic stress and to its resolution. As well as to the nutrients that circulate in your bloodstream and either support or starve the enzymatic processes that maintain epigenetic balance. To the accumulated burden of inflammation. And, critically for what we are discussing today, to the senescent cell load in your tissues.

Research in epigenetic clocks, computational models that use patterns of DNA methylation across the genome to calculate biological age as distinct from chronological age, has confirmed what many of us have observed clinically for years: two people of the same birth year can have biological ages that differ by decades. Senescent cell accumulation accelerates epigenetic aging. And interventions that reduce senescent cell burden have been shown to slow or partially reverse epigenetic clock progression.

What this means practically is significant. Your age is not written in stone. It is written in the choices you make at the cellular level every day, the nutrients you provide, the inflammation you resolve or sustain, and the senescent burden you reduce or allow to accumulate. The science of epigenetics has given us something remarkable: evidence that biological aging is malleable. That the cells writing your aging story can, to a meaningful degree, be given a different pen.

 

Senolytics: The Science of Clearing What Should Have Gone

The recognition that senescent cells drive aging has prompted one of the most exciting areas of longevity research of the past decade: the search for senolytics, which are compounds that selectively trigger the clearance of senescent cells without harming healthy ones.

Senescent cells survive the apoptosis they should undergo partly because they upregulate certain pro-survival pathways, mechanisms that suppress the cell death signals that would normally eliminate them. Senolytics work by targeting these pro-survival mechanisms, restoring the cell’s ability to receive and respond to apoptotic signals, and allowing the immune system to complete the clearance process it was failing to accomplish on its own.

The early senolytic research used pharmaceutical compounds, most notably dasatinib, a leukemia drug, combined with quercetin. The results in animal studies were striking enough to generate significant excitement. In mouse models, periodic senolytic treatment improved physical function, extended health span, reduced age-related pathology, and, in some models, extended lifespan. Human clinical trials are ongoing, and early results are promising.

But the pharmaceutical route is not the only path to senolytic activity. Several plant-derived polyphenols have demonstrated meaningful senolytic or senomorphic (SASP-suppressing) activity in cell studies and, increasingly, in human clinical contexts. Quercetin, one of the most widely studied, has demonstrated selective pro-apoptotic effects in senescent cells that are not observed in healthy proliferating cells. Fisetin, a flavonoid found in strawberries, apples, and onions, has shown even more potent senolytic activity in preclinical studies than quercetin in some models, with one landmark paper reporting a 25–50% reduction in senescent cell markers in mouse tissues following treatment. Curcumin, the active compound in turmeric, exerts senomorphic effects, reducing SASP cytokine secretion and modulating the NFκB inflammatory signaling that senescent cells exploit. Fucoidan, a complex polysaccharide derived from brown seaweed, has attracted research interest for its immunomodulatory properties and its capacity to support the natural killer cell activity that governs immune surveillance of senescent cells.

These are not fringe compounds. They are among the most studied phytochemicals in nutritional biochemistry. And when formulated together at meaningful concentrations and combined with the nutritional cofactors, zinc and Vitamin C, that support their activity, they create a synergistic senolytic environment that goes significantly beyond what any single compound can achieve alone. This is the premise behind ZinoGene+, a supplement I use in my clinical work that combines seaweed fucoidans, curcumin, quercetin, fisetin, piperine, zinc, and Vitamin C into a formulation specifically designed around senolytic and SASP-suppressive mechanisms. I am transparent with my clients about why I recommend it: the ingredient profile is clinically coherent, the mechanism is scientifically grounded, and the results I have observed, particularly in skin quality, energy, and inflammatory burden, are consistent and meaningful.

 

The Lifestyle Architecture of Cellular Youth

Senolytics are a powerful tool. But they work within a context, and that context matters enormously. The cellular environment that either accelerates or decelerates senescence accumulation is shaped daily by choices that are entirely within your control.

Sugar and glycation. Advanced glycation end products, AGEs, are formed when glucose molecules attach non-enzymatically to proteins and lipids. They accumulate in tissues, cross-link collagen fibers, stiffen cell membranes, and generate oxidative stress. They also promote senescence directly, by damaging cellular structures and impairing the mitochondrial function that healthy cells depend on. Reducing dietary sugar is not simply about caloric management. It is about reducing one of the primary biochemical drivers of cellular aging.

Gluten and intestinal permeability. For a significant proportion of women, particularly those with particular HLA genotypes or compromised gut microbiome diversity, gluten exposure contributes to intestinal permeability: the loosening of the tight junctions between intestinal epithelial cells that allows luminal contents, including lipopolysaccharide from gram-negative bacteria, to enter systemic circulation. The systemic inflammatory activation this produces is, from a cellular aging perspective, chronic SASP amplification. Every inflammatory signal that reaches your tissues adds to the burden that senescent cells are already creating.

Sleep and cellular repair. The restorative processes of the night shift are not metaphorical. During deep sleep, autophagy, the cellular self-cleaning mechanism that clears damaged organelles and misfolded proteins, reaches its daily peak. HGH secretion, which governs tissue repair and regeneration, occurs primarily in the early hours of sleep. The glymphatic system, the brain’s waste-clearance network, operates almost exclusively during sleep. Poor sleep quality is not simply tiring. It is a profound impediment to the cellular renewal processes that counterbalance senescence accumulation during waking hours.

Polyphenols and mitochondrial support. Colorful plant foods are not just nutritionally dense. They are epigenetically active. Polyphenols from berries, pomegranate, green tea, dark leafy vegetables, and olive oil modulate the activity of sirtuins, the family of proteins that regulate cellular stress responses, mitochondrial function, DNA repair, and epigenetic modifications. Sirtuins are directly implicated in the rate of biological aging. Their activity is supported by NAD+ availability, which in turn is influenced by niacin intake, exercise, fasting, and the presence of polyphenol-rich foods.

Omega-3 fatty acids and membrane resilience. The phospholipid composition of cell membranes, governed substantially by the omega-3 to omega-6 ratio, directly influences cellular susceptibility to inflammatory stress and to senescence. A membrane rich in EPA and DHA maintains fluidity, supports efficient receptor signaling, and generates the specialized pro-resolving mediators that actively orchestrate inflammatory resolution. A membrane depleted of EPA and DHA is rigid, pro-inflammatory, and far more susceptible to the oxidative damage that triggers senescence. Fatty acid status testing, the bloodspot test I use with all my clients, makes this measurable and correctable rather than a matter of guesswork.

Ascorbic acid and the collagen-senolytic connection. Vitamin C in its ascorbic acid form is simultaneously one of the most powerful cellular antioxidants available and a critical cofactor in collagen synthesis, specifically in the hydroxylation of proline and lysine that gives collagen fibers their structural integrity. At higher therapeutic doses, ascorbic acid supports the oxidative detoxification that accompanies senescent cell clearance. It is among the most important nutritional supports during any period of intentional cellular renewal.

 

Your Epigenetic Age Is Not Fixed

I want to return to epigenetics here, because I think this is where the deeper significance of this entire conversation lives.

When a senescent cell secretes SASP molecules into surrounding tissue, those molecules do not simply cause local damage. They alter the epigenetic state of neighboring cells, influencing DNA methylation patterns, activating stress-response pathways, and shifting the gene expression profiles of healthy cells toward pro-inflammatory, pro-aging phenotypes. Senescence, in other words, is epigenetically contagious. A local accumulation of zombie cells can propagate an aging epigenetic signature outward through tissue in a cascade.

The reverse is also true. Environments that are anti-inflammatory, nutrient-rich, senolytically active, and low in glycation and oxidative stress shift the epigenetic landscape back toward youthful gene expression patterns. This is not speculation. Epigenetic clock research, including the work behind the Horvath clock, the GrimAge clock, and increasingly refined next-generation methylation models, consistently shows that lifestyle and nutritional interventions are among the most powerful determinants of the rate at which the epigenetic clock ticks.

This is the core of what I believe, and what I have built my practice around: the body is not simply declining. It is responding constantly, dynamically, and epigenetically to the environment we create for it. The cells writing your aging story are listening. Every meal, every night of deep sleep, every reduction in inflammatory burden, every senolytic compound that clears a zombie cell, these are not small decisions. They are instructions. They are the signals your epigenome uses to decide which version of your biology to express.

Younger-looking skin is not a vanity goal. It is a biomarker. It reflects what is happening in your tissues, the inflammatory load, the collagen matrix integrity, the microvascular health, the cellular renewal rate. When the inside is working well, the outside reflects it. Every time.

 

A Seven-Day Experiment in Cellular Renewal

I want to invite you to experience what this looks like in practice. Not as an abstract concept but as something you can see on your own face, in your own mirror, in the span of a single week.

I am running a free 7-day Glow From Within Cellular Reset Challenge, and the protocol is built around exactly the science I’ve outlined here. Participants receive a structured daily routine that includes a targeted senolytic supplement protocol using ZinoGene+, a sequence of therapeutic anti-aging tonics designed to support liver detoxification, insulin regulation, and cellular antioxidant protection, and a simple no-sugar, no-gluten food framework that removes the two most significant dietary drivers of cellular inflammation and glycation.

The results have been consistent and often surprising. Smoother fine lines. Brighter skin tone. Reduced puffiness. Improved energy. Clients who have done this protocol tell me that by Day 5 they can see a visible difference, not in spite of doing it for only a week, but precisely because they are working at the right level. When you address cellular senescence, reduce SASP-driven inflammation, remove glycation promoters, and support epigenetic renewal simultaneously, the skin responds. It is the most visible organ, and it reflects what is happening at the cellular level faster than almost anything else.

If you would like to join the challenge or receive the protocol document, reach out to me directly. This is free to participate in. All I ask is that you commit to the week and share your before and after selfies, because seeing the results on real faces is the most powerful education I know how to offer.

 

Brigitte Spurgeon is a Board-Certified Functional Genomics Practitioner and Doctor of Orthomolecular Nutrigenomics. She works remotely with clients across the US, Canada, Europe, Asia, Africa, and Australia, offering personalized nutrigenomics consultations and the Glow From Within Cellular Reset Challenge. To join the challenge or learn more about working together, visit www.brigittespurgeon.com

As an Independent Partner with Zinzino, Brigitte uses bloodspot fatty acid testing and ZinoGene+ as part of her clinical protocols.

This article is for educational purposes and does not constitute medical advice.

Youth Athlete Nutrition Crisis: Why Young Athletes Break Down

Youth Athlete Nutrition Crisis: Why Young Athletes Break Down

Athlete Nutrition

If you are a parent, coach, athlete interested in youth athlete nutrition, or a woman who was a competitive athlete in her teens and is only now connecting the dots between those years and how your body feels today, this article is for you.

There is a pattern I have started to see, and once you see it, you can’t unsee it.

A fifteen-year-old girl is training six days a week. She’s fast, dedicated, the kind of athlete coaches dream of. Her parents are proud, but exhausted, ferrying her to early-morning sessions and weekend competitions and physiotherapy appointments for injuries that never quite resolve. Then one of three things happens:
• Her periods stop, or never properly arrive.
• She fractures a bone in her foot that should not fracture in a healthy fifteen-year-old.
• She simply stops improving, i.e. plateaus then slides backwards, and no one can work out why.

A sixteen-year-old boy is in the same picture. He is leaner than he was a year ago, despite eating what looks like lots of food. He catches every virus going through the school. His mood has flattened. His coach mentions, almost in passing, that he just doesn’t have the same spark in training.

These aren’t separate stories. They’re the same story, expressed through different bodies. And the answer is rarely what the medical system reaches for first.

What these young athletes have is, almost always, a fueling problem. Not a talent, discipline, or psychological problem. A biochemical problem that conventional sports medicine still routinely misses, and that the supplement industry actively makes worse.

I want to walk you through what is actually happening, because if you are raising, coaching, or treating a young athlete, this information can change the trajectory of their career, and more importantly, their long-term health.

 

Teenage Athletes Are Not Small Adults

This sounds obvious, but it is missed constantly in practice.

A teenage athlete is doing three biologically demanding things simultaneously: training at intensities approaching elite adult levels, navigating the most rapid period of growth and sexual maturation since infancy, and building the peak bone mass that will protect their skeleton for the rest of their lives. That bone-building window closes in the early twenties. Whatever is laid down now is, literally, the bank they draw from for the next sixty years.

Each of these processes — training, growth, bone accrual — carries its own energy and nutrient cost. Stack them together, and the metabolic demand on a fourteen-year-old elite swimmer or a sixteen-year-old cross-country runner is staggering.

In practical terms, this often means 3,000 to 4,000 calories a day for a female endurance athlete in her mid-teens, and considerably more for many young male athletes. Most are not eating anywhere near this. The reasons are layered:

• Sport culture rewards leanness.
• Social media has distorted how teenage girls relate to food and their bodies.
• Training schedules leave little time to eat.
• High training loads suppress appetite through changes in hunger hormones, a recognized biological effect that many athletes and coaches do not know exists.
• Well-meaning adults, raised in a diet culture that has confused thinness with health, often do not see the warning signs.

The result is what the International Olympic Committee now formally calls Relative Energy Deficiency in Sport, RED-S. It is not anorexia. It is not always disordered eating in any clinical sense. What it is, very often, is an unintentional and chronic gap between what a young body needs and what it is being given.

 

What Under Fueling Actually Does to a Young Body

When energy availability drops below what a body needs to train, grow, repair, and run basic metabolism, the body makes a choice. It downregulates the functions it considers non-essential to immediate survival. The hierarchy is consistent and biologically logical.

Reproductive function goes first

In female athletes, this means menstrual disruption. It starts with irregular cycles, then missed periods, then the complete absence of menstruation. The mechanism is suppression at the hypothalamus, which collapses the downstream hormone cascade that drives estrogen production. In male athletes, the equivalent is reduced testosterone It’s less obvious, but with real consequences for mood, muscle mass, bone, and recovery.

Many young female athletes, and the adults around them, interpret the absence of periods as a convenience, or as evidence that training is going well. It’s the opposite. The body is declaring that it can’t afford to reproduce because it can’t afford the energy cost. This is a serious clinical signal.

Bone remodeling slows

The young athlete who fractures a metatarsal during a normal training week is not unlucky. She is showing you that her skeleton is no longer keeping pace with the demands placed on it. Stress fractures in adolescents almost always indicate energy deficiency, often compounded by low estrogen or testosterone, and by inadequate vitamin D, calcium, and K2.

Roughly 90 percent of adult bone mass is laid down by age eighteen. A girl who under-fuels through her competitive teenage years walks into her thirties with a skeleton several years older than it should be, and into the perimenopausal years, when estrogen-driven bone loss accelerates, with significantly less in reserve than her peers.

This is where the story of the teenage athlete connects directly to the health of the menopausal woman. The body keeps a record. What is built, or not built, in youth tends to surface decades later.

Thyroid output falls

Under fueling reliably suppresses the active thyroid hormone, T3 through reduced conversion from T4, and through downregulation at the hypothalamic level. This is not thyroid disease in the conventional sense. It is a metabolic adaptation that expresses itself as fatigue, cold intolerance, brain fog, and a stubborn performance plateau that no amount of additional training will move. TSH and T4 often look normal on standard panels. Free T3 and reverse T3 tell the real story.

Immune function falters

The teenager who catches every cold, who is always slightly unwell, or who takes longer to recover from minor illness is not a victim of coincidence or weakness. Chronic under fueling suppresses immune defenses at multiple levels. Recurrent illness in a young athlete is a symptom, not a personality trait.

Mood and mental performance decline

Serotonin and dopamine, the neurotransmitters that regulate mood, motivation, and the capacity to engage with hard training, require specific amino acids, cofactors, and a functioning methylation pathway to be produced. A teenager who is chronically under fueled is not producing enough of them. The flatness, the irritability, the lost spark: these are biochemistry, not character.

 

The Nutrients That Make or Break a Young Athlete

The deficiencies I see are remarkably consistent across this population. Here is what I look for and why.

Iron

This is the single most common deficiency I see in young female athletes, and it is consistently under-investigated. Menstruating girls lose iron monthly. Endurance training adds further losses through sweat and the mechanical destruction of red blood cells with each foot strike. Growth demands more. The iron requirement of a fifteen-year-old female cross-country runner is dramatically higher than her peers.

The mistake most clinicians make is checking only hemoglobin. By the time hemoglobin drops, iron depletion has been developing for months. Ferritin, the storage form, drops first. A young athlete with ferritin below 30 ng/ml is already underperforming, regardless of whether her hemoglobin reads normal. Many elite athletes function best with ferritin above 50.

Vitamin D

Indoor-sport athletes, athletes training in northern latitudes, and athletes with darker skin are routinely deficient. Vitamin D affects bone, immune function, muscle force production, and mood. I look for serum levels in the 50–80 ng/ml range, well above the conventional threshold, which was set to prevent rickets, not to support an elite athlete’s physiology.

Calcium, Magnesium, and Vitamin K2

These work as a system. Calcium alone, without the cofactors that direct it into bone, is at best wasted and at worst deposited where it should not be. Magnesium is depleted by sweat and training stress, and it is required for vitamin D to activate. K2 directs calcium into bone rather than soft tissue. Young athletes need all three, first from food, and then precision supplemented where intake falls short.

Omega-3 EPA and DHA

Training generates inflammation. Adaptation depends on it. But chronic, unresolved inflammation impairs recovery and accelerates the systemic toll of high training loads. Adequate EPA and DHA are precursors to the molecules that actively resolve inflammation, not merely oppose it. They also support ongoing brain development and, critically for contact-sport athletes, appear to play a meaningful role in concussion recovery.

Most teenage athletes on a standard fish oil capsule are not getting what they think. Omega-3 index testing, measuring EPA and DHA as a percentage of red blood cell membrane fatty acids, is the only way to know with certainty.

 

The Genomic Layer

Two young athletes on identical training plans and identical diets will respond differently. Much of that difference is genomic.

Variants in the MTHFR gene affect how folate is metabolized and how well the body clears homocysteine, with downstream implications for neurotransmitter production, recovery, and the safety of standard B-vitamin supplementation.

Variants affecting vitamin D receptors influence how efficiently a given serum vitamin D level translates into actual cellular activity. Other variants shape antioxidant capacity, mitochondrial function, fast-twitch to slow-twitch fiber ratio, and caffeine metabolism.

This is not theoretical. Personalized nutrition informed by functional genomics is what differentiates the athletes who break down from the athletes who keep building.

 

What Actually Helps

The intervention is rarely glamorous, which is part of why it is overlooked.

• Fuel first.

Caloric intake matched to training load and growth. Carbohydrate treated as fuel, not as a category to be feared. Protein distributed across the day rather than concentrated in one meal. Real, varied fats included rather than restricted.

• Protect the menstrual cycle.

A regular cycle is one of the most reliable signals that a young female athlete’s physiology is well-resourced. Its absence is a medical issue, and not a convenience. It should never be masked with hormonal contraception without addressing the underlying cause.

• Test what actually matters.

Ferritin, transferrin saturation, 25(OH)D, RBC magnesium, zinc, B12, free T3, reverse T3, and an omega-3 index. Standard bloodwork misses most of what is relevant in this population.

• Prioritize sleep.

Recovery and growth hormone release peak during sleep. A young athlete sleeping six hours a night is not able to optimize training gains regardless of how many sessions she completes. Adolescents have a naturally delayed circadian rhythm, so early-morning training carries costs that need to be understood and managed.

• Personalize.

Genomic data, functional lab work, and clinical observation, integrated. Not a generic protocol applied to an individual body.

 

The Longer View

The decisions made, and the deficits accumulated, in the teenage athletic years cast a long shadow.

Many of the adult women I work with today were competitive athletes in their teens and twenties. The patterns I see are remarkably consistent: thyroid systems that never fully recovered from years of under fueling; declining bone density; hormonal systems entering perimenopause already running on debt. The body keeps a meticulous record.

This is not a reason for guilt for anyone reading this who has lived that history. It is a reason for clarity about what we owe the next generation of athletes coming through.

If we can fuel them properly now, support their physiology rather than override it, and approach their development with the respect that young bodies deserve, we change the trajectory of the rest of their lives. Not only their athletic careers.

 

The Question Worth Asking

If you are watching a young athlete struggle with recurrent injury, fading performance, missed periods, frequent illness, or the quiet loss of spark, the most useful question is not “what’s wrong with her?”

It’s: what is she not being given enough of?

That is the question orthomolecular medicine begins with. And in young athletes, the answer is almost always the same: energy, key nutrients, recovery, and the kind of informed, personalized approach that recognizes a developing body for what it is: a remarkable system that responds beautifully when it is properly resourced, and breaks down quietly when it is not.

The talent in our young athletes deserves better than the broken system currently surrounding them. So do the futures they are building in their bones.

 

Is this resonating with your story or with someone you love?

Whether you are a parent trying to protect your child’s health, a coach wanting to be better for your athletes, or a woman looking back at your own athletic years and recognizing these patterns in your body today, I am here to help.

My practice integrates functional genomics, orthomolecular medicine, and targeted nutrition to find and address root causes. I work remotely with clients across North America, Europe, Africa, Asia, and Australia.

Book a free call or learn more at www.brigittespurgeon.com

Brigitte Spurgeon is a Doctor of Orthomolecular Nutrigenomics and Functional Genomics Practitioner. She works with clients worldwide to prevent and reverse chronic disease through personalized, root-cause nutrition, which includes youth athlete nutrition.

This article is for educational purposes and does not constitute medical advice.

Your Genes and Your Weight: How Nutrigenomics Changes the Conversation on Metabolic Health

Your Genes and Your Weight: How Nutrigenomics Changes the Conversation on Metabolic Health

Nutrigenomics

If you have ever followed exactly the same diet as someone else — a friend, a colleague, a sibling — and had completely different results, you have already experienced nutrigenomics in practice.

One person loses weight easily on a low-carbohydrate approach. Another person follows the same protocol diligently and loses almost nothing. One person takes a standard B-complex and their energy transforms. Another takes the same supplement and feels worse. One person reduces saturated fat and their cholesterol drops dramatically. Another person makes the identical change and their numbers barely shift.

These are not mysteries. They are the predictable results of biochemical individuality — the fact that each of us carries a unique genetic blueprint that profoundly shapes how we process food, metabolize nutrients, regulate inflammation, manage blood sugar, and store fat. Nutrigenomics is the science of understanding that blueprint and using it to inform genuinely personalized nutrition.

I became obsessed with nutrigenomics because of the clarity it offered to my own life experiences. Despite years of being an endurance athlete and following clean nutrition, I continued to struggle with hormonal balance and metabolic resilience during certain periods of my life. Standard nutrition advice never worked for me. Understanding my own genetic terrain and nutrient deficiencies did. And it changed everything about how I work with my clients.

 

What Nutrigenomics Actually Is

Nutrigenomics examines the interaction between your genetic variants — known as single nucleotide polymorphisms, or SNPs — and the nutrients, foods, and dietary patterns you are exposed to. It works in two directions simultaneously.

Nutrigenetics examines how your genes affect your response to nutrition: which nutrients you need more of, which you process poorly, which dietary approaches are likely to be beneficial or counterproductive for your specific physiology. Nutrigenomics also examines how what you eat affects the expression of your genes — because our genetic code is not fixed destiny. Nutrients act directly on gene expression, switching pathways on and off, regulating enzyme production, and influencing which genetic risks materialize and which do not.

The practical application of this is what I do in my practice. I process raw genetic data files from my clients and generate detailed reports that reveal which variants are present, what they mean biochemically, and how nutrition, targeted supplementation, and lifestyle modifications can address the specific pathways those variants affect. I then walk each client through their results and build a protocol that is grounded in their actual genetic physiology — not a generic template.

 

The Key Genes in Metabolic Health and Weight

Several genetic variants have direct and well-studied implications for metabolic health, weight regulation, and the conditions my clients most commonly struggle with.

FTO — the fat mass and obesity gene. FTO variants are among the most widely studied in metabolic health research. Certain variants increase leptin levels while reducing HDL cholesterol, creating an environment of persistent hunger and metabolic disadvantage. Individuals with the higher-risk FTO genotype respond particularly well to personalized dietary interventions and benefit substantially from understanding and working with their specific metabolic predispositions rather than applying generic weight loss approaches.

PPARG — the adipogenesis and insulin sensitivity gene. PPARG regulates how fat cells are formed and how sensitive tissues are to insulin. Variants in this gene influence carbohydrate and fat metabolism and determine in part how a person responds to different dietary macronutrient ratios. Someone with particular PPARG variants may have a significantly different metabolic response to a high-fat diet than someone without them — information that makes generic dietary advice at best ineffective and at worst counterproductive.

FADS1 and FADS2 — the fatty acid desaturase genes. These genes encode the enzymes responsible for converting the shorter-chain omega-3 and omega-6 fatty acids from diet into the longer-chain forms — EPA, DHA, and arachidonic acid — that the body actually uses. Variants in FADS1 and FADS2 significantly affect this conversion efficiency, meaning that some people cannot effectively produce anti-inflammatory DHA and EPA from plant-based omega-3 sources and require preformed EPA and DHA directly. This is one of the reasons I recommend fatty acid testing — because understanding both the genetic conversion capacity and the actual membrane fatty acid ratio gives a complete picture of an individual’s omega-3 status and what is needed to correct it.

MTHFR — the methylation gene. I have dedicated an entire blog to MTHFR, but in the context of metabolic health, its implications deserve mention here. Methylation — the biochemical cycle that MTHFR governs — is involved in insulin regulation, inflammation modulation, gene expression, and the production of the neurotransmitters that influence appetite, mood, and energy. Impaired methylation contributes to elevated homocysteine, which drives vascular inflammation, and to disrupted neurotransmitter balance, which affects the brain’s regulation of hunger and satiety. Addressing MTHFR is not peripheral to metabolic health — it is often central to it.

TNF and IL-6 — the inflammatory genes. Variants in genes encoding inflammatory cytokines like TNF-alpha and interleukin-6 determine in part how robustly the body mounts an inflammatory response and how quickly it resolves it. Those with higher-risk variants may experience more pronounced inflammatory responses to dietary fat, to gut dysbiosis, or to metabolic stress — driving the chronic low-grade inflammation that impairs insulin signaling, disrupts hormone balance, and makes weight loss physiologically difficult. Knowing these variants helps prioritize anti-inflammatory strategies and informs dietary fat choices in ways that generic guidelines cannot.

 

Why Generic Nutrition Advice Will Never Be Enough

Standard dietary guidelines are designed around population averages. They represent what tends to be beneficial for most people most of the time. But metabolic individuality is not marginal — it is the norm. The variation between individuals in how they respond to the same dietary inputs is not small. It is enormous. And for people struggling with weight, insulin resistance, hormonal imbalance, or chronic inflammation that does not respond to standard approaches, that variation is not an academic footnote. It is the reason they have not been getting better.

The conventional nutrition model asks: what should people eat? Nutrigenomics asks: what should this person eat, given their specific genetic, metabolic, and biochemical context? These are fundamentally different questions, and they produce fundamentally different answers.

A woman with FADS2 variants affecting her fatty acid conversion capacity needs more preformed EPA and DHA than someone without those variants — and she needs it in a tested, bioavailable form, not just a generic fish oil capsule. A man with PPARG variants affecting his insulin sensitivity may need a significantly different carbohydrate approach than his partner with a different genetic profile. Someone with compound MTHFR variants needs specific forms of B vitamins — standard forms will not work in their methylation cycle and may actively impair it.

This is not complexity for its own sake. It is precision — the difference between an intervention that works and one that doesn’t.

 

Genes Are Not Destiny

I want to be clear about something important. Understanding your genetic variants is not about receiving a fixed sentence. Genes are not destiny — they give us direction. What nutrigenomics reveals is not what will inevitably happen to you, but what is likely to happen if your nutrition and lifestyle are not calibrated to your specific biology.

The same FTO variant that predisposes someone to excess weight under a standard Western diet may have minimal metabolic consequences when that person understands their specific nutrient needs and eats accordingly. The MTHFR variant that has been driving elevated homocysteine for years can be managed effectively with the right forms of B vitamins. The FADS2 conversion deficit that has been leaving someone chronically omega-3 deficient despite years of fish oil supplementation can be corrected when the actual membrane ratio is tested and the right form and dose of supplementation is applied.

Nutrigenomics does not offer a cure. It offers clarity — a clear, personalized picture of the biological terrain that has been shaping your health, and a roadmap for working with that terrain rather than against it. For people who have spent years doing everything right and still not getting the results they expect, that clarity is not just useful. It is often transformative.

 

What This Looks Like in Practice

In my nutrigenomics consultations, I process raw genetic data and generate a detailed report covering the variants most relevant to my client’s health goals and symptoms. I then conduct a thorough consultation in which I walk them through what their results mean in plain language — what each variant affects, what it means for their specific situation, and what changes to nutrition, supplementation, and lifestyle are indicated.

The report and consultation give clients something most people have never had: a genuine baseline — a biochemically grounded understanding of their individual physiology that they can carry forward for life. Rather than chasing the next diet trend or supplement recommendation, they understand what their body actually needs. Interventions stop being trial and error. They become targeted and evidence based.

This is the future of personalized nutrition. And for many of my clients, it is the first time in years — sometimes decades — that they have finally understood why what they were doing wasn’t working, and what will.

Brigitte Spurgeon is a Board-Certified Functional Genomics Practitioner and Doctor of Orthomolecular Nutrigenomics. She works remotely with clients across the US, Canada, Europe, Asia, Africa, and Australia, offering personalized nutrigenomics consultations, the Metabolic Pathway Strategy, and the Holistic Healing Strategy. To learn more or inquire about working together, visit www.brigittespurgeon.com

This article is for educational purposes and does not constitute medical advice.

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