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Evidence levels in this article
This article draws on material from different levels of evidence, which are worth distinguishing. Well-established: the role of insulin resistance, sleep apnoea, kidney dysfunction, physical inactivity, and sodium intake in hypertension — supported by RCTs and international guidelines. Plausible with moderate evidence: autonomic imbalance, magnesium deficiency, CoQ10, omega-3, and exercise-based interventions. Emerging or mechanistically plausible: gut permeability, oral microbiome, estrobolome effects on blood pressure — biologically interesting but not yet supported by robust clinical trials in hypertensive populations. Where the evidence level is relevant, it is noted throughout.
Most people with high blood pressure are on medication that brings the number down. That is not the same as understanding why the number was up in the first place.
Conventional hypertension management — measure, classify, and treat to target — is effective and evidence-based. It significantly reduces the risk of stroke, heart attack, and renal failure. But blood pressure medication addresses the level of pressure, not necessarily the biological factors driving it. For some patients, particularly those with concurrent metabolic dysfunction, sleep disorders, or lifestyle contributors, understanding and addressing those upstream factors alongside medication can be clinically valuable.
Cardiologist Dr Mark Houston has written extensively on the functional drivers of hypertension. He describes the condition as "a correct but dysregulated vascular response" in which "the blood vessel is an innocent bystander" — a framing from his 2014 paper in the Journal of Clinical Hypertension and his broader body of work on nutritional and integrative approaches to cardiovascular disease. That framing is deliberately provocative and sits outside mainstream cardiology consensus. Hypertension is a recognised clinical condition that requires medical management and monitoring. What Houston's framing usefully draws attention to is that blood pressure elevation is often the downstream result of identifiable, modifiable processes — and asking what those processes are is a reasonable complement to conventional treatment.
Composite patient voice — common presentation in clinic
"I've been on two blood pressure medications for four years. My readings are controlled, according to my doctor. But I still feel awful — tired, foggy, and I've gained twelve kilos since I started them. Nobody has ever asked me why my blood pressure was high."
Melbourne patient, 2025
Controlled blood pressure is an important treatment success — it meaningfully reduces cardiovascular event risk. But it does not necessarily tell us which underlying factors contributed to the hypertension in the first place. For some patients, there are still modifiable metabolic, sleep, lifestyle, or vascular factors worth investigating alongside medication. That is the clinical gap I work in.
Quick Answer
High Blood Pressure — What the Number Is Actually Telling You
- Hypertension is more than a number to suppress. It reflects the interaction of vascular, metabolic, nervous-system, renal, and hormonal factors — and the clinical task is to identify which of those factors are most active in each individual.
- Five interconnected areas are particularly relevant to investigate in many hypertension presentations: metabolic dysfunction, autonomic imbalance, inflammatory burden, endothelial dysfunction, and multisystem contributors including sleep, thyroid, and nutrient status. These represent my clinical framework, not a medical taxonomy — and conventional drivers including kidney function and medication effects sit alongside them.
- Blood pressure medication meaningfully reduces cardiovascular risk when the number is controlled. For some patients, modifiable underlying drivers — insulin resistance, sleep apnoea, autonomic imbalance, nutrient deficiency — may still be worth investigating alongside medication.
- Identifying whether hypertension has a secondary reversible cause — kidney disease, sleep apnoea, endocrine disorder, or medication effect — is an important first step in conventional workup, and should be done by your GP or specialist.
- The naturopathic approach identifies which drivers are active in each individual and addresses them systematically, working alongside medical management, not against it.
In this article
- Reframing Hypertension: Signal, Not Disease
- Driver 1: Insulin Resistance
- Driver 2: Autonomic Imbalance and Sympathetic Dominance
- Driver 3: Gut Permeability and Inflammatory Burden
- Driver 4: Endothelial Dysfunction and Nitric Oxide Depletion
- Driver 5: Multisystem Contributors
- The ROOT Method for Hypertension
- Frequently Asked Questions
First step — exclude secondary hypertension
Before exploring functional contributors, conventional medical evaluation should exclude secondary causes of hypertension: kidney disease, renal artery stenosis, primary aldosteronism, phaeochromocytoma, obstructive sleep apnoea, thyroid dysfunction, and medication effects (NSAIDs, oral contraceptives, decongestants). Secondary hypertension accounts for a meaningful minority of cases and some causes are reversible with specific treatment. This evaluation is your GP's or specialist's domain — naturopathic assessment is most useful once secondary causes have been considered.
Reframing Hypertension: Signal, Not Disease
Blood pressure exists for a reason. Its biological purpose is to ensure adequate tissue perfusion — to get blood, oxygen, and nutrients to every part of the body efficiently. When the system works properly, vessels dilate when flow needs to increase (via nitric oxide) and constrict when it needs to be redirected (via angiotensin-II). Vascular health is a persistent, dynamic balance between these two mechanisms.
When blood pressure becomes chronically elevated, it usually means that balance has shifted — something is driving persistent constriction, reducing the ability of vessels to dilate, or increasing the body's perceived need for higher perfusion pressure. Several interacting mechanisms contribute to chronic hypertension, including inflammation, oxidative stress, endothelial dysfunction, and autonomic dysregulation — often overlapping in individual patients.
On medication
Nothing in this article suggests stopping or reducing blood pressure medication. In many situations, blood pressure medication is necessary and appropriate, and withdrawal without medical supervision carries real cardiovascular risk. The goal of functional assessment is to identify and address the drivers of hypertension alongside medical management — not to replace it. Any changes to medication should be made in consultation with your prescribing doctor, based on serial blood pressure monitoring over time.
Insulin resistance is increasingly recognised as a significant contributor to hypertension, particularly in patients with concurrent metabolic syndrome, abdominal adiposity, or prediabetes. As cells become resistant to insulin's signal, the pancreas compensates by producing more insulin. Research suggests this compensatory hyperinsulinaemia may contribute to blood pressure elevation through several mechanisms, which are still being characterised in human studies.
Insulin resistance can develop well before fasting glucose becomes abnormal, meaning that normal fasting glucose does not necessarily exclude early metabolic dysfunction. Fasting insulin and HOMA-IR are not standard diagnostic tests for hypertension and are not recommended in routine hypertension guidelines. They may provide additional metabolic context in selected patients — particularly those with concurrent features of insulin resistance or metabolic syndrome — where a more comprehensive metabolic picture is clinically useful. These results should be interpreted alongside, and not instead of, conventional cardiovascular assessment. A fasting insulin and HOMA-IR calculation — not on a standard Medicare panel, specifically requested as private pathology — will tell a completely different story.
Limitations of fasting insulin and HOMA-IR
Fasting insulin assays are not standardised across Australian laboratories, which limits direct numerical comparison between results from different providers. HOMA-IR is a calculated index with meaningful inter-individual variation. These markers are most useful as directional indicators of metabolic status in clinical context — not as diagnostic thresholds. Reference ranges used in functional medicine (often HOMA-IR above 2.0 as concern) differ from those used in diabetes research and are not validated against hypertension-specific outcomes. Interpretation should be conservative and contextual.
Important — supplements and medication interactions
Supplement selection and dosing should be individualised, particularly where antihypertensive, anticoagulant, diabetes, or thyroid medication is being used. Several of the interventions listed in this article can interact with medications or may not be appropriate for everyone. Discuss any supplementation with your prescribing doctor before starting. The interventions below represent clinical approaches used in practice — they are not prescriptions.
Clinical approach — insulin resistance and hypertension
- Protein-first meal sequencing — eating protein and non-starchy vegetables before carbohydrates has been associated with reduced postprandial glucose and insulin responses in some studies; a low-burden practical modification worth trialling
- Reduce refined carbohydrates and sweetened beverages — the highest-yield dietary change for lowering fasting insulin
- Shift caloric timing earlier in the day — insulin sensitivity follows a diurnal pattern and is generally higher in the morning; earlier caloric loading may support metabolic health though individual variation is significant
- Resistance training — increases GLUT4 transporters in muscle cells, improving glucose uptake independent of insulin
- Post-meal movement — short walks after meals are associated with reduced postprandial glucose levels in research; a practical and low-risk addition to daily routine
- Myo-inositol — supports insulin receptor signalling; evidence is strongest in PCOS; discuss appropriate dosing with your practitioner as evidence specifically in hypertension is limited
- Berberine — activates AMPK and has supporting evidence for improving insulin sensitivity; not a replacement for metformin or diabetes medication; dosing and suitability should be discussed with your GP particularly if you are on hypoglycaemic agents
The autonomic nervous system governs blood pressure on a moment-to-moment basis. In its healthy state, sympathetic activation (fight-or-flight) is a short-term emergency response, and parasympathetic tone (rest-and-digest) is the dominant baseline. In some people with chronic hypertension, this balance appears shifted: sustained sympathetic dominance with reduced parasympathetic buffering may become habitual, though the extent to which this is a cause versus consequence of hypertension varies between individuals.
The perceived need for fight-or-flight — whether from genuine physical threat, unresolved psychological stress, chronic pain, sleep disruption, or blood sugar instability — naturally elevates blood pressure. That is the system working correctly. The problem is when the perceived threat never resolves, and the nervous system never fully returns to parasympathetic baseline.
Autonomic imbalance drives hypertension through increased sympathetic outflow, impaired vagal tone, electrolyte disruption (sodium retention, magnesium and potassium excretion), increased heart rate and reduced heart rate variability, and chronic vasoconstriction that over time promotes vascular remodelling and stiffness.
Stressors in this context include not just psychological pressure but physiological and biochemical stress: infections, blood sugar instability, toxin exposure, sleep deprivation, excessive stimulant use, and impaired gut barrier function all activate sympathetic pathways and sustain the hypertensive state. Identifying which stressors are most active for each individual is where clinical assessment becomes genuinely useful.
Clinical approach — autonomic imbalance
- Slow nasal breathing with extended exhale — associated with reduced heart rate and blood pressure in research; multiple short daily practices appear beneficial; evidence supports inclusion as a complementary approach
- Re-establish circadian rhythm — sleep quality and duration have established associations with cardiovascular health including blood pressure; morning natural light exposure and consistent sleep/wake timing support circadian regulation
- RBC magnesium assessment — magnesium depletion is extremely common in chronically stressed individuals and directly impairs vasodilation and parasympathetic tone; magnesium glycinate 300 to 400mg elemental magnesium daily in divided doses — note that product labels often list the compound weight, not the elemental magnesium content; check the label
- Reduce stimulatory load in the evening — caffeine half-life varies between individuals and can affect sleep quality; limiting stimulating content and screen exposure before bed supports sleep onset and quality, which has cardiovascular relevance
- Adaptogenic herbs — ashwagandha has supporting evidence for cortisol and stress response modulation in some RCTs; holy basil has limited but plausible evidence; note that ashwagandha may lower blood pressure and should be used with caution alongside antihypertensive medication
- Melatonin (low dose, 0.3 to 3mg) — some evidence for modest nocturnal blood pressure reduction, particularly in non-dipper hypertension; primarily useful for sleep quality support; check for interactions with antihypertensive medication
- Nervous system-regulating movement — yoga, tai chi, meditative walking; different mechanism from aerobic exercise and specifically supports parasympathetic recovery
Identifying which drivers are most active requires testing, not guesswork. A free discovery call identifies what assessment is most relevant for your specific presentation.
Book a free discovery call →Gut-derived inflammation is an emerging area of research in cardiometabolic health. When intestinal barrier integrity is compromised, bacterial lipopolysaccharides (LPS) from gram-negative bacteria can cross into systemic circulation and activate immune pathways, potentially producing IL-6, TNF-alpha, and reactive oxygen species. Whether and to what extent this contributes to hypertension in individual patients remains incompletely defined — the biological mechanisms are plausible and consistent with research in cardiometabolic disease generally, but should not be presented as established causal relationships. What is better established is that chronic low-grade inflammation broadly contributes to endothelial dysfunction and vascular remodelling, and that the gut can be a significant source of such inflammation in some individuals.
There is also a specific oral component. The oral microbiome contains nitrate-reducing bacteria that are part of the nitric oxide production pathway: dietary nitrates from vegetables are converted by oral bacteria to nitrite, then to bioavailable nitric oxide in the gut and bloodstream. Frequent use of strong antibacterial mouthwash has been associated in research with reductions in systemic nitric oxide bioavailability, raising the question of whether routine antimicrobial mouthwash use may influence blood pressure in some individuals. The evidence is mechanistically plausible but not yet definitive at a population level.
Clinical approach — gut and inflammatory burden
- Consider gut assessment where clinically indicated — where significant gut symptoms, recurrent infections, or inflammatory markers suggest gut involvement, a GI Microbiome Map can provide useful information on dysbiosis and barrier markers; this is an adjunctive and emerging area, not a standard part of hypertension investigation
- High-nitrate vegetables — beetroot, rocket, chard, celery; dietary nitrate is converted to nitrite and then to nitric oxide via oral and gut bacteria; some RCTs of beetroot juice show modest short-term blood pressure reductions; thorough chewing supports this pathway
- Avoid antibacterial mouthwash — switch to salt water or xylitol-based alternatives that preserve beneficial oral bacteria
- Omega-3 fatty acids (2 to 4g EPA+DHA daily) — meta-analyses support modest blood pressure-lowering effects; anti-inflammatory properties are biologically plausible; dose, formulation quality, and baseline omega-3 status affect response
- Polyphenol-rich diet — berries, dark chocolate, green tea; associated with improved endothelial function and cardiovascular outcomes in observational research; mechanistic studies suggest effects on nitric oxide pathways and oxidative stress, though translation to clinical blood pressure reduction varies
- Gut barrier support where clinically indicated — L-glutamine, zinc carnosine; evidence for each is largely mechanistic or from gut-specific conditions; their role in hypertension specifically is indirect and based on the proposed gut-inflammation pathway rather than direct hypertension RCTs
The endothelium — the single-cell layer lining the interior of blood vessels — is where vascular tone is regulated. It produces nitric oxide in response to shear stress from blood flow, physical activity, and specific nutritional inputs. Nitric oxide signals smooth muscle to relax, producing vasodilation and reducing blood pressure. As the endothelium becomes damaged and dysfunctional, this capacity diminishes.
In many patients with hypertension, the issue is not only inadequate nitric oxide production. It is also excessive nitric oxide destruction. Oxidative stress from hyperglycaemia, insulin resistance, hypoxia (from obstructive sleep apnoea), and inflammatory burden all produce reactive oxygen species that rapidly degrade nitric oxide before it can act. Where impaired nitric oxide bioavailability is contributing to endothelial dysfunction, supporting production and reducing destruction are both relevant clinical considerations.
Elevated uric acid has been associated with endothelial dysfunction and impaired nitric oxide bioavailability in some observational research, though its causal significance in hypertension remains debated. Dietary patterns high in fructose and alcohol can contribute to elevated uric acid alongside genetic susceptibility, kidney handling, and body composition. Moderating these is a reasonable dietary consideration where uric acid is elevated.
Clinical approach — endothelial dysfunction
- Regular aerobic movement — exercise is one of the best-evidenced lifestyle interventions for blood pressure reduction; shear stress from blood flow stimulates eNOS activity; aim for at least 150 minutes per week of moderate intensity activity per Australian guidelines
- Optimise sleep and address sleep apnoea — OSA is a recognised contributor to elevated blood pressure; nocturnal hypoxia can impair endothelial function; clinical assessment for OSA is warranted where blood pressure is difficult to control and sleep symptoms are present
- Coenzyme Q10 — supports mitochondrial energy production; meta-analyses suggest modest blood pressure reduction in some populations though trial quality varies; most relevant where statin use or age-related depletion is suspected; discuss dosing with your practitioner
- Vitamin C (500mg twice daily) — antioxidant support; some evidence for modest blood pressure effects, potentially via reduced oxidative degradation of nitric oxide; most relevant where dietary intake is poor; evidence for supplementation specifically in normovitaminotic individuals is weaker
- Monitor and reduce uric acid — reduce fructose and alcohol; some preliminary evidence suggests tart cherry may modestly reduce uric acid, though clinical evidence is limited; reducing fructose and alcohol remains the most evidence-supported dietary approach
- Garlic — mince or crush and allow to rest for 10 minutes to activate allicin; meta-analyses show modest blood pressure reduction effects though effect sizes vary across trials and preparation method affects bioavailability
- Potassium from food sources — avocado, leafy greens, legumes; dietary potassium supports blood pressure via natriuresis; do not supplement potassium without medical supervision, particularly on ACE inhibitors, ARBs, or potassium-sparing diuretics where hyperkalaemia risk is real
Beyond the drivers above, several other conditions and nutritional factors may contribute to hypertension and are worth considering in a comprehensive assessment.
Kidney function and RAAS regulation
The kidneys play a central role in long-term blood pressure regulation through sodium and fluid balance and the renin-angiotensin-aldosterone system (RAAS). Kidney disease can both cause and result from hypertension, and renal function assessment is a fundamental part of conventional hypertension evaluation. Secondary hypertension from renal artery stenosis, primary aldosteronism, and other conditions should be excluded by your GP or specialist as part of conventional workup. Naturopathic assessment complements this medical workup rather than replacing it. The dietary factors most relevant to kidney-related blood pressure include sodium intake, adequate potassium from food sources, and hydration.
Thyroid dysfunction
Thyroid dysfunction can affect cardiovascular physiology and may contribute to abnormal blood pressure in some patients. Conventional assessment centres on TSH and free T4, and these should be the starting point. Where clinical history or symptoms suggest thyroid involvement, further assessment including free T3 and thyroid antibodies may be considered in selected patients, guided by clinical context rather than routine screening. It is worth noting that TSH threshold definitions for subclinical hypothyroidism vary between guidelines, and treatment decisions should be made with a GP or endocrinologist.
Sleep apnoea
Obstructive sleep apnoea (OSA) is a recognised contributor to hypertension and a cause of secondary and treatment-resistant hypertension in a subset of patients. Nocturnal hypoxia repeatedly activates the sympathetic nervous system during sleep, producing morning blood pressure surges and sustained daytime elevation. Blood pressure that is consistently higher in the morning than the evening, or that is difficult to control despite adequate medication, warrants OSA investigation.
Nutrient deficiencies
Magnesium depletion directly impairs vasodilation and is extremely common in chronically stressed individuals, in those on diuretics or PPIs, and in those with high alcohol or caffeine intake. Low magnesium has been associated with elevated blood pressure and increased vascular reactivity in some studies. Standard serum magnesium is commonly used clinically and will identify overt deficiency. RBC magnesium may detect depletion in some patients where serum appears normal — a recognised phenomenon, though the clinical significance and optimal threshold for supplementation remain debated. Where symptoms and clinical context suggest deficiency, a supplementation trial may be warranted regardless of which test is used. Elevated ferritin has been associated with oxidative stress in some research contexts. Where unexplained hypertension is present without obvious metabolic drivers, iron studies including ferritin may be worth reviewing — though elevated ferritin has many causes including inflammation and should be interpreted carefully rather than automatically attributed to iron overload.
Sedentary behaviour and muscle mass loss
Skeletal muscle is an important site of glucose disposal, and loss of muscle mass with age — sarcopaenia — can contribute to worsening insulin sensitivity over time. Resistance training supports muscle mass, insulin sensitivity, and has independent evidence for modest blood pressure reduction. It is a well-supported component of cardiovascular health management, particularly in older adults, and is worth including alongside aerobic exercise.
Our Naturopathic Approach: The ROOT Method for Hypertension
ROOT stands for Review, Order, Observe, Treat. This is our clinical practice framework — not a validated diagnostic or treatment protocol with RCT evidence. What it offers is a systematic way of assessing the modifiable metabolic, autonomic, gut, endothelial, and multisystem contributors that standard cardiovascular investigation does not routinely explore. The evidence for individual components within it varies: some are well-established (addressing sleep apnoea, insulin resistance, physical activity), others are emerging (gut permeability, oral microbiome).
How these drivers connect
Hypertension rarely has a single cause. The following shows how upstream inputs feed through interconnected mechanisms to produce chronic vascular dysfunction.
The following represents a clinical framework for thinking about modifiable contributors to hypertension — not a validated causal diagram. Individual contributions will vary significantly between patients.
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Related reading
Understanding why — not just managing the number
If Your Blood Pressure Is Controlled but You Still Feel Unwell, the Underlying Drivers Have Not Been Addressed
Where standard cardiovascular investigation has not fully explained your blood pressure picture, a naturopathic assessment can explore additional modifiable contributors — metabolic, sleep-related, nutritional, and autonomic — that conventional workups do not routinely cover. Results are discussed with Domenic in a clinical consultation, and recommendations are made in the context of your existing medical management. The goal is to identify factors worth addressing alongside your GP and cardiologist, not to replace that care. A free 20-minute discovery call is the right starting point.
What Happens When You Book a Free Discovery Call
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Here is what actually happens:
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Frequently Asked Questions
References and Further Reading
- Houston MC. Hypertension is not a disease — it is a correct but dysregulated vascular response. J Clin Hypertens. 2014;16(4):236-239. doi: 10.1111/jch.12188. Wiley
- Brands MW. Chronic blood pressure control. Compr Physiol. 2012;2(4):2481-2494. doi: 10.1002/cphy.c110012. PMID: 23720253
- Lastra G, Syed S, Kurukulasuriya LR, et al. Type 2 diabetes mellitus and hypertension: an update. Endocrinol Metab Clin North Am. 2014;43(1):103-122. doi: 10.1016/j.ecl.2013.09.005. PMID: 24582093
- Kapil V, Rathod KS, Khambata RS, et al. Sex differences in the nitrate-nitrite-NO pathway: role of oral nitrate-reducing bacteria. Free Radic Biol Med. 2020;152:375-382. doi: 10.1016/j.freeradbiomed.2019.12.010. PMC6628144
- Barbaro NR, Fontana V, Modolo R, et al. Increased arterial stiffness in resistant hypertension is associated with inflammatory biomarkers. Blood Press. 2015;24(1):7-13. doi: 10.3109/08037051.2014.949254. PMID: 25198671
- Gabb GM, Mangoni AA, Anderson CS, et al. Guideline for the diagnosis and management of hypertension in adults — 2016. Med J Aust. 2016;205(2):85-89. doi: 10.5694/mja16.00526. PMID: 27456633 [Australian hypertension guideline 2016; the National Heart Foundation of Australia has published updated blood pressure guidance — readers should refer to nhf.org.au for the most current Australian recommendations]
- McEvoy JW, McCarthy CP, Bruno RM, et al. 2024 ESC Guidelines for the management of elevated blood pressure and hypertension. Eur Heart J. 2024;45(38):3912-4018. doi: 10.1093/eurheartj/ehae178. PMID: 39210715 [Current international guideline]
- Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA Hypertension Guidelines. J Am Coll Cardiol. 2018;71(19):e127-e248. doi: 10.1016/j.jacc.2017.11.006. PMID: 29146535
- Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC Heart Failure Guidelines. Circulation. 2022;145(18):e895-e1032. [Renal and RAAS considerations in blood pressure management]
- Drager LF, Togeiro SM, Polotsky VY, Lorenzi-Filho G. Obstructive sleep apnea: a cardiometabolic risk in obesity and the metabolic syndrome. J Am Coll Cardiol. 2013;62(7):569-576. doi: 10.1016/j.jacc.2013.05.045. PMID: 23770180
- Cornelissen VA, Smart NA. Exercise training for blood pressure: a systematic review and meta-analysis. J Am Heart Assoc. 2013;2(1):e004473. doi: 10.1161/JAHA.112.004473. PMID: 23525435
- Australian Institute of Health and Welfare (AIHW). High blood pressure 2023. AIHW, Australian Government. aihw.gov.au
- Uribarri J, del Castillo MD, de la Maza MP, et al. Dietary advanced glycation end products and their role in health and disease. Adv Nutr. 2015;6(4):461-473. doi: 10.3945/an.115.008433. PMID: 26178030
About the Author
Domenic Pisanelli, BHSc Naturopathy, is a Melbourne naturopath with 25 years of clinical experience. His practice focuses on metabolic health, cardiovascular risk factors, gut health, hormonal health, and chronic fatigue. He uses targeted functional pathology to identify the root cause drivers of chronic conditions and builds personalised protocols through the ROOT Method clinical framework. He practises at Vital Health and Natural Medicine, 195A Sunshine Ave, Kealba VIC 3021, and offers telehealth nationally. ATMS registered. This article is for educational purposes only and does not constitute medical advice. High blood pressure requires medical monitoring and management.
