The Blood Pressure Paradigm

Summary

High blood pressure is a major cardiovascular risk factor — and it is also often a downstream marker of broader physiological dysregulation, rather than a single isolated fault.

Contemporary research shows that hypertension is closely linked to endothelial dysfunction, oxidative stress, low-grade inflammation, immune-vascular signalling, autonomic nervous system imbalance, metabolic dysfunction, sleep and circadian disruption, and renal–electrolyte stress.

Lowering blood pressure with medication reduces cardiovascular risk and is often necessary. However, long-term outcomes are strongest when blood pressure control is paired with correction of upstream biological drivers, rather than treating the blood pressure number alone.

A regulation-first approach — addressing sleep and circadian timing, breathing and airway function, nutrient sufficiency, metabolic stability, vascular signalling (including nitric oxide biology), stress physiology, and recovery — allows blood pressure to normalise as a by-product of restored regulation, rather than a forced outcome.

— Christopher Pickard, DC
Functional Nutritionist | Health Coach | Regulation-First Blood Pressure Specialist
30+ years clinical experience

Blood pressure is one of the most frequently measured parameters in medicine — and one of the most misunderstood.

In conventional care, elevated blood pressure is often framed as a primary disease entity requiring numerical suppression. This framing exists for good reason: sustained hypertension directly increases the risk of stroke, myocardial infarction, heart failure, kidney disease, and vascular damage, and lowering blood pressure reduces these risks at a population level (Ettehad et al., The Lancet, 2016; NICE NG136).

However, from a systems-biology and vascular-physiology perspective, blood pressure is also a compensatory and regulatory response.

The cardiovascular system raises pressure to maintain:

• tissue perfusion

• oxygen and nutrient delivery

• vascular wall integrity

• filtration pressure at the kidney

when regulatory systems are under strain.

This distinction matters.

Because lowering the number without addressing the reason the number rose can leave the underlying biology unchanged — or displaced into another form of dysfunction.

Model 1: Blood Pressure as a Primary Malfunction

• Blood pressure is “too high”

• The system is assumed to be failing

• Medication is used to force the number down

• Success is defined primarily by the reading

This model is appropriate and often lifesaving in acute, high-risk, or secondary hypertension contexts. It is also supported by large outcome trials showing reduced cardiovascular events with BP reduction.

Model 2: Blood Pressure as a Regulatory Signal

• Blood pressure reflects total system load

• The body is assumed to be adaptive but dysregulated

• The goal is restoring regulation, not silencing signals

• Blood pressure improves as physiology improves

This model aligns with modern understandings of:

• vascular and endothelial biology

• neuro-immune interactions

• autonomic nervous system regulation

• metabolic–renal integration

• systems and functional medicine frameworks

Both models matter. The error is using only the first.

Large bodies of research identify several recurring mechanisms in the development and maintenance of hypertension:

• Endothelial dysfunction

• Oxidative stress

• Low-grade vascular inflammation

• Immune system activation within the vasculature

• Neurohormonal and sympathetic overactivation

(Montezano & Touyz, Hypertension, 2014; Harrison et al., Hypertension, 2021)

These mechanisms describe how blood pressure rises — but not necessarily why the system entered this state.

Across decades of clinical practice, the following upstream factors repeatedly appear in people with persistent or treatment-resistant hypertension — and are increasingly supported by research:

1. Sleep & Circadian Disruption

Short sleep duration, circadian misalignment, and especially obstructive sleep apnoea are strongly associated with hypertension via intermittent hypoxia, sympathetic activation, and endothelial dysfunction
(Pepin et al., Journal of Human Hypertension, 2024)

2. Chronic Sympathetic Nervous System Activation

Sustained stress signalling elevates vascular tone, renin–angiotensin activity, and sodium retention — contributing to persistent BP elevation
(Grassi et al., Journal of Hypertension, 2015)

3. Breathing, Airway & Nitric Oxide Availability

The nasal airway is a major source of nitric oxide (NO), a critical regulator of vascular tone and endothelial health
(Lundberg & Weitzberg, Free Radical Biology & Medicine)

Mouth breathing, sleep apnoea, and poor nasal airflow reduce effective NO signalling and are independently associated with hypertension.

4. Oral Microbiome Disruption

Oral bacteria play an essential role in the nitrate → nitrite → nitric oxide pathway.
Several trials show that antiseptic mouthwashes impair this pathway and can modestly raise blood pressure in some individuals, though findings vary by population and product
(Kapil et al., American Journal of Hypertension; Woessner et al., Nitric Oxide, 2016)

5. Mineral & Electrolyte Insufficiency

Higher potassium intake consistently lowers blood pressure in meta-analyses of randomised trials, particularly in salt-sensitive individuals
(Filippini et al., European Heart Journal, 2020)

Magnesium supplementation shows modest BP-lowering effects, especially where deficiency exists
(Zhang et al., Hypertension, 2016)

6. Metabolic Instability & Insulin Resistance

Hyperinsulinaemia increases renal sodium retention and sympathetic activity, linking blood sugar dysregulation to hypertension
(Reaven, Diabetes Care)

7. Renal Load & Fluid Regulation

Kidney function, sodium handling, and pressure–natriuresis remain central to long-term BP regulation
(Guyton, Circulation)

Nitric oxide is a key signalling molecule governing:

• vascular dilation

• arterial compliance

• endothelial health

• blood pressure regulation

Research demonstrates that:

• The nasal passages produce NO continuously

• Humming markedly increases nasal NO output (≈15-fold in classic studies)

• Oral bacteria are required for dietary nitrate conversion to NO

(Lundberg et al., American Journal of Respiratory and Critical Care Medicine)

This provides a plausible mechanistic link between:

• mouth breathing

• sleep apnoea

• poor oral health

and elevated blood pressure.

Regular physical activity is one of the most effective non-pharmacological tools for reducing blood pressure and cardiovascular risk.

However, physiology follows a Goldilocks principle.

In dysregulated individuals, excessive intensity, volume, or poor recovery can increase sympathetic load, impair sleep, and blunt expected BP benefits.

Evidence supports tailoring exercise to:

• recovery capacity

• autonomic balance

• metabolic status

rather than assuming “more is always better”
(Pescatello et al., Hypertension, 2015)

Antihypertensive medications:

• reduce cardiovascular events

• save lives

• are often necessary

They do not, however, correct upstream drivers such as sleep apnoea, insulin resistance, mineral insufficiency, or autonomic dysregulation.

If blood pressure rises when medication is reduced or stopped (under medical supervision), this is physiological feedback, not personal failure — indicating unresolved regulatory load.

(Abrupt withdrawal of some medications can cause rebound hypertension and must be supervised.)

Blood pressure improves most reliably when the body is:

• well-rested and circadian-aligned

• adequately nourished

• metabolically stable

• well-oxygenated

• neurologically regulated

• supported in recovery

In this context, blood pressure normalisation becomes a by-product of restored regulation, not a forced outcome.

I do not treat blood pressure as an isolated number.

I treat the system that is asking for higher pressure.

This approach is informed by:

• functional blood chemistry analysis

• vascular and autonomic physiology

• systems-based clinical reasoning

• pattern recognition across 30+ years of practice

• continuing professional development and advanced training in cellular and metabolic health

Christopher Pickard, DC
Functional Nutritionist | Health & Performance Coach

• 30+ years clinical experience

• Specialist focus on blood pressure and cardiometabolic regulation

• Host of weekly educational blood pressure webinars

• Featured guest on The Energy Blueprint podcast with Ari Whitten

Free education, webinars, and resources available at:
https://www.beatbloodpressure.com

https://www.thepainreliefcentres.co.uk/

Book a consultation: https://stan.store/heroichealth/p/blood-pressure-consultation

1. Blood Pressure, Risk & Outcomes

1. Ettehad D, et al.
   Blood pressure lowering for prevention of cardiovascular disease and death: a systematic review and meta-analysis.
   The Lancet. 2016;387(10022):957–967.
   → Demonstrates reduced cardiovascular events and mortality with BP lowering across risk groups.

2. NICE Guideline NG136
   Hypertension in adults: diagnosis and management.
   National Institute for Health and Care Excellence (UK), updated regularly.
   → Confirms BP as a major modifiable risk factor while emphasising lifestyle and individualised care.

3. Whelton PK, et al.
   2017 ACC/AHA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults.
   Hypertension. 2018;71:e13–e115.
   → Global reference standard for BP thresholds, risk, and management.

2. Hypertension as a Systems & Vascular Disorder

4. Harrison DG, et al.
   Inflammation, immunity, and hypertension.
   Hypertension. 2021;77:1181–1196.
   → Details immune activation and vascular inflammation as central mechanisms.

5. Montezano AC, Touyz RM.
   Oxidative stress, Noxs, and hypertension.
   Hypertension. 2014;63:923–931.
   → Foundational work on oxidative stress and vascular dysfunction.

6. Carretero OA, Oparil S.
   Essential hypertension: Part I—definition and etiology.
   Circulation. 2000;101:329–335.
   → Classic overview of multifactorial drivers of hypertension.

3. Autonomic Nervous System & Stress Physiology

7. Grassi G, et al.
   Sympathetic neural mechanisms in human hypertension.
   Journal of Hypertension. 2015;33:197–206.
   → Demonstrates chronic sympathetic overactivity in hypertension.

8. Thayer JF, Lane RD.
   The role of vagal function in the risk for cardiovascular disease.
   Biological Psychology. 2007;74:224–242.
   → Links autonomic imbalance with cardiovascular risk.

4. Sleep, Circadian Rhythm & Obstructive Sleep Apnoea

9. Pepin JL, et al.
   Hypertension and sleep: overview of a tight relationship.
   Journal of Human Hypertension. 2024.
   → Modern synthesis of sleep disruption and BP regulation.

10. Somers VK, et al.
    Sleep apnea and cardiovascular disease.
    Journal of the American College of Cardiology. 2008;52:686–717.
    → Landmark paper linking OSA to hypertension mechanisms.

11. Morris CJ, et al.
    Circadian misalignment increases cardiovascular disease risk factors.
    Proceedings of the National Academy of Sciences (PNAS). 2016;113:E1402–E1411.
    → Experimental evidence for circadian disruption and cardiometabolic stress.

5. Nitric Oxide, Endothelial Function & Oral Microbiome

12. Lundberg JO, Weitzberg E.
    Nitric oxide signaling in health and disease.
    Free Radical Biology & Medicine. 2013;55:3–8.
    → Authoritative overview of NO biology.

13. Lundberg JO, et al.
    Humming increases nasal nitric oxide.
    American Journal of Respiratory and Critical Care Medicine. 2002;166:144–145.
    → Demonstrates ≈15-fold increase in nasal NO with humming.

14. Kapil V, et al.
    Physiological role for nitrate-reducing oral bacteria in blood pressure control.
    American Journal of Hypertension. 2013;26:1–8.
    → Establishes oral bacteria as essential for nitrate–NO BP effects.

15. Woessner M, et al.
    Effects of oral antiseptic rinses on blood pressure.
    Nitric Oxide. 2016;52:38–44.
    → Shows disruption of nitrate reduction; BP effects vary by context.

16. Bondonno CP, et al.
    Nitrate, nitric oxide, and cardiovascular health.
    Molecular Aspects of Medicine. 2018;61:83–91.
    → Reviews dietary nitrate and vascular outcomes.

6. Electrolytes & Nutrient Status

17. Filippini T, et al.
    Potassium intake and blood pressure: a dose–response meta-analysis.
    European Heart Journal. 2020;41:416–425.
    → Strong evidence for potassium’s BP-lowering effect.

18. Zhang X, et al.
    Effects of magnesium supplementation on blood pressure.
    Hypertension. 2016;68:324–333.
    → Meta-analysis showing modest BP reductions, strongest in deficiency.

7. Metabolic Health & Insulin Resistance

19. Reaven GM.
    Insulin resistance, hypertension, and coronary heart disease.
    Diabetes Care. 1991;14:195–202.
    → Foundational link between hyperinsulinaemia and BP regulation.

20. Ferrannini E, et al.
    Insulin resistance and blood pressure.
    Journal of Hypertension. 1997;15:1367–1374.

8. Renal Physiology & Long-Term BP Control

21. Guyton AC.
    Blood pressure control—special role of the kidneys and body fluids.
    Circulation. 1991;83:1043–1060.
    → Seminal work on pressure–natriuresis and kidney control of BP.

22. Hall JE, et al.
    Renal mechanisms of hypertension.
    Hypertension. 2015;65:123–130.

9. Exercise, Recovery & BP Regulation

23. Pescatello LS, et al.
    Exercise and hypertension.
    Hypertension. 2015;65:1003–1010.
    → Gold-standard review of exercise dose, intensity, and BP response.

24. Niebauer J, et al.
    Hypertension in athletes.
    European Journal of Preventive Cardiology. 2019;26:157–166.
    → Discusses complexity of BP in highly trained individuals.

10. Medication, Withdrawal & Deprescribing

25. Fares H, et al.
    Rebound hypertension and antihypertensive withdrawal.
    Journal of Clinical Hypertension. 2012;14:150–155.

26. Sheppard JP, et al.
    Withdrawal of antihypertensive medication in older people.
    JAMA Internal Medicine. 2020;180:542–551.
    → Demonstrates that some patients remain normotensive after supervised withdrawal.