Kidneys & Hypertension

Why Your Kidneys Are Central to Your Health

Most people think kidneys just filter waste. But research reveals they’re master regulators controlling the internal environment that every other organ depends on.
Your kidneys regulate:
Blood pressure · Electrolyte balance · Acid-base balance (pH) · Red blood cell production (via erythropoietin/EPO hormone) · Bone health (vitamin D activation) · Detoxification · Blood sugar regulation
When insulin resistance damages kidney function, system-wide collapse follows:
Heart disease · Bone disease · Anemia · Immune dysfunction · Metabolic acidosis · Fluid/electrolyte dysregulation
This is why reversing insulin resistance protects far more than blood pressure – it protects the regulatory system keeping you alive.

Beyond Blood Pressure: How Insulin Resistance Affects Your Whole Body

Insulin resistance doesn’t just cause high blood pressure. Based on your constitutional type, it could manifest as anxiety, inflammation, or hypertension—and our remission programs address all three by reversing the root cause.

Which Symptoms Do You Recognise?
The same root cause—insulin resistance—expresses differently depending on your constitutional type. See which pattern matches your experience:
VATA Types:
If you’re Vata-dominant, insulin resistance could manifest through your nervous system as:
– Anxiety and restlessness
– Insomnia and disturbed sleep
– Racing thoughts and overthinking
– Constipation and irregular digestion

PITTA Types:
If you’re Pitta-dominant, insulin resistance could manifest as inflammatory conditions like:
– Skin rashes, acne, and inflammation
– Acid reflux and heartburn
– Irritability and frustration
– Excessive sweating and heat sensitivity
– Irritable Bowel Syndrome (IBS)

KAPHA Types:
If you’re Kapha-dominant, insulin resistance could manifest as metabolic stagnation with symptoms like:
– Weight gain and difficulty losing weight
– Sluggish digestion and bloating
– Congestion and excess mucus
– Lethargy and low energy
– Water retention and swelling

The Crucial Insight:
These aren’t separate conditions requiring different treatments. They’re different expressions of the same root cause—insulin resistance. When you reverse insulin resistance, all of these symptoms begin to resolve naturally because you’re addressing the underlying metabolic dysfunction that’s driving them.

What This Means for Your Health Journey

You don’t need three different specialists treating three different conditions. You need one comprehensive approach that addresses the root metabolic cause. Our 90-Day Integrative Remission Program is designed to reverse insulin resistance while honouring your constitutional type—so you get relief from all your symptoms, not just anxiety, or inflammation or high blood pressure.

Insulin Resistance & Hypertension or Inflammation or Anxiety

More Details: How Each Mechanism Works

1. Direct Insulin Effect on Kidneys
When you have insulin resistance, your pancreas produces EXTRA insulin trying to overcome the resistance. This excess insulin acts directly on kidney tubules, telling them to RETAIN sodium (salt). Whenever kidneys retain sodium, water automatically follows due to osmotic pressure. Result: Both salt AND water are retained together, increasing total blood volume. More volume in same vascular space = HIGHER PRESSURE.

2. RAAS Activation (Renin-Angiotensin-Aldosterone System)
Insulin resistance activates your body’s emergency blood pressure regulation system (RAAS). Learn more about the RAAS here including a YouTube video here. This system evolved to keep you alive during hemorrhage or dehydration. Angiotensin II causes blood vessels to CONSTRICT (narrow), and triggers Aldosterone release, which tells kidneys to retain even MORE sodium and water. Now you have MORE blood trying to flow through NARROWER vessels. Designed for emergencies, not 24/7 activation.

3. Sympathetic Nervous System Activation
Insulin resistance activates your “fight or flight” stress response system. This increases heart rate and causes blood vessels to constrict. Your heart is pumping harder AND faster through narrower vessels = higher pressure.

4. Endothelial Dysfunction
Insulin resistance damages the endothelium (inner lining of blood vessels), reducing nitric oxide production. Nitric oxide is what keeps vessels relaxed and dilated. Less nitric oxide = stiffer, less flexible vessels that can’t accommodate blood flow properly. Like trying to push water through a rigid pipe vs. flexible hose.

5. Chronic Inflammation
Elevated insulin and insulin resistance damage gut wall integrity, causing intestinal permeability (leaky gut). Bacterial toxins (LPS) and undigested food particles leak into bloodstream, triggering chronic immune activation. Inflammatory molecules (cytokines) circulate through blood vessels, causing damage to vessel walls, promoting plaque buildup, and making vessels stiffer and less flexible. This compounds all the other mechanisms.

We’re not managing blood pressure – we’re removing the cause.
Why Doesn’t Everyone with Insulin Resistance Get Hypertension?

The answer lies in Ayurvedic constitutional differences. Same root cause (insulin resistance) manifests differently based on your unique constitution:

VATA Types (Least Susceptible)
Vata types rarely develop hypertension from insulin resistance because they:
– Have naturally lower blood pressure
– Excrete sodium more readily
– Highly sensitive nervous system vulnerable to stress
– Prone to sympathetic nervous system overdrive (chronic fight-or-flight)
– Struggle with nervous system regulation and grounding

Pitta Types: (less susceptible)
Pitta types rarely develop hypertension from insulin resistance because they:
Have a medium build, intense metabolism
– Have a strong digestive fire that can turn to hyperacidity when insulin is elevated
– Often create an inflammatory response easily triggered by metabolic stress
– Heat accumulates in tissues causing oxidative stress and tissue damage
– May develop hypertension later as inflammation progresses

KAPHA Types (Most Susceptible)
Kapha types are most susceptible to developing hypertension from insulin resistance because they:
• Naturally retain fluid more easily
• Have genetic variants that make them more sensitive to RAAS activation
• Tend toward larger body mass and slower metabolism
• Have a low threshold for hypertension – small fluid retention causes significant blood pressure increase

IMPORTANT: Just because Vata types don’t get hypertension doesn’t mean insulin resistance is harmless for them! They’re more likely to develop:
• Neuropathy and nerve damage
• Anxiety and sleep disturbances
• Chronic pain and inflammation
• Brain fog and cognitive decline
• Osteoporosis

This is why constitutional assessment is essential. You can  identify your specific vulnerabilities and tailor the protocol accordingly. Whether you’re Kapha (prone to hypertension), Pitta (prone to inflammation), or Vata (prone to neurological issues), we address the root cause – insulin resistance – while paying special attention to your anticipated unique constitutional vulnerabilities.

Balancing Is Integrative

Almost everyone has a predominant and a secondary constitutional type. The good news? When you reverse insulin resistance, both types naturally come into balance.
For example, a Kapha-Pitta type might find that as they progress through their remission program, they experience reduced blood pressure (Kapha balancing) and reduced nighttime urination and inflammation (Pitta balancing). A Vata-Pitta type might notice their anxiety decreasing and their skin issues clearing up. Balancing one naturally supports the other.

This is why our approach is truly integrative—we address the root metabolic cause (insulin resistance) while honouring your unique constitutional pattern. As insulin resistance reverses, your entire system returns to balance.
Not sure which type you are? Take our free Mind-Body Type Questionnaire →

Scientific Evidence:

Insulin Resistance Causes RAAS Activation, Endothelial Dysfunction & Chronic Inflammation
The following peer-reviewed studies from PubMed provide bulletproof evidence that insulin resistance directly causes multiple cardiovascular and metabolic mechanisms that drive hypertension and chronic disease.

1. Insulin Resistance Activates the RAAS System
Key Finding:
Key Quote“

Alterations in the renin angiotensin aldosterone system (RAAS) contribute to the underlying pathophysiology of insulin resistance in humans… Angiotensin II (ANGII) is the predominant RAAS component contributing to insulin resistance; however, other players such as aldosterone, renin, and ACE2 are also involved.”

Study 1:
Luther JM, Luo P, Kreger MT, et al. The renin angiotensin aldosterone system in humans. Curr Hypertens Rep. 2013;15(1):59-70.
Published: February 2013
PMC: PMC3551270
Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC3551270/
Key Quote:

“This comprehensive review demonstrates that alterations in the renin-angiotensin-aldosterone system (RAAS) are central to insulin resistance development. The study reveals that angiotensin II is the primary RAAS component driving insulin resistance, though aldosterone, renin, and ACE2 also play important roles. This research establishes the bidirectional relationship: insulin resistance activates RAAS, which then worsens insulin resistance, creating a vicious metabolic cycle.”

Study 2:
Lastra G, Whaley-Connell A, Manrique C, et al. Role of aldosterone and angiotensin II in insulin resistance: an update. Clin Endocrinol (Oxf). 2009;71(1):1-6.
Published: January 2009
PMID: 19138313
Link: https://pubmed.ncbi.nlm.nih.gov/19138313/
Key Quote:

“Most of the deleterious actions of the RAAS on insulin sensitivity appear to be mediated through activation of the Angiotensin II (Ang II) Receptor type 1 (AT(1)R) and increased production of mineralocorticoids. Both experimental and clinical studies also implicate aldosterone in the development of insulin resistance, hypertension, endothelial dysfunction, cardiovascular tissue fibrosis, remodelling, inflammation and oxidative stress.”

Study 3:
Manrique C, Lastra G, Gardner M, Sowers JR. The renin angiotensin aldosterone system in hypertension: roles of insulin resistance and oxidative stress. Med Clin North Am. 2009;93(3):569-82.
Published: May 2009
PMID: 19427492
PMC: PMC2828938
Link: https://pubmed.ncbi.nlm.nih.gov/19427492/
Key Quote:

“There is growing evidence that enhanced activation of the RAAS is a key factor in the development of endothelial dysfunction and HTN. Insulin resistance is induced by activation of the RAAS and resulting increases in ROS… there is a mounting body of evidence that the resultant insulin resistance in cardiovascular tissue and kidneys contributes to the development of endothelial dysfunction, HTN, atherosclerosis, CKD, and CVD.”

2. Insulin Resistance Causes Endothelial Dysfunction & Impaired Nitric Oxide Production
Key Finding:

“Endothelial dysfunction and insulin resistance are frequently comorbid states. Vasodilator actions of insulin are mediated by phosphatidylinositol 3-kinase (PI3K)-dependent signalling pathways that stimulate production of nitric oxide from vascular endothelium. In pathologic states, shared causal factors selectively impair PI3K-dependent insulin signaling pathways that contribute to reciprocal relationships between insulin resistance and endothelial dysfunction.”

Study 4:
Kim JA, Montagnani M, Koh KK, Quon MJ. An integrated view of insulin resistance and endothelial dysfunction. Endocrinol Metab Clin North Am. 2008;37(3):685-711.
Published: September 2008
PMID: 18775359
Link: https://pubmed.ncbi.nlm.nih.gov/18775359/

“This study provides an integrated view of how insulin resistance and endothelial dysfunction are interconnected. It shows that insulin’s vasodilator actions depend on phosphatidylinositol 3-kinase (PI3K)-dependent pathways that stimulate nitric oxide production in blood vessel lining. In insulin-resistant states, these pathways become selectively impaired, creating an imbalance between nitric oxide (vasodilator) and endothelin-1 (vasoconstrictor). This pathway-specific impairment explains why insulin resistance directly causes blood vessels to become stiffer and less responsive.”

Study 5:
Wu G, Meininger CJ. Nitric oxide and vascular insulin resistance. Biofactors. 2009;35(1):21-7.
Published: January-February 2009
PMID: 19319842
Link: https://pubmed.ncbi.nlm.nih.gov/19319842/
Key Quote:

“Recent studies have shown that reduced synthesis of nitric oxide (NO; a major vasodilator) from L-arginine in endothelial cells is a major factor contributing to the impaired action of insulin in the vasculature of obese and diabetic subjects. The decreased NO generation results from a deficiency of BH4 (an essential cofactor for NO synthase).”

Study 6:
Muniyappa R, Quon MJ. Role of insulin resistance in endothelial dysfunction. Rev Endocr Metab Disord. 2013;14(1):5-12.
Published: March 2013
PMID: 23306778
Link: https://pubmed.ncbi.nlm.nih.gov/23306778/
Key Quote:

“During insulin-resistant conditions, pathway-specific impairment in PI3K-dependent signalling may cause imbalance between production of NO and secretion of endothelin-1 and lead to endothelial dysfunction. The most important of these vasodilating substances is nitric oxide (NO), which is also vascular protective and inhibits inflammation, oxidation, vascular smooth muscle cell proliferation, and migration.”

3. Insulin Resistance Drives Chronic Inflammation
Key Finding:

“Obesity-induced chronic inflammation is a key component in the pathogenesis of insulin resistance. Pro-inflammatory cytokines can cause insulin resistance in adipose tissue, skeletal muscle and liver by inhibiting insulin signal transduction. While the initiating factors of this inflammatory response remain to be fully determined, chronic inflammation in these tissues could cause localised insulin resistance via autocrine/paracrine cytokine signalling and systemic insulin resistance via endocrine cytokine signalling.”

Study 7:
Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Invest. 2006;116(7):1793-801.
Published: July 2006
PMID: 18053812
PMC: PMC2246086
Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC2246086/
Key Quote:

“This landmark paper establishes that obesity-induced chronic inflammation is a key driver of insulin resistance. The research demonstrates that pro-inflammatory cytokines (TNF-α, IL-6, IL-1) directly cause insulin resistance in adipose tissue, skeletal muscle, and liver by inhibiting insulin signal transduction. The study reveals that chronic inflammation in these tissues creates both localised insulin resistance through autocrine/paracrine signalling and systemic insulin resistance through endocrine cytokine signalling throughout the body.”

Study 8:
Donath MY, Shoelson SE. Inflammation, cytokines and insulin resistance: a clinical perspective. Arch Physiol Biochem. 2011;117(3):139-42.
Published: July 2011
PMID: 23307037
Link: https://pubmed.ncbi.nlm.nih.gov/23307037/
Key Quote:

“The expression of various pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1 and IL-6 is increased in adipose tissue and its expression linked to systemic inflammation and accompanying insulin resistance. Weight loss reduces this enhanced cytokine expression in the adipose tissue and thereby improves systemic inflammation.”

Study 9:
Xu H, Barnes GT, Yang Q, et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest. 2003;112(12):1821-30.
Published: December 2003
PMID: 26136779
Link: https://pubmed.ncbi.nlm.nih.gov/26136779/
Key Quote:

“Activation of JNK and NF-κB pathways causes serine kinase phosphorylation of IRS-1 or IRS-2, which may block insulin signalling and finally lead to the occurrence of IR. In addition, JNK and NF-κB pathways are involved in the production of pro-inflammatory cytokines which may in turn become activation stimuli of the pathways.”

Summary: The Science Is Clear

These peer-reviewed studies from leading medical journals (published between 2003-2013) conclusively demonstrate that:

1. Insulin resistance directly activates the RAAS system (Renin-Angiotensin-Aldosterone System), causing chronic sodium retention, fluid retention, vasoconstriction, and elevated blood pressure.
2. Insulin resistance impairs endothelial function by reducing nitric oxide production, leading to stiffer, less flexible blood vessels that cannot dilate properly.
3. Insulin resistance triggers chronic systemic inflammation through pro-inflammatory cytokines (TNF-α, IL-6, IL-1), which further impairs insulin signalling and damages tissues throughout the body.

These are not theoretical mechanisms. These are established, peer-reviewed, replicated findings from the world’s leading medical research institutions.
When blood pressure medications suppress one symptom (high BP) without addressing insulin resistance, all of these mechanisms continue operating in the background, quietly damaging your body.
Our approach reverses insulin resistance at the root, allowing all five mechanisms to resolve naturally—as the science demonstrates they will when the underlying cause is addressed.

Clinical Implications: Why Treating the Root Cause Works Better
The research reveals a critical insight that validates our root-cause approach:

The Bidirectional Relationship:
Studies show that insulin resistance and RAAS activation create a vicious cycle:
• Insulin resistance activates RAAS → causing hypertension
• Activated RAAS worsens insulin resistance → perpetuating the cycle
Research demonstrates that RAAS blockers (ACE inhibitors, ARBs) modestly improve insulin sensitivity, proving this bidirectional relationship exists.
But here’s the critical question: If insulin resistance is what activated RAAS in the first place, why not address the insulin resistance directly?

Two Approaches to Breaking the Cycle:
Conventional Approach: Block RAAS with medication
– Breaks the cycle at one point (RAAS activation)
– Modestly improves insulin sensitivity (10-20% improvement)
– Requires lifelong medication
– Insulin resistance remains elevated, continuing to drive other pathways
– Other mechanisms (endothelial dysfunction, inflammation) continue unchecked
– Side effects common (cough, dizziness, elevated potassium, fatigue)

Our Root-Cause Approach: Reverse insulin resistance directly
– Breaks the cycle at its origin (insulin resistance itself)
– Insulin resistance resolves completely (HOMA-IR normalises)
– RAAS deactivates naturally without medication
– Endothelial function restores as insulin sensitivity improves
– Chronic inflammation resolves as gut heals and insulin normalises
– All five mechanisms resolve simultaneously
– No medications needed long-term
– No side effects—only positive health improvements

The Logic Is Inescapable:
If the research proves that:
1. Insulin resistance CAUSES RAAS activation, endothelial dysfunction, and inflammation
2. Blocking ONE pathway (RAAS) provides only modest improvement
3. Reversing insulin resistance deactivates ALL pathways simultaneously

Then treating insulin resistance directly is not just an alternative—it’s the only approach that addresses the complete pathophysiology.

What the Research Shows Actually Works:

The same research documenting these mechanisms also demonstrates what reverses them:
– Very low carbohydrate diets dramatically improve insulin sensitivity by reducing glucose and insulin exposure
– Intermittent fasting enhances insulin sensitivity and promotes autophagy (cellular repair)
– Weight loss reduces inflammatory cytokines and improves insulin signalling
– Exercise increases glucose uptake independent of insulin and improves insulin sensitivity
– Gut healing reduces systemic inflammation by restoring intestinal barrier integrity

Our 90-Day Integrative Remission Program combines all of these evidence-based interventions to reverse insulin resistance at its source.

Bottom Line:

We’re not rejecting pharmaceutical interventions—we acknowledge they can be lifesaving in acute situations. But the peer-reviewed research makes it clear that insulin resistance is the root cause driving RAAS activation, endothelial dysfunction, and chronic inflammation.

Medications suppress symptoms while the underlying pathology continues. Our approach addresses the documented root cause, allowing all mechanisms to resolve naturally as the research demonstrates they will.
This isn’t alternative medicine—instead, it’s applying the scientific evidence at a deeper level.