Hypertension

Insufficient sodium intake and hypertension

“It was observed that a poor patient prognosis is associated with either a very high and a very low 24h urinary sodium excretion. This relationship does not depend on BP, aging, diabetes, chronic kidney disease, or cardiovascular disease” (Grillo et al., 2019).

Multiple studies have found that lowering salt intake (Graudal et al., 2020):

• triggers the body’s sodium-conserving hormones (renin and aldosterone)
• raises stress hormones (adrenaline and noradrenaline)
• elevates blood lipids such as cholesterol and triglycerides.
• is linked to a higher risk of death.

Too low sodium intake can promote hypertension by:

• activating hormonal and sympathetic responses – which increases cardiovascular stress (Kong et al., 2016)
• triggering the RAAS – which leads to vasoconstriction and fluid retention (Judge & O’Donnell, 2021)
• increasing norepinephrine levels – which elevates heart rate and vascular resistance (Kong et al., 2016)
• raising fasting insulin levels and reducing insulin sensitivity – which by causes sodium retention, activates stress responses, and impairs vascular function (DiNicolantonio & O’Keefe, 2023)

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2. Ratio of sodium and potassium

The sodium to potassium ratio

• The sodium-potassium ratio is the amount of sodium compared to potassium.
• The ideal ratio of sodium to potassium in the body for good health is generally considered to be around 1:2 or 1:3, meaning that potassium intake should be approximately double to triple that of sodium intake.
• Most people consume too much sodium relative to potassium from their diet (Woodruff, 2020).

Sodium to potassium ratio and hypertension

• A high sodium-to-potassium ratio is a stronger predictor of hypertension than either sodium or potassium levels alone (Perez & Chang, 2014).
• The high ratio exacerbates the adverse effects of sodium on blood pressure while diminishing the protective benefits of potassium (Perez & Chang, 2014).

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3. Sodium sensitivity

Sodium sensitivity
“Sodium-sensitive” people are those whose blood pressure rises more than average in response to higher sodium intake.

Key causes of sodium sensitivity include (Frame & Wainford, 2017; Kim, 2024):

• impaired kidney sodium excretion – due to genetic differences, reduced nephron number, age-related decline, or kidney damage
• dysregulated renin–angiotensin–aldosterone system (RAAS) – as a result of genetic variants, altered receptor sensitivity, low renin activity, or neurohormonal imbalances
• vascular and endothelial dysfunction – including reduced nitric oxide production, which impairs vasodilation and sodium excretion
• genetic variants affecting kidney function, RAAS components, sodium transporters/channels, and vascular regulation

Addressing sodium sensitivity
Sodium sensitivity can be at least partially reversed or improved with targeted nutrition, lifestyle changes, and other interventions.

Addressing sodium excess or deficiency

How much sodium/salt?

• Conventional medical advice is to limiting sodium intake to ≤2,300 mg/day, which is the equivalent of a little less than a teaspoon of salt.
• However, Mente et al. (2021) reported in their review that adverse health risks rise when daily total sodium intake is below 3,000 mg and above 5,000 mg. These amounts are the equivalent of 1.5 teaspoons and 2.5 teaspoons of salt.

• Steps to reduce sodium excess and an elevated sodium to potassium ratio include:

  • increase potassium intake by consuming fresh vegetables and fruit
  • ensuring proper hydration – the standard recommendation for daily water intake is about 8–10 cups (2–2.5 litres) for most adults. This includes water from all beverages and food
  • avoid processed foods that are high in sodium

Steps to ensure adequate sodium/salt

• avoid processed foods that are high in sodium
• use a good-quality salt
• drink water with a pinch of salt (for sodium) and a little lemon juice (for potassium)
• salt meals to taste

Good types of salt to use:

• Himalayan pink salt
• Celtic sea salt (greyish colour)
• Sea salt

Minimize use of refined table salt as it is highly processed, has reduced trace minerals, and often contains anti-caking agents.

Diets that can support acceptable sodium consumption include:

• DASH diet
• Mediterranean diet
• Low carbohydrate diets (e.g. ketogenic)
• Paleolithic (Paleo) Diet
• any whole-food-based diet

Stress

• Stress is the body’s natural reaction to changes or challenges.
• The stress response is a complex, adaptive mechanism that helps the body cope with immediate threats, preparing for “fight-or-flight”.
• While beneficial in short bursts, prolonged activation of the stress response can lead to negative health effects such as cardiovascular disease, chronic inflammation, and weakened immune function.
• A repeated or prolonged activation of the stress response can cause damage to the blood vessels, heart, and kidneys and may contribute to sustained elevations in blood pressure (Spruill, 2010; Stress and High Blood Pressure, n.d.).

Key ways stress promotes hypertension include:

• activating the sympathetic nervous system (SNS)
• stimulating the release of cortisol, epinephrine, and norepinephrine
• activating the renin-angiotensin-aldosterone system (RAAS)
• increasing sodium retention and fluid volume
• promoting unhealthy behaviour (such as poor diet, excessive alcohol consumption, smoking, and lack of physical activity)
• increasing body inflammation

Stress, epinephrine, and norepinephrine

• The sympathetic nervous system (SNS) responds to stress by secreting the hormones norepinephrine and epinephrine – which increase how fast and forcefully the heart beats and promote blood vessel constriction (Stress and High Blood Pressure, n.d.).

• A study by Inoue et al. (2021) found that elevated levels of the stress hormones norepinephrine, epinephrine, dopamine (and cortisol) in the urine were related to increased risk of hypertension.

Stress and cortisol

• Elevated cortisol levels contribute to hypertension through several mechanisms, involving direct and indirect effects on the cardiovascular system, kidneys, and other regulatory pathways.
• Key ways cortisol can contribute to hypertension include:
  • enhancing the sensitivity of body tissues to epinephrine and norepinephrine (Barbot et al., 2019)
  • mimicking the effects of aldosterone – which increases sodium retention by the kidneys (Funder, 2017)
  • increasing the sensitivity of blood vessels to vasoconstrictors (Yang & Zhang, 2004)
  • impairing the function of the endothelium (the inner lining of blood vessels), reducing its ability to produce nitric oxide (Sher et al., 2020)
  • stimulating the renin-angiotensin-aldosterone system (RAAS)
  • contributing to insulin resistance – which is associated with an increase in blood pressure (Underwood & Adler, 2013)
  • promoting weight gain, particularly central obesity (Parvanova et al., 2024)
  • contributing to insulin resistance, which is associated with an increase in blood pressure (Underwood & Adler, 2013)

Addressing stress
Ensure adequate intake of stress-response-supporting nutrients including:

• B-vitamins (especially vitamin B6)
• vitamin C
• vitamin D
• magnesium
• zinc
• omega-3 fatty acids (e.g. fish oils)

Incorporate actions that help mitigate stress including (Understanding the Stress Response, 2011):

• physical activity
• deep abdominal breathing
• breathing, focus on a soothing word (such as peace or calm)
• visualization of tranquil scenes
• repetitive prayer
• yoga
• tai chi

Inflammation

Inflammation is the body’s immune response to injury, infection, or harmful stimuli.
It involves the activation of immune cells and the release of signalling molecules like cytokines.

Inflammation is a normal part of the body’s defense to injury or infection. However, inflammation is damaging when it occurs in healthy tissues or lasts too long (months or years).

Causes of chronic inflammation include (Inflammation, n.d.):

• environmental chemicals
• poor nutrition
• imbalanced microbiome
• sleep issues
• stress
• personal environment

Key ways inflammation promotes hypertension include:

• damaging the endothelium (the inner lining of blood vessels) – which reduces its ability to make nitric oxide (Drożdż et al., 2023)
• increasing the stiffness and thickness of the vascular walls (Rios et al., 2024)
• activating the RAAS – which increases angiotensin II, a potent vasoconstrictor, and aldosterone, which promotes sodium and water retention (Satou et al., 2018)
• generating reactive oxygen species (ROS) – which damages the endothelium, exacerbates NO depletion, and promotes vasoconstriction and vascular stiffness (Barrows et al., 2019)
• activating immune cells within the blood vessels – resulting in the release of pro-inflammatory cytokines and enzymes, perpetuating vascular inflammation (Zhang et al., 2023)
• stimulating the sympathetic nervous system – which promotes increased heart rate and vasoconstriction
• damaging the kidneys and impairing their ability to filter sodium effectively (Hao et al., 2024)

Adipose tissue and inflammation

• In conditions like obesity, inflamed adipose tissue releases pro-inflammatory cytokines such as TNF-α and IL-6 (Kern et al., 2001).
• These cytokines directly contribute to systemic inflammation and vascular dysfunction, promoting hypertension.

Insulin resistance

• Insulin is a hormone that regulates the use and storage of sugar and carbohydrates as well as fats and protein by the body.
• Increased levels of insulin have been found in patients with hypertension (Burke et al., 2001).

Insulin resistance

• Insulin resistance is the state in which the body’s cells become less responsive to the hormone insulin, resulting in:
  • increased insulin production by the pancreas
  • increased levels of insulin in the blood
  • increased blood sugar levels

Causes of insulin resistance include:

• diet high in carbohydrate and sugar
• multiple nutrient deficiencies including:
  • vitamin D, chromium, magnesium, and zinc
• increased amounts of body fat (insulin resistance can be diagnosed through blood tests, especially fasting plasma glucose, and glycated hemoglobin (HbA1c)).

Insulin resistance and hypertension

• Insulin resistance and elevated insulin promote hypertension by (Wang et al., 2017):
  • promoting sodium retention by the kidneys
  • enhancing sympathetic nervous system activity
  • causing endothelial dysfunction
  • increasing vascular and kidney resistance (impedes blood flow)
  • increasing systemic inflammation
• Elevated insulin is a marker of insulin resistance. A meta-analysis of eleven studies on insulin resistance and incidence of hypertension found that people with the highest fasting insulin had a 54% increased risk of hypertension (Wang et al., 2017).
• Excessive insulin has been shown to increase the amount of sodium reabsorbed by the kidneys (Tiwari et al., 2007) which can result in increased blood pressure (Sarafidis & Bakris, 2007).
• Insulin stimulates nitric oxide production. However, excess insulin, as seen in the context of insulin resistance, promotes factors that cause vasoconstriction.
• insulin resistance itself does not directly affect blood pressure, but the combined effects of insulin resistance – elevated blood sugar and blood lipids (fats and cholesterol) – can damage the kidneys and vascular system making hypertension worse (da Silva et al., 2020).

Addressing insulin resistance
Steps to decrease insulin resistance include:

• decreasing consumption of sugars and carbohydrates, for example:
  • high-sugar drinks, juices
  • bread, baked goods, pastries
  • potatoes and other starchy vegetables
  • rice
• increasing physical activity and moderate-intensity exercise
• reducing excess body fat – especially visceral fat

Homocysteine

What is homocysteine?

• Homocysteine is an amino acid that is produced in the body. It is made in the body by the metabolism of methionine as part of the methionine cycle.
• Homocysteine has important roles in metabolism, but in excess is harmful to the body.

Homocysteine levels are regulated by:

1. converting it to methionine
2. converting it into other molecules, like glutathione

Causes of elevated homocysteine include:

• deficiencies of vitamin B2, B6, folate, vitamin B12, choline, and betaine
• genetic issues (polymorphisms/SNPs) that affect methionine and folate cycle enzymes

Key ways elevated homocysteine promotes hypertension include:

• increasing production of reactive oxygen species (unstable molecules that react with other molecules), especially superoxide, which (Pushpakumar et al., 2014):
  • damage the endothelial cells that line the inside of blood vessels
  • promote vascular inflammation and stiffness
• decreasing available nitric oxide by (Zhang et al., 2000):
  • inactivating it through oxidative (loss of electron) reactions
  • inhibiting the enzyme nitric oxide synthase (the enzyme that makes nitric oxide)
• stimulating the proliferation of vascular smooth muscle cells causing thickening of arterial walls and narrowing of the arterial space (Yasar et al., 2021)
• increasing vascular inflammation (Yuan et al., 2023)
• increasing expression of adhesion molecules (special proteins on the surface of cells) on the inner lining of blood vessels), which cause increased white blood cell migration into the artery walls, resulting in (Pushpakumar et al., 2014):
  • chronic vascular inflammation
  • arterial damage and stiffness
• up-regulating angiotensin II activity which causes (Li et al., 2018):
  • vasoconstriction
  • sodium retention
  • sympathetic nervous system activation

Addressing elevated homocysteine

• Optimize the amounts of nutrients that regulate homocysteine levels:
  • B-vitamins, especially vitamin B2, vitamin B6, folate, vitamin B12
  • methyl donor molecules: choline, betaine, SAMe
  • minerals: zinc, magnesium
• Increase intake of leafy greens, legumes, and vegetables, eggs, fish, and meat.
• Reduce alcohol and coffee intake (if excessive).

Obesity

• Obesity is a complex chronic condition characterized by excessive accumulation of body fat.
• Key causes of obesity include:
  • excessive calorie intake, especially from sugar and carbohydrate foods
  • intake of poor-quality foods
  • physical inactivity
  • psychological factors like stress, emotional eating, and mental health disorders
  • some medical conditions like hypothyroidism
  • certain medications
  • genetics

Obesity and hypertension

• Multiple studies have demonstrated that excess weight is predictive of hypertension (Lobato et al., 2012) and that overweight and obesity are responsible for 65-75% of the risk of hypertension in various populations (da Silva et al., 2020).
• A study by (Aronow, 2017) found that the occurrence of hypertension in nearly 20,000 Canadians between the ages of 18 and 74 rose along with increases in body mass index.
• Results from the Cardiovascular Risk in Young Finns Study (Juhola et al., 2012) showed that the risk of hypertension in adulthood was increased 1.65 times by being overweight or being obese in childhood.

Key ways obesity promotes hypertension include:

• activating the sympathetic nervous system (SNS) – which leads to increased blood volume and blood vessel constriction (Rahmouni et al., 2005)
• triggering the renin angiotensin aldosterone system (RAAS) – which stimulates production of hormones angiotensin II and aldosterone, leading to increased sodium and water retention and blood vessel constriction (da Silva et al., 2020; Rahmouni et al., 2005)
• contributing to endothelial dysfunction – which results in blood vessel constriction and increased arterial pressure, and decreased availability and responsiveness of nitric oxide (Lobato et al., 2012)
• promoting kidney dysfunction – due to the accumulation of fat in and around these organs (da Silva et al., 2020; Rahmouni et al., 2005)
• promoting metabolic dysfunctions such as high insulin, and blood sugar, and insulin resistance – which contribute to inflammation and oxidative stress (da Silva et al., 2020)

Smoking

This webpage focuses on the effects of smoking cigarettes and cigars, but the information is also relevant for vaping and other forms of tobacco consumption.

Smoking is known to increase hypertension by various factors including:

• increasing oxidative stress
• causing inflammation
• increasing coagulation in the blood

Components from smoking that promote hypertension:

• nicotine
• cadmium
• carbon monoxide

Smoking and nicotine
Cigarette smoking:

• results in sympathetic neural arousal that lasts for 24 hours of the day (Benowitz et al., 2002)
• increases blood pressure and heart rate regardless of how it is acquired – for example smoking and chewing gum (Benowitz & Burbank, 2016)
  Nicotine:
• causes blood-vessel constriction (Braverman, 1992)
• causes the release of epinephrine and norepinephrine – which increase blood pressure by increasing the rate and force of heart beats (Benowitz & Burbank, 2016)

Smoking and cadmium

• Cigarettes contain cadmium, which is known to increase blood pressure (Aramjoo et al., 2022).

Smoking and inflammation (Benowitz & Burbank, 2016)

• Smoking causes chronic inflammation
• Chronic inflammation damages arterial vessels, promoting constriction and blood clotting – resulting in increased blood pressure (Benowitz & Burbank, 2016).

Smoking and oxidative stress
Oxidative stress is the condition in the body where the protective capacity of antioxidant molecules is exceeded by reactive oxygen species (free radicals).

• Smoking causes oxidative stress which damages endothelial cells. This damage (Benowitz & Burbank, 2016):
  • decreases nitric oxide production
  • depletes endogenous (made by the body) antioxidants
  • increases inflammation – which further depletes antioxidants
  • causes platelet activation – which increases the production of reactive oxygen species (free-radicals)
  • damages lipids (fatty compounds) in cell membranes – which promotes cell membrane dysfunction, and makes them less flexible

Smoking and carbon monoxide (Benowitz & Burbank, 2016)

• Cigarette smoke contains carbon monoxide.
• Carbon monoxide reduces oxygen-carrying capacity in the blood – which is compensated for by an increase in red blood cells.
• More red blood cells result in increased blood viscosity (“thicker blood”) – which is a contributor to hypertension.

Toxic metals

Cadmium

• Cadmium is a metal that occurs naturally and persists as an environmental toxicant (Aramjoo et al., 2022).
• Toxic metals bind tissues and interfere with the functions of essential minerals (Sears, 2018).
• Cadmium can accumulate in the liver, kidneys, and central nervous system (CNS) and can contribute to high blood pressure (Aramjoo et al., 2022).

Effects of cadmium exposure can include (Aramjoo et al., 2022; Biersner, n.d.):

• cardiovascular issues, including hypertension
• kidney damage (renal tubular damage)
• kidney stones
• pulmonary edema
• skeletal damage from bone demineralization
• pulmonary emphysema
• upper respiratory tract irritation
• lung cancer
• prostate cancer

Sources of cadmium exposure include (Aramjoo et al., 2022):

• cigarettes
• dietary (wheat, potato, rice, leafy vegetables, cereal crops – in large amounts)
• drinking water
• soil
• air pollution

Cadmium and hypertension

• Blood and hair levels of cadmium have been shown to be correlated with high blood pressure has been shown in both males and females (Aramjoo et al., 2022).
• Key ways cadmium promotes hypertension include:
  • increasing oxidative stress and inflammation
  • increasing levels of epinephrine and norepinephrine
  • damaging the smooth muscle lining the arteries
  • affecting kidney function
  • disrupting calcium signalling
• It has been demonstrated that cadmium activates inflammation and oxidative stress in the body, which can lead to (Gökalp et al. 2009; Aramjoo et al., 2022):
  • endothelial dysfunction
  • decreased availability of nitric oxide
  • increased blood vessel constriction

Cadmium, epinephrine, and norepinephrine

• Cadmium and other heavy metals inactivate the enzyme catechol-O-methyltransferase (COMT), which increases levels of epinephrine and norepinephrine (Houston, 2007).
• Epinephrine and norepinephrine increase blood pressure by increasing the rate and force of heart beats (Benowitz & Burbank, 2016).
• Cadmium increases the half-life of noradrenaline in vascular smooth muscle tissue (da Cunha Martins et al., 2018).

Other effects of cadmium that promote hypertension

• damaging vascular smooth muscle cells (da Cunha Martins et al., 2018)
• affecting kidney function through its interference with the renin-angiotensin system (Júnior et al. 2020; Aramjoo et al., 2022)
• disrupting calcium equilibrium, and affecting blood vessel responses to calcium signalling (Biagioli et al. 2008; Aramjoo et al., 2022)

Lead

• Lead is a naturally occurring toxic metal which is a pervasive environmental toxin.
• An abundance of research has shown a connection between chronic lead exposure and increased blood pressure (Vaziri, 2008).
• A study of data from the National Health Nutrition and Examination Survey (NHANES 1999–2016) by Tsoi et al. (2021), showed increased levels of lead in the blood were associated with increased risk of hypertension.

Sources of lead exposure

• Lead exposure via water, soil, and other sources remains a worldwide health concern (Nigg et al., 2008).

Common sources of lead exposure (Common Sources of Lead, n.d.; Campbell, 1995):

• lead-based paint
• children’s toys and jewelry
• mini blinds
• imported candy
• lead water pipes
• drinking water
• newsprint
• organ meats
• tobacco
• cosmetics
• workplace and hobby hazards
• traditional home remedies and cosmetics
• lead-glazed ceramic ware, pottery and leaded crystal
• contaminated soil
• car batteries
• leaded gas (which may persist in the environment still) (Eschner, 2016)

Lead absorption and release

• After lead is absorbed, it is distributed in the blood, bone, and soft tissues of the body (Vaziri, 2008).
• The majority of lead is stored in the bone where it persists over time (Vaziri, 2008).
• The gradual release of lead from bone can be a continued source of toxicity. The rate at which lead is released from the bone is increased in conditions such as, pregnancy, lactation, peri-menopause, menopause, osteoporosis, and hyperthyroidism, with which there is an intensified loss or turnover of bone (Vaziri, 2008; Nash et al., 2003).

Lead exposure can be identified by:

• 24-hour urine challenge test using a chelating compound
• hair mineral/toxic metal analysis
• lead blood tests

Key ways lead promotes hypertension include (Tsoi et al., 2021; Vaziri, 2008):

• increasing oxidative stress – which leads to reduced availability of nitric oxide (a molecule that signals blood vessels to relax) and increased inflammation
• promoting inflammation – which results in damage to endothelial tissue and causes vascular dysfunction (Vaziri, 2008)
• enhancing sympathetic nervous system activity – which promotes blood vessel constriction and causes the heart to beat faster and more forcefully (Nash et al., 2003)
• impacting blood pressure regulation by the renin angiotensin aldosterone system (RAAS) – which leads to increased blood volume and blood vessel constriction (Nash et al., 2003)
• increasing production of prostaglandins (signalling molecules) – which promote  blood vessel constriction
• increasing production and activity of endothelin (a peptide hormone) – which promotes blood vessel constriction and increased arterial pressure
• displacing calcium in pathways that regulate contraction of arterial smooth muscle cells – which can lead to excessive contraction and vasoconstrictions

Lead and endothelial dysfunction (Tsoi et al., 2021):

• increases oxidative stress
• activates nuclear factor-κB and causes inflammation that damages endothelial cells and causes vascular dysfunction
• inhibits endothelial tissue repair and repopulation (Vaziri, 2008)

Lead and calcium

• Lead competes with calcium for utilization in the body.
• Elevated lead levels result in changes in cellular calcium levels that result in increased vascular resistance by altering contractile activity in the walls of small arteries and arterioles (Tsoi et al., 2021).

Lead and oxidative stress

• Lead promotes oxidative stress by chemical processes that involve the generation of highly reactive oxygen species (free radicals). Key reactions involved include (Vaziri, 2008):
  • the Fenton reaction
  • the Haber-Weiss Reaction

Lead and prostaglandins

• Prostaglandins:
  • are signalling molecules with diverse and crucial roles in the human body
  • often act as mediators of inflammation and homeostasis (self-regulating processes in the body)
• Lead is known to (Vaziri, 2008):
  • increase production of prostaglandins that increase vasoconstriction
  • lower production of prostaglandins that promote vasodilation

Addressing toxic metal accumulation

• Environmental and dietary sources of toxic metal exposures need to be identified and removed as much as possible.
• Many patients will improve with a basic protocol of a healthy diet, supplementation of essential nutrients, exercise, and rest.
• Sweating from exercise or sauna can also help remove toxic metals (Sears, 2018).
• It is important to work with a practitioner that is trained in detoxification when addressing excessive or chronic heavy metal exposure or accumulation.