Contributing Factors
Contributing factors are substances, contexts or conditions that have roles in the causation or promotion of hypertension.
Alcohol
- Alcohol, commonly known as ethanol or ethyl alcohol, is the intoxicating component found in varying concentrations in alcoholic beverages like beer, wine, and spirits.
- Alcohol consumption is a known contributor to hypertension
- Studies in both men and women have demonstrated that alcohol consumption increases blood pressure (Mori et al., 2015).
Key ways alcohol promotes hypertension include (Richardson, 2021):
- increases blood levels of renin – which
- increases blood vessel constriction
- decreases fluid output in the urine
- increases cortisol production – which stimulates the release of epinephrine and norepinephrine
- decreases baroreceptor sensitivity – results in a lack of blood vessel expansion to accommodate blood pressure increases
- increases the amount of calcium that binds to blood vessels – which makes them more prone to constrict
- decreases the hormone vasopressin – which causes the body to retain water
Caffeine
- Caffeine is compound in certain plants that has stimulant properties.
- Caffeine consumption has been shown to be associated with hypertension (Braverman, 1992).
Common sources of caffeine include:
- coffee
- tea (black, green)
- soft drinks
- energy drinks
- chocolate
- medications
Common symptoms of too much caffeine include (Greden, 1974):
- jitteriness
- irritability
- nervousness
- insomnia
- anxiety
Coffee, caffeine, and hypertension
- coffee consumption has been shown to be associated with increased systolic and diastolic blood pressure. A study by Jee et al., (1999) showed that on average, for every cup of coffee consumed, systolic pressure increased by 0.8 mm Hg and diastolic pressure by 0.5 mm Hg.
Key ways caffeine promotes hypertension include:
- depleting B vitamins, vitamin C, potassium, magnesium, calcium, and zinc (Scott, 2011) – nutrients known to be involved with blood pressure regulation
- blocking adenosine receptors
Caffeine and adenosine receptors
- Adenosine is a chemical compound in the body that relaxes and dilates blood vessels when it binds to adenosine receptors.
- Caffeine blocks adenosine receptors, resulting in an elevated level of circulating adenosine in the body. The increased amounts of adenosine contributes to hypertension by increasing (Supplements et al., 2014):
- sympathetic nervous system stimulation/input, which increases heart rate
- epinephrine and norepinephrine secretion – which intensifies force of contraction and excitability of the heart, and increases heart rate and blood vessel constriction
- the amount of resistance blood encounters as it flows through the arteries (peripheral resistance)
- renin secretion, triggering formation of angiotensin II, which increases blood volume and blood vessel constriction
Caffeine metabolism and hypertension
- Caffeine is metabolized (detoxified) by the liver
- The liver enzyme CYP1A2 metabolizes the majority of caffeine for excretion in the urine, however people having a genetic variant for the enzyme can have a slower rate of caffeine metabolism (Cornelis & El-Sohemy, 2007).
- A study by Palatini et al. demonstrated an increased risk of hypertension among slow caffeine metabolizers, and a decreased risk among fast metabolizers, as coffee consumption rose among both groups (Palatini et al., 2009).
Addressing caffeine consumption
- The blood pressure response to caffeine varies from one person to another.
- 400 mg a day is considered by the Food and Drug Administration to be safe for most people (“Caffeine’s Effects on Blood Sugar and Blood Pressure,” 2022).
- With existing hypertension it is recommended to (“Caffeine’s Effects on Blood Sugar and Blood Pressure,” 2022):
- limit caffeine intake to 200 mg per day
- consume away from activities that cause a natural increase in blood pressure (exercise, physical labour, stressful events),
- avoid it altogether
Amounts of caffeine in various drinks (Caffeine, n.d.):
- coffee (8 ounces) – 95–200 mg
- cola (12 ounces) – 35–45 mg
- energy drink (8-ounces) – 70–100 mg
- tea (8-ounces) – 14–60 mg
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)
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
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 (impeding of blood flow)
- increases 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 and a 54% increased risk of hypertension (Wang et al., 2017).
- Excessi nsulin 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
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)
- Data from 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
Lead and hypertension
Lead can promote hypertension by (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 damage to endothelial cells and vascular dysfunction
- inhibits endothelial tissue repair and repopulation Fujiwara et al. (26) via (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 promoted 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
- prostaglandins are signalling molecules with diverse and crucial roles in the human body
- prostaglandins 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.