Functional Nutrition Evaluation

ANTHROPOMETRICS:
BLOOD PRESSURE
Companion Guide

nsight.org

Version 14
Table of Contents

Determination of Blood Pressure

from the Functional Medicine
Perspective......................................3

Patient Positioning...........................3

Order of Exam..................................3

Clinical Exam Findings....................4

Clinical Considerations for

Modifiable Lifestyle Factors.............6

Orthostatic Hypotension................11

Functional Medicine
Matrix Model..................................13

Conclusion.....................................13

Acknowledgements.......................14

Blood Pressure References............14

Additional Resources.....................15

© 2018 The Institute for Functional Medicine

“Vascular aging parallels aging.” — M. Houston

Determination of Blood Pressure from the Functional Medicine Perspective

Blood pressure determination, part of the ABCDs of Functional Nutrition Evaluation allows the clinician to
consider the root causes of endothelial dysfunction associated with inflammation, immune dysfunction, and
oxidative stress imbalances. The correct determination of blood pressure and appropriate interventions can change
the trajectory of health and disease. A comprehensive program that includes diet and nutrition and optimal exercise
to influence healthful weight and body composition changes can decrease the 90-percent risk of developing
hypertension during a person’s lifetime.1

Equipment Needed
n Stethoscope with diaphragm and bell
n Blood pressure cuffs: pediatric, small, regular, and large adult, as well as thigh sizes
n Aneroid blood pressure gauge and cuffs
n Oscillatory blood pressure device and cuffs

n Oxygen saturation monitor

n Vascular doppler

Patient Positioning
Arm Blood Pressures: The patient should be seated in a chair with their feet on the ground and their back
supported. The clinician needs to have access to both arms. Blood pressure is taken with the arm forward, parallel
to the floor, and at the level of the heart, with the arm resting comfortably on a table. It is preferable to take two
readings, 1-2 minutes apart and then average the measurements to obtain the blood pressure.2,3
Leg Blood Pressures: The patient is prone, lying on the exam table with the legs supported (not hanging past
the end of the table) to check popliteal pressures, and then rotates to supine to check pressures of the lower leg by
auscultating the dorsalis pedis or the posterior tibial artery using the bell of the stethoscope or a vascular doppler.
Standing, Sitting, and Lying Blood Pressures and Pulse (Orthostatic Blood Pressure determination):
It may be necessary to obtain standing blood pressures to check for postural effects in older adults or those with
diabetes, autonomic dysfunction, or on antihypertensive medications.
Patient lies supine for at least 2 minutes before the blood pressure and pulse is recorded. Patient then transitions
to a seated position; after 2 minutes, blood pressure and pulse is taken. Patient then transitions to a standing
position; after 2 minutes the blood pressure and pulse is taken again. Any symptoms of dizziness, lightheadedness, or
palpitations should be noted.

Order of Exam
Exam Techniques and Methods
n Note that blood pressures can be affected by the patient drinking caffeine or alcohol, smoking or using smokeless
tobacco, and taking over the counter medications within 12 hours prior to taking the blood pressure.
n Before taking the reading, have patient sit for 5 minutes in a quiet comfortable environment, with the arms

free of restrictive clothing.

n Clinician should sit or stand to be at eye level with gauge. Use the appropriate cuff size for the patient

(20% wider than the diameter of the extremity). A new patient should have pressures checked in both arms
and both legs.

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Lying, Sitting, and Standing Bilateral Arm Pressures
n Determine the blood pressures in first the left arm then the right arm.
n Discrepancies in the systolic pressures should be no greater than 5 mm Hg.
Arm Pressures
n Place deflated cuff 2.5 cm above antecubital space. Ensure that fit is snug and firm around the arm with the
bladder over the brachial artery.
n Palpate brachial pulse. Rapidly inflate cuff until brachial pulse is no longer felt.

n Place bell of stethoscope over brachial artery location and inflate to 30 mm above pulse loss and then deflate at

a rate of 2–3 mm Hg/sec.

n Record systolic blood pressure at first Korotkoff sound and diastolic blood pressure at fifth Korotkoff sound.

n Repeat blood pressure on the other arm. Arm readings should not differ by more than 5 mm Hg.

n The arm with the higher of the two readings should be recorded in the chart and used when taking future

blood pressure readings.

n Elevated blood pressure readings in the office should be followed with blood pressure evaluations at home or

a 24-hour ambulatory blood pressure evaluation prior to starting medications. (This can help rule out possible
white coat hypertension when readings are taken in the office.)
Leg Pressures (the patient starts prone)
n Popliteal Pressures: Place thigh cuff above the popliteal fossa. After determining location of popliteal artery
pulse, follow the same procedure as for arm pressures to determine the mmHg.
n Ankle pressures are determined by placing the appropriate size cuff on the lower leg and after palpating the

dorsalis pedis pulse or the posterior tibial artery pulse then following the same procedure as for arm pressures.
Ankle/Arm Index (Ankle Brachial Index)
n The ankle/arm index equals the ankle pressure divided by the brachial artery pressure. Normal values are 1.0
or greater. An ankle/arm index of <0.9 has a sensitivity of 88% and specificity of 82%3 for peripheral vascular
disease. An elevated ankle brachial index is associated with stiffening of the soft tissues of the lower extremity;
seen in some diabetics or those with marked peripheral vessel atherosclerosis.

Clinical Exam Findings

An elevated blood pressure determination either in the clinic, at home, or with continuous ambulatory blood
pressure monitoring needs to be evaluated further. Normal and abnormal elevations in blood pressure are
highlighted in Table 1.
Co-morbidities and other risk factors help to further stratify risk. A person’s age, smoking history, pulse pressure,
dyslipidemia and blood pressure further increase the associated risk of elevated blood pressure and resultant organ
damage and influence the degree and aggressiveness of needed interventions (Table 1).
Abnormal Findings and Symptoms4–7
n Hypertension (see Table 1)
n Hypotension
n Transient dizziness—possibly due to hypovolemia (20 mm drop in systolic and diastolic pressure with an increase

in pulse of greater than 20 bpm), autonomic dysfunction (no increase in pulse from sitting to standing with
change in blood pressure and increased dizziness), baroreceptor dysfunction, or normo-pressure hydrocephalus.
Asymmetric measurement of blood pressures may suggest subclavian/brachial occlusion or steal syndrome. Marked
discrepancies between arm and leg pressures may suggest coarctation of the aorta. Greater than a 5 mmHg difference
in arm blood pressures is abnormal. Spinal cord injury, regional pain syndromes, or autonomic dysfunction can
impact the proximal/distal symmetry of blood pressures.

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Table 1: Blood Pressure (mmHg) Risk Assessment

Normal Prehypertension Grade 1 HTN Grade 2 HTN

Risk Factors SBP <120 and SBP 120 –129 and SBP 130 –139 or SBP ≥ 140 or
or Disease DBP <80 DBP <80 DBP 80-89 DBP ≥ 90

No Other Risk Average Risk; Low Added Risk; Moderate Added Risk; High Added Risk;
Factors No BP intervention Lifestyle changes, Lifestyle changes for Lifestyle changes
needed exercise and diet several months then and consider
interventions drug treatment if drug treatment
BP uncontrolled

1–2 Risk Factors Low Added Risk; Moderate Added Risk; High Added Risk; Very High Added Risk;
Lifestyle changes, Lifestyle changes for Lifestyle changes Lifestyle changes
exercise and diet several months then and consider drug and immediate
interventions drug treatment if treatment drug treatment
BP uncontrolled

>3 Risk Factors, Moderate Added Risk; High Added Risk; High Added Risk; Very High Added Risk;
Metabolic Lifestyle changes for Lifestyle changes Lifestyle changes Lifestyle changes
Syndrome or several months then and consider and consider and immediate
Other Disease drug treatment if drug treatment drug treatment drug treatment
BP uncontrolled

Diabetes Moderate Added Risk; High Added Risk; High Added Risk; Very High Added Risk;
Lifestyle changes for Lifestyle changes Lifestyle changes Lifestyle changes
several months then and consider and consider and immediate
drug treatment if drug treatment drug treatment drug treatment
BP uncontrolled

Established CV Very High Added Risk; Very High Added Risk; Very High Added Risk; Very High Added Risk;
or Renal Disease Lifestyle changes Lifestyle changes Lifestyle changes Lifestyle changes
and immediate and immediate and immediate and immediate
drug treatment drug treatment drug treatment drug treatment

*Adapted from the JNC6 risk stratification, JNC7 grade guidelines. For drug treatment interventions refer to JNC8 guidelines below.
BP = Blood pressure; DBP = diastolic blood pressure; SBP= systolic blood pressure; CV = cardiovascular; HTN = hypertension

Clinical Variables Influencing Prognosis (Risk Factors) Signs/Symptoms of Subclinical Organ Damage
1. Elevated Systolic or Diastolic Blood Pressures Influencing Prognosis
2. Age (>60) n Electrocardiogram showing left ventricular hypertrophy (LVH)
3. Race/Ethnicity
>38 mm
4. Smoking
n ECHO documented LVH (males >125 g/m2, females >110 g/m2)
5. Elevated Pulse Pressure in the elderly
n Carotid wall thickening (CIMT>0.9 mm) or plaque
6. Dyslipidemia
n Carotid-femoral pulse wave velocity >12 m/sec
n Total cholesterol >5.0 mmol/L (190 mg/dL)
n Ankle/Arm Index <0.9
n Low-density lipoprotein (LDL) >3.0 mmol/L
n Increase in plasma creatinine
(115 mg/dL)
n High-density lipoprotein (HDL): males <1.0 mmol/L Males: 115-133 mmol/L (1.3-1.5 mg/dL)
(40 mg/dL), females <1.2 mmol/L (46 mg/dL) Females: 107-124 mmol/L (1.2-1.4 mg/dL)
n Triglycerides >1.7 mmol/L (150 mg/dL) n Low glomerular filtration rate (<60 mL/min/1.73 m2) or creatinine

7. Fasting plasma glucose 5.6-6.9 mmol/L (102-125 mg/dL) clearance <60 mL/min
8. Abnormal 1 or 2 hour glucose tolerance test n Microalbuminuria 30-300 mg/24 hr or albumin/creatinine ratio
9. Abdominal obesity (waist circumference males >102 cm >22 (males) or >31 (females) mg/g creatinine
or >40 in, females >88 cm or >35 in) n Established cerebrovascular disease, stroke, or transient ischemic
10. Family history of premature cardiovascular disease
attack
(males <55, females <65) n Heart disease: myocardial infarction, angina, coronary
11. Diabetes mellitus
12. Autoimmune disease
revascularization, congestive heart failure, stent
n Renal disease: diabetic nephropathy, renal impairment, proteinuria
13. Heavy metal burden (lead, cadmium, arsenic, etc.)
n Peripheral artery disease or advanced retinopathy
14. Infections of the mouth, teeth, or gums

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Clinical Considerations for Modifiable Lifestyle Factors
Initiation of treatment outlined by JNC 8 is shown in Figure 1. The guidelines for treatment are influenced by age,
presence or absence of diabetes or chronic kidney disease, and race. The pharmacologic treatment interventions
vary depending on mechanisms (diuretic, calcium channel blockage, angiotension converting enzyme inhibition, or
angiotensin receptor blockage). Therapeutic lifestyle interventions should be addressed at all levels. These would include
sleep, nutrition, movement and exercise, mindfulness changes in thoughts and emotions, as well as relationships and habits.

Figure 1. JNC 8 Algorithm for Blood Pressure Goals and Intervention Management

Adult Age > 18 Years

Diet and Lifestyle Therapeutic Interventions Concurrent

With All Stages of Intervention

Blood Pressure Goal and Therapy Intervention Based on Age, Race, Diabetes,
and Chronic Kidney Disease

Age > 60 Age < 60 All Ages with All Ages

No DM or CKD No DM or CKD DM, no CKD with CKD

Goal SBP<150 mmHg Goal SBP<140 mmHg Goal SBP<140 mmHg Goal SBP<140 mmHg
Goal DBP<90 mmHg Goal DBP<90 mmHg Goal DBP<90 mmHg Goal DBP<90 mmHg

Black Non Black All Races

Initiate thiazide-type diuretic or Initiate thiazide-type diuretic or ACEI, Initiate ACEI or ARB, alone or in
CCB, alone or in combination ARB, CCB, alone or in combo combination with other class

DM = diabetes mellitus; CKD = chronic kidney disease; SBP = systolic blood pressure; DBP = diastolic blood pressure; CCB = calcium channel blocker;
ACEI = angiotensin converting enzyme inhibitor; ARB = angiotensin receptor blocker

There are many diet and lifestyle habits that are associated with abnormal blood pressure. These have been well
documented in review articles that focus on nutrition-associated impacts on hypertension.4,5,8,9 Less-healthy diets are
often low in protein, potassium, and magnesium while being high in trans fats and sodium.
Nutritional interventions include eating healthy proteins, fats and oils, limiting simple carbohydrates, and adding
specific types of fiber. Attention to dietary minerals, soluble vitamins, and a wide variety of phytonutrients from
colorful vegetables and fruit is essential. Often adding a single food item can have a significant effect on systolic
blood pressure. Some of these effects are listed in Table 2.

Table 2: Improving Nutrition Improves Blood Pressure4,5,8,9

Nutrient Effect on Blood Pressure

Protein Reduces sympathetic activity, induces natriuresis, inhibits tyrosine kinase, reduces vascular
smooth muscle hypertrophy, lowers superoxide anion, decreases aldosterone. Whey protein
stimulates glutathione production.18-20 Carnitine limits end organ damage.22,23
n 1.5–1.8 g/kg body weight /day of non-animal protein
n Whey 30 g/day (ACEI)
n Carnitine 1g/bid
n Sardine muscle protein 3 g/d (ACEI)
n Bonito protein 1.5 g/d (natural ACEI)
n Soy protein 40 g/d (activates PPARs)
n Arginine up to 10 g/d from food or supplement; precursor vascular nitric oxide.23
n Taurine 6 g/day induces mild diuresis, vasodilation, increases atrial natriuretic factor,
improves insulin sensitivity, reduces homocysteine levels

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Table 2: Improving Nutrition Improves Blood Pressure4,5,8,9 (cont.)

Nutrient Effect on Blood Pressure

Fats Emphasize polyunsaturated/monounsaturated fats, limited saturated fats, no trans fats

n EPA and DHA 1:1-4:1 ratio 3–4 g/d
n Olive oil 40 gm/d
n Sesame oil : 35 g/d

Carbohydrates n Fiber: Oatmeal fiber, psyllium, glucomannan, or betaglucan improves insulin sensitivity

Minerals n Sodium (Na): reduce to 2400 mg/d

n Potassium (K): increase to 60–120 mEq/d; 5:1 ratio K:Na
n Magnesium: 500–1000 mg/d
n Calcium: 500–1000 mg/d in food or mixed supplement.
n Zinc: 25-50 mg/d inhibits NFkB

Vitamins n Vitamin D to maintain adequate serum levels (36-50 ng/mL); many people need 5000 iu/d
to obtain and maintain optimum levels
n Vitamin E: 100 iu Vitamin E/1 g EFA
n Vitamin C: 250–500 mg twice a day if lack of adequate ascorbates from fruits/vegetables
n B2 (riboflavin): 25 mg/d
n Vitamin B6: 5 mg/kg/d reduces sympathetic nervous system activity, improves
insulin sensitivity
n Methyl folate or folinic acid if the patient is hyperhomocysteinemic
n B12 If the patient is hyperhomocysteinemic

Phytonutrients n Dark chocolate and cocoa: up to 100 gm/d

(or foods providing n Lycopene: 10 mg; found in tomato, guava, watermelon, papaya, apricots
phytonutrients) n Green tea, black tea: >600cc
n Quercetin: 500 mg twice a day
n Celery: high in 3-N butyl phthalide, apigeniin; 4 large sticks/d
n Garlic: 2–4 cloves/d
n Wakame seaweed: 3–4 g/d
n Pomegranate juice: 330 ml/d

ACEI = Angiotension converting enzyme inhibitor; EFA = essential fatty acid; EPA = eicosapentaenoic acid; K = potassium; N = nitrogen; NFkB = nuclear factor kappa B;
PPARs = peroxisomal proliferator-activated receptors

Diet, nutrition, and lifestyle interventions functionally change cellular systems and improve hypertensive
vascular disease.8,9
A more extensive listing of lifestyle and therapeutic dietary interventions that can reduce blood pressure is
provided in Table 3.

Table 3: Lifestyle Interventions for Reducing Blood Pressure by Many Mechanisms4,5,8,9

Lifestyle Change Mechanism

Stop or limit caffeine Caffeine causes:

n Vasoconstriction
n Norepinephrine levels
n Pulse wave velocity
n Plasma renin activity

Limit alcohol to 1 drink/d Alcohol elevates:

(8 oz wine, 2 oz hard n Blood pressure
liquor, 24 ounce beer) n Plasma renin activity
n Aldosterone
n Cortisol

Evaluate and address Increasing heavy metal burden of lead, arsenic, cadmium, or mercury increases:
heavy metal burden n Endothelial dysfunction
n Oxidative stress

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Table 3: Lifestyle Interventions for Reducing Blood Pressure by Many Mechanisms4,5,8,9 (cont.)
Lifestyle Change
Stop smoking tobacco
Discontinue medications
that increase BP
Aerobic and resistance
exercise and physical
training.
Exercise should include:
n 60 min/d of combined
aerobic and resistance
exercise
n Aerobic 30 minutes
60-80% of Maximal
aerobic capacity
(= 220–age)
n 4200 kj/week achieves
maximal reduction of
CV risk
Behavior Modifications
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Mechanism
Tobacco increases
n Vasoconstriction
n Sympathetic tone
n Norepinephrine levels
n Renin angiotensin levels
n Carbon monoxide levels
n Platelet aggregation
n Coagulation risk
n Oxidative stress
n Inflammatory markers
Medications such as
n Oral contraceptives
n NSAIDs and COX2 inhibitors (interfere with beta blockers, ACE inhibitors, ARBs)
n Antihistamines, decongestants
n Corticosteroids, mineralocorticoids, and anabolic steroids.
n Sympathomimetics and amphetamine-like drugs.
n Carbenoxolone or licorice
n TCA, MAO inhibitors
n Ergot alkaloids
n Diet pills and energy pills
n Heavy metal toxins: lead, cadmium, thallium, mercury, arsenic in herbal or
nutritional supplements
n Erythropoietin compounds
n Cyclosporin and tacrolimus
n Bromocriptine
n Metoclopramide
n Digitalis, disulfaram
n Lithium
Exercise improves
n Endothelial nitric oxide synthase
n Endothelial function
n Nitric oxide levels
n Coronary artery flow
n Systemic vascular compliance
n Insulin sensitivity
n Respiratory excursion (PFT, FEV1 lung function tests)
n Frontal lobe oxygen delivery
All of the following can lower blood pressure by a number of many autonomic nervous
system, endocrine, and neurotransmitter blood pressure influencers:
n Stress management
n Biofeedback, relaxation
n Pilates, Yoga
n Psychotherapy
n Hypnosis
n Meditation
n Spiritual and religious practices
© 2018 The Institute for Functional Medicine 8
Table 3: Lifestyle Interventions for Reducing Blood Pressure by Many Mechanisms4,5,8,9 (cont.)

Lifestyle Change Mechanism

Weight Reduction To ideal body weight (60% of hypertensive patients are 20% over ideal body weight)
Decrease in weight of 4–5 kg decreases systolic BP by 7 points, diastolic by 5 points.
Decreases waist circumference
Weight loss improves:
n Cardiac output
n Left ventricular filling pressure
n Insulin sensitivity
n Catecholamine levels
n Systemic vascular compliance
n Sodium retention
n Sympathetic tone
n Plasma renin activity
n Aldosterone levels
n hs CRP
n TNF, IL-6, inflammatory markers, and oxidative stress

ACE = angiotension converting enzyme; ARB = angiotension receptor blocker; MAO = monoamine oxidase; NSAID = nonsteroidal anti-inflammatory drug; TCA = tricyclic antidepressant;
hs CRP = high sensitivity C-reactive protein; TNFα = tumor necrosis factor; IL-6 = interleukin-6

Using nutrition as an antihypertensive is accomplished by understanding the therapeutic class of the food, much
as we understand the therapeutic classes of pharmaceutical interventions. The abilities of food to act as angiotensin
converting enzyme inhibitors, angiotensin receptor blockers, and beta and calcium channel blockers are real.
The diuretic, renin-inhibitory, vasodilatory, and central alpha agonist activities of foods and supplements are listed
in Table 4.9

Table 4: Natural Antihypertensive Compounds Categorized by Class9

Antihypertensive Therapeutic Class Food (ingredients) Nutrients

Angiotensin-Converting Enzyme Corn protein (zein) Omega-3 fatty acids

Inhibitors Egg yolks Zinc
Fish (bonito, dried salted fish, fish sauce, Pycnogenol
sardines, tuna) Melatonin
Garlic
Gelatin
Hawthorne berry
Milk protein (casein)
Pomegranate
Sea vegetables (kelp)
Seaweed (wakame)
Wheat germ (hydrolyzed)
Whey (hydrolyzed)
Angiotensin Receptor Blockers Celery N-acetyl cysteine
Fiber-rich foods Taurine
Garlic Gamma linolenic acid
Monounsaturated fatty acids (olive oil) Oleic acid
Potassium
Vitamin B6 (pyridoxine)
Vitamin C
Resveratrol
Coenzyme Q-10
Beta Blockers Hawthorne berry

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Table 4: Natural Antihypertensive Compounds Categorized by Class9 (cont.)

Antihypertensive Therapeutic Class Food (ingredients) Nutrients

Calcium Channel Blockers Celery N-acetyl cysteine

Garlic Taurine
Hawthorne berry Eicosapentaenoic acid
Monounsaturated fatty acids Docosahexanoic acid
Oleic acid
Omega-3 fatty acids
Calcium
Magnesium
Vitamin B6
Vitamin C
Vitamin E
Alpha lipoic acid
Central Alpha Agonists Celery Taurine
Fiber Gamma linolenic acid
Garlic Potassium
Protein Zinc
Vitamin B6
Vitamin C
Coenzyme Q-10
Direct Renin Inhibitors Vitamin D
Direct Vasodilators Celery Arginine
Fiber Taurine
Garlic Alpha linolenic acid
Monounsaturated fatty acids Omega-3 fatty acids
Soy Calcium
Magnesium
Potassium
Vitamin C
Vitamin E
Flavonoids
Diuretics Celery L-carnitine
Hawthorne berry Taurine
Protein Gamma linolenic acid
Fiber
Calcium
Magnesium
Potassium
Vitamin B6
Vitamin C
Vitamin E: high gamma/delta
tocopherols and tocotrienols
Coenzyme Q-10
Adapted from: Houston M. The role of nutrition and nutraceutical supplements in the treatment of hypertension. World J Cardiol. 2014;6(2):38-66. Used with permission.

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Orthostatic Hypotension
The normal blood pressure response. When an adult assumes an upright position, there is a pooling of 500 to
1000 cc of blood in the splanchnic circulation and the lower extremities, which triggers a rapid decrease in venous
return to the heart. The reduced ventricular filling leads to a drop in cardiac output and a resultant drop in blood
pressure. The fall in blood pressure causes a reflex compensation of the central and peripheral sympathetic response,
with a decreased parasympathetic outflow involving baroreceptors. The increased sympathetic outflow increases
peripheral vascular resistance, venous return, and cardiac output, limiting the fall in blood pressure.32 This is the
normal baro-reflex response: an increase in heart rate and vascular resistance to maintain cardiac output and blood
pressure.33 Most of the time this reflex is intact; there is usually a small drop in systolic blood pressure (5 mmHg), an
increase in diastolic blood pressure (5 mmHg), and an increase in pulse rate of up to 10 beats per minute. Greater
changes in systolic and diastolic pressures or pulse rate, warrant further work-up.
An abnormal blood pressure response. In patients with symptomatic orthostatic hypotension, one or more steps
in this reflex process result in a greater decline in blood pressure without a normal compensation in heart rate.34
There are many conditions and diseases associated with symptomatic orthostatic hypotension. Nutrition adequacy
plays a role in improving many of these conditions.
The prevalence of postural change in blood pressure increases with older age and with higher blood pressure levels
regardless of age.35 Aging individuals who develop cardiac, endocrine, or neurodegenerative conditions and are
treated with medications are more likely to have symptomatic orthostatic hypotension.32-34,36,37 For example, up to
25 percent of diabetic patients have altered autonomic response to position change and symptomatic orthostatic
hypotension.37 Examples of the medications and the associated conditions that exacerbate orthostatic hypotension
are summarized in Table 5. Heat intolerance, adrenal insufficiency, or situational or induced malnutrition (starvation,
anorexia nervosa, complications of bariatric surgery) also are associated with orthostatic hypotension. Specific
genetic single nucleotide polymorphisms affecting nutrient availability are being identified and may play a weak role
in maintaining the reflexes of normal blood pressure.38

Table 5: Medications and Associated Medical Conditions that Cause or Exacerbate Orthostatic Hypotension36

Medication/Substance Associated Medical Conditions

Alcohol Social habits, anxiety, depression

Alpha Blockers —terazosin Benign prostatic hypertrophy

Antidepressents — selective serotonin reuptake Depression, Insomnia
inhibitors, trazodone, monoamine oxidase inhibitors,
tricyclic antidepressants

Antihypertensives (sympathetic blockers) Hypertension

Antiparkinson’s — levodopa, pramipexole, ropni Parkinson’s
Antipsycotics— olanzapine, resperidone Psychosis, schizophrenia
Beta-blocker drugs— propranolol, metoprolol Hypertension, arrhythmias
Diuretics — hydrochlorothiazide, furosemide, Hypertension
spironolactone
Hypoglycemics— Insulin Diabetes mellitus, insulin resistance
Muscle relaxants— tizanidine, valium, cyclobenzaprine Muscle spasms, lumbalgia
Narcotic-opiate derivatives— morphine, oxycodone Pain syndromes, addiction
Phosphodiesterase inhibitors— sildenafil, tadalifil Erectile dysfunction, conditions of intravascular nitric
oxide insufficiency
Sedative/hypnotic drugs— temazepam Insomnia, anxiety (short-term)
Vasodilator drugs— nitroglycerin, hydralazine, calcium Hypertension, angina
channel blockers

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A severe form of orthostatic hypotension includes reflex syncope.Vasovagal syncope, situational syncope, cardiac
sinus syncope, and atypical forms lead to an altered, neurally-mediated, transient loss of consciousness due to
vasodilation, bradycardia, systemic hypotension, and cerebral hypoperfusion.39 Nutrition intervention would be
considered as a secondary, not primary intervention in these conditions.40
Therapeutic uses of nutrition in symptomatic hypotension are entertained by addressing the root causes of the
conditions. Increasing protein in the sarcopenic orthostatic patient might be the intervention of choice when
the reasons for the sarcopenia are fully considered. Many underlying disease dysfunctions have nutrition levers.
Interventions can be quite specific: e.g., improving insulin response in the person with metabolic syndrome,
lessening the peak insulin levels and the resultant physiologic effects of insulin leading to increased orthostasis, or
addressing vitamin D deficiency in the elder with orthostatic hypotension.41,42 Reflexes that maintain blood pressure
are also influenced by nutrition.
The extensive range of interventions for the hypertensive patient reflects the many roles of nutrition in maintaining
a healthy blood pressure. The literature offers nutritional considerations for orthostatic hypotension in specific
conditions.42–45 For example, in postural orthostatic tachycardia (POTS), vitamin B1245 and vitamin D43,44 have
been identified as therapeutic treatments. In the case of orthostatic hypotension in the elderly, addressing alpha
hydroxylation insufficiency by using calcitriol in the vitamin D-deficient patient is therapeutic.42 Whether the
patient is a diabetic with neuropathy or a severely depleted anorexic, a Functional Medicine workup addressing the
adequacy of the diet as far as macronutrients, protein, healthy fats and oils, carbohydrates, and the many minerals
and vitamins that are needed to maintain the physiologic reflexes associated with a healthy blood pressure must
be completed.37,46–48

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Functional Medicine Matrix Model
When addressing the underlying causes of elevated blood pressure, consideration must be given to each of the areas
of possible system imbalance shown in the Functional Medicine Matrix in Figure 2. This figure highlights some of
the antecedents, triggers, and mediators of hypertension, as well as diet and lifestyle influences.

Figure 2. Hypertension: Findings and Potential Areas of Clinical Imbalance

FUNCTIONAL MEDICINE MATRIX

Retelling the Physiology and Function: Organizing the Patient’s Clinical Imbalances
Patient’s Story

Antecedents
Assimilation Defense & Repair
(e.g., Digestion, (e.g., Immune,
(Predisposing Factors— Absorption, Microbiota/GI, Inflammation,
Genetic/Environmental) Respiration) Infection/Microbiota)

Mental Emotional
e.g., cognitive e.g., emotional
Structural function, regulation, grief, Energy
Integrity perceptual sadness, anger, (e.g., Energy
Regulation,
Triggering Events (e.g., from Subcellular patterns etc.
Membranes to Mitochondrial
(Activators) Function)
Musculoskeletal
Structure)

Spiritual
e.g., meaning &
purpose,
Communication relationship with Biotransformation
Mediators/Perpetuators (e.g., Endocrine,
something greater
& Elimination
(Contributors) Neurotransmitters, Immune (e.g., Toxicity,
messengers) Detoxification)

Transport
(e.g., Cardiovascular, Lymphatic System)

Modifiable Personal Lifestyle Factors

Sleep & Relaxation Exercise & Movement Nutrition Stress Relationships

Name: Date: CC: © 2015 Institute for Functional Medicine

Version 3

Conclusion
The correct measurement of blood pressure is part of the ABCDs of Functional Nutrition Evaluation. Improving
blood pressure to low-risk or normal levels requires an evaluation of underlying nutritional causes of chronic
disease. The practitioner must understand systemic imbalance and how to intervene to correct the root causes of
blood pressure abnormalities. This means addressing and correcting the drivers of oxidative stress and immune
or inflammatory imbalance causing endothelial dysfunction. Elevated blood pressure is a symptom of imbalance;
improving blood pressure to normal levels promotes health instead of disease.

“You are as old as your arteries.” — W. Osler

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Acknowledgements
IFM would like to acknowledge and thank the development team for their research, organization, and creation of the ABCDs of Functional
Nutrition Physical Exam series. P. Michael Stone MD, MS and topic specific contributors developed the materials. The Functional Nutrition
Evaluation; Blood Pressure materials were co-developed with Mark Houston, MD. The development team also included Kristi Hughes, ND,
Nicole Dotson, ND, Deanna Minich, PhD, and Nicholas Morgan, ND, who all did excellent work in support of the materials.
To cite: Stone PM, Houston M: Functional Nutrition Evaluation; Anthropometrics: Blood Pressure Companion Guide. Federal Way (WA):
Institute for Functional Medicine: 2016.

Blood Pressure References

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3. McGee S. Peripheral vascular disease. In: McGee S. Evidence-based physical diagnosis: expert consult. 3rd ed. New York: Saunders, 2012. p. 462
4. Houston MC. The role of cellular micronutrient analysis, nutraceuticals, vitamins, antioxidants and minerals in the treatment of hypertension and cardiovascular disease. Ther Adv Cardiovasc Dis.
2010;4(3):165-183.
5. Houston M. Treatment of hypertension. In: Houston M. Handbook of hypertension. Hoboken NJ: Wiley Blackwell, 2009. pp. 61-74.
6. Houston M. Nutrition and nutraceutical supplements in the treatment of hypertension. Expert Rev Cardiovasc.Ther. 2010; 8(6): 821-833.
7. Medline Plus. Blood pressure measurement. http://www.nlm.nih.gov/medlineplus/ency/article/007490.htm, Accessed 10/22/13.
8. Houston MC. The role of nutrition, nutraceuticals, vitamins, antioxidants, and minerals in the prevention and treatment of hypertension. AlternTher. 2013; 19(supplement 1):32-49.
9. Houston M. The role of nutrition and nutraceutical supplements in the treatment of hypertension. World J Cardiol. 2014; 26:6(2):38-66.
10. Beitzke M, Pfister P, Fortin J, Skrabal F. Autonomic dysfunction and hemodynamics in vitamin B12 deficiency. Auton Neurosci. 2002 Apr 18;97(1):45-54.
11. Savica V, Bellinghieri G, Kopple JD. The effect of nutrition on blood pressure. Annu Rev Nutr. 2010 Aug 21;30:365-401. doi: 10.1146/annurev-nutr-010510-103954
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17. Harrington JM, Fitzgerald AP, Kearney PM, McCarthy VJ, Madden J, Browne G, et al. DASH diet score and distribution of blood pressure in middle-aged men and women. Am J Hypertens. 2013 Nov;
26(11):1311-20. doi: 10.1093/ajh/hpt106. Epub 2013 Aug 6..
18. Fekete AA, Givens DI, Lovegrove JA. The impact of milk proteins and peptides on blood pressure and vascular function: a review of evidence from human intervention studies. Nutr Res Rev. 2013 Oct 18:1-
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20. Marshall K. Therapeutic applications of whey protein. Altern Med Rev. 2004 Jun; 9(2):136-56.
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22. Ruggenenti P, Cattaneo D, Loriga G, Ledda F, Motterlini N, Gherardi G, et al. Ameliorating hypertension and insulin resistance in subjects at increased cardiovascular risk: effects of acetyl-L-carnitine therapy.
Hypertension. 2009 Sep; 54(3):567-74. doi: 10.1161/HYPERTENSIONAHA.109.132522. Epub 2009 Jul 20.
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drudis.2010.03.014. Epub 2010 Apr
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32. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res 2011; 21:69.
33. Mathias CJ. Orthostatic hypotension: causes, mechanisms, and influencing factors. Neurology 1995;45(4 Suppl 5):S6-S11.
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44. Chaudhari SA, Sacerdote A, Bahtiyar G. 1- hydroxylation defect in postural orthostatic tachycardia syndrome: remission with calcitriol supplementation. BMJ Case Rep. 2012 Aug 13;2012. pii:
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Dec 23
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Additional Resources:
JNC8
James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee
(JNC 8). JAMA. 2013 Dec. doi: 10.1001/jama.2013.284427.
Weber MA, Schiffrin EL, White WB, Mann S, Lindholm LH, Kenerson JG, et al. Clinical practice guidelines for the management of hypertension in the community: a statement by the American Society of
Hypertension and the International Society of Hypertension. J Clin Hypertens. 2014 Jan;16(1):14-26. doi: 10.1111/jch.12237.
JNC7 http://www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.htm
JNC6 http://www.nhlbi.nih.gov/health-pro/guidelines/archive/hypertension-jnc6
DASH Diet http://www.nih.gov/news/pr/apr97/Dash.htm
National High Blood Pressure Education Program http://www.nhlbi.nih.gov/about/nhbpep/indes.htm,
http://www.nhlbi.nih.gov/hbp/index.html.

Video Resources:
Campbell NR, Chockalingam A, Fodor JG, McKay DW. Accurate, reproducible measurement of blood pressure. CMAJ: Canadian Medical Association Journal. 1990;143(1):19-24.
Handler J. The Importance of Accurate Blood Pressure Measurement. The Permanente Journal. 2009;13(3):51-54.
Kurtz KJ. Bruits and Hums of the Head and Neck. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990
Chapter 18. Available from: https://www.ncbi.nlm.nih.gov/books/NBK289/
Ogedegbe G, Pickering T. Principles and techniques of blood pressure measurement. Cardiology clinics. 2010;28(4):571-586. doi:10.1016/j.ccl.2010.07.006.
Pessi, T. et al. Bacterial signatures in thrombus aspirates of patients with myocardialinfarction. 2013, Circulation 12(11):1219-1228. doi: 10.1161/CIRCULATIONAHA.112.001254.
Pickering TG, et al. Recommendations for blood pressure measurement in humans and experimental animals. Circulation. 2005 Feb 8;111(5):697-716.
Tolonen H, et al. Challenges in standardization of blood pressure measurement at the population level. BMC Medical Research Methodology. 2015;15:33. doi:10.1186/s12874-015-0020-3.
Wong DH et al. Acute cardiovascular response to passive leg raising. Crit Care Med. 1988 Feb;16(2):123-5.

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nsight.org

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