the russ hedrick r. r. center nutritional guide · 2018-08-16 · the russ hedrick r. r. center...

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE i

The Russ Hedrick Recovery Resource Center

Nutritional Guide to Optimize Recovery and

Ameliorate Post-Acute Withdrawal Symptoms

2018

Library of Congress cataloging-in publication

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© 2018 Rajan Masih

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THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE ii

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE iii

Acknowledgements

The authors wish to acknowledge the many

people who made this book possible.

Margaret Rioux

Jerrena Auville

Teresa Landis

Bob Borror

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE iv

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE v

Authors

Editors in Chief

Raj Masih MD, MPH, MPHN

Regional Health Promotion and Wellness

Coordinator PHG Petersburg, WV

Michael Landis MBA, AADC

Executive Director, PHG Petersburg, WV

Barbra Masih MS, CRC, PLPC

Substance Abuse Counselor, PHG Petersburg,

WV

Wade Rohrbaugh, Certified Recovery Coach,

CCAR, FAADP

Coordinator of the Russ Hedrick Recovery

Resource Center, Petersburg, WV

Christian J. Landis

Garrett Community College, Deep Creek, MD

Contributing Authors

Krystal Bates

Nutritional Expert, Charlotte, NC

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE vi

Kabeer Masih, MS

Texas Tech University School of Medicine EL

Paso, Texas

Justin Bates BS

University of San Francisco, CA

Brandon Bates, BS

News Anchor, WBIR, Knoxville, TN

Kevin Knowles, CCAR, FAADP

Berkeley County Community Recovery

Services Coordinator

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE vii

Dedications

This book is dedicated to my mother Catherine

Masih

&

Russ Hedrick

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE viii

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE ix

Table of Contents Pages

Background

Dopamine Deficiency Syndrome in

Addictions

Role of Nutrition

2016 Study of 1850 Patients with

Substance use Disorder

Research Questions

Research Objectives


Addictions

Organization of the US Healthcare System

for Addictions Treatment

What is Dopamine

6 Phenylalanine Rich Foods

18 Top Foods for Dopamine

Central Nervous System effects of

Dopamine Restoration

Decreased Dopamine Transporters in a

Methamphetamine Abuser

The Cocaine Abuser’s Brain

D2 Receptors + Anhedonia

PET Scan Imaging

Effect on Energy

Effect on Sleep

Effect on Mood

Effect on Cravings

Effect on Restless Leg Symptoms

Engagement in Counseling and Goal

Setting Objectives

Pathophysiology of nutritional

deficiencies that occur with Substance

Use Disorder


THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE x

for Addictions Treatment

What is Dopamine

Central Nervous System Effects of

Dopamine Restoration

Whole Foods High in l-Tyrosine

Cheese (Parmesan)

Soy Foods (Roasted Soybeans)

Lean Beef & Lamb (Roast Beef)

Lean Pork (Chops, cooked)

Fish & Seafood (Salmon, cooked)

Chicken & Turkey (Chicken Breast,

cooked)

Seeds & Nuts (Pumpkin Seeds)

Eggs & Dairy (Eggs)

Beans & Lentils (White Beans, cooked)

Wholegrains (Wild Rice, cooked)

Phenyalanine Rich Foods:

Soy Foods (Roasted Soybeans)

Cheese (Parmesan)

Seeds & Nuts (Pumpkin Seeds)

Lean Beef & Lamb (Roast Beef)

Chicken & Turkey (Chicken Breast,

cooked)

Lean Pork (Chops, cooked)

Fish & Seafood (Tuna, cooked)

Eggs & Dairy (Eggs)

Beans & Lentils (Pinto Beans, cooked)

Wholegrains (Kamut, cooked)

Magnesium Rich Foods

Foods Rich in Zinc

Sample Food for Dopaminergic

Potentiation

Fava Bean Dopamine Delights (Dr. Oz,

2017)

References

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE xi

THE RUSS HEDRICK R. R. CENTER NUTRITIONAL GUIDE 1

Background

Substance Use Disorder (SUD) is a

primary, chronic brain disorder, characterized

by compulsive substance use, withdrawal, and

repeated use despite adverse consequences

(ASAM, 2017).

One of the primary pathological

mechanisms underlying SUD is impairment in

the dopamine reward system in the nucleus

accumbens and the amygdala of the brain. The

decreased metabolism of dopamine in the D2

receptors of the nucleus accumbens and the

amygdala results in a decreased dopaminergic

reward in response to normal pleasurable

stimuli (Volkow, 2007). This condition is

known as dopamine deficiency syndrome or

reward deficiency syndrome.

According to the CDC, in 2016, more

than 23,000,000 Americans suffered from SUD.

Less than 10% received any kind of treatment

at all, and those that received treatment are very

likely to relapse within one year (CDC, 2016).

Treatment for substance use disorder has

traditionally included behavioral modification,

detoxification, treatment modalities utilizing

counseling, and medication assisted treatment

utilizing medication such as methadone,

Suboxone, and Vivitrol (ASAM, 2017). In 2016


54,000 Americans died from opioid overdoses

(CDC, 2017).

Research conducted into the nutritional

and metabolic status of people with substance

use disorder who are currently in detox are eye-

opening and reveal a variety of nutritional

deficiencies including deficiencies in serum

zinc levels, vitamin D, vitamin C, vitamin B-

12, and lower than normal serum albumin

levels (Willis, 2016). People with substance use

disorder who are successful in going through

detoxification frequently suffer from anhedonia

meaning they are unable to derive pleasure

from normal stimuli. In response to this, people

with substance use disorder frequently turn to

consuming large amounts of caffeine, foods

containing simple sugars, carbonated

beverages, and nicotine products (Willis, 2016).

It may take months to years for brain

physiology and chemistry to normalize or

approach normalcy in the dopamine reward

system of the D2 receptors. This period of

months to years is a period of great

vulnerability to relapse, but is also a potential

time for targeted nutritional interventions.

More and more, the treatment of

addiction has become a multimodal integrated

treatment model utilizing trained specialists in

addiction medicine, counseling, behavioral

therapies, 12- step Self-Help modalities, and


alternative and complementary interventions

such as mindfulness, meditation, and

acupuncture. The role of the dietetics

professional, and the targeted nutritional

intervention as part of an integrated treatment

approach to the disease of addiction has not

been widely accepted and no formal programs

exist on a national or international level. Given

the stimulation of the dopamine D2 receptors

by food products it stands to reason that

nutritional interventions including dietary

optimization can play an important role in the

facilitation of normal brain physiology and

biochemistry in an effort to ensure a successful

launch into recovery.


Addictions:

Dopamine Deficiency Syndrome (DDS)

also known as Reward Deficiency Syndrome

has been described before by others (Blum,

2011) (Volkow, 2007). Single Photon CT Scan

(SPECT) and Positron Emission Tomography

(PET) of the brain have been utilized to

extensively study the role of DDS in addiction,

particularly opioid addiction (Volkow, 2007).

These brain imaging studies have confirmed

that individuals with OPRD-1 and OPRM-1

genotypes are predisposed to not only

dopamine deficiency in the limbic system and


nucleus accumbens of the brain, but are also

susceptible to opioid and alcohol addiction

(Volkow, 2007). Dopamine deficiency

syndrome has also been associated with food

addiction (Volkow, 2007).

Individuals with DDS have been shown

to have reduced dopamine release (in the

physiological “pleasure centers” of the brain

including the nucleus accumbens and the limbic

system) and reduced dopamine metabolism in

response to normal “pleasurable stimuli” such

as food, sex, love, and normal physiologically

“satisfying stimuli” such as holding one’s

newborn baby, receiving recognition, or

interacting with nature (Volkow, 2007). Thus,

even as small children they never receive the

sensation of abject pleasure associated with the

normal physiological circumstances and events

that trigger the release of dopamine in the

limbic system (Volkow, 2007) (Blum, 2011).

Compounds such as simple sugar,

caffeine, and nicotine which are capable of

releasing dopamine in the limbic system of the

brain to the magnitude of 2-4 times more than

the normal physiologic release in response to

pleasurable stimuli become novel and create

intense sensations of euphoria and pleasure in

individuals with DDS (Blum, 2011). For the

first time in their lives these individuals with

DDS may experience a sensation of “normalcy”


and pleasure in response to sugar, caffeine, or

nicotine (Volkow, 2007) (Blum, 2011). This

then induces neuroplastic and neuro-adaptive

responses in the mesolimbic system and pre-

frontal cortex of the brain in individuals with

DDS, and dopamine release takes on “salience”

and the “brain expects it” (Volkow, 2007)

(Blum, 2011).

Children with DDS may exhibit

maladaptive behaviors such as overeating,

binge-eating, consuming and craving large

quantities of sugary foods and sugary beverages

(Volkow, 2007) (Blum, 2011). Additionally,

these children may exhibit pathologic behaviors

such as obsessively playing video games, or

“acting-out”.

Later in life if these susceptible

individuals with the genotypes for DDS are

exposed to alcohol or other drugs such as

marijuana, opioids, cocaine, or

methamphetamine, the neuroplastic and neuro-

adaptive changes in the mesolimbic system and

pre-frontal cortex become attenuated leading to

a pattern of craving and recurrent misuse. As

use continues, tolerance invariably develops,

thus more and more of the substance is required

to cause sufficient dopamine release. Additional

neuro-adaptive changes occur at a cellular

level, whereby, if the individual does not have

the drug in their system for a period of time,


they experience synaptic irritability and axonal

depolarization leading to the classic symptoms

of drug withdrawal (Volkow, 2007) (Blum,

2011). This then creates an intolerable

physiologic state to the individual wherein the

drug must be obtained at all costs to alleviate

the symptoms of withdrawal. Axonal

depolarization at the Dopamine D-2 receptor is

mediated by Na/K ATPase inhibition and leads

to severe depression, anxiety, insomnia, muscle

pain, tremor, intense fatigue, and possible

seizures (Rosen, Klintmam, et al., 2003).

Protracted use of these drugs and alcohol

can cause significant dopamine depletion

particularly in the Dopamine D-2 receptors, and

this is magnified by decreased dopamine

sensitivity at the synaptic end-plate (Rosen,

Klintmam, et al., 2003). Functional MRI (f-

MRI) and SPECT imaging during acute and

post-acute withdrawal demonstrate functional

depletion of dopamine metabolism in the limbic

system (Rosen, Klintmam, et al., 2003).

This state of dopamine depletion,

decreased dopamine sensitivity, and decreased

dopamine metabolism during acute and post-

acute withdrawal syndrome (PAWS) is the

primary mechanism behind relapse, and

represents the single most important barrier to

treatment success (Blum, 2011). This state of

dopamine depletion also represents a potential


breakthrough area for targeted nutritional

interventions that will be explored further in

this paper and Nutrition Research proposal.


Pathophysiology of nutritional deficiencies

that occur with Substance Use Disorder:

Vitamin C: Johnson and associates (2003)

have described the slow reduction in serum

ascorbic acid levels that occur with chronic

opiate addiction. Through an independent

action on the liver, opiates can inhibit synthesis

of ascorbic acid binding globulin levels

resulting in significant deficiencies in available

Vitamin C levels. Studies from China with

chronic opium smokers have revealed scurvy as

a major cause of morbidity (Zhou and Han,

1998).

Vitamin D: Vitamin D deficiency has been

described before in chronic Marijuana smokers


(Chester, 2011). Vitamin D deficiency can lead

to accelerated osteoarthritis, osteopenia,

frequent fractures and altered immune status

with increased susceptibility to infections with

gram positive bacteria.

Vitamin B-12: Cyanocobalamin deficiency is

commonly found in cocaine and

methamphetamine users due to it being a

substrate in stimulant metabolic pathways

(Kolger, Murray, et al. 1998).

Folic Acid: Alcohol abuse can cause depletion

of folic acid leading to deficiency syndrome

with megaloblastic anemia and neurologic

sequelae such as alcohol-induced seizure

disorder (AISD) (Talbott, 2002).

Thiamine: Thiamine deficiency is common in

alcoholics and can lead to neuro-psychiatric

symptoms such as Wernicke-Korsakoff

syndrome, Wernickes’s encephalopathy, and

Korsakoff Psychosis. Cognitive impairment is

also a consequence of thiamine deficiency in

alcoholics (Talbott, 2002).

Zinc: Zinc deficiency is common in alcoholics

and lead to poor wound healing, prostate

problems, and accelerated development of

alcoholic liver disease (Talbott, 2002).


Additionally, zinc deficiency attenuates opioid

withdrawal symptoms in chronic opioid abusers

(Talbott, 2002).

Magnesium: magnesium deficiency has been

well described in chronic alcoholics (Talbott,

2002). Proposed mechanisms for magnesium

deficiency include gastro-intestinal losses,

malabsorption and chelation. Additionally,

alcohol independently induces magnesium

excretion leading to profound hypomagnesemia

(Talbott, 2002). Symptoms of hypomagnesemia

include seizures, tremors, irritability, sleep

deprivation and concurrent refractory

hypokalemia (Talbott, 2002).

Protein deficiencies: Protein malnutrition has

been reported in both cocaine and

methamphetamine abusers (Mohs, 1990). The

profound anorexigenic effect of these stimulant

drugs leads to loss of appetite, decreased

protein intake, and decreased endogenous

protein synthesis in skeletal muscle (Mohs,

1990) leading to significant muscle wasting and

weight loss.

Alcoholics similarly are often protein deficient,

exhibiting serum hypoalbuminemia which

contributes to ascites, pleural effusions, and a

predisposition to enteric infections in ascetic

fluid (Talbott, 2002).


Optimizing these nutritional deficiencies

is critical for successful recovery from opioid

and alcohol addiction (Blum, 2016).


for Addictions Treatment:

The United States is currently

experiencing an epidemic. In 2016 more than

54,000 people died from opioid overdoses in

the United States. Currently deaths from opioid

overdoses exceed those from firearms and

automobile accidents combined (CDC, 2017).

According to the CDC approximately 144

people buying reading from opioid overdoses

(CDC, 2017).Synthetic drugs such as fentanyl,

carfentanyl, and acetyl- fentanyl are

increasingly mixed with heroin and brought in

to the US from Mexico by criminal drug cartels

(DEA, 2017).In October of 2017 President

Donald Trump declared a state of emergency to

deal with the opioid crisis. This has allowed

many new resources and innovative treatment

modalities to become widely integrated into the

Healthcare System. In spite of this surge in

resources and federal attention, and the death

rate from opioid overdoses continues to climb

(CDC, 2017). Many Federal authorities believe

that the true plateau of this epidemic has not

been reached yet.


Treatment for substance use disorder in

the United States broadly falls into two

categories: medical model and traditional

models. In October of 2016, the Surgeon

General of the United States addressed

Congress and declared addiction a chronic brain

disease and not a “moral failing” (US Surgeon

General Dr.Vivek Murthy, 2016). He

encouraged the Federal government and

physicians to recognize this and to adopt the

medical model of treatment for addiction.

The medical model of treatment involves

the use of detoxification, inpatient treatment,

intensive outpatient treatment, and medication

assisted treatment (MAT) (Rosen, Klintmam, et

al., 2003).Typically, detoxification is an

inpatient process in a medically supervised

setting. This is for those patients who are at-risk

of significant withdrawal symptoms up such as

seizures. Detoxification can last anywhere from

5 to 10 days. The usual inpatient treatment for

substance use disorder is 20 to 60 days long,

and is conducted in a formal treatment center

(Rosen, Klintmam, et al., 2003). Inpatient

treatment consists of the use of medications in

conjunction with counseling and behavioral

modification therapy. Intensive outpatient

therapy usually less from six months to a year

and is conducted by trained substance abuse

counselors (Rosen, Klintmam, et al., 2003).


Medication assisted treatment (MAT) is

always medically supervised and conducted by

a Physician. The goals of medication assisted

treatment include preventing withdrawal

symptoms, reducing cravings, and facilitating

recovery. Medications that are utilized in this

form of treatment include methadone,

Suboxone, Vivitrol, Campral and Antabuse.

These forms of treatment often involve

replacing one addictive drug with another, and

are extremely expensive. The cost of Vivitrol

injection is $1100 per month (Alkemes, 2017).

The cost of 6 months of injectable

buprenorphine is $ 6400 (Alkemes, 2017).

Conversely, traditional addiction

treatment consists of mutual support meetings

including Alcoholics Anonymous, Narcotics

Anonymous, Cocaine Anonymous or faith-

based initiatives such as Celebrate Recovery or

Refuge Recovery (Fried, Febo, Waite, et al.,

2016).

What is Dopamine?

Dopamine is in neurotransmitter in the

central nervous system and an adrenergic

agonist in the peripheral nervous system (Blum,

2011). Dopamine produces psychotropic effects

including mood elevation, euphoria, satisfaction

and empathy in physiologic doses (Blum,


2011). Additionally, dopamine plays a role in

movement, blood pressure control and

temperature regulation. Dopamine is

synthesized from the amino acids L-tyrosine

and phenylalanine by the enzyme amino acid

decarboxylase (AADC), in the presence of

pyridoxal 5-phosphate, ionic zinc and

magnesium (Blum, 2011).

Adequate levels of bioavailable substrate

(L-tyrosine) and phenylalanine are needed to

synthesize dopamine in the central nervous

system. L-tyrosine and phenylalanine have

excellent bioavailability when given as an

intravenous infusion (2.75% Travasol Amino

Acid with Dextrose), and is rapidly taken up by

the adrenal glands and the central nervous

system (CNS) (Blum, 2016).

Central Nervous System Effects of

Dopamine Restoration:

Studies in opioid dependent patients

demonstrated excellent bioavailability of both

L-tyrosine and phenylalanine when consumed

orally both as a neuronutraceutical (Blum,

2011) and through consuming 0.8 gms/Kg of

protein containing whole foods (Volkow,

2015). Trachtenberg, Ramsey and associates

(2014) demonstrated increased central nervous

system metabolic restoration of dopamine in the


limbic system compared to controls after 8

weeks of a proprietary supplement containing

11mg of L-tyrosine and 170 mg of

phenylalanine, along with 51 mg of Magnesium

chloride, with 14 mg of zinc per serving

administered 4 times daily. This increased

dopamine restoration in the limbic system was

associated with decreased cravings, increased

program compliance, and greater sobriety at 1

year compared to controls.

Koob and Simon (2009) demonstrated

enhanced recovery rates at 3, 6, and 9 months

compared to controls in opioid dependent

patients who underwent nutritional education,

counseling and a specialized neuronutritive diet

composed of 0.8 gms/Kg of protein, zinc,

pyridoxine, and magnesium oxide through

whole foods. Study subjects in this cohort were

not allowed to consume caffeinated beverages,

nicotine, or simple sugar containing products

for the first 90 days of the program.

Wiss (2016) studied the effects of an

extract of mucuna pruriens in opiate addicts,

and found that taking this extract 3 times a day

for 30 days boosted CNS dopamine levels

compared to controls in a small study.

Additionally, this extract was found to increase

levels of the neurotransmitter norepinephrine

which also plays an important role in mood and

depression (Wiss, 2016).


A 2015 study by Ciubotariu and

associates demonstrated the positive effects of

zinc supplementation in opioid dependent

patients to increase dopamine levels and to

reduce symptoms of opioid withdrawal

(Ciubotariu, Ghiciuc, et al., 2015). Their study

demonstrated increased dopamine metabolism

in the nucleus accumbens by SPECT and f-MRI

imaging compared to controls.

In addition to dietary supplementation

with dopamine precursors and the use of

targeted whole foods to enhance dopamine

synthesis in the CNS, many studies have shown

the benefits of targeted nutrition education to

enhance long-term recovery. Empowering

patients with life-long learning related to

nutritional solutions to dopamine deficiency

syndrome have been shown to have positive

outcomes (Grant, Haughton, et al., 2004).

The Society for the Study of Addiction

(SSA, 2017) promotes the use of inpatient daily

intravenous infusions of amino acid complexes

containing L-tyrosine and phenylalanine in

addiction to zinc and magnesium for 30 days as

an adjunct to motivational interviewing and

cognitive behavioral therapy in treatment

centers endorsed by the organization (SSA,

2017).

Thus, there exists a large volume of

empirical research data on the importance of


dopamine deficiency syndrome in patients with

addiction, and the ability of whole foods

containing optimal levels of L-tyrosine and

phenylalanine along with zinc and magnesium

to optimize CNS dopamine levels in the limbic

system. Early optimization of CNS dopamine

levels are associated with improved outcomes

including sobriety and recovery. This stands in

stark contrast to the pharmaceutical industry

backed, medical model of addiction which

promotes the use of potentially harmful and

equally addictive pharmacologic products such

as Methadone and Suboxone.


Whole Foods High in l-Tyrosine

Cheese (Parmesan) Tyrosine

100g

Per ounce

(28g)

Per cubic inch

(10g)

1995mg

(228% RDI)

559mg

(64% RDI)

200mg

(23% RDI)

Other Cheeses High in Tyrosine (%RDI per

ounce): Gruyere (57%), Swiss (54%), Edam

(47%), Reduced-Fat Mozzarella (45%), Blue

Cheese (41%), Monterey & Hard Goat’s

Cheese (38%), and Cottage Cheese (21%).

Soy Foods (Roasted Soybeans) Tyrosine

100g

Per cup

(93g)

Per ounce

(28g)

1497mg

(171% RDI)

1392mg

(159% RDI)

419mg

(48% RDI)

Other Soy Foods High in Tyrosine (%RDI per

ounce): Koyadofu (Dried, Frozen Tofu) (51%),

Soy Flour (42%), Soy Chips (33%), Tempeh

(21%), Fried Tofu & Natto (18%), Sprouted

Soybeans, stir-fried (15%), and Silken Tofu

(10%).


Lean Beef & Lamb (Roast Beef) Tyrosine

100g

Per piece

(296g)

Per 3oz

(85g)

1386mg

(158% RDI)

4103mg

(469% RDI)

1178mg

(135% RDI)

Other Cuts of Beef & Lamb High in Tyrosine

(%RDI per 3oz, cooked): Grilled Steak (133%),

Beef Sirloin & Beef Ribs (127%), Beef

Tenderloin (122%), Lamb Shoulder (116%),

New Zealand & Australian Lamb (112%), and

Stewing Lamb 110%.

Lean Pork (Chops, cooked) Tyrosine

100g

Per chop

(180g)

Per 3oz

(85g)

1228mg

(140% RDI)

2210mg

(253% RDI)

1044mg

(119% RDI)

Other Cuts of Pork High in Tyrosine (%RDI

per 3oz, cooked): Bacon (150%), Low Fat

Ground Pork (130%), Pork Sirloin (117%),

Pork Ribs (112%), Ham (111%), Loin of Pork

(110%), Pork Tenderloin and Pork Shoulder

(103%).


Fish & Seafood (Salmon, cooked) Tyrosine

100g

Per 1/2 fillet

(155g)

Per 3oz

(85g)

1157mg

(132% RDI)

1793mg

(205% RDI)

983mg

(112% RDI)

Other Fish & Seafood High in Tyrosine (%RDI

per 3oz, cooked): Tuna (98%), Snapper (86%),

Mackerel (85%), Shrimp (84%), Halibut (83%),

Haddock (76%), Cod (66%), and Crab (64%).

Chicken & Turkey (Chicken Breast, cooked) Tyrosine

100g

Per breast

(181g)

Per 3oz

(85g)

1155mg

(132% RDI)

2091mg

(239% RDI)

982mg

(112% RDI)

Other Cuts of Chicken & Turkey High in

Tyrosine (%RDI per 3oz, cooked): Fat-Free

Ground Turkey (109%), Stewing Chicken

(108%), Turkey Breast (106%), Turkey Leg

Meat (105%), Chicken Wing (99%), Turkey

Wing (97%), Chicken Drumstick (94%) and

Turkey Drumstick (90%).


Seeds & Nuts (Pumpkin Seeds) Tyrosine

100g

Per cup

(129g)

Per ounce

(28g)

1093mg

(125% RDI)

1410mg

(161% RDI)

306mg

(35% RDI)

Other Seeds & Nuts High in Tyrosine (%RDI

per ounce): Peanuts (31%), Sesame Seeds

(24%), Sunflower Seeds (21%), Chia Seeds

(18%), Pine Nuts, Macadamia Nuts, Flaxseeds

& Pistachio Nuts (16%), and Almonds (14%).

Eggs & Dairy (Eggs) Tyrosine

100g

Per cup

(243g)

Per egg

(50g)

499mg

(57% RDI)

1213mg

(139% RDI)

250mg

(29% RDI)

Other Dairy Foods High in Tyrosine (%RDI per

cup):Fat-free Natural Yogurt (81%), Natural

Yogurt (49%), Skimmed Milk (48%), Semi-

Skimmed Milk (47%), Buttermilk (45%),

Whole Milk (44%), Sour Cream (34%), and

Butter (11%).


Beans & Lentils (White Beans, cooked)

Tyrosine

100g

Per cup

(179g)

Per tablespoon

(11g)

274mg

(31% RDI)

490mg

(56% RDI)

30mg

(3% RDI)

Other Beans & Lentils High in Tyrosine (%RDI

per cup, cooked): Adzuki Beans (59%), Lentils

(55%), Split Peas (54%), Roman (Cranberry)

Beans (53%), Kidney Beans & Black Beans

(49%), Broad Beans (Fava Beans) (47%), Pinto

Beans (46%), and Chickpeas (Garbanzo Beans)

(41%).

Wholegrains (Wild Rice, cooked)

Tyrosine

100g

Per cup

(164g)

Per 1/2 cup

(82g)

169mg

(19% RDI)

277mg

(32% RDI)

139mg

(16% RDI)

Other Wholegrains High in Tyrosine (%RDI

per cup, cooked): Raw Oats (102%), Teff

(38%), Kamut (27%), Brown Rice (22%),

Millet (21%), Bulgur (19%), Quinoa & Cous

Cous (18%).


Phenyalanine Rich Foods:

Soy Foods (Roasted Soybeans) Phenylalanine

100g

Per cup

(93g)

Per ounce

(28g)

2066mg

(236% RDI)

1921mg

(220% RDI)

578mg

(66% RDI)

Other Soy Foods High in Phenylalanine (%RDI

per ounce): Koyadofu (Dried, Frozen Tofu)

(75%), Soy Flour (58%), Soy Chips (44%),

Tempeh (29%), Sprouted Soybeans, stir-fried

(28%), Fried Tofu (27%), Boiled Soybeans

(18%) and Silken Tofu (14%).

Cheese (Parmesan) Phenylalanine

100g

Per ounce

(28g)

Per cubic inch

(10g)

1922mg

(220% RDI)

538mg

(61% RDI)

192mg

(22% RDI)

Other Cheeses High in Phenylalanine (%RDI

per ounce): Gruyere (56%), Swiss (53%), Edam

(46%), Monterey (41%), Reduced-Fat

Mozzarella & Colby (40%), Hard Goat’s

Cheese (39%), 8and Cottage Cheese (22%).


Seeds & Nuts (Pumpkin Seeds) Phenylalanine

100g

Per cup

(129g)

Per ounce

(28g)

1733mg

(198% RDI)

2236mg

(256% RDI)

485mg

(55% RDI)

Other Seeds & Nuts High in Phenylalanine

(%RDI per ounce):Watermelon Seeds (65%),

Peanuts (39%), Sunflower Seeds (38%),

Almonds (36%), Pistachio Nuts (35%), Chia

Seeds (32%), Flaxseeds (31%), Sesame Seeds

(30%), and Cashew Nuts (25%).

Lean Beef & Lamb (Roast Beef) Phenylalanine

100g

Per piece

(296g)

Per 3oz

(85g)

1464mg

(167% RDI)

4333mg

(495% RDI)

1244mg

(142% RDI)

Other Cuts of Beef & Lamb High in

Phenylalanine (%RDI per 3oz, cooked): Lamb

Shoulder & Beef Sirloin (141%), Australian &

New Zealand Lamb (135%), Beef Ribs (134%),

Stewing Lamb & Beef Rib Eye Steak (133%),

Beef Pot Roast (132%), and Beef Tenderloin

(129%).


Chicken & Turkey (Chicken Breast, cooked) Phenylalanine

100g

Per piece

(181g)

Per 3oz

(85g)

1294mg

(148% RDI)

2342mg

(268% RDI)

1100mg

(126% RDI)

Other Cuts of Chicken & Turkey High in

Phenylalanine (%RDI per 3oz, cooked):

Stewing Chicken (128%), Fat-Free Ground

Turkey (120%), Chicken Wings (117%),

Turkey Breast (110%), Chicken Thighs

(109%), Chicken Drumsticks & Turkey Leg

Meat (106%), and Turkey Wings (103%).

Lean Pork (Chops, cooked) Phenylalanine

100g

Per chop

(180g)

Per 3oz

(85g)

1288mg

(147% RDI)

2318mg

(265% RDI)

1095mg

(125% RDI)

Other Cuts of Pork High in Phenylalanine

(%RDI per 3oz, cooked):Bacon (157%), Low

Fat Ground Pork (131%), Pork Sirloin (123%),

Pork Tenderloin & Pork Ribs (118%), Ham

(114%), Loin of Pork (111%), and Pork

Shoulder (108%).


Fish & Seafood (Tuna, cooked) Phenylalanine

100g

Per 1/2 fillet

(154g)

Per 3oz

(85g)

1101mg

(126% RDI)

1696mg

(194% RDI)

936mg

(107% RDI)

Other Fish & Seafood High in Phenylalanine

(%RDI per 3oz, cooked):Lobster (108%),

Salmon (101%), Snapper (100%), Mackerel

(99%), Crab (97%), Halibut (96%), Haddock

(88%), and Cod (71%).

Eggs & Dairy (Eggs) Phenylalanine

100g

Per cup

(243g)

Per egg

(50g)

680mg

(78% RDI)

1652mg

(189% RDI)

340mg

(39% RDI)

Other Dairy Foods High in Phenylalanine

(%RDI per cup): Fat-free Natural Yogurt

(88%), Natural Yogurt (53%), Skimmed Milk

(49%), Semi-Skimmed Milk (48%), Buttermilk

(47%), Whole Milk (45%), and Sour Cream

(35%).


Beans & Lentils (Pinto Beans, cooked) Phenylalanine

100g

Per cup

(171g)

Per tablespoon

(11g)

531mg

(61% RDI)

908mg

(104% RDI)

58mg

(7% RDI)

Other Beans & Lentils High in Phenylalanine

(%RDI per cup, cooked): White Beans (108%),

Adzuki Beans (105%), Kidney Beans (103%),

Cranberry (Roman) Beans (102%), Lentils

(101%), Mung Beans (98%), Black Beans

(94%), and Chickpeas (Garbanzo Beans)

(89%).

Wholegrains (Kamut, cooked) Phenylalanine

100g

Per cup

(172g)

Per 1/2 cup

(86g)

300mg

(34% RDI)

516mg

(59% RDI)

258mg

(30% RDI)

Other Wholegrains High in Phenylalanine

(%RDI per cup, cooked): Teff (59%), Quinoa

(39%), Wild Rice & Millet (37%), Cous Cous

(33%), Bulgur & Brown Rice (30%),

Buckwheat Groats (25%), and Pearled Barley

(23%).


Magnesium Rich Foods

(Men RDA 400 milligrams and Women RDA

310 milligrams a day)

Spinach — 1 cup: 157 milligrams (40% DV)

Chard — 1 cup: 154 milligrams (38% DV)

Pumpkin seeds — 1/8 cup: 92 milligrams (23%

DV)

Yogurt or Kefir — 1 cup: 50 milligrams (13%

DV)

Almonds — 1 ounce: 80 milligrams (20% DV)

Black Beans — ½ cup: 60 milligrams (15%

DV)

Avocado — 1 medium: 58 milligrams (15%

DV)

Figs — ½ cup: 50 milligrams (13% DV)

Dark Chocolate — 1 square: 95 milligrams

(24% DV)

Banana — 1 medium: 32 milligrams (8% DV)

Other foods that are also high in magnesium

include: salmon, coriander, cashews, goat

cheese and artichokes.


Foods Rich in Zinc

Food

Milligrams (mg)

per

serving

Percent

DV*

Oysters, cooked, breaded and

fried, 3 ounces

74.0 493

Beef chuck roast, braised, 3

ounces

7.0 47

Crab, Alaska king, cooked, 3

ounces

6.5 43

Beef patty, broiled, 3 ounces 5.3 35

Breakfast cereal, fortified

with 25% of the DV for zinc,

¾ cup serving

3.8 25

Lobster, cooked, 3 ounces 3.4 23

Pork chop, loin, cooked, 3

ounces

2.9 19

2Baked beans, canned, plain

or vegetarian, ½ cup

2.9 19

Chicken, dark meat, cooked,

3 ounces

2.4 16

Yogurt, fruit, low fat, 8

ounces

1.7 11

Cashews, dry roasted, 1

ounce

1.6 11

Chickpeas, cooked, ½ cup 1.3 9

Cheese, Swiss, 1 ounce 1.2 8

Oatmeal, instant, plain,

prepared with water, 1 packet

1.1 7

Milk, low-fat or non- fat, 1

cup

1.0 7

Almonds, dry roasted, 1

ounce

0.9 6


Food

Milligrams (mg)

per

serving

Percent

DV*

Kidney beans, cooked, ½ cup 0.9 6

Chicken breast, roasted, skin

removed, ½ breast

0.9 6

Cheese, cheddar or

mozzarella, 1 ounce

0.9 6

Peas, green, frozen, cooked,

½ cup

0.5 3

Flounder or sole, cooked, 3

ounces

0.3 2

Sample Food for Dopaminergic Potentiation:

Fava Bean Dopamine Delights (Dr. Oz, 2017)

Makes 12 crostini

Ingredients:

12 brown rice crackers

3 tbsp extra virgin olive oil

Salt and freshly ground black pepper

1 cup fava beans, shelled

1/2 small Spanish onion

1 organic garlic clove

1 tbsp finely diced red pepper

10 black olives (pitted)

6 sprigs tarragon, leaves only

Directions:


Cook the fava beans in boiling water for 2

minutes. Drain and rinse under cold running

water. Purée the beans in a food processor with

the onion, garlic, olives, the remaining 1 tbsp

olive oil, and the tarragon leaves. Season with

salt and pepper to taste.

Just before serving, spread the fava bean

paste onto the rice crackers. Garnish with the

diced red pepper and a sprinkling of black

pepper.

Menus will be developed by the RD to

ensure that each meal delivers the goals of

providing 0.8 gm/Kg of l-tyrosine and

phenylalanine, zinc, and magnesium while

avoiding caffeine and simple sugars in an effort

to provide adequate dopamine precursor

substrate to boost dopamine levels in the limbic

system.


References

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