# doping2017

Игорь

MINISTRY OF PUBLIC HEALTH OF UKRAINE

ZAPOROZHYE STATE MEDICAL UNIVERSITY

DEPARTMENT OF PHYSICAL REHABILITATION,

SPORTS MEDICINE, PHYSICAL TRAINING AND HEALTH

Doping and athlete's

nutrition

Zaporozhye

2017

1

UDC 615.27+642]:796.07(075.8)

BBC 75я73

D73

Ratified on meeting of the Central methodical committee

of Zaporozhye State Medical University

(protocol N 3 from 02.03.2017)

and it is recommended for the use in educational process for foreign students.

Compilers:

Mikhalyuk E. L. - MD, PhD, Professor, Head of Department of Physical

Reabilitation, Sports Medicine, Physical Training and Health of Zaporozhye State

Medical University;

Tkalich I. V. - MD, Assistant of Department of Physical Reabilitation, Sports

Medicine, Physical Training and Health of Zaporozhye State Medical University;

Cherepok O. O. - MD, PhD, Assistant of Department of Physical Reabilitation,

Sports Medicine, Physical Training and Health of Zaporozhye State Medical University.

Reviewers:

Klapchuk V. V. , MD, PhD, Professor, Head of Department of Physical

Reabilitation, Zaporozhye National Technical University.

Bogdanovskaya N. V., PhD, Professor, Head of Department of Physical

Reabilitation, Zaporozhye National University.

Doping and athlete's nutrition: the educational and methodical

D7

manual / comp. : E. L. Mikhalyuk, I. V. Tkalich, O. O. Cherepok. –

3

Zaporozhye : [ZSMU], 2017. - 77 p.

Educational and methodical manual is made up on the basis of the working curriculum

and the program on «Physical rehabilitation and sports medicine» for medical students of the

medical educational institutions of the ІІІ-ІV accreditation levels for direction of education

"Medicine" 1101, for branches of study 7.110101 and 7.110104, according to the educational-

qualifying characteristic and the educational-professional program authorized by orders of

Ministry of Health of Ukraine as of 16.04.03 No. 239 and of 28.07.03 No. 504, and the

experimental curriculum of Ministry of Health of Ukraine developed on principles of the

European credit-transfer system and authorized by order of Ministry of Health of Ukraine as of

31.01.2005, No. 52.

The educational and methodical manual is intended for independent work of students of

medical faculties at preparation for practical employment on «Physical rehabilitation and sports

medicine» subject.

Discussed and approved at a meeting of the Cyclic Methodical Committee from Therapeutic

Disciplines of Zaporozhye State Medical University (the record No 5 as of 16.02.2017).

© Zaporozhye State Medical University, 2017

2

CONTENTS

1. Foreword................................................................................... Page 4.

2. The concept of doping.............................................................. Page 5.

3. 2017 Prohibited List................................................................. Page 6.

4. The growing competition between technical and

biological research and detection methods.......................................... Page 16.

5. The impact of doping on health................................................ Page 21.

6. Calling into question sports institutions: the

Sociological point of view.................................................................. Page 25.

7. Individual factors and the critical age question........................ Page 29.

8 . Energy drinks........................................................................... Page 32.

9. Eating disorders.......................................................................... Page 52.

10. Eating disorders in male athletes.............................................. Page 54.

11. Consequences of eating disorders........................................... Page 57.

12. References.............................................................................. Page 74.

Foreword

3

Pierre de Coubertin, founder of the modern Olympic games, was one of the

first to point out the necessity of protecting sport from the dangers threatening it as

an institution. In 1923, in a speech delivered in Rome, he denounced "the intrusion

of politics into sports, the increasingly venal attitude towards championship, the

excessive worshipping of sport, which leads to a belief in the wrong values,

chauvinism, brutality, overworking, overtraining, and doping".

Human's ability to resist extreme factors appreciably depends on individual

features of physiological reactivity of an organism, the speed of involving and

urgent efficiency adaptation mechanisms. Mechanisms of adaptation to various

environmental influences and physical loads have common and individual

features. Hereditary features of reactivity to a humoral stimulus and the character

of metabolisms which are under genetic control and are interconnected to the

development, structure and actions of skeletal muscles are a probable basis of

individual differences arising in adaptation. The specific metabolic capacities

usually are related to aerobic potential realization during loads of different power

and specific of athletes' aerobic-anaerobic energy potential utilization for sports

event.

Eating disorders are devastating psychiatric conditions. They have an

unacceptably high mortality rate and invoke considerable morbidity among those

affected. Athletes are at greater risk for eating disorders given the pressure to

achieve a body composition that optimizes performance.

This corresponds to the academic program for the 4th- year English-speaking

students of the Medical department upon studying “

4

I. The aims.

In order to enhance their performance, sportsmen use specific "methods" which

optimize the qualities needed for their sport, on the basis of various physiological,

biological, and psychological factors. According to a widespread opinion,

"upstream" doping, used for the above-mentioned aim, is "bad" and should be

distinguished from "downstream", or "good" doping, meant to help athletes recover

their physiological and biological balance. In fact, both types of doping are

complementary, since they artificially boost the body's abilities, the second type of

doping aiming to make up for the negative effects of the former.

Aerobic potential can be increased by increasing the blood's oxygen transfer

capacity. This is very important in sports requiring staying power, rely on the

body's energy metabolism, or require intense effort and varying sources of energy.

After long-lasting or intense effort, glycogen reserves must be restored. A specially

adapted nutritional strategy and drugs are then needed to modify the metabolic

process. Methods include altitude training, self-transfusion, more recently,

recombinant EPO, and of course glucocorticoids, etc. When the aim is to

increase strength and muscular power and improve technique, protein, natural or

synthetic anabolic agents are frequently used, in combination with hyperprotein

diets and muscle-building exercises. The balance between the increase in muscle

mass and the loss of fat mass can be maintained thanks to growth hormones

associated with aminoacids or other drugs with anabolic properties (but whose

initial medical purpose is other), or with nutritional supplements. To postpone

fatigue and enable the body to reach its utmost limits, one can use antalgics,

cardio-respiratory analeptics, central nervous system stimulants, several of which

are strong anti-depressants and stimulants.

In sports where body features or size, tall or short, are important, such as body-

building, the shape of the body can be modified through hormonal manipulations.

Various drugs are used to fight stress, facilitate sleep, remain in good physical

5

shape, such as benzodiazepine derivatives and amphetamines, cannabinoids,

alcohol, beta-blockers. For disciplines where it is important to stay alert, the

sleeping-waking rhythm can be controlled thanks to amphetamines or more recent

drugs. Last, cultural and invidual factors also play a role in drug-taking

behaviour. On the one hand, as concerns men, value is placed on the

mesomorphic body type and muscular strength; physical stereotypes are spread by

the media and the athletic subculture. On the other hand, one must take into

account factors such as low self-esteem, or other psychological problems linked to

for example to one’s body image and which existed prior to drug-taking. Illicit

drugs are of course taken on the sly. Several ways of hiding the fact exist: diluting

urine, hemodilution, reducing kidney tubular secretions or the

testosterone/epitestosterone ratio.

2017 Prohibited List

SUBSTANCES AND METHODS PROHIBITED AT ALL TIMES (IN AND

OUT-OF-COMPETITION)

S0. NON-APPROVED SUBSTANCES.

Any pharmacological substance which is not addressed by any of the

subsequent sections of the List and with no current approval by any governmental

regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical

or clinical development or discontinued, designer drugs, substances approved only

for veterinary use) is prohibited at all times.

6

S1. ANABOLIC AGENTS.

Anabolic agents are prohibited.

1.Anabolic Androgenic Steroids (AAS):

a. Exogenous* AAS, including: 1-androstenediol (5a-androst-1-ene-3ß, 17ß-diol

); 1-androstenedione (5a-androst- 1-ene-3,17-dione); bolandiol (estr-4-ene- 3ß,17ß-

diol); bolasterone; boldenone; boldione (androsta-1,4-diene-3,17-dione);

calusterone; clostebol; danazol ([1,2] oxazolo[4’,5’:2,3]pregna-4-en-20-yn-17aol);

dehydrochlormethyltestosterone (4-chloro-17ß-hydroxy-17amethylandrosta-1,4-

dien-3-one); desoxymethyltestosterone (17a-methyl- 5a-androst-2-en-17ß-ol);

drostanolone; ethylestrenol (19-norpregna-4-en-17aol); fluoxymesterone;

formebolone; furazabol ( (17a-methyl[1,2,5] oxadiazolo[3’,4’:2,3]-5a-androstan-

17ß-ol); gestrinone; 4-hydroxytestosterone (4,17ß-dihydroxyandrost-4-en-3- one);

mestanolone; mesterolone; metandienone (17ß-hydroxy-17amethylandrosta-1,4-

dien-3-one); metenolone; methandriol; methasterone (17ß-hydroxy-2a,17a-

dimethyl-5aandrostan-3-one); methyldienolone (17ß-hydroxy-17a-methylestra-4,9-

dien-3-one); methyl-1-testosterone (17ß-hydroxy-17a-methyl-5a-androst- 1-en-3-

one);


methylnortestosterone


(17ß-hydroxy-17a-methylestr-4-en-3-one);

methyltestosterone; metribolone (methyltrienolone, 17ß-hydroxy-17amethylestra-

4,9,11-trien-3-one); mibolerone; nandrolone; 19-norandrostenedione (estr-4-ene-

3,17-dione); norboletone; norclostebol; norethandrolone; oxabolone; oxandrolone;

oxymesterone; oxymetholone; prostanozol (17ß-[(tetrahydropyran-2-yl)oxy]-

1’Hpyrazolo[3,4:2,3]-5a-androstane); quinbolone; stanozolol; stenbolone; 1-

testosterone (17ß-hydroxy-5a-androst- 1-en-3-one); tetrahydrogestrinone (17-

hydroxy-18a-homo-19-nor-17apregna-4,9,11-trien-3-one).and other substances

with a similar chemical structure or similar biological effect(s).

b. Endogenous** AAS when administered exogenously: Androstenediol

(androst-5-ene-3ß,17ß- diol); androstenedione (androst-4- ene-3,17-dione);

dihydrotestosterone


(17ß-hydroxy-5a-androstan-3-one);


prasterone

(dehydroepiandrosterone, DHEA, 3ß-hydroxyandrost-5-en-17-one); testosterone;

7

and their metabolites and isomers, including but not limited to: 5a-androstane-

3a,17a-diol; 5aandrostane-3a,17ß-diol; 5a-androstane- 3ß,17a-diol; 5a-androstane-

3ß,17ß-diol; 5ß-androstane-3a,17ß-diol; androst- 4-ene-3a,17a-diol; androst-4-ene-

3a,17ß-diol; androst-4-ene-3ß,17a-diol; androst-5-ene-3a,17a-diol; androst-5- ene-

3a,17ß-diol; androst-5-ene-3ß,17adiol; 4-androstenediol (androst-4- ene-3ß,17ß-

diol); 5-androstenedione (androst-5-ene-3,17-dione); androsterone; 3ß-hydroxy-5a-

androstan-17-one; epi-dihydrotestosterone; epitestosterone; etiocholanolone; 7a-

hydroxy-DHEA; 7ß-hydroxy-DHEA; 7-keto-DHEA; 19-norandrosterone; 19-

noretiocholanolone.

2. Other Anabolic Agents, including but not limited to: Clenbuterol, selective

androgen receptor modulators (SARMs, e.g. andarine and ostarine), tibolone,

zeranol, and zilpaterol.

For purposes of this section:

* “exogenous” refers to a substance which is not ordinarily produced by the

body naturally. ** “endogenous” refers to a substance which is ordinarily produced

by the body naturally.

S2. PEPTIDE HORMONES, GROWTH FACTORS, RELATED

SUBSTANCES AND MIMETICS.

The following substances, and other substances with similar chemical structure

or similar biological effect(s), are prohibited:

1. Erythropoietin-Receptor agonists: 1.1. Erythropoiesis-Stimulating Agents

(ESAs) including e.g. darbepoietin (dEPO); erythropoietins (EPO); EPO-Fc; EPO-

mimetic peptides (EMP), e.g. CNTO 530 and peginesatide; methoxy polyethylene

glycol-epoetin beta (CERA);

1.2. Non-erythropoietic EPO-Receptor agonists, e.g. ARA-290; asialo EPO;

carbamylated EPO.

2. Hypoxia-inducible factor (HIF) stabilizers, e.g. cobalt and FG-4592; and HIF

activators, e.g. argon, xenon;

8

3. Chorionic Gonadotrophin (CG) and Luteinizing Hormone (LH) and their

releasing factors, e.g buserelin, gonadorelin and leuprorelin, in males;

4. Corticotrophins and their releasing factors, e.g. corticorelin;

5. Growth Hormone (GH) and its releasing factors including: Growth Hormone

Releasing Hormone (GHRH) and its analogues, e.g. CJC-1295, sermorelin and

tesamorelin; Growth Hormone Secretagogues (GHS), e.g. ghrelin and ghrelin

mimetics, e.g. anamorelin and ipamorelin; GH-Releasing Peptides (GHRPs), e.g.

alexamorelin, GHRP-6, hexarelin and pralmorelin (GHRP-2).

Additional prohibited growth factors: Fibroblast Growth Factors (FGFs);

Hepatocyte Growth Factor (HGF); Insulin-like Growth Factor-1 (IGF-1) and its

analogues; Mechano Growth Factors (MGFs), Platelet-Derived Growth Factor

(PDGF); Vascular-Endothelial Growth Factor (VEGF) and any other growth factor

affecting muscle, tendon or ligament protein synthesis/ degradation,

vascularisation, energy utilization, regenerative capacity or fibre type switching.

S3. BETA-2 AGONISTS.

All beta-2 agonists, including all optical isomers, e.g. d- and l- where relevant,

are prohibited.

Except:

• Inhaled salbutamol (maximum 1600 micrograms over 24 hours);

• Inhaled formoterol (maximum delivered dose 54 micrograms over 24 hours);

• Inhaled salmeterol in accordance with the manufacturers’ recommended

therapeutic regimen.

The presence in urine of salbutamol in excess of 1000 ng/mL or formoterol in

excess of 40 ng/mL is presumed not to be an intended therapeutic use of the

substance and will be considered as an Adverse Analytical Finding (AAF) unless

the Athlete proves, through a controlled pharmacokinetic study, that the abnormal

result was the consequence of the use of the therapeutic inhaled dose up to the

maximum dose indicated above.

9

S4. HORMONE AND METABOLIC MODULATORS.

The following hormones and metabolic modulators are prohibited:

1. Aromatase inhibitors including, but not limited to: aminoglutethimide;

anastrozole; androsta-1,4,6-triene- 3,17-dione (androstatrienedione); 4-androstene-

3,6,17 trione (6-oxo); exemestane; formestane; letrozole and testolactone.

2. Selective estrogen receptor modulators (SERMs) including, but not limited to:

raloxifene; tamoxifen and toremifene.

3. Other anti-estrogenic substances including, but not limited to: clomiphene;

cyclofenil and fulvestrant.

4. Agents modifying myostatin function(s) including, but not limited, to:

myostatin inhibitors.

5. Metabolic modulators:

5.1. Activators of the AMP-activated protein kinase (AMPK), e.g. AICAR;

and Peroxisome Proliferator Activated Receptorδ (PPARδ) agonists, e.g. GW 1516;

5.2. Insulins and insulin-mimetics;

5.3. Meldonium;

5.4. Trimetazidine.

S5. DIURETICS AND MASKING AGENTS.

The following diuretics and masking agents are prohibited, as are other

substances with a similar chemical structure or similar biological effect(s).

Including, but not limited to:

- Desmopressin; probenecid; plasma expanders, e.g. glycerol and intravenous

administration of albumin, dextran, hydroxyethylstarch and mannitol.

- Acetazolamide; amiloride; bumetanide; canrenone; chlortalidone; etacrynic acid;

furosemide; indapamide; metolazone; spironolactone; thiazides, e.g.

10

bendroflumethiazide, chlorothiazide and hydrochlorothiazide; triamterene and

vaptans, e.g. tolvaptan.

Except: - Drospirenone; pamabrom; and ophthalmic use of carbonic anhydrase

inhibitors (e.g. dorzolamide, brinzolamide).

- Local administration of felypressin in dental anaesthesia.

The detection in an Athlete’s Sample at all times or In-Competition, as applicable,

of any quantity of the following substances subject to threshold limits: formoterol,

salbutamol, cathine, ephedrine, methylephedrine and pseudoephedrine, in

conjunction with a diuretic or masking agent, will be considered as an Adverse

Analytical Finding unless the Athlete has an approved TUE for that substance in

addition to the one granted for the diuretic or masking agent.

PROHIBITED METHODS.

M1. MANIPULATION OF BLOOD AND BLOOD COMPONENTS.

The following are prohibited:

1. The Administration or reintroduction of any quantity of autologous, allogenic

(homologous) or heterologous blood, or red blood cell products of any origin into

the circulatory system.

2. Artificially enhancing the uptake, transport or delivery of oxygen. Including,

but not limited to: Perfluorochemicals; efaproxiral (RSR13) and modified

haemoglobin products, e.g. haemoglobin-based blood substitutes and

microencapsulated haemoglobin products, excluding supplemental oxygen.

3. Any form of intravascular manipulation of the blood or blood components by

physical or chemical means.

M2. CHEMICAL AND PHYSICAL MANIPULATION.

11

The following are prohibited:

1. Tampering, or Attempting to Tamper, to alter the integrity and validity of

Samples collected during Doping Control. Including, but not limited to: Urine

substitution and/or adulteration e.g. proteases.

2. Intravenous infusions and/or injections of more than 50 mL per 6 hour period

except for those legitimately received in the course of hospital admissions, surgical

procedures or clinical investigations.

M3. GENE DOPING.

The following, with the potential to enhance sport performance, are prohibited:

1. The transfer of polymers of nucleic acids or nucleic acid analogues;

2. The use of normal or genetically modified cells.

SUBSTANCES AND METHODS PROHIBITED IN-COMPETITION

In addition to the categories S0 to S5 and M1 to M3 defined to the left, the

following categories are prohibited In-Competition:

PROHIBITED SUBSTANCES

S6. STIMULANTS.

All stimulants, including all optical isomers, e.g. d- and l- where relevant, are

prohibited. Stimulants include:

a: Non-Specified Stimulants: Adrafinil; amfepramone; amfetamine;

amfetaminil; amiphenazole; benfluorex; benzylpiperazine; bromantan;

clobenzorex; cocaine; cropropamide; crotetamide; fencamine; fenetylline;

fenfluramine; fenproporex; fonturacetam [4- phenylpiracetam (carphedon)];

furfenorex; mefenorex; mephentermine; mesocarb; metamfetamine(d-); p-

12

methylamphetamine; modafinil; norfenfluramine; phendimetrazine; phentermine;

prenylamine and prolintane. A stimulant not expressly listed in this section is a

Specified Substance.

b: Specified Stimulants: Including, but not limited to: Benzfetamine; cathine**;

cathinone and its analogues, e.g. mephedrone, methedrone, and a-

pyrrolidinovalerophenone; dimethylamphetamine; ephedrine***; epinephrine****

(adrenaline); etamivan; etilamfetamine; etilefrine; famprofazone; fenbutrazate;

fencamfamin; heptaminol; hydroxyamfetamine (parahydroxyamphetamine);

isometheptene;


levmetamfetamine;


meclofenoxate;

methylenedioxymethamphetamine; methylephedrine***; methylhexaneamine

(dimethylpentylamine); methylphenidate; nikethamide; norfenefrine; octopamine;

oxilofrine (methylsynephrine); pemoline; pentetrazol; phenthylamine and its

derivatives;


phenmetrazine;


phenpromethamine;


propylhexedrine;

pseudoephedrine*****; selegiline; sibutramine; strychnine; tenamfetamine

(methylenedioxyamphetamine), tuaminoheptane; and other substances with a

similar chemical structure or similar biological effect(s).

Except:

- Clonidine

- Imidazole derivatives for topical/ ophthalmic use and those stimulants included

in the 2017 Monitoring Progam*.

* Bupropion, caffeine, nicotine, phenylephrine, phenylpropanolamine,

pipradrol, and synephrine: These substances are included in the 2017 Monitoring

Program, and are not considered Prohibited Substances.

** Cathine: Prohibited when its concentration in urine is greater than 5

micrograms per milliliter.

*** Ephedrine and methylephedrine: Prohibited when the concentration of

either in urine is greater than 10 micrograms per milliliter.

**** Epinephrine (adrenaline): Not prohibited in local administration, e.g. nasal,

ophthalmologic, or co-administration with local anaesthetic agents.

13

***** Pseudoephedrine: Prohibited when its concentration in urine is greater

than 150 micrograms per milliliter.

S7. NARCOTICS.

Prohibited: Buprenorphine; dextromoramide; diamorphine (heroin); fentanyl

and its derivatives; hydromorphone; methadone; morphine; oxycodone;

oxymorphone; pentazocine; and pethidine.

S8. CANNABINOIDS.

Prohibited: Natural, e.g. cannabis, hashish and marijuana, or synthetic ∆ 9-

tetrahydrocannabinol (THC). Cannabimimetics, e.g. “Spice”, JWH-018, JWH-073,

HU-210.

S9. GLUCOCORTICOIDS.

All glucocorticoids are prohibited when administered by oral, intravenous,

intramuscular or rectal routes.

SUBSTANCES PROHIBITED IN PARTICULAR SPORTS

P1: ALCOHOL:

Alcohol (ethanol) is prohibited In-Competition only, in the following sports.

Detection will be conducted by analysis of breath and/or blood. The doping

violation threshold is equivalent to a blood alcohol concentration of 0.10 g/L.

- Air Sports (FAI)

- Automobile (FIA)

- Archery (WA)

- Powerboating (UIM)

-

P2: BETA-BLOCKERS:

14

Beta-blockers are prohibited In-Competition only, in the following sports, and

also prohibited Out-of-Competition where indicated.

- Archery (WA)* ;

- Automobile (FIA);

- Billiards (all disciplines) (WCBS);

- Darts (WDF);

- Golf (IGF);

- Shooting (ISSF, IPC)*;

- Skiing/Snowboarding (FIS) in ski jumping, freestyle aerials/halfpipe and

snowboard halfpipe/big air;

- Underwater sports (CMAS) in constant-weight apnoea with or without

Including, but not limited to: Acebutolol; Labetalol; Alprenolol;

Levobunolol; Atenolol; Metipranolol; Betaxolol; Metoprolol; Bisoprolol;

Nadolol; Bunolol; Oxprenolol; Carteolol; Pindolol; Carvedilol;

Propranolol; Celiprolol; Sotalol; Esmolol; Timolol.

The growng competition between technical and biological research

and detection methods.

1. The rules enforced by the medical commission of the IOC.

The definition of doping established by the medical commission of the

"International Olympic Committee" is based on the prohibition of certain types of

pharmaceuticals. This definition also bans new substances which may have been

developed by laboratories specifically for doping purposes.A& ) &

HODS

2. Drugs which are detectable thanks to present testing methods.

All natural or synthetic doping drugs have a common physical and chemical

characteristic, which is low molecular weight (under 500) (see table II). They can

thus be detected by the usual analytical methods, such as gas chromatography,

together with mass spectrometry.

15

The only problem with the detection of xenobiotics is the fact that analysts

have to work with small samples, which are not always best suited to this type of

testing. However, as concerns endogenous substances, their detection does not

constitute sufficient proof of doping for the institutions in charge of enforcing the

law.

Table II: example of the molecular weight of several molecules

Example


of Molecular


Mass

Type of active substance

substance

(Mw)

Amphetamine

135

a. Stimulants

Cocaine

303

b. Natural or synthetic anabolic Nandrolone

274

agents

Testosterone

288

Dextromoramide

392

c. Narcotics and analgesics

Propoxyphene

339

Morphine

285

Pindolol

248

d. Beta-blockers

Acebutol

336

Propanolol

259

Ethacrinic


acid 303

e. Diuretics and masking drugs

Furosemide

330

Canrerone

340

HGH

22,400

f. Peptide hormones

LH

30,000

EPO

30,400

More recently, recent research in organic synthesis and genetic engineering has

produced new substances which are similar to natural peptide hormones (f) — a

combination of aminoacids which can stimulate the endogenous secretion of

substances such as androgenous steroids (hCG, LH, etc.) or corticoids (ACTH).

These molecules have a much heavier molecular weight than the others (see table

16

II). They are present in the body at very low levels of concentration, with

considerable variations from one person to the next, and are influenced by

environmental parameters such as effort, stress and/or fatigue. It is thus very

difficult to distinguish between natural and artificial variations.

3. The problem of natural or semi-synthetic or synthetic substances.

A certain number of substances normally used in specific medical circumstances

are now being used in top level sports because of their positive effect on several

physiological functions which play a role in sports. Erythropoietin (EPO) was thus

developed to treat anemia by stimulating the synthesis of red blood cells. Since it

increases corpuscular mass and oxygen transfer capacity, this drug has been used

for the past ten years in aerobic sports and as a rule all intense aero-anaerobic

disciplines, whether practised continuously or alternately. In healthy subjects, it

raises hemoglobin and hematocrite levels and improves staying and maximum

aerobic power. Its use — through injections, as in standard medical practice — is

simpler than transfusions which can cause problems and accidents. For the time

being, anti-doping tests cannot detect EPO. It is commercialized under various

denominations and sold in France at the Pharmacie Centrale des Hôpitaux.

Other drugs, either hardly commercialized or still awaiting market

authorization, are known for their ability to increase oxygen transfer capacity, such

as reticular haemoglobin, developed from a human molecule mainly used in

hemorrhagic emergencies, in order to avoid having to determine the blood type for

selective corpuscle transfusions. This is also the case of fluoro-carbons which are

even more convenient since they keep well. They can also be used as a recovery

activator after intensive effort. So far, no control procedure, in terms both of

prevention and testing, exists for this type of drug. A solution to this problem

should be found before it is commercialized, if possible.

The possibility of increasing muscular mass and acting on the anabolic or

catabolic properties of the metabolism is extremely interesting for top-level sports.

17

The use of androgens and anabolic agents has become increasingly widespread

over the past 20 years, especially with the development of synthetic anabolic

agents whose anabolic power is 30 to 50 times higher than that of natural

androgens. The growth hormone (hGH) developed by genetic engineering has

made it possible to avoid testing positive on synthetic anabolic agents. The

recombinant growth hormone is available on the market. It is used in all sports

where performance is linked to muscular mass, as well as in aero-anaerobic sports,

including team sports. The production of IGF1 (Insulin-like growth factor),

which completes the physiological action of the growth hormone, by genetic

engineering complicates the issue. IGF1 used together with the growth hormone

provides optimal results with smaller doses of both drugs and fewer side-effects.

This may explain the standardization of a certain body shape and the disappearance

of indirect signs of use of the single growth hormone. The availability of a second

IGF2 opens new prospects in the field of energy metabolism.

To a lesser degree, interleukin 3 can be used singly or with another drug to

enhance growth and stimulate corpuscle production. G-CSF is a growth enhancer

which acts mainly on white corpuscles. Although it does not have any known

effect on performance, it may help resist infections.

Analyzing peptide hormone levels in blood, especially the chorionic gonadotropin

hormone (hCG), the growth hormone and EPO is thus of utmost importance.

Synthetic peptide hormones presently in use have a chemical structure which is

identical, or at least very similar to that of natural hormones, and it is impossible to

distinguish their physical or chemical characteristics. Their dosage is at present

determined by immunology techniques, but quantitative standards would be

necessary to determine the exogenous presence of such substances.

4. Organizing the tests

Sports officials organize sports events, but the task of detecting illegal drugs is

devolved to others. If an athlete tests positive, s/he is punished by sanctions. Three

possible cases can occur:

18

- In the first case, tests show the presence of a banned substance which enhances

performance more than would simple training. In this case, there is no question

that this person must be sanctioned.

- In the second case, the tests show the presence of an illegal drug which does not

necessarily enhance performance. Sanctioning the athlete for this would be unfair,

since it would create an unequal situation between athletes and non-athletes, the

latter not being tested.

- In the last case, the test does not reveal any illegal doping substance because it is

"masked", new, or (temporarily) undetectable as an exogenous substance. In this

case, testing is impossible, though justified.

The world of sport is understandably quite ill-at-ease regarding this complex

issue. Indeed, sportsmen are used to dealing with extremely strict rules, in the

sense that all that is not explicitly forbidden is allowable. This principle is actually

what motivates technical progress, which in turn leads to a modification of the

rules.

Another important problem concerns the tests' underlying principle: indeed, sports,

as an institution, focuses on performance, not on the actors, whereas anti-doping

tests focus on the actors, in other words on the athletes as individuals.

Considered necessary, though imperfect, these tests are at the same time perceived

as imposed by external authorities; they are usually criticized and condemned on

principle, and when it comes to the actual testing procedure, attitudes are often

unclear: upon arrival of the physician in charge of carrying out the tests, athletes

and organizers often join forces. If an athlete is tested positive, the entire "family"

falls necessarily under suspicion, which leads to a tightening of group bonds.

When a case of doping is announced, the athlete and his entourage usually protest

loudly. Sports officials thus finds themselves in a contradictory situation: they ban

doping and base their authority on this prohibition, but at the same time, when

doping cases occur and persons are sanctioned, they express surprise, doubt, and

19

minimize the issue. The attitude of sporting authorities is thus far from clear,

especially if we consider that a century ago, doping was a poor man's resource to

earn some profit from sports, and that today, doping has become extremely

expensive. "Scientific" doping, with the accompanying "masking" procedures, is

affordable only to the rich. Improving the efficiency of antidoping tests does not

mean increasing the frequency of testing but carrying them out more efficiently, for

example by monitoring the athlete during the training period, and especially by

improving detection methods and reducing the margin of error on the tested

samples.

The task of laboratories specializing in drug detection is quite complex. To search

for the possible presence of one of 300 illegal drugs and/or their metabolites, at

any possible level of concentration in a selective and small urine sample, without

any chemical diagnosis to help direct the search in any specific direction, requires

extremely precise procedures in terms of sample preparation, methodology and

interpretation of results. Every year, the list of banned substances gets longer and

longer, which means that laboratory researchers must constantly revise and

improve their detection methods. Such a task is almost impossible when results

must be ready within 24 hours.

5. Present detection techniques.

Detection techniques are practically the same in all laboratories with

international accreditation. The first analytical stage, called the "fast" stage, is

based on immunological or radioimmunological methods, separative methods such

as gas chromatography and liquid chromatography (GC and HPLC) and methods

associating two techniques, such as chromatography/mass spectrometry (GS-MS,

HPLC-MS), chromatography/atomic emission detection (GC-AED).

Obviously, it is important to attain a maximum degree of sensitivity at this level,

in order to avoid falsely negative tests.

20

At this initial level of analysis, the samples can be sorted out so as to determine

those containing illegal substances, or, more generally speaking, those which do

not look quite normal.

The second stage of analysis consists in formally identifying the substances

(illegal or not) detected during the first stage and searching for various possible

metabolites, determining their level of concentration and identifying the drug as

precisely as possible by looking for other characteristic active ingredients or

vehicles.

The impact of doping on health.

1. Potentially fatal risks.

In 1886, Arthur Linton died during the Bordeaux-Paris race. In 1904, the

marathon runner Thomas Hicks collapsed after winning the Saint-Louis Olympics:

he had taken strychnine. Dorando Pietri died in London in 1908 for the same

reason. In 1960, the cyclist K. Jensen died during the 100 km road run in the

Rome Olympics. The drug Ronicol was blamed. In 1967, Tom Simpson, a

professional world cycling champion, collapsed and died while climbing the Mont

Ventoux after having taken amphetamines. In 1975, anabolics killed Kangasniesmi,

a weight lifter. His muscles gave in under the weight and the iron bar fell down,

breaking his spine.

These grave accidents, and there are many more, are well-known. It would be

difficult to ignore them, since they happened during competitions, in view of the

public and TV cameras. This, however, is only the visible part of the damage done

by doping: indeed, little is known about its effects once the athlete has left the

sports arena or given up his/her career. We do know for a fact that several great

champions suffered from serious health problems after leaving sport. And we also

know that there is a direct relationship between certain drugs and certain health

problems, such as heart disease or cancer: the existence of a causal relationship

21

between doping and disease thus appears increasingly probable. However, an

additional difficulty resides in the fact that some substances are very often used

together with another, main, drug, that some substances of the same nature (but

bearing different names) are used together, and that these cocktails undeniably

have a positive effect on performance.

1.1.

P

otentially dangerous drug cocktails .

No single drug can satisfy the numerous demands made on athletes to improve

performance, stimulate staying power, sustain effort during training, eliminate

stress. For this reason, s/he can be tempted to use drug cocktails, either as

"scientific doping" and/or as "easy" doping, the latter being used by athletes with

limited financial means. These "cocktails" can be made up of different drugs

whose combined effect increases their power, or of similar drugs with different

names, which, when taken together, bring the dosage to toxic levels. Among these

combinations: amphetamines combined with corticoids, cardio-respiratory

analeptics or cocaine, caffeine or ephedrin; EPO with aspirin and/or an

anticoagulant, or natural or synthetic glucocorticoids; to recover strength, a

combination of glucose-enriched serum added to insulin, IGF1, and as a

supplement, androgens, GH, beta 2-agonists. The list of possible combinations is

much longer, since cocktails are elaborated and adapted according to need.

Pharmacodependency.

Several doping substances used by athletes are considered by psychiatrists as

addictive, leading to drug abuse and dependence, and their psychological effects

and impact on behaviour have been described in the context of the study of

dysfunctions linked to drug use (cf. DSM-IV, American Psychiatric Association,

1994). Caffeine intoxication can lead to nervousness, overexcitement, insomnia, or

attacks of anxiety in certain persons. Cocaine or amphetamine intoxication can

cause hyperactivity, anxiety, stereotyped and repetitive behaviour, anger and

violent behaviour, altered judgement. Their chronic use can cause dulled

22

emotions, fatigue, sadness, social withdrawal, or, as concerns cocaine, persecution

mania and aggressiveness. According to De Mondenard (1991), marijuana, which

is used by some athletes either for its disputed stimulating effect or for the feeling

of calm it provides before an event, can sometimes cause anxiety, dysphoria and

social withdrawal.

2. Clinical and biological signs indicating an iatrogenic disease.

Drug abuse can lead to the development of iatrogenic diseases which must be

diagnosed early and with precision. The drugs used — generally in combination

and at high dosages — provoke changes in the person taking them, modifies in

his/her homeostasis, behaviour, and morphology. As a result, a clinical and

biological semiology of doping with a diagnostic tree should urgently be drawn

up as a diagnostic tool for physicians. Such a medicalized approach to doping

could lead to further investigation of the problem by specialists and to the

establishment of certificates of inaptitude to sport. This approach is only possible

in the framework of a system centered on the long-term monitoring of athletes,

conducted in specialized centers, by teams of clinical specialists in sports

medecine and thanks to sophisticated equipment for the evaluation of the athletes'

functional ability to sustain effort. This medical/athletic monitoring would be

computerized and carried out in close collaboration with the athlete's personal

physician.

3. Psychopathological problems.

Knowledge about the possible psychological and behavioral effects of drugs on

athletes stems exclusively from publications describing isolated cases of

pathological reactions to the use of anabolic steroids, and from experimental

research carried out on animals, voluntary human subjects, either healthy or taking

23

these drugs for therapeutic reasons, or still, from more or less systematic

comparisons conducted within small groups of athletes, both taking and not taking

drugs.

For example, problems linked to body image occur more frequently than

average in body-builders taking anabolic steroids. These subjects often suffer from

"reverse anorexia", feelings of dissatisfaction regarding their body, and bulimia.

Amateur weight-lifters of the male sex taking high doses of anablic steroids are

more aggressive towards objects and verbally aggressive during training. Their

periods of waking are longer and they are more irritable, anxious, suspicious and

negative. Mood changes are more frequent and personal relationships more

difficult when they are "on" drugs than when they are "off", or than in non-users.

4. Numerous determining factors.

Due to rising financial stakes and the toughening of the competition for

recognition and fame, athletes and their entourage tend to search for additional

ways of improving performances, even if it means disobeying the rules established

by the sports federations. Today, science has developed very effective drugs to

enhance performance and hasten the recovery of athletes facing increasing

constraints (schedule, competitions, events, etc.). Many athletes use drugs. The

wealthier athletes use them under the supervision of competent professionals,

while the others, in order to "stay in the race", resort to self-medication on the basis

of advice or information gathered in stadiums ("poor man" doping), unaware of the

risk they run. The analysis of determining factors shows that both sociological and

personal factors must be taken into account.

Calling into question sports institutions: the sociological point of view.

A sociological study of the doping issue must be based on the analysis of

relationships between sports actors holding various positions and whose interests

differ. With the development of sports as a business, the interaction between two

24

different rationales, that of athletic performance and that of profit, has become

increasingly complex, leading us to raise the question of the power of sports.

Competition sports are dominated by a complex system of interdependent

actors:

- the federations, whose aim, among others, is to ensure that rules and traditions

are respected,

- the athletes, who compete mainly for glory; however, through their unions and

associations, they demand recognition as professional players, as well as better

working conditions,

- the educators and coaches who wish to protect their interests, as opposed to those

of their employers (the clubs),

- the referees, employed by federations or professional leagues, who wish to

improve their working environment (professionalization, protection against

violence and pressure, etc.),

- the professional clubs (Unions of professional football clubs, basketball clubs,

etc.) who aim to some profit from their investment in sports, either in financial

terms or in terms of public image, etc.),

- the consultants, sometimes grouped together in multinational firms (International

Management Group, News Corporation, etc.), who manage the athletes' business.

Some of them own TV channels, shares in broadcasting rights for the more popular

sporting events,

- showbusiness companies, which try to reconcile the interests of the public with

those of their clients (sponsors, sports announcers) and those of the actors (the

athletes).

- companies selling sports and leisure equipment (equipment makers, distributors,

service companies, etc.) and sponsors,

- the specialized medical (sports physicians), paramedical, pharmaceutical

professions;

- journalists hunting for pictures, declarations, revelations which could be of

interest to news editors wishing to satisfy their readers'/viewers' demands,

25

- academics and researchers who publish articles and speak out on the subject and

thus wield some influence on public opinion and on the various actors involved,

- persons practising sports or sports fans, who, as consumers (of lessons, images,

clothing, equipment, etc.), support the entire system. Due to their numbers

(evaluated in terms of audience, number of copies sold, etc.), they play a very

important role (events postponed to ensure better attendance, scandals stifled so as

not to shock, etc.). Thanks to them, sponsors, businessmen and professional

athletes are able to earn a living.

When high level sports are governed by federations or olympic bodies, thanks to

state support or because of these institutions' monopoly over the award system

(their titles being the only "noble" titles), the rules of the game remain stable and

more or less protected against attacks of businessmen wishing to adapt the rules of

sport to public demand. However, when federations have little authority, sport can

turn into show business, opening the way for corruption, cheating and rule

changes.

1. Playing with the rules: a risky game.

As the stakes involved in competition sports grow higher, the rule is to get

around the rules. Not to take risks with the rules, or not being able to ensure one's

protection if suspected of cheating can mean being left out of the race. Those who

have nothing or not much to lose are the first to resort to cheating to attain their

goal. Those on the higher rungs of the social ladder are in a much better position

than others to play that dangerous game without getting caught. Persons who have

access to information, to more or less legal ways of getting round the rules

(waivers, corruption, or getting those in charge of enforcing the rules to close their

eyes), and resort to all kinds of loopholes to get around the law, move ahead faster

and remain in dominant positions longer than those who have no way of doing so.

(A "wealthy" club or athlete, in terms of both money and information, has easier

access to the services of physicians, or of laboratories specialized in doping and

masking drugs than "poor" clubs or athletes). To explain why certain athletes,

26

federations, physicians, referees, resort to cheating, it is necessary to question the

entire international sports system, nowadays entirely focused on the tough

competition for medals and money. Not to take drugs when others are taking them

would mean to lose. In this context, a special study on the side effects of the drugs

most used by athletes ought to be commissioned and results publicized among

regularly competing athletes. Players' and athletes' unions or associations would be

in the best position to carry out these information campaigns, since they can

protect athletes who are already locked in the system — forced to take drugs, or

addicted. Of course, athletes are under very high pressure, if only because only the

"best" are selected for competition; the pressure is exerted by actors who have an

interest in seeing "their" athletes win — federations, TV channels, consulting

firms, directors of professional clubs, coaches, event organizers, sponsors, etc.

There is a direct link between doping and the question of power relationships

between these various actors. Internationally recognized associations and unions

(such as in golf or tennis) would thus be the best source of information and

protection for athletes.

2. The declining authority of the federations.

Two processes are responsible for the decline of the power of federations.

In the first place, sports are now practised by all, whereas before World War II, the

working classes, women, and adults over 50 did not practise sports. The growing

TV audience for sports events has generated new sources of profit, leading to the

professionalization of the most popular sports. The sponsors of "show-business

sport" represent a counter-authority for federations, whose power stems from two

main sources: the monopoly on "noble sports" titles, which are a hundred years old

for the more traditional disciplines, and a network of clubs and volunteer educators

who coach millions of athletes and organize their activities. These two elements

are essential to the development of a sports elite, for the benefit of showbusiness

managers, independent professional leagues, sponsors, etc. The recruitment by

private companies of an elite trained in state subsidized clubs (professional clubs

27

or teams) is reminiscent of the transfer to the private sector of graduates of the

French state subsidized grandes écoles system. The second reason for the decline

of the power of federations is the development of other types of sports ("leisure"

sports, "street" sports) which, according to national surveys, draws as large a

public as there are licensed athletes, in other words about 12 million people. Along

with the emergence of these "new" sports, there has been a change of attitude

towards federations, which tend to be considered as service providers rather than

authorities. Athletic excellence is viewed differently from one generation to the

next; nowadays, the winner (according to the rules) is not necessarily the "best"

player. "Excellence" is less a question of measurable, objective performance than

one of self-expression and style, mirroring the aspirations of a generation. "Fun"

sports remain competitive, of course, but creativity and artistic expression are

nevertheless central. These "new" sports include skateboarding, rollerblading,

acrobatic biking, break-dancing, border-crossing, jumping contests, etc.

Demographic and social transformations may explain why the principles which

dominated 19th and 20th-century sports no longer correspond to the expectations

of most members of today's new generations. Though institutional sports have

managed so far to preserve the illusion that their principles were universal, it now

appears that they are not eternal; they only hold true in a world where the values,

beliefs and ideals they represent are shared by all.

Individual factors and the critical age question.

1. Varying degrees of susceptibility.

In addition to sociological factors, individual factors also play a significant

role. Group pressure and financial interests can drive most, if not all, athletes to

28

dope themselves. Nevertheless, doping behaviour — the age at which an athlete

will begin to use drugs and the development of addiction — is also determined by

individual factors. In this respect, it should be noted that there are many former top

athletes among chronic drug users. Heroin or any other drug thus acts a

replacement for sport, which for them was practically a drug in itself.

Several reasons have been suggested to explain this phenomenon. On the one hand,

the daily and mechanical practise of sports blocks unpleasant thoughts and

anesthetizes the mind, in the same way as heroin. Furthermore, when a person

attempts to exceed his/her physical limits, the body secretes endorphin which acts

as an endogenous drug. Although no specific study has been carried out on the

relationship between sports, doping and drug addiction, enough scientific data

exists to show that there is a great deal of inequality among athletes in this respect.

1.1. Temperamental factors.

Personal temperament also determine the choice of behaviour in a given

situation. It is a known fact that differences in behaviour are determined for a large

part by biological factors, in particular as concerns reactivity towards the

environment and need for stimulation. Thus, it has been shown that highly reactive

persons tend to prefer situations which have low stimulating power, and conversely

for persons with low reactivity. The need for strong sensations and new and

intense experiences is governed by the need to reach a high level of sensorial

activation. However, the forms of behaviour aimed at reaching this level of

activation may vary a great deal: drugs and alcohol, danger, adventure (dangerous

sports, mountain-climbing, hang gliding, etc...). In the understanding that each

individual has his/her own personal optimal level of activation and his/her own

way of reaching it, one can see how persons who enjoy taking risks may be liable

to use psychostimulants or drugs.

1.2. Motor activity as a source of gratification.

29

Physical exercise requires the participation of the body's physiological systems

and modifies its homeostasis. In particular, it modifies the activity of several

cerebral neurotransmitter systems. In animals, heavy exercise, prolonged exercise

and overexercising have opposite effects. For most neurotransmitters, the release

increases, then decreases (with slowing down of activity) if the exercising lasts a

long time. Furthermore, it is a known fact that exercising can lead to hormonal

changes, by increasing the secretion of prolactin, of the growth hormone and

corticosteroids. Some of these hormones have a powerful effect on most

neurotransmitter systems. These neurotransmitter systems are both the target of

doping substances and the providers of gratification. As a result, it is easily

conceivable that proneness to addiction should entail doping behaviour, with

doping substances taken together with other drugs. This is all the more true for

persons with a need for strong sensations.

2. Adolescence: a period of major risk.

2.1. Taking doping substances together with drugs: the risk for teenagers and top

athletes.

The subject of doping is usually exclusively related to sports, since doping

drugs are used to enhance performance, as opposed to other forms of addictive

behaviour. In fact, in recent years, the parallel between doping and drug addiction

has become increasingly obvious, and some authors, such as P. Laure (1995), have

been considering whether one should not "regard doping not only as a way of

enhancing performance but also, and most importantly, as a new form of drug

addiction". Indeed, it has long been known that the use of "doping" substances

such as amphetamines, and more recently, anabolic steroids, can lead to drug abuse

and physical and psychological dependence. Between 1980 and 1990, several

epidemiological surveys were conducted in United States high schools. Their aim

was to evaluate teenagers' consumption of anabolic steroids, possibly in

combination with other drugs. This represents a new phenomenon among

teenagers, whether or not they practice sports, and the reason they gave for

30

taking drugs was the wish to improve physical appearance and muscular strength.

According to the surveys, 2 to 4% of teenagers of both sexes, but mostly boys, had

used anabolic steroids. The average age at which they begin is 14 (ranging from 8

to 17), and the proportion of users is slightly higher among those practising

sports. Recent surveys conducted in American and Canadian high schools show

that teenagers practising sports admitted to having taken anabolic steroids in order

to improve their performance, but that they also drank, smoked and used other

drugs, in the same way as those who did not practise sports.

The first surveys conducted on the drug habits of young American

athletes date back to the early 1980s. These surveys showed that athletes took

psychoactive drugs just as did their non-athletic peers. Subsequent studies carried

out in the early 90s do not confirm the generally accepted idea that sports students

use more drugs and drink more alcohol than others. Neither do they confirm the

existence of an anabolic doping "epidemic" in American colleges. Recent studies

carried out in Canada among athletes of both sexes underscore the importance of

alcohol and caffeine consumption. In conclusion, the various epidemiological

surveys conducted in the United States and Canada, in various environments, with

students practising competition sports, or not practising sports, show that there are

not many differences in the choice of drugs in general, whether these are legal,

such as alcohol, illicit, or "doping" substances. The distinction between use and

abuse is not clearly marked.

2.2. Psychopathological disorders underlying the abuse of psychoactive drugs

Certain psychiatric disorders are more frequently observed among young drug

addicts, a fact which raises the question of whether these disorders play a role in

determining a subject's proneness to drug-taking. Depending on the survey,

emphasis is laid on some substances rather than others, but globally, all are

involved (tobacco, alcohol, marijuana, hard drugs such as cocaine). The vast

majority of users are male. However, "externalized" disorders are not the only

explanations for drug addiction among these teenagers. "Internalized" or

31

"emotional" disorders — mood changes, anxiety — are also frequently observed. It

is important to determine whether these observations apply to doping substances as

well.

Important semiological similarities have been observed between the

behavioural and biological characteristics of athletes and those of persons suffering

from eating disorders. Thus, amenorrhea, which often happens in cases of mental

anorexia, is a frequent problem among long-distance runners. These connections

show that the intensive practise of sports is often in itself a form of addiction. In

the same line of thought, one may note that eating disorders are extremely frequent

among young female gymnasts. Another disorder, hyperactivity with attention

deficiency may be an underlying problem in cases of drug abuse. Given its

frequency among children, as well as among teenagers and adults, it would be

particularly interesting to study its incidence in a large sample of young athletes

and correlate this disorder with drug and/or doping substance abuse. This disorder

affects 2 to 3% of the adult population. Drug abuse usually begins during

adolescence or in early adulthood, and affects 10 to 20% of adults.

Energy drinks.

Health hazard data on energy drinks were found to be limited

and therefore the hazard assessment was based on individual

ingredients.

Caffeine was identified as the ingredient with the greatest potential for

intakes of possible health concern. On this basis, excess consumption of

energy drinks would be expected to result in health consequences similar to

those from excess exposure to caffeine. The more mild and transient health conseq

uences could include anxiety, headache and insomnia and these health

consequences can become chronic conditions.

More severe health consequences may include irregular heartbeat, heart attack

and,

very

rarely, death.

Currently,

the

potential

for

taurine

and glucuronolactone to interact with caffeine is unknown and therefore

they

32

may or may not exacerbate the effects of caffeine. In addition, the

health effects of excessive intake of taurine and glucuronolactone are also

unknown.

Using exposure modelling, the potential health risk posed by energy drink

consumption was examined. However, no Canadian intake data for energy

Drinks were available. Therefore, for the purpose of modelling intake, it

was assumed that energy drinks are consumed in a manner similar to

that of caffeinated carbonated soft drinks. In the worst case modelling exposure

scenario, energy

drinks were substituted for caffeinated carbonated

soft drinks on a volume basis. The energy drink caffeine concentration was set

to

320 ppm

(80

mg

of

caffeine/250

ml

serving)

for

modelling purposes. In the most conservative scenario, all caffeinated carbonated s

oft drinks were replaced by a typical energy drink for consumers who drink

these beverages. The results of this conservative estimate showed that

slightly less than 30% of male and female adults, about 15% of pregnant woman an

d more than 50% of the children and adolescents, amongst consumers who

drank

caffeinated carbonated

soft

drinks,

were

above

Health

Canada’s recommended maximum daily caffeine intake.

This extreme scenario only applies to that subset of the population that

consumes caffeinated carbonated soft drinks, which does not exceed 8% of

young children (1‐8 years old), 22% of older children (9‐14 years old), 32% of ado

lescents, 20% of the adult population and 13% of pregnant females.

In critically reviewing the outcomes of this exposure modelling, it

appeared that the corresponding health concerns for children and adults

would be limited to remote, based on this scenario, in view of the

parental control that should exist and would limit access of these products

to to children, as well as the ability of adults and pregnant women to monitor their

own caffeine intake.

This hypothetical scenario and its outcomes could not be as easily excluded for

adolescents, given that energy rinks tend to be marketed to this subset of the

33

population, which is less likely to adhere to consumption recommendations than

adults. The existence of larger volume containers (e.g., 710 ml) increases the

likelihood of exceeding caffeine recommended intakes in one consumption

setting. Specific risk management measures to address potentially high caffeine

levels in larger volume energy drink products would therefore be desirable.

It is acknowledged that various data gaps would need to be addressed

to improve the exposure assessment

and the overall risk

characterization. In particular, data related to the evolving consumption patterns of

these products by the various subsets of the population, in Canada, needs to be gat

hered.

Health Canada’s proposed risk management approach

for energy drinks, announced in October 2011 and updated in 2012, limits the

concentration and total amount of caffeine in these products and requires that

caffeine and nutrition information be displayed on product labels.

These measures support the mitigation of risks related to overconsumption of

caffeine from this type of product that are within the possible areas of

intervention available to a federal food regulator. A more concerted approach

(e.g., education, awareness and regulation) and more research would

be needed to ascertain the effectiveness of the various measures taken

by regulators and other stakeholders.

Defining a typical energy drink.

Defining products known as energy drinks For the purpose of thi

s document, a typical energy drink is characterised

by the ingredients and ingredient levels shown in Table 1. Ingredients include

caffeine, taurine, glucuronolactone, inositol and a variety of B vitamins. The

basis for this characterisation is the formulation of the most commonly sold

products of this category of

beverages, such as the product known as Red Bull.

Although Health Canada does not have a definition or standard for

products

known

as

energy

drinks,

other food regulators have reached a decision on this aspect of these products. For

34

example, Australia and New Zealand categorizes energy drinks as ‘formulated

caffeinated beverages’ which are defined under the Australia New Zealand

Food Standards Code as “a non‐alcoholic water‐based flavoured beverage

which contains caffeine and may contain carbohydrates, amino acids,

vitamins and other substances, including other foods, for the purpose

of enhancing mental performance”.

In Europe, the Ireland Food Safety Promotion Board (FSPB) established a

committee consisting of external experts to research the health effects

of ‘stimulant drinks’ (energy drinks). The committee noted in its final

report that there is no agreed definition in the regulatory framework for

products referred to as energy drinks or ‘stimulant drinks’. For the purposes

of the report, the term ’stimulant drinks’ was adopted. The

committee defined

stimulant

drinks

as

“beverages,

which

typically contain caffeine, taurine and vitamin(s), and may contain an

energy

source (e.g. carbohydrate), and/or other substance(s), marketed for the

specific

purpose

of providing

real

or

perceived

enhanced

physiological and/or performance effects” (FSPB, 2003).

Major components of energy drink products During the preparation of this

manuscript, energy drinks were marketed in Canada under the Natural Health

Products (NHP) Regulations. At the time, it was estimated that over 300 energy

drink product submissions were before Health Canada for consideration as

NHPs. Only twelve were assessed and received a license. Approximately half

of the 300 product submissions

were either refused a license or withdrawn by the petitioner.

either refused a license or withdrawn by the petitioner.

A number of products were also on the Canadian market

under the provisions of the Unprocessed Product Licensing Regulations. Table

below lists the major ingredients and levels typically found in the products

that were in the queue for consideration to be licensed as an NHP.

Substance Formulation of products known as Energy Drinks (mg. per 250 ml

35

serving)

Caffeine 50 – 200 80

Taurine 10 – 2000 1000

Glucuronolactone 600 – 1200 600

niacin 10 – 40 18a

vitamin B6 5 – 10 2

vitamin B12 0.002 ‐ 0.2 0.001

pantothenic acid 5 – 10 6

thiamine 0.5 ‐ 5 2

riboflavin 0.5 ‐ 5 1.65

Inositol 50‐200 50

Serving size is typically 250‐473 ml.


Health Effects of Energy Drinks.

The research on energy drinks is largely limited to a small number of clinical

studies (about 12 studies) and case reports.

The clinical studies tended to have small numbers of participants (less than 100 su

bjects) and focused on very specific health effects. These studies mostly examined

the effect

of

energy

drink

consumption

on

behaviour

and physical activity; therefore, the parameters examined were limited and not

necessarily

significant

from

a

health

and safety perspective. Other studies assessed the consequences of consuming the

combination of energy drinks and alcohol.

Calories.

Except for sugar‐free versions, energy drinks, like many beverages, contain sugars

in the form of sucrose, glucose, and/or high‐fructose corn syrup. The sugar content

varies among energy drinks but ranges from 21 to 34 grams per 237 ml. can

(Clauson et al. 2008). This sugar content is similar to that of carbonated

caffeinated soft drinks.

36

During each heartbeat, blood pressure varies between

a maximum (systolic) and a minimum (diastolic) pressure. constitutes the vast maj

ority of calories in these products. A 250 ml. serving of a typical energy drink

contans 110 calories, which is similar to the 86‐130 calories in the same volume

of a carbonated caffeinated soft drink (USDA Nutrient Database, 2011).

Health Effects of Energy Drinks and Sports Activity Energy drinks are

frequently marketed to individuals interested in athletics and an active

lifestyle.

The ain ingredients in energy drinks purported to enhance sport performance

are

caffeine

and

carbohydrates.

The

term “energy drink”

itself

implies that its consumption might enhance physical activity.

Energy drinks should not be confused with ’sports drinks’. Sports drinks

are typically a mixture of carbohydrates and electrolytes formulated to

enhance athletic performance and prevent dehydration, and, unlike energy

drinks, they do not contain caffeine. Conversely, energy drinks contain

caffeine which is a stimulant and therefore they are not considered suitable to re‐

establish normal body function after exercise (e.g. normal heart rate).

Studies investigating the use of energy drinks have generally found an

improvement in endurance performance.

The consumption of 500 ml of a Red Bull energy drink 40 minutes before a s

imulated

cycling

time

trial

in

12

trained

cyclists

significantly improved endurance performance compared to a non‐caffeinated,

sugar‐free

placebo.

Significantly

increased

upper

body

muscle endurance but had no effect on anaerobic peak or average power

during

repeated Wingate cycling tests in healthy young adults, when compared to a

non‐caffeinated, isoenergetic, control beverage. Pre‐workout energy drink

consumption, significantly improved some physiological adaptations to combined

aerobic and resistance training, when compared to a non‐caffeinated, sugar‐

free control drink. Lastly, a study investigating the use of a sugar‐free energy

drink (Red Bull) found that there was no difference in run time‐to‐

37

exhaustion or perceived exertion in young adults when compared to non‐

caffeinated sugar‐free placebo. Overall the studies’ result suggest that the

consumption of energy drinks may enhance physical ability but it is not

clear whether the effect is due to the presence of caffeine, sugar or both of these co

nstituents in the energy drink.

Energy drinks, like other beverages containing added sugars, are

often associated with a high caloric intake. These drinks are not to be

considered “sports drinks” as they contain at least one ingredient that is a

stimulant (caffeine). Despite some study results suggesting that energy drink

consumption prior to exercise may have some performance benefits, there are

concerns, as caffeine may delay the return to a resting heart rate. Limited study res

ults have shown increases in systolic blood pressure and heart rate associated

with moderate intakes of energy drinks (2 servings). However, across the

various studies, transitory changes in blood pressure did not

reach hypersensitive levels with consumption of energy drinks. These effects were

deemed to be similar to the effects on blood pressure demonstrated in conjunction

with caffeine intake.

There were insufficient toxicological data to characterize the health hazard

associated with energy drinks as a single product.

As a consequence, the major individual ingredients were assessed for hazard

identification and hazard characterization, and this was considered a means

to gain insight into the hazard characterization of energy drinks.

Energy drinks can be generally characterised as containing the following

ingredients: caffeine, taurine, glucuronolactone, inositol and a variety of B

vitamins, including thiamine, niacin, vitamin B6, vitamin B12, pantothenic

acid and riboflavin.

The

dietary

sources,

nutritional

aspects

and

toxicity

of

these ingredients are reviewed below.

Caffeine.

38

Caffeine

is

consumed

as

a

natural

constituent

of

coffee, tea, chocolate and other natural sources, such as guarana and yerba mate. It

is also used as a food additive and is present in certain carbonated soft drinks. It is

also present in some therapeutic products, such as cold remedies and

allergy medicines. In Canada, it is estimated that male and female adults

have a respective mean intake of 281 and 230 mg. of caffeine per day.

These amounts are about three times the 80 mg of caffeine present in a

single 250 ml. serving of a typical energy drink.

When a single serving of a caffeinated beverage containing 40‐

120 mg of caffeine is consumed the main biological effect of caffeine is that

it acts as a stimulant and promotes alertness,

stimulant enhances cognitive performance, relieves fatigue and promotes

physical endurance. A single serving can also cause transient adverse

effects, such as insomnia, headaches and nervousness in caffeine‐sensitive

individuals.

It was concluded that a healthy adult could tolerate a maximum intake

of 400 mg of caffeine per day (equivalent to 6 mg/kg bw/day for a 65 kg adult). Th

is amount of caffeine was not associated with adverse effects such

as general toxicity, cardiovascular effects, effects on bone status, changes

in behaviour,

effects

on

male

fertility

or

increased incidence of cancer.


Further, the assessment concluded that reproductive‐

aged women could tolerate a maximum intake of up to 300 mg.

caffeine per day (equivalent to 4.6 mg/kg bw/day for a 65 kg. adult), based on

reproductive considerations (spontaneous abortion, retarded fetal growth).

Finally children, aged 4 to 12 years, were considered to tolerate a maximum of 45

to 85 mg. of caffeine per day (equivalent to 2.5 mg/kg bw/day for a child

weighing 18 to 34 kg.), based on transient mild behaviour changes.


There

were

insufficient

data

to

recommend

a

daily

maximum intake of caffeine for adolescents, aged 13 to 18 years.

39

However, the adult recommendation could be considered inappropriate

since

many adolescents may have a lighter body weight

may have a lighter body weight More importantly, adolescents are less

developed than adults and their growing bodies may be more susceptible

to adverse effects of caffeine.

One author has suggested that caffeine may adversely affect the growing

adolescent brain.

Alternatively, adolescents may be less habituated to consuming caffeine

and therefore may be more susceptible. In any case, there is

substantial uncertainty

as

to

whether

the

adult

recommendation should be applied. As a precaution, it would be prudent to recom

mend that an adolescent have a daily intake of caffeine no greater than the amount

calculated from the dose

used

to

determine

the

recommended

maximal intake for children (2.5 mg/kg bw/day) and the individual adolescent

body weight (estimated range of adolescent body weights: 40‐70 kg.). This

dose would suggest that adolescents could consume 100 to 175 mg. of

caffeine daily, depending on the individual body weight of the adolescent.

It should be noted that all of these recommended maximum intakes of

caffeine are considered a daily amount that would be the result of

cumulative consumption

throughout

the

day.

The

ingestion

of

the daily maximum intake in a brief period of time, that is 1‐2 hours, may cause

adverse reactions, such as insomnia, headache, stomach ache, nervousness,

nausea or more serious reactions. For example, studies have shown that a

single ingestion of more than 250 mg. of caffeine by a healthy adult can also

cause an increase in blood pressure while more than 450 mg. of caffeine may

result in tachycardia.

Taurine.

Taurine is an amino acid that is naturally present in the diet. Specifically, it is

found

in

meat

and

seafood.

Estimates of

human

daily intake of taurine range from 40 mg. to 400 mg. These dietary levels of

40

taurine

are

relatively

low

compared

with

the 1000 mg. of taurine present in a single serving of a typical energy drink.


Taurine is also synthesized in the liver from the

amino acid cysteine, as well as from other sulphur compounds. It has a role in seve

ral biological processes, including the formation of bile salt, cell membrane

stability, the modulation of calcium flow and neuronal excitability (FSPB

2002). Taurine is considered essential for the normal development of infants

and consequently it is a standard ingredient in infant formula, such that

newborns ingest about 280 mg daily (equivalent to a dose of 17 mg/kg bw/day).

Taurine is one of the most abundant amino acids in the human body.

Human studies suggest that taurine is readily absorbed from consumed

food and that plasma level of taurine peak within an hour after ingestion

(SCF 2003). This observation is consistent with the findings of a

study where rats received taurine as a single oral dose of

300 mg/kg bw. It was observed that the exogenous taurine is quickly

absorbed

into

the

body,

equilibrates

with endogenous pools of taurine

and that excess amounts are rapidly eliminated by the kidneys. The study also sho

wed that a 14‐day repeat treatment with taurine did not change the fate of

the last single oral dose, which suggests that the body can

metabolically handle relatively large amounts of taurine daily. The acute oral toxici

ty of taurine is considered relatively low, such that no adverse effects have

been observed

following a single administration in rats up

p to 7000 mg/kg bw or in humans up to 150 mg/kg bw (equal to 10,500 mg for a 7

0 kg. adult).


In short‐

term studies with human subjects, the ingestion of up to 6000 mg per day for 42 da

ys and 1500 mg per day for 90 days showed no evidence of adverse

effects (SCF 2003). In a 90‐day study in rats, taurine was administered by

gavage to groups of animals (20animals/sex/dose) at doses of 0, 300, 600

or 1000 mg/kg bw/day. No taurine‐related changes of standard toxicological

41

parameters were observed. The exception was a dose‐related behavioural

change (increased activity, self‐injury) that was observed in all three treated

groups and in both sexes of the test animal (SCF 2003).

A developmental toxicity study in mice showed that when orally

administered at a dose of 4000 mg/kg bw/day on days 7 to 14 of gestation,

taurine was not a teratogen, that is, it did not cause birth defects.

In

the

additional

studies

conducted,

taurine

has

not shown any mutagenic or genotoxic potential in bacterial or mammalian cell in

vitro assay systems.

There are no long‐term toxicity or carcinogenicity studies conducted to assess the

carcinogenic potential of taurine; however, there is no indication that taurine

is a carcinogen based on short‐term toxicity studies.

In over thirty studies with adult, child and infant subjects, the use of taurine

has

not

demonstrated

any

safety concerns. Most of these studies involved the ingestion of taurine on a daily

basis with doses in the range of 3000 to 6000 mg for periods of up to one month or

longer without any apparent adverse health effects (EFSA 2009).

One double‐blind study in human volunteers (14 subjects) showed that a

combination of caffeine and taurine, at levels present in a typical

energy drink, had no effect on short‐term memory, as indicated by

an abbreviated version of a standard test for short‐term memory. However,

this combination did induce a decrease in heart rate and an increase in

mean arterial blood pressure.

This finding is unexpected since caffeine generally stimulates heart rate. Furt

her investigation into the combination of these two substances is warranted.

D‐Glucurono‐γ‐lactone.

D‐Glucurono‐γ‐lactone (glucuronolactone) is the γ‐lactone of glucuronic acid.

It is a normal human metabolite and formed from glucose and glucuronic acid.

It seems to be found naturally in only a small number of foods such as wine and pl

ant gums (e.g. guar gum, gum Arabic). An estimate of the mean daily intake

42

is 1.2 mg/day and a high daily intake is suggested to be 2.3 mg/day (SCF

1999).

These

intake

values

are

very

small when compared to the intake of glucuronolactone of 600 mg from the consu

mption of a single serving of a typical energy drink. It is claimed that

glucuronolactone is a quick energy source and may assist in the detoxification

of xenobiotics (SCF 1999).

Human and rat studies show that when ingested, glucuronolactone is

rapidly absorbed, metabolised and excreted as glucaric acid, xylitol and L‐

xylulose.

These compounds

are

not

considered

to

be

toxicologically significant (ANZFA 2001). In contrast to humans, mice and

rats

have

an

additional

metabolic

pathway

that allows them to use glucuronic acid to synthesize vitamin C. Rodents can

also

use

exogenous

glucuronolactone

to yield glucuronic acid and then generate vitamin C. This additional pathway in

the

rodent

created

some uncertainty with respect to the appropriateness of rodents as a model for

humans.

However, further examination of the issue has determined that the

rodent metabolic pathway is relatively minor in the animal’s handling of

glucuronolactone, which suggests that toxicological results from rodents are

relevant to the human situation.


The acute oral toxicity of glucuronolactone is very low, such that in mice

the oral LD50 is greater than 20000 mg/kg bw. The short‐

term oral toxicity of glucuronolactone was assessed in a study where groups of

rats

(20 animals/sex/dose)

were

administered

a

single

daily gavage dose of 0, 300, 600 or 1000 mg/kg bw, for up to 90 days (SCF 2003).

The results showed no treatment‐related deaths, no significant difference in

body

weights,

food consumption,

hematological

or

clinical

chemistry parameters.

Urinalysis

showed

that

males

treated

43

with 1000 mg/kg bw group had urine with a lower pH than the control group, and

males in the 600 and 1000 mg/kg groups had a lower specific gravity than

the control group. Results from histopathological examination showed

vacuolisation

and

inflammatory

changes localised to the papilla of the kidney in females such that at doses of 0,

300,

600

and

1000

mg/kg

bw/day,

the incidences were respectively 11/20, 9/20, 11/20 and 11/20.


In a second 90‐day study in rats, the toxicity

of glucuronolactone was assessed with specific focus on the kidneys (SCF 2009).

The previous gavage study was repeated with an additional four sets of

animals

(20 animals/sex/dose)

that

received

glucuronolactone

in drinking water; with both routes of administration animals received nominal dos

es of 0, 300, 600 or 1000 mg/kg bw for 90 days. There were no treatment‐related

deaths, no effects on clinical observations, food or water consumption, body

weights,

clinical

parameters,

organ

weights

or

clinical chemistry parameters related to renal function. Lastly there were no test m

aterial‐related gross or microscopic findings. This included the kidneys

which showed typical amounts of background lesions for this strain of rat.

There

was

no

test

material‐

related vacuolisation of the cells lining the collecting tubules of the

kidney. This suggests that the kidney lesions observed in the first study were not

significant, since the drinking water administered in the second

study was more relevant to the human situation. Reproductive and developmental

toxicity studies for glucuronolactone were not available but were

not considered

necessary

to

conduct,

as

part

of

the

safety evaluation since glucuronolactone in the body hydrolyses to glucuronic acid,

which is an endogenous metabolite in humans and present in normal human diets.

Glucuronolactone

was

shown

not

to

be

mutagenic

in

a bacterial reverse mutation system.

Inositol.

44

Myoinositol (inositol) is a constituent of phosphatidylinositol, a phospholipid,

which plays an essential role in growth, metabolism regulation and

signal transduction.

Inositol

is

a

normal

component

of

human tissue and can be synthesized in some tissues. It is a normal part of food der

ived from plants in the form of phytate and from animals in the form of free

and phosphorylated inositol and as inositol phospholipid. It is estimated

that adults ingest about 500 to 1000 mg of inositol daily. This amount

is

relatively large compared to the 50 mg of inositol present in a single

serving of a typical energy drink.


The toxicity associated with inositol is very low. In

mice the oral LD50 is reported to be 10000 mg/kg bw. There are no reproductive

or developmental toxicity studies or genotoxicity studies that assessed

inositol. Although inositol was not tested as a carcinogen, several

studies assessed

its

ability

to

prevent

cancer

development

in mouse models. The results showed that a 3% level in the diet (equivalent to a do

se of 6000 mg/kg bw/day) did not increase cancer formation.

In humans, inositol has been used as an experimental therapy for

depression,

panic

disorder,

and

obsessive compulsive disorder. There is a report of people consuming up to 20,000

mg of inositol daily for 2 weeks. Another report cites the administration of

18g.

of

inositol

daily

for

6

weeks.

In

these reports and several others, no adverse effects were observed.

B Vitamins.

Most energy drinks contain added B vitamins including thiamine, riboflavin,

niacin, vitamin B6, vitamin B12, and pantothenic acid.

Thiamine (Vitamin B1).

Thiamine is widely found in foods, including meat, legumes, and whole or

enriched grain products. The Recommended Dietary Allowance (RDA)8 for

thiamine for adult males is 1.2 mg/day and for adult females, 1.1 mg/day (IOM

1998). Based on data from the Canadian Community Health Survey (CCHS)

45

(2004), the 95th percentile of dietary intake indicates that adults consume up to

4

mg

of

thiamine

per

day.

The

formulation

of

a typical energy drink product as described in Table 1 does not contain thiamine; h

owever, other energy drinks may contain up to 5 mg. of thiamine per serving.

The US Institute of Medicine (IOM) was not able to set a tolerable upper intake lev

el (UL) for thiamine due to the lack of data on adverse effects (IOM 1998). In

addition, the European Commission concluded that while it is not possible

to

derive

a

UL

for

thiamine,

current

levels

of intake from all sources do not represent a health risk for the general population

(European Commission 2001). However, the Australia New Zealand Food

Authority (ANZFA) set a maximum limit for thiamine of 20 mg/250 ml. in formula

ted caffeinated beverages as a conservative limit that was based on a maximum one

‐day quantity of 40 mg thiamine (ANZFA 2001). Orally ingested thiamine has

a long history of use as a supplement without reported adverse effects.

There are no reports of adverse effects of oral thiamine, even at dosages of

several

hundred

milligrams

per

day (European Commission 2001). A Canadian evaluation of micronutrient safety

classified thiamine as a nutrient with no known adverse effects (Program on Food

Safety 1996).

Riboflavin (Vitamin B2).

Riboflavin is found in a wide variety of foods but

milk and milk products are thought to contribute the majority of

dietary

riboflavin. Eggs, meat, and legumes also provide riboflavin in significant

quantities.

The RDA for riboflavin for adult males is 1.3 mg/day and for adult females, 1.1 m

g/day. Based on data from CCHS (2004), the 95th percentile

of dietary intake indicates that adults consume up to 4.5 mg of riboflavin per

46

day.

The

typical

energy

drink

product formulation, as described in Table 1, contains 1.65 mg. of riboflavin per 25

0 ml serving while other energy drinks may contain up to 5 mg of riboflavin per se

rving.

ANZFA set a maximum limit for riboflavin of 20 mg/day in

formulated caffeinated beverages based on the composition of Red Bull

and knowledge of regular consumption of 500 ml per day of this product (ANZFA

2001).

The toxicity of riboflavin is considered to be extremely low due in part

to ready excretion of excess amounts. Available sub‐chronic data from

human studies

and

pharmacokinetic

studies

do

not

show reported effects on oral toxicity of riboflavin. Apart from a

few

minor

gastrointestinal

disorders,

which

are

not clearly related to riboflavin intake, it is free from serious side effects.

Niacin (Vitamin B3).

Niacin is the term used to describe vitamin B3; nicotinic acid and nicotinami

de are two different forms of niacin. The best dietary sources of niacin include

tuna,

beef,

other

meats,

and

cereal

grains. The RDA for niacin for adult males is 16 mg/day and for adult females, 14

mg/day (IOM 1998). Based on data from CCHS (2004), the 95th percentile of

dietary intake indicates that adults consume up to 76.7 mg. of niacin per day.

The

typical

energy

drink,

as

defined

in

Table

1, contains 18 mg of niacin per 250 ml serving while other energy drinks may

contain

up

to

40

mg

of

niacin

per serving. The niacin in these products is generally present in the form of nicotin

amide and is most likely added due to its role in energy metabolism.

The Institute of Medicine (IOM) in the United States (1998) set a UL of

35 mg/day for niacin based on the adverse effect of flushing. Flushing is

first observed after excess niacin intake and is generally observed

at lower doses than are other effects. Flushing that results in patients deciding

47

to

change

the

pattern

of

niacin

intake (i.e., reduce the amount taken at a time or withdraw from treatment) was sel

ected as the most appropriate endpoint on which to base a UL. Although

nicotinamide appears not to be associated with flushing effects, a UL for

nicotinic acid that is based on flushing is considered protective against

potential adverse effects of nicotinamide (IOM 1998).

The Expert Group on Vitamins and Minerals (Food Standards Agency 2003)

set a guidance level of 560 mg/day for nicotinamide as the limited data on

the occurrence of nicotinamide toxicity indicates that it is quite low.


There

is

no

evidence

of

adverse

effects

from

the consumption of normal levels of niacin in foods. Adverse effects have been obs

erved with intakes of nicotinamide greater than 3000 mg/day compared with

intakes

of nicotinic

acid

of

1500

mg/day

(ANZFA

2001).

Adverse effects can be observed following high intakes of nicotinic acid, which

may be achieved through consumption of pharmacological preparations or

dietary supplemental products. Adverse effects associated with the use of

nicotinic acid as a drug, especially in doses of 1 g or more per day include:

Pyridoxine (Vitamin B6).

Excellent sources of vitamin B6 in commonly consumed foods

are

bananas,

navy beans, and walnuts. The RDA for vitamin B6 for adult males is 1.3‐1.7

mg/day and for adult females, 1.3‐1.5 mg/day (IOM 1998).

The typical energy drink, as described in Table 1, contains 2 mg of vitamin B6

per

250

ml

serving

while

other

energy

drinks

may contain up to 10 mg of vitamin B6 per serving.

Health Canada’s Category Specific Guidance for Temporary Marketing

Authorization:

Caffeinated

Energy

Drinks

(March 2012) set a daily maximum level of 450 mg/day for the addition of nicotina

mide to energy drinks.

48

ANZFA set a maximum limit for vitamin B6 of 10 mg/day in formulated

caffeinated

beverages

based

on

history

of

use,

rather than the U.S. UL (ANZFA 2001).


There

are

no

safety

concerns

in

relation

to

vitamin

B6 intake from food sources. However, adverse neurological effects have been

detected in humans after very high doses (>500 mg/day, equivalent to

approximately 8 mg/kg/day)13. Minor neurological symptoms may be

apparent at doses of 100 mg/day or more if consumed for long periods. There are n

o subgroups that are known to be unusually susceptible to the adverse effects of vit

amin B6 (European Commission 2000).

Cobalamin (Vitamin B12).

The only dietary sources of vitamin B12 for humans are from animal products,

which have derived their cobalamins from microorganisms. The best sources

of cobalamins are meat and meat products, poultry and eggs. The RDA for

vitamin B12 for adult males and females is 2.4 mcg/day (micrograms/day)

(IOM 1998). Based on data from CCHS (2004), the 95th percentile of

dietary intake indicates that adults consume up to 6 mcg of vitamin B12 per

day.

The

typical

amount

used

for energy drinks, as described in Table 1, contains 1 mcg of vitamin B12 per 250

ml serving while other energy drinks may contain up to 20 mcg of vitamin B12 per

serving. IOM was not able to set a UL for vitamin B12 due to the lack of data

on

adverse

effects

(IOM

1998).

Similarly,

the European Commission concluded that it is not possible to derive a UL for vita

min B12 as there are no clearly defined adverse effects produced from this

vitamin (European Commission 2000). ANZFA set a maximum limit for

vitamin

B12

of

10

mcg/day

in

formulated

caffeinated beverages based on history of use. No adverse effects have been

associated with excess vitamin B12 intake from food or supplements

in healthy individuals (European Commission 2000). 14 4.6.6 Pantothenic acid (Vi

tamin B5) Meats (especially liver), egg yolk, legumes, and whole grain

49

cereals

are

good

sources

of

pantothenic

acid.

The adequate intake (AI) for pantothenic acid for adult males and females is 5 mg/

day (IOM 1998). CCHS (2004) did not have any dietary intake data on

pantothenic acid; however, another source indicates that average intakes of

adults range between 3‐12 mg/d (European Commission 2002).

The typical energy drink, contains 6 mg of pantothenic acid per 250 ml.

acid per 250 ml. contains 6 mg of pantothenic acid per 250 ml.

serving while other energy drinks may contain up to 10 mg. of

pantothenic acid per serving.

IOM was not able to set a UL for pantothenic acid due to the lack of data on adver

se effects (IOM 1998). In addition, the European Commission concluded that

while it is not possible to derive a UL for pantothenic acid, current levels

of intake from all sources do not represent a health risk for the general population

ANZFA set a maximum limit of 10 mg/day for pantothenic acid in

formulated caffeinated beverages based on the

composition of

the reference product known as Red Bull™ and knowledge of regular consumption

of 500 mL per day of this product (ANZFA 2001).

There

are

no

reports

of

pantothenic

acid

or

panthenol toxicity in humans. Minor gastrointestinal effects such as occasional diar

rhea and water retention occurred only at very high intakes (10‐20 g/day)

Health hazard data on energy drinks are extremely limited and

therefore

the

hazard assessment was based on individual ingredients. Caffeine was

identified as the ingredient in energy drinks having the greatest potential

for

intakes

of

health

concern.

Assuming

no

additional caffeine from the diet, it was determined that no more than 5 servings

per

day

of

a

typical

energy

drink

should

be consumed by the general adult population. At this level of consumption, the lev

els of taurine and glucuronolactone in a typical energy drink are not expected

to pose a health hazard in the short term. Although there are limited

50

hazard

data

on

energy

drinks

as

formulated

in

the published literature, actual use of energy drinks has been associated with some

adverse reactions. However, due to the absence of long‐term safety data on

high levels of consumption of taurine and glucuronolactone, the potential

interaction

of

these

substances

with

caffeine, and for most consumers, the known addition of caffeine from

other

dietary

sources,

it

was

concluded

that

the long‐

term consumption of 5 servings of energy drinks per day

could

not

be

considered to represent no health concern for the general adult population.

Also, the evidence examined suggests that most of the B vitamins and other constit

uents of a typical energy drink would not pose a health hazard in the short

term, but long‐term safety data were not available for this level of consumption.


The health hazard assessment concluded that the general adult population could

consume 2 servings of a typical energy drink per day with no expected

negative health consequences. This conclusion was based on the safety of

the non‐caffeine ingredients of energy drinks (i.e. taurine, glucuronolactone, inosit

ol and B vitamins) at this level of consumption, and the fact that caffeine from othe

r dietary sources in addition to that in 2 servings of energy drinks would not pose

a health risk to the general adult population.

More specifically, the respective mean daily intakes of caffeine from all

dietary sources for adult Canadian males and females are 281 and 230 mg.

With body weights of 80 and 65 kg., theses intakes are equivalent to a daily dose

of 3.5 and 3.1 mg/kg bw, respectively (Statistics Canada, Canadian

Community Health Survey, 2004). The consumption of two servings of a

typical

energy

drink

containing

80

mg

of

caffeine

per serving would result in the addition of 160 mg caffeine to the diet. In males, thi

s would result in a daily dose of 5.5 mg/kg bw and in females, a daily dose of 6.0

mg/kg bw.16

Health

Canada’s

recommended

maximum

51

daily intake of caffeine for adults is 6.5 mg/kg bw or about 400 mg for an adult

weighing 65 kg.

Given that the addition of two servings of a typical energy drink to the

diet would not exceed the recommended maximum daily intake of caffeine,

it can be concluded that this level of consumption would not pose an additional hea

lth hazard based on the caffeine content of these products. The consumption of

energy drinks by subpopulations, such as children and pregnant

and breastfeeding women, is not generally recommended. Based on caffeine conte

nt, consumption

of

such

drinks

by

any

group

should

be limited to their recommended maximum daily intake of caffeine.

Excess consumption of energy drinks would be expected to result in health conseq

uences similar to those from excess exposure to caffeine.

Eating disorders.


In the USA, it is estimated that 10 million women, and 1 million men will

suffer from a clinically significant eating disorder in their lifetime. Given the

secretive nature and denial surrounding eating disorders, these numbers likely

grossly underrepresent the total disease burden in the US population. In a Finnish

community study, approximately half of all individuals with anorexia nervosa had

not yet been identified by the healthcare system. Worldwide, rates of eating

disorders in Western societies parallel those in the USA, whereas in developing

countries, the likelihood of disease is considerably less.16–11 Among athletes,

estimating the prevalence of eating disorders remains somewhat elusive.

Disordered eating is more prevalent among athletes than non-athletes, Illustrating

the relative importance of this problem in the athletic community. The majority of

studies investigate the prevalence of eating disorders in female athletes. In a study

of 522 elite female athletes and 448 nonathlete controls completing a disordered

eating questionnaire, clinical examination and interview,13 18% of athletes were

diagnosed with an eating disorder compared to only 5% of non-athlete controls. In

52

addition, athletes tended to under-report disordered eating symptoms on

questionnaires compared to the control group. A similar but larger study

including 1620 athletes and 1696 controls found similar results—20% of female

athletes met criteria for an eating disorder, compared to 9% of female controls.12

Even among female athletes the rates of eating disorder vary by sport and have

generally been higher in sports with weight classes (such as rowing), aesthetic

sports (such as gymnastics or figure skating) and sports where having a low body

mass is seen as advantageous (such as cross-country or cycling). These

conclusions were supported by Sundgot-Borgen’s study that found rates of eating

disorders in aesthetic sports and weight-dependent sports were 25%, compared to

12% in other sports. In the 2004 study the prevalence of eating disorders in

aesthetic sports was 42%, in endurance sports it was 24%, in technical sports it

was 17% and in ballgame sports it was 16%. Similarly, in a 2015 study of 108

elite German athletes who were age-matched with 108 non-athlete controls, rates

of eating disorders were 17% in aesthetic sports, 2% in ball sports and 2% in non-

athletes.14 Additional studies suggest that the prevalence of disordered eating

behaviours (such as binging, using saunas, taking laxatives or diuretics, self-

inducing vomiting, etc) is higher in the college-aged population, even in the

absence of a formal eating disorder diagnosis.15 Similar to the trend in eating

disorder prevalence, athletes in lean sports exhibited more disordered eating

behaviours than non-lean sport athletes. Glazer found that disordered eating

scores on standardised questionnaires were higher in athletes than non-athletes,

and highest in athletes within physique salient sports. An Australian study also

found that disordered eating behaviours and body dissatisfaction were higher in

lean sports, regardless of level of competition.

In some studies as much as 70% of athletes in weight class sports

were dieting or exhibiting abnormal eating behaviours to reduce their weight

before competition.

Eating disorders in male athletes.

53

An increasingly large body of research also indicates that eating disorders and

disordered eating are significant problems among male athletes. In general,

male athletes have a lower prevalence of eating disorders than female athletes, but

a higher prevalence than male non-athletes. In one study, 20% of female athletes

and 8% of male athletes met criteria for an eating disorder, compared to 9% of

female controls and 0.5% of male controls. Another study of male and female

rowers supported this trend by showing that male athletes had higher rates of

pathological eating behaviours than the general male population–12% of men had

reported at least two binge eating episodes per week, 3% of men had self-induced

vomiting and rates of rapid weight fluctuation and fasting were even higher in

male athletes than female athletes (57% vs 25%). Similar to the trend seen in

elite female athletes, male athletes in lean sports are more likely to suffer from an

eating disorder than those in other sports. In a 2004 study rates of eating disorders

in male athletes in antigravitation sports were 22%, as compared to 9% in

endurance sports and 5% in ball game sports. In a study by Rosendahl, et al, the

prevalence of eating disorders among male athletes was 10% in endurance sports,

17% in weight class sports and 42% in antigravitation sports. As was observed in

the female athlete population, numerous studies focusing specifically on male

athletes in lean sports have found similarly high rates of disordered eating in this

population, even in the absence of a formal eating disorder diagnosis. In a survey

of 732 male collegiate athletes in the USA, Chatterton and Petrie found that male

athletes who participated in weight class sports were more likely to engage in

pathological eating and weight control behaviours and be symptomatic

compared to male athletes in endurance sports or ball game athletes.

The importance of eating disorders in athletes is further emphasised by

concerns that rates of eating disorders are increasing in the general population

among individuals age 15–19 years old. While this may be partially explained by

changes to DSM-V criteria and greater awareness surrounding the Female Athlete

Triad, it may also reflect broader cultural changes including public health efforts

to reduce the burden of obesity.

54

DIAGNOSTIC CRITERIA.

The majority of the studies mentioned above were conducted using definitions of

eating disorders from the Diagnostic and Statistical Manual of Mental Disorders

(DSM). The release of the DSM has provided several important updates to the

diagnostic criteria (tables 1–3).

One study found that according to DSM IV criteria, 81% of adolescents and

75% of adults who presented for treatment of eating disorders were classified as

‘eating disorder not otherwise specified’ (EDNOS) because they did not meet all

of the criteria for one type of eating disorder. The changes in the DSM are

intended to reduce the number of diagnoses which fall into the EDNOS category

(or its renamed counterpart), which should facilitate more accurate descriptions of

patient symptoms and also further research on eating disorders. Several studies

have shown reductions in EDNOS diagnosis rates using the DSMV criteria. The

criteria for anorexia nervosa have undergone the greatest number of revisions.

Previously, individuals were required to have a weight less than 85% of normal.

This has been updated to state that significantly low weight is ‘less than minimally

normal weight in adults or less than expected weight in children and adolescents.’

Additionally patients no longer need to explicitly endorse a fear of weight gain;

this can now be inferred from patient behaviours. This change is likely to be

particularly beneficial in the athlete population, because athletes may deny

symptoms in an effort to continue competing. Lastly, amenorrhoea has been

discarded as a diagnostic criterion for anorexia. Studies found that women who

otherwise met criteria for anorexia but still had regular (or irregular) menses did

not differ clinically from women with similar symptoms plus amenorrhoea.6

Removing amenorrhoea as a diagnostic requirement also facilitates the

diagnosis of anorexia in men, postmenopausal women and adolescents with

delayed menarche.

55

The new definition for bulimia nervosa in the DSMV reduced the required

frequency of binge episodes and compensatory behaviours from twice per week to

an average of once per week over a period of 3 months. This change was made

because the frequency of binge episodes did not significantly impact prognosis or

treatment, and it caused more EDNOS diagnoses. The DSM V also created a new

diagnosis that had previously fallen under EDNOS—binge eating disorder.

Lastly, the miscellaneous category previously called EDNOS has been changed to

two categories—‘other specified feeding or eating disorder,’ and ‘unspecified

feeding or eating disorder.’ The first of these categories is used for individuals who

have a specific reason why they do not meet criteria for one of the types of

eating disorder. For example, it would include a patient who had lost significant

weight but was still within the normal weight range despite meeting all other

criteria for anorexia. The second category is used in situations where the clinician

cannot or does not clarify the reasons why the patient fails to meet full criteria for

an eating disorder.

COMMON COMORBIDITIES.

Individuals affected by eating disorders commonly suffer from other mental

health conditions, including depression, anxiety, obsessive-compulsive disorder

and substance use disorder. In a Canadian study almost half of all patients with

eating problems were also found to have mood or anxiety disorders. Similarly,

in a Swedish study half of patients with eating disorders had depression and one-

quarter endorsed substance abuse. Lifetime prevalence of substance abuse in

patients with bulimia nervosa is at least 30%.

Furthermore, among patients with bulimia nervosa, those with comorbid

psychiatric conditions were more likely to report suicidal ideation and history of

suicide attempts. Binge eating disorder has been found to significantly co-occur

with depression, bipolar disorder, anxiety, bulimia nervosa, kleptomania and body

dysmorphic disorder. Limited data exists regarding the relationship between eating

56

disorders and comorbid mental health conditions in female and male athletes. A

study in British athletes found a positive and significant relationship between

eating psychopathology and risk of subsequent depressive symptoms 6 months

later.35 Importantly, clinicians caring for an athlete with an eating disorder should

consider and evaluate for other mental health conditions.

In addition to the aforementioned mental health conditions, premorbid medical

conditions can increase the likelihood of subsequent eating disorders and

contribute significantly to the morbidity of eating disorders. For example,

individuals with type 1 diabetes mellitus are at higher risk for eating disorders later

in life—in a German study, one in three females with type 1 diabetes and one in six

males with type 1 diabetes had disordered eating and insulin restriction. Data on

athletes with type 1 diabetes and eating disorders is unknown. Gastrointestinal

conditions such as chronic constipation, gastroesophageal reflux disease

(GERD), coeliac disease, lactose intolerance, delayed gastric emptying,

gastroparesis and superior mesenteric artery syndrome may all occur as a result of

eating disordered behaviour,and in some cases may predate the eating disorder,

thereby contributing to its onset.

CONSEQUENCES OF EATING DISORDERS.

There are both health and performance consequences of eating disorders.

Health consequences Eating disorders have wide-ranging health consequences,

including one of the highest mortality rates of any mental health condition.

Risk of premature death is 6–12 times higher in women with anorexia

nervosa.41 Crude mortality rate is approximately 5% per decade.In 1994 the death

of US gymnast Christy Henrich from anorexia nervosa was a devastating example

of the extent to which athletes will manipulate their dietary intake and exercise to

achieve what is perceived as an ideal body image. Death is most often caused by

suicide or cardiac arrhythmia—suicide accounts for 20% of deaths among

patients with anorexia nervosa, and 23% of deaths among patients with bulimia

57

nervosa.42 43 Particularly worrisome is the finding that among individuals with

an eating disorder, overexercise (common among competitive athletes) is the

disordered eating behaviour which is most strongly associated with suicidal

behaviour.

Death from cardiac arrhythmia may result from electrolyte disturbances

associated with self-induced vomiting, laxative abuse and diuretic use, especially

among those with extremely low body weight. While cardiac consequences of

eating disorders—especially anorexia nervosa—are considered a significant

contributor to morbidity and mortality, a recent meta-analysis of mortality rates in

anorexia nervosa was unable to elucidate exact cause of death, aside from medical

causes versus suicide.

Disordered eating behaviours such as restricted dietary intake, excessive

exercise, binge eating, self-induced vomiting, laxative abuse, diuretic use,

regurgitation and eat and spit, can affect nearly every system of the human body.

While some individuals practice a single behaviour such as restriction, studies

suggest that up to a third of individuals engage in two or more pathogenic

behaviours.Furthermore, individuals who report using multiple compensatory

behaviours have more severe presentations of eating disorders, lower levels of

functioning and increased rates of general psychopathology.

As athletes may approach the medical care team for evaluation of an ‘eating

disorder consequence’ rather than seeking care directly for an eating disorder,

sports medicine clinicians should be aware of the signs and symptoms of

restricting and purging behaviours (table 1).

Table 1

№

System

Signs

58

Symptoms

1

General

Marked or sudden weight loss, gain or fluctuation;

Failure to gain expected weight in child/adolescent who is still growing and

developing;

Hypothermia, cold intolerance

Fatigue

2

Oral/dental

and throat

Oral trauma/lacerations;

Dental erosion or caries;

Perimolysis;

Parotid enlargement;

Recurrent sore throats;

3

Gastro-intestinal

Epigastric discomfort and/or abdominal pain;

Early satiety and delayed gastric emptying;

Gastroesophageal reflux;

Hematemesis;


59

Haemorrhoids, rectal fissures and rectal prolapsed;

Constipation;

Diarrhoea;

4

Endocrine

Irregular or missed menses;

Loss of libido;

Infertility

5

Neuro-psychiatric

Memory loss/poor concentration;

Insomnia;

Depression, anxiety;

Obsessive compulsive behavior;

Self-harm;

Suicidal ideation attempt;

Seizures;

6

Cardio-respiratory

Chest pain;

Palpitations;

Hypotension;

Bradycardia;

60

Other cardiac arrhythmias;

Shortness of breath; Oedema;

7

Musculo-skeletal

Low bone mineral density;

Stress fractures;

Fragility fractures

8

Dermato-logical

Lanugo hair;

Hair loss;

Yellowish skin discolouration;

Calluses or scars on the dorsum of the hand (Russell’s sign);

Poor skin healing;

Evidence of self-harm (superficial

lacerations in various stages of healing)

People at normal weight may also have an eating disorder. Do not rely on weight

or BMI alone to diagnose or rule-out an eating disorder. Awareness of the broad

array of signs and symptoms that may be present can facilitate early identification

of patients struggling with an eating disorder.

Among female athletes with eating disorders, especially those with restricted

dietary intake, a commonly recognized consequence is the Female Athlete Triad.

The Triad describes three distinct but inter-related conditions including low energy

availability, menstrual dysfunction and low bone mineral density. Low energy

availability (whether inadvertent, intentional or psychopathological), can result

61

from low energy intake relative to high energy expenditure during training and is

the underlying factor contributing to negative effects on reproductive and skeletal

health.

While not as extensively studied, there is increasing research on the health

consequences of disordered eating in the male athlete. In a subset of male athletes,

especially those participating in sports emphasizing leanness, parallels to the Triad

have been described that include low energy availability - with or without

disordered eating, hypogonadotropic hypogonadism or other gonadal steroid

effects and low bone mineral density. Similar to the female athlete, male athletes

with low energy availability (with or without disordered eating) may be

predisposed to stress fractures and bone stress injuries. However, our current

understanding of the mechanisms of nutrition and low energy availability on

neuroendocrine function and bone health in males is limited compared to that for

female athletes and further research is needed.

Performance consequences

Athletic performance suffers as a result of eating disorders. Female athletes with

anorexia nervosa and a body mass index (BMI) <16.5, and those with bulimia

nervosa purging four or more times per day should be categorically restricted from

participation in sport. Additionally, low energy availability leading to the loss of

fat and lean body mass, electrolyte abnormalities and dehydration all contribute to

poor sport performance. A study of junior elite female swimmers, found that those

with energy restriction and ovarian suppression had poor sport performance

compared to cyclic swimmers.68 Even among high school athletes, those with

disordered eating behaviours were more than twice as likely to sustain a

musculoskeletal injury during their competitive season.

SCREENING FOR EATING DISORDERS IN ATHLETES

the Preparticipation Physical Examination (PPE)

The PPE includes several questions aimed at identification of disordered

eating behaviours:

1. Do you worry about your weight?

62

2. Are you trying to, or has anyone recommended that you gain or lose weight?

3. Are you on a special diet or do you avoid certain types of food?

4. Have you ever had an eating disorder?

5. Have you ever taken any supplements to help you gain or lose weight or

improve your performance?

Additional questions on the PPE questionnaire screen for downstream

consequences of eating disorders including menstrual dysfunction (in female

athletes), and stress fractures, mood disturbance and substance use (in female and

male athletes).70 Clinicians should maintain a high index of suspicion for

disordered eating since some studies show that athletes tend to under-report

disordered eating behaviours on questionnaires.

The Female Athlete Triad Coalition has published an 11-question screening

tool that aims to identify disordered eating, menstrual dysfunction and low bone

mineral density. It is recommended that these questions be administered to

athletes during the preparticipation examination.

Recommended screening questions for the female athlete triad.

Recommended questions:

1. Have you ever had a menstrual period?

2. How old were you when you had your first menstrual period?

3. When was your most recent menstrual period?

4. How many periods have you had in the past 12 months?

5. Are you presently taking any female hormones (oestrogen, progesterone, birth

control pills)?

6. Do you worry about your weight?

7. Are you trying to or has anyone recommended that you gain or lose weight?

8. Are you on a special diet or do you avoid certain types of foods or food groups?

9. Have you ever had an eating disorder?

10. Have you ever had a stress fracture?

11. Have you ever been told you have low bone density (osteopenia or

osteoporosis)?

63

These questions should be included as a part of the preparticipation physical

examination (PPE).

DIAGNOSIS AND EVALUATION OF ATHLETES WITH EATING

DISORDERS.

Sports medicine providers serve an important role in evaluating disordered eating

and diagnosing eating disorders. Physicians, athletic trainers, sport psychologists,

sport dietitians and physical therapists interact with athletes and active persons,

and may have an opportunity to identify eating disordered behaviours.

Early identification and early intervention are associated with better outcomes.

Referral of an athlete suspected of engaging in unhealthy eating behaviours to a

physician with expertise in the evaluation and management of eating disorders,

and especially with additional knowledge regarding the interaction with

competitive sport, is a key step. As is often the case in medicine, ‘the mystery is in

the history,’ and given the secretive nature of eating disorders, this adage is

particularly applicable when caring for athletes with eating disorders. Questions

such as, ‘what percentage of your waking hours do you spend thinking about food,

weight and body image?’ and ‘in what ways does your weight affect the way you

think about yourself?’ are but a few questions that often open up a dialogue about

feelings, eating behaviours and health consequences. A more complete list of

questions to consider integrating into the medical history when evaluating an

athlete suspected of having disodered eating or an eating disorder can be found in

table 2.

A review of systems and a comprehensive physical examination (table 1) can

further aid in the identification of disordered eating behaviours and health

consequences, leading to diagnosis as well as subsequent treatment. Laboratory

evaluation and additional diagnostic testing are often required to better assess

health consequences. Both historical and physical examination findings should

guide the laboratory and additional diagnostic evaluation (table 3). Female

athletes who develop menstrual dysfunction and/or evidence of low bone mineral

density—the Female Athlete Triad—should undergo testing of their reproductive

64

hormones and evaluation of their bone mineral density as defined in the 2014

Female Athlete Triad Coalition Consensus Statement on Treatment and Return to

Play of the Female Athlete Triad.

Table 2. Eating behaviour questions.

№

Topic

Questions

1

Questions to start

- How have you been feeling in general? How do you

the

feel about yourself?

conversation

- Do you mind if we talk about your eating habits?

2

Initial critical

- Are there foods or food groups that you avoid eating?

questions

- How do you feel about dieting in general?

-How do you feel about your body size?

- In what ways does your weight affect the way you

think about yourself?

- What percentage of your waking hours do you spend

thinking about weight, food and body image?

3

Diet and dieting

- Do you worry that you have lost control of how much you

eat?

- Are you happy with your eating behaviour?

- Do you eat in secret?

- What did you have for breakfast today/yesterday?

Lunch? Dinner? Snacks?

- Do you count your calories? Watch fat grams?

Avoid certain foods?

65

- Do you ever eat a lot in one sitting—enough that

you feel sick afterward?

- Are you worried because sometimes you can’t stop

eating?

4

Vomiting/purging

- Do you make yourself throw-up because you feel

Uncomfortably full?

Do you use diuretics, laxatives or diet pills?

5

Weight and

- When you look in the mirror, what do you see?

self-perception

- What do you think you should weigh? What are you doing

to reach or maintain that weight?

- Have you recently lost or gained a lot of weight in a short

period of time?

- What was your lowest weight in the last year? Your

highest weight?

6

Exercise and

- Do you exercise above and beyond what is required for

training

your sport?

- Do you feel anxious if you miss a workout?

7

Family and

- Does your family have any history of obesity, eating

support

disorders, depression, mental illness or substance abuse

(parents or other family members)?

- Who are your primary sources of emotional support? How

do they support you?

8

Health female

- When did you have your first period? Are your periods

patients

regular? When was your last period?

- Do you have constipation? Diarrhoea?

- Are you ever dizzy? Weak? Tired? Have you ever fainted?

- Do you get cold easily?

- Have you lost any hair? Grown new hair? Do you have

dry skin?

- Do you ever feel bloated? Have abdominal pain?

- Do you have muscle cramps, bone pain?

66

Consider these questions for engaging patients and their family members in

meaningful discussion that can help to identify the eating disorder.

Table 3 Eating disorder laboratory evaluation and diagnostic testing.

№

Lab/test

When to use

1 Basic blood chemistry: serum All patients with suspected eating

electrolytes; renal function (BUN, Cr); disorder.

calcium; liver function tests; thyroid

stimulating hormone (TSH); complete

blood count (CBC), differential and

platelets; urinalysis.

2 Additional blood chemistry: iron studies; Malnourished and severely symptomatic

vitamin D; vitamin B12; magnesium; patients.

phosphorous.

3 Additional blood chemistry: serum Patients with delayed menarche—no

luteinizing hormone; follicle stimulating menses by age 15.

hormone; prolactin; estradiol; thyroid Absence/delay of secondary sexual

stimulating hormone (TSH)—if not characteristics by age 13.

previously obtained; urine pregnancy test. Secondary amenorrhea (no menses for

three consecutive months).

4 Toxicology screen.

Patients with suspected substance use.

5 Radiological imaging: dual energy X-ray DXA for patients with amenorrhoea for

absorptiometry (DXA), radiographs, 6 months or more of prolonged

advanced imaging.

oligomenorrhoea (<6 periods in 24

months);

Radiographs to evaluate for stress

fractures, or more advanced imaging if

needed ECG.

6 ECG

Patients with syncope, recurrent near

syncope, palpitations, resting supine

67

heart rate <50 bpm.

Rapid weight loss; weight <80% of

ideal body weight.

Hypophophatemia.

TREATMENT OF DISORDERED EATING AND EATING DISORDERS IN

ATHLETES.

Once a diagnosis of disordered eating or an eating disorder has been made, a

knowledgeable and experienced multidisciplinary team of healthcare

professionals should care for the athlete, with a goal of personalised patient-

centered care (figure 1).

Figure 1 Multidisciplinary care. Multidisciplinary care of patients affected by eating disorders

should include a physician, dietitian and mental health professional. Regular communication

between team members facilitates clinically relevant information exchange, and cohesive,

comprehensive, patient-centered care.

The first step in treatment is determining the level of care. Can the athlete be

treated in an outpatient setting, or does he or she require a higher level of care in

68

the hospital or in a residential treatment setting? Deteriorating physical and/or

mental health are the primary reasons prompting a higher level of care—exam-

ples include rapid uncontrolled weight loss, severe electrolyte abnormalities,

syncope, suicidal intent and inability to function in one’s environment. The

majority of individuals can be treated in an outpatient setting using the

multidisciplinary team care model. In the athletic setting the team often consists of

a physician, a sports dietitian, a mental health professional and the

athletic trainer.

Communication among team members is critically important. The individual

affected by the eating disorder must feel like he or she is receiving a cohesive and

consistent message from the treatment team. While each member of the team

plays a unique role in supporting the athlete’s recovery from the eating disorder,

there is considerable crossover in the care that team members provide—with the

physician talking about nutrition, or the dietitian discussing feelings and function

alongside calories and carbohydrates. Setting aside time for the team to ‘round’

and share important information about the athlete can help to facilitate care.

Additional health professionals may have a consulting role in the care of the

athlete affected by an eating disorder (such as psychiatry, or gastroenterology).

For younger athletes still living at home, engagement and alignment with parents

or guardians is critically important.

Knowing that chaotic or disruptive family situations (such as divorcing

parents) can contribute to the development of an eating disorder, it is imperative

that the multidisciplinary treatment team understands the environment in which the

athlete lives, and takes that into account when developing and implementing

treatment plans.

The primary role of the physician is to address the eating disordered behaviours

and their health consequences, and to support and reinforce the treatment plans of

the dietitian, mental health professional and others involved in the athlete’s care.

Healthcare visits are typically monthly, although may be more or less frequent

69

depending on the athlete’s stage of recovery. Medical care should focus on the

following areas:

▸ Function—Assessing day-to-day functioning

– How have you been doing since your last visit?

– Is there a time of day that your behaviours are better or

worse?

– What helps you succeed (with changing behaviours, with

treatment, etc)?

– Are you taking your medications as prescribed?

– Additional questions to develop rapport and further assess

patient functioning (eg, ‘How is school? Practice? Work?

Family/Friends?’).

▸ Physical health discussion—Discussing health-related topics,

such as:

– A targeted symptom review: sleep, bowel habits, energy,urination, palpitations,

syncope/near-syncope, menstruation, other issues or concerns – Eating behaviours

—restriction, binging, purging, etc

– Exercise and training behaviours—healthy and unhealthy;

issues related to clearance and return to play

▸ Mental status—Assessing the patient’s mental health with a standard mental

status examination (MSE) and discussion of various topics, such as body image,

stressors, and mental health issues.

▸ Physical health examination—Checking and recording the following:

– Vital signs—blinded weight, height, BMI, blood pressure, heart rate,

temperature

▸ Change in weight since last visit

– Physical examination if necessary—throat, heart, lungs, extremities, etc

– Repeated tests/examination items from diagnosis as necessary

▸ Medications—Prescribing and managing medications as needed.

70

▸ Other health needs as necessary—Reviewing menstrual function, digestive

issues, bone health, endocrinology manifestations, etc.

Medication use

Medications are often prescribed to patients with eating disorders to treat comorbid

conditions such as depression and anxiety, or to manage physical complications.

Target symptoms should be established with the patient and regularly monitored.

Sports medicine physicians should be aware of the unique interaction between

medications and sport participation. For example, medications that induce

orthostatic hypotension should not be prescribed to a gymnast who experiences

many changes in posture and position. Likewise, sedating medications may not

be tolerated by student athletes attending school, practice or trying to complete

evening homework tasks.

CLEARANCE AND RETURN TO PLAY CONSIDERATIONS

One of the most important areas of concern for the team physician involves the

decision-making process regarding clearance and return to play. For female

athletes with disordered eating behaviours and health consequences related to those

behaviours, the Female Athlete Triad: Cumulative Risk Assessment in the 2014

Female Athlete Triad Coalition Consensus Statement on Treatment and Return to

Play of the Female Athlete Triad can serve as a guide to physicians making

clearance and return to play decisions. The risk assessment tool takes into account:

dietary restriction, BMI, menstrual history (delayed menarche, oligomenorrhoea,

amenorrhoea), bone mineral density and history of stress reaction or fracture. Each

risk factor carries a point value, and the numeric score suggests whether an athlete

should receive full clearance, provisional/limited clearance or restriction from

participation. While this risk assessment tool can help to guide clearance and return

to play decisions for athletes with disordered eating and eating disorders,

physicians should combine these recommendations with their own clinical

71

decision-making skills, and need not use the tool in isolation. Of note, athletes

diagnosed with anorexia nervosa who have a BMI <16 kg/m² or athletes with

moderate-to-severe bulimia nervosa (purging >4 times/week) should be

categorically restricted from training and competition. Female athletes who fall

into moderate and high- risk categories should have a written contract completed

and signed by the athlete and each member of the multidisciplinary team. While

a similar evidence-based scoring system with concomitant clearance

recommendations has not yet been developed for male athletes, the IOC has

proposed a return to play model based on a red light (high risk), yellow light

(moderate risk), green light (low risk) system.

PREVENTION

Efforts to prevent disordered eating behaviour among athletes should be aimed

at athletes, coaches, athletic administrators and parents. Primary prevention efforts

work to expand athlete knowledge about healthy eating, pathological eating

behaviours and their consequences, and what to do if you or a teammate are

thought to have an eating disorder. Athletes should be educated that dietary

restriction and/or purging behaviour in pursuit of optimal weight and body

composition will negatively impact sport performance and result in adverse health

consequences. In one study, a peer-led educational programme for athletes resulted

in improved bulimic pathology even 1 year after the intervention, and researchers

noted an increase in the number of athletes who sought medical care because they

had become concerned that they might have symptoms of the Female Athlete

Triad. Likewise, athletes, coaches and parents should be informed that the loss of

menstruation is not a positive adaptation to high-intensity training and sport

participation, and represents a state of low energy availability stemming from

either intentional or unintentional dietary restriction. Studies have shown that

educational programmes directed at coaches are successful in increasing their

knowledge about eating disorders in athletes, including recognition and

management. However, it is not yet clear whether this increased awareness

72

translates to improved outcomes among athletes. The National Collegiate Athletic

Association (NCAA) has developed educational materials for coaches, athletic

administrators and athletes in an effort to prevent eating disorders. They identify

10 strategies for coaches and administrators, which aim to reduce the likelihood of

disordered eating and eating disorders among their athletes:

1. Be aware of the symptoms of disordered eating.

2. Consult a registered dietitian who specialises in sport, particularly a Board

Certified Specialist in Sports Dietetics (CSSD) to prescribe appropriate nutrition

for optimal sport performance.

3. De-emphasise weight: Be aware of how you are communicating to athletes

about weight and performance. Focus on ways for athletes to enhance their

performance that do not involve weight.

4. Keep an open dialogue with athletes about the importance of nutrition and

staying injury-free for optimal athletic performance.

5. Recognise that the body composition and training required for optimal health

and performance are not identical for all athletes.

6. Screen student-athletes before the start of the season for risk factors of

disordered eating using a validated screening instrument.

7. Ensure that all stakeholders (coaches, strength and conditioning coaches, athletic

trainers, student-athletes, student-athlete affairs administrators and athletics

department staff) are educated about the factors that put athletes at risk for

disordered eating.

8. Understand your institution’s referral protocol for student-athletes who are in

need of assistance with nutrition or disordered eating issues.

9. Encourage help-seeking for all mental health concerns, including disordered

eating.

10. Develop a plan with other stakeholders (such as university counselling

services or a sports registered dietitian) for how to identify and treat student-

athletes with eating disorders.

73

Finally, sports medicine physicians should use the preparticipation evaluation as

an opportunity to educate the parents of younger athletes about disordered eating

and common health consequences. Emphasising the role of nutrition in optimising

performance and health is an important strategy to avoid unhealthy dietary

manipulation.

While females are affected more commonly than males (at nearly a 9:1 ratio),

both sexes are at greatest risk for eating disorder in sports where leanness

confers a competitive advantage. Athlete medical teams need to systematically

screen athletes (both male and female) as a part of the preparticipation evaluation.

Once diagnosed, referral to an experienced multidisciplinary team is considered

best practice. In addition to the team physician, dietitian and mental health

professional, athletic trainers play a key role as the ‘eyes and ears’ of the healthcare

team on the practice field and in the training room and oftentimes

serve as the confidant and support person for the athlete who is struggling with

and recovering from an eating disorder.

Sports medicine physicians play a key role in evaluation, diagnosis and

treatment, including clearance and return to play. Utilising established

recommendations that guide clearance and return to play decision-making can ease

difficult decisions, and promote transparency and accountability in support of a

healthy athlete.

74

RECOMMENDED LITERATURE

1. Sports Nutrition Manual : Sports Nutrition Professional / Mark P. Kelly, Scott

Skinner, Ron J. Clark, Charles DeFrancessco, F. Campitelli. - 2nd ed. -

National Federation of Professional Trainers, 2006. – 100 p.

2. Glazer J. Eating disorders among male athletes / J. Glazer // Curr. Sports Med.

Rep. – 2008. – Vol. 7, № 6. – P. 332–337.

3. Dieting and disordered eating in German high school athletes and nonathletes /

J. Rosendahl, B. Bormann, K. Aschenbrenner [et al.] // Scand. J. Med. Sc.

Sports. - 2009. - Vol. 19, № 5. - P. 731-739. doi: 10.1111/j.1600-

0838.2008.00821.x.

4. Eating Disorders [Electronic resource] : AED Report. - 2nd ed. - Academy for

Eating


Disorders,


2011.


-


Access


mode


:

http://eatingdisorders.ucsd.edu/resources/docs/AED%20Report.pdf

5. 2014 Female athlete triad coalition consensus statement on treatment and

return to play of the female athlete triad: 1st International Conference held in

San Francisco, California, May 2012 and 2nd International Conference held in

Indianapolis, Indiana, May 2013 / M. J. De Souza, A. Nattiv, E. Joy [et al.] //

Br. J. Sports Med. – 2014. – Vol. 48. – P. 289. doi:10.1136/bjsports-2013-

093218

75

6. Sports Nutrition: A Practice Manual for Professionals / M. Dunford. - 4th ed. -

American Dietetic Association, 2006. – 547 p.

7. World Anti-Doping Agency (WADA) [Electronic resource] : - Access mode :

https://www.wada-ama.org/

76

Оригінал-макет підготовлено на кафедрі фізичної реабілітації, спортивної медицини, фізвиховання

і здоров`я ЗДМУ

Тиражування - кафедра фізичної реабілітації, спортивної медицини, фізвиховання і здоров`я ЗДМУ

69035, м. Запоріжжя, пр. Маяковського, 26

____________________________________________________________________________________________

77