INTERNATIONAL ACADEMY OF PREVENTIVE MEDICINE34 CORPORATE WOODS. SUITE 46910950 GRANDVIEWOVERLAND PARK. KANSAS 66210

JOURNAL of theInternational Academy of

PREVENTIVE MEDICINE

Crackdown On CancerReviewed by Steven Cordos, D.o., FAPM 45

Book ReviewAcquired Immune Deficiency Syndrome:

Let the JIAPM Be A HotlineLeon R. Pomeroy, Ph.D. 46

Editor-in-Chief - Leon R. Pomeroy, Ph.D.Co-Editors Stevan Cordas, D.O.

Paul J. Dunn, M.D.

In This Issue . ..ARTICLES

Why Look Elsewhere ... for HealthDr. Vernon A. Nord

Overcoming Motivational Obstacles toSmoking Cessation and OtherPreventive Health Measures

Stuart Wakefield, Ph.D., and Leon R. Pomeroy, Ph.D.Serum Lipids, Prostaglandins,

and Marine OilsJeffrey S. Blond, Ph.D.

Holistic Applications To Ear DisordersPaul Yanick. Jr., PhD., C.C.CA.

Food Allergy As An EtiologicalFactor In Arthropathies: A Survey

Marianne Reinhardt Taylor

An Orthomolecular Approach ToFeline Leukemia Prevention and Control

Wendell O. Belfield, D.V.M.Editorial

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5

10

16

24

28

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40 1983 Feline Leukemia Preventian and Contral

An Orthomolecular Approach ToFeline Leukemia Prevention and Control

Wendell O. Belfield, D.V.M.

Journal of IAPM

DR. WENDELL O. BELFIELDisa graduate of Tuskegee In-stitute, School of VeterinaryMedicine. He served in theMeat Inspection Division ofthe U.S. Department of Agri-culture and as a captain inthe U.S. Air Force. Dr. Bel-field has published severalpapers on new and unor-thodox therapies and surgi-cal procedures. He has been

-til in private practice for over20 years and established the first Orthomolecular VeterinaryHospital in the United States. Dr. Belfield is the author of twobooks on vitamins and minerals for dogs and cats, How ToHave A Healthier Dog (Doubleday), and The Very Healthy CatBook (McGraw Hill).

TerminologyOrthomolecular by definition means "right

molecule" and refers to a new branch of medicinedeveloped by Dr. Linus Pauling. "OrthomolecularMedicine is the preservation of health and thetreatment of disease by the provision of the opti-mum molecular constitution of the body, espe-cially Ihe optimum concentration of substancesthai are normally present in the body and arerequired for life."

INTRODUCTION

Leukemia may be defined as any malignantneoplastic proliferation of Ihe leukocyles, Iheirprecursor, or allied cell types, when these neo-plastic cells are found in the circulating blood.This disease is thought to occur in all warmblooded animals, but it is more frequent in the calthan in any other mammal commonly given veter-inary care.

The causative agent, in recent years, was foundto be a virus and Ihe leukemias are classifiedaccording to the cells affected such as lympho-cytic, lymphoblastic, monocytic, elc. Severalcells of a series are occasionally presenl in essen-tially similar proportions, and in such cases, theleukemia is named according to Ihe cell series, forexample, myelogenous or lymphogenous. In man,studies have shown that a reasonable correlationcan be made between the cell type, physical find-ings, and course of illness. Thus, the prefixes"chronic" and "acute" are used. Our limited expe-rience with leukemia in animals does nol permitus as yet to do this with any degree of reliability(Feline Medicine and Surgery, 1964).

FeLV DiseasesThe FeLV virus can and will cause the follOWingdiseases:

1. Lymphosarcoma (LSA)2. FeLV Non - regenerative Anemia3. FeLV Panleukopenia-like syndrome4. Myelogenous Leukemia5. Thymic atrophy6. FeLV Secondard Immunosuppressive Diseases

(Hardy. Wm. Do, Jr., 1979,)While all six of these diseases are extremely

importanl, the two most often seen in my practiceare the Thymic atrophy which affecls the kittensof FeLV infected queens. The virus causes degen-eration of the thymus resulting in a deficiency inthe cell mediated immune response. FeLV Second-ary Immunosuppressive Diseases in which Ihevirus is an immunosuppressive agent and is indi-rectly responsible for several chronic secondarydiseaSes (stomatitis, abscesses, upper respiratory in-fections). More cats die from these FeLV inducedimmunosuppresive disorders than die from LSA(Hardy, 1979).

This study was stimulated by a paper writtenby Dr. Francis M. Pottenger, Jr. M.D. of Monrovia,California (October 9, 1945). Dr. Pottenger per-formed feeding experiments with cats to determinethe effect of heat-treated foods upon growthand development. This experiment stemmedfrom the facl that he suffered steady mortalityamong the cats on which adrenalectomies wereperformed for the purpose of standardizingadrenal cortical material. He found Ihat feedingcooked meat scraps, together with raw milk andcod-liver oil were poor surgical risks, eventhough his technique was good. As his cat supplyincreased il was necessary 10 find a new source ofmeat. The new source came from a butcher andincluded muscle, bone and viscera. The raw meatwas fed each day to the same group of cals.Within a very short time the cats in those penssurvived the operations, the unoperated catsappeared 10 be in better health, and the kittenswere born vigorous. The contrast in apparenthealth between Ihe cals in the pens fed on rawmeat scraps and those fed on the cooked meatscraps was so starlling that he decided to do afeeding experiment. To summarize Dr. Pot-tenger's findings - Ihose felines fed the raw mealdiets were heallhy and producing healthy normalprogeny. Those females fed the cooked meats

Journal of IAPM Feline Leukemia Prevention and Control 1983 41

were irritable and dangerous to handle. Themales were more docile and unaggressive. Catsreceiving the cooked meat scraps reproducedheterogeneous strain of kittens, each of the litterbeing different in skeletal pattern. Abortions inthese queens were common, about 25 percent inthe first generation and about 70 percent in thesecond generation. Queenings were generallydifficult, many cals dying in labor. Mortalityrates of the kittens were high and were often toofrail to nurse. At times the queen would steadilydecline in health following the birth of the kit-tens, dying from some obscure tissue exhaustionabout three months after queening. Others expe-rience increasing difficulty with subsequentpregnancies. Some failed to become pregnant.Osteomyelitis was common, cardiac lesions,hyperopia and myopia, thyroid disease, nephri-tis, hepatitis, orchitis, oophoritis, pa,'alysis,meningitis, cystitis, arthritis and many otherdegenerative lesions. Vermin and intestinal para-sites were abound. Skin lesions and allergieswere frequent. being progressively worse fromone generation to the next.

The cats receiving raw meat and raw milk re-produced in homogeneity from one generation tothe next. Abortions were uncommon, lilte,'saveraged five and the mother cats nursed theiryoung in a normal manner. The cats in these penshad good resistance to vermin, infections, andparasites. They possessed excellent equilibrium;they behaved in a predictable manner. Theirorganic development was complete and func-tioned normally.

Since this study was done in the late thirties,the,'e was even less knowledge of feline diseasesthan now. It is reasonable to assume some ofthese cats may have had leukemia or related dis-eases. It was apparent to me, after reading Dr.Pottenger's paper that the raw meat containedsubstances that the cooked meats did not. It isgenerally known that most vitamins are de-stroyed during the cooking process.

The owners of cattery number one CaliforniaCattery enlisted my help to sol ve a se,'ious leukemiaproblem in their cattery. Of the felines testingpositive for FeLV, some females were not conceiv-ing, some aborting, several adults dying andnumerous kittens dying between the ages of 2-12months. The situation was so bad at this catterythat the local veterinary school recommended thecattery be closed. Because of the wo,'k Dr. Pollengerhad done thirty years earlier, t hypothesized theproblem to be one of nutrition. There were six catsin this callery that routinely tested positive to theIFA test. These six were divided into two groups,one with an oral multiple vitamin (RDA recom-mendations) and the other group with the same'olultiple vitamin plus 500 mg of sodium ascorbate[non-acid vitamin C]. This callel'y, biannually was

tested for FeLV by a team of medical students as aclinical pathology exercise. Six months after thestudy began the three cats on the straight RDAmultiple vitamins were still positive for FeLV. Thethree on the RDA multiple vitamins plus 500 mg ofsodium ascorbate were negative. The multiplevitamin group in six months were still positive forFe LV.

The vitamin C group consisted of one male andtwn barren females, ages two and three respectively.Several months later both females were bred, bothconceived. The two-year-old female had fourhealthy kittens all of which lived. the three-year-oldfemale had three kittens all of which were alive as ofthe writing of this paper.

The non-vitamin C group were then placed onthe vitamin C regiment and when tested sixmonths later were all negative for FeLV. Thesethree are now very active in the callery's breedingprogl'am.

Callery number two was newly formed three yearsago. The breeding stock had been tested (IFAmethod) for FeLV. My first introduction to thiscallery was testing a new adult female being intro-duced into the ca ttery for breedi ng purposes. Threeblood smears (glass slides) were submitted to thelaboratory for the IFA test - the test was positivefor FeLV, and the animal was asymptomatic.Because of the positive IFA blood test, the felinewas placed on an ascorbate regiment. Ten weekslater, three more blood smears were resubmilledand the test was negative for Fe LV. This negativeresult brought a phone call from the laboratorypathologist. "This animal was positive a month anda half ago and now it's negative, what are youdoing?" There were fi ve such cases in the past threeyears at this callery. We are now in the third gener-at ion of offsprings and the enlire callery is negativefor FeLV.

At no time were these Fe LV carriers isolated fromthe other members of the catteries. who were alreadyon the ascorbate regiment. In fact, they were treatedno differently than the others and permitted tosocialize.

A third cattery in 1978 lost 90% of its killens in aone-year period. AUlopsies revealed no cause ofthe sudden infant death (SID). Each day the ownerwould find a killen dead for no reason. One minutealive and apparently well, the next minute dead.These felines, like the other catteries previouslymentioned were on a vitamin and mineral RnA. Thequeens all tested positive to the !FA leukemia test.To the RDA vitamin and mineral supplement weadded 20-50 mg of sodium ascorbate to the 2-hour-old kittens and maintained this level daily. with oraldosages to weaning. Post-weaning. the vitamin Clevel was increased to 100-250 mg and maintainedto adulthood. It was requested that the kittens betaken off the vitamin C to determine the effects,

42 1983 Feline Leukemia Prevention and Control Journal of IAPM

TYPES OF ASCORBATES {VITAMIN CJFigure 2:

Norsworthy of San Antonio [1977], made theobservation that anemia is the most consistentfinding of these leukemia diseases and the mecha-nism for its development are not completely under-stood. Most cases involve depression of the bonemarrow. Sollmann, Torald (194B), in discussingchronic lead poisoning, indicates that there isdegeneration and atrophy of the whole marrowtissue. The blood changes as a whole indicateincreases deslI'uction of the corpuscles. It is myopinion that the anemia associated with FeLV canbe lead-induced, and is worthy of more investiga-tion. Moreover,the entire predisposition of FeLV canvery likely be charged to chronic lead poisioningsince the M.l.T.I'eport had brought out the possibil-ity of reduced antibody product ion and suppressedimmune response by the presence of lead.

Dr. Carl C. Pfeiffer's book on zinc and othermicro-nutrients discusses the high concentrationsof lead in pet food. He also discussed the positiveeffects of Vitamin C on heavy metals includinglead. Dr. Pfeiffer (1978) wrote "under physiologicalconditions. vitamin C acts as a strong reducingagent to bring melal ions and affect their movementacross biological membranes." Dr. Chattejee, et ai,has reported on the dietary intake of metal ions andvitamin C metabolism. They have fouod Ihatadministration of any of the heavy melals - cad-mium. lead or mercury -to rats. reduces the levelsof vitamin C in both the liver and kidneys. Lead wasadministered in these experiments at a dose of 10mgl100 g body weight raised vitamin C levels intissues to above the control levels. Animal studiesiodicale that zinc aod vitamin C may serve as anti-dotes for lead poisoning. In the Journol of labora-tory and Clinical Medicine (1939) vitamin C re-versed lead poisoning in humans who had come 10contact with lead filings.

Ascorbate RegimentAscorbic acid, in mega doses, is not recom-

mended because of the 3.0 pH. This vitamin C willcause gastric upset. flatulence, acidosis and diar-rhea. Also, due to the tartness most felines will notconsume it when mixed with food. On the otherhand, the ascorbates, [Fig. 2) are neutral [pH 7.4]and do not have the negative side effects of ascorbicacid.

pH 7.4

ASCORBIC ACID - pH 3.0

SODIUM ASCORBATEPOTASSIUM ASCORBATEr.ALCIUM ASCORBATEMAGNESIUM ASCORBATEZINC ASCORBATEMANGANESE ASCORBATE

DiscussionIt is apparent that the FeLV virus is immunosup-

pressive and raises havoc with felines. but we fellthat befol'e the enlrance of the vil'us into the bodythere are other factors Ihat permit the virus to gaina foothold in the animal. In other words, if the bodydefenses are up to the task, the virus would not beable to propagate and cause the problems theseanimals have been plagued with.

While corresponding with a Southern Californiaorganization dedicated to the eradication of felineleukemia. I was informed that. after extensive test-ing of FeLV animals, one of the puzzling findingswas Ihat all of the felines had high levels of lead.Upon further investigation we discovered that allfelines tested for lead were being fed commercialcat foods. My inquiry to those catteries I hadworked with revealed that the cats were being fedcommercial cat food. An investigation of literaturerevealed a study by Fox, Aldrich and Boylen ofM.l.T. (1976). This group did a study for lead con-tent in 78 random samples of pet food purchased 10local grocery outlets, and on 25 individual rationsfor laboratory animals. The lead content of 46 sam-ples of cat food ranged from 0.1 to 7.6 microgramsper gram. . .

In man, as in other animals, lead exerts Its tOXICeffect on a number of target organs, including thenervous syslem, the kidneys and the erythropoiet icsystem. By inhibiting some enzyme systems, leadexerts widespread biologic effects. Some of thesechanges are subtle: lead has been shown to reducethe resistance of mice to bacterial infection and toreduce antibody formation and suppressed immuneresponse to pseudorabies virus in rabbits [Fox. etal,1976).

One interesting fact brought oul by this studywas that twenty-one of the tested cat foods con-tained more than 1.0 ppm of lead: of these, 10 hadmore the 2.0 ppm. If an adult, 4.5 kg cat consumedthis food at a rate of 53 g/kg body weight/day, theamount of daily ingested lead would be 0.023-1.434mg. This lead intake is 0.1-4.6 times the daily inges-tion [0.3 mg/day] considered potentially toxic forchildren. Moreover, the feline burden of lead/kgbody weight would be much higher than a childsince a 2-3 year old child weighs considerably morethan an adult cat [Fox, et aI1976).

however, the owners in the three catteries refused tocooperate for fear of losing any more animals.Figure 1:

ORAL FELINE DOSAGES OF SODIUM ASCORBATEKITTENS - PRE-WEANED

(2 hours TO 5 wks.J 20mg.- 50mg.KITTENS - POST-WEANED

(5 wks. TO 6 mo.) 100mg-250mg.ADULTS - MALES & FEMALES

(6 monlhs"'l 500mg.-750m~.PREGNANT QUEE S 750mg.-l.0g.

Journal of fAPM Feline Leukemia Prevention and Control 1983 43

Affects of Ascorbate on immune componentsThe mechanism by which ascorbate may be

in valved in the control of infect ion is by way of theimmune system. The leukocytes, in particular, con-tain high concentrations of ascorbate, 1.0 micro-gram per milligram of protein. Mononuclear phag-ocytes contain a higher concentration. 2.0 micro-grams per milligram of protein with both peritonealand alveolar macrophages being rich in ascorbate.It has been established the leukocyte ascorbatequality decreases following virus infection and afterwhich returns to normal levels. Leukocytesabsorb large amounts of ascorbate when theymigrate into an area of infection. Ascorbate levelsin leukocytes have shown to decrease in responseto a variety of exogenous agents, many of which areassociated with depressed immunological func-tion. As was implied above, viral infection rapidlydepletes leukocyte ascorbate (Thomas, W.R. andHolt, PC., 1978).

Barton and Roath (1976) have surveyed leuko-cyte ascorbate levels in patients with a variety ofabnormal leukocyte states and other hematologicaldisorders. Levels below the normal range werefound in most cases of chronic myeloid leukemiaand chronic lymphatic leukemia, and in greaterthan 1/3 of patients with acute leukemias, lymph-omas, glandular fever, myelofibrosis, polycy-thaemia, polymorphleukocytosis, purpura andthose receiving cytotoxic drugs (Thomas and Holt,1978).

PhagocylesTh'e direct involvement of ascorbate in neutro-

phil phagocytosis is probable since both ascorbateand dehydroascorbate are consumed in these cellsduring phagocytosis. Ascorbate appears to playarole in a number of neutrophil functions includingincreased chemotaxis, incl'eased particulate inges-tion, enhanced lysozyme meditated non-oxidativekilling, protection against the toxic effects ofsuperoxide anion radical, inhibition of thehalideperoxide-myeloperoxidase system without apronounced bactericidal effect and stimulation ofthe hexose monophosphate shunt (Leibovitz andSiegal. 1978), A more positive effect of exogenousascorbate has been observed in neutrophils defi-cient in ascorbate, Steroid therapy depletes leuko-cyte ascorbate and also inhibits the phagocyticactivity of human neutrophils, as judged bynitroblue tetrazolium reduction during phagocyto-sis of latex particles or by counting the accumula-tion of latex particles [Thomas, et ai, 1978),

InterferonTexas Reports on Biology and Medicine (1977)

reported that in interferon, a protein produced by anynucleated cells of the body, seems to be the primarydefense against viruses, Interferon production isstimulated only by the presence of viruses and is

not observed when the body is not being challengedby a vi I'US, There are two types of interferon whichare linked to the chromasomes, One type attacksthe virus intracellularly, surrounds it and preventspropagation, The other attacks the virus extracel-lularly and thought to destroy the virus by attack-ing the nucleic acid within the virus, In 1974, Siegalreported mice fed on an ascorbate supplementeddiet displayed augmented levels of circulatinginterferon after stimulation with murine leukemiavirus, and later (1975) demonstrated a similar phe-nomenon in vetro employing cultures of murine Lcells and embryonic fibroblasts stimulated poly-nucleotides, Dahl and Degre (1976) had a similarfinding to Siegel. Thomas and Holt (1978) ob-served that leukocyte interferon assayed in lungfibroblasts titrated 0,2-0,3 log" units higher in thepresence of 5.0 mg ascorbate than in the absence ofthe ascol'bates.

AntibodiesThe early literature on ascorbate and immunity

suggests an important role for ascorbate in thehumoral immune response, The addition of ascor-bate to immunizing doses of antigen appeared toincl'ease antibody production and deprivationapparently reduced the response,

At the time of this clinical study, the only testfor leukemia was the !FA test. More recently theAntibody Titer Test (FeLV antibody test) is nowavailable to aid the clinician in determining thedegree of involvement of the leukemia virus, How-ever, the standard test for FIP [Feline InfectiousPeritonitis), a related viral disease, is determinedby an antibody titer test. One patient was testedfor FIP and had a titer of 1:400, This patient wasplaced on the vitamin C plus RDA vitamins andminerals and routinely retested one year later andthe antibody titer was "0", The feline was retestedin two days because we felt a discrepancy in thelaboratory; the test once again read "0", J queriedthe laboratory pathologist and he informed me, "thetest indicated the virus had been destroyed and, tohave antibodies there must be a virus." This animalwith no FIP antibodies has been exposed to otherfelines with FIP titers of 1:400 and developed notiter.

Antibody production is dependent on the pres-ence of microorganisms in the body and do notappear for some six or seven days after infestation.It may be postulated that antibody production isthe final line of defense for the body and ant ibodiesmay not be needed when the primary immunologi-cal defense [interferon, leukocytes, etc.) is function-ing at maximum capacity.

ConclusionIn veterinary research there are no reports on the

effects of exogenous ascorbate on the immune sys-tem of felines. Research is lacking because themembers of our profession feel the 40 mg per kilo of

44 19B3 Feline Leukemia Prevention and Canlrol Journal of fAPM

ANIMAL

REFERENCES

Subramanian, N.. et al. Detoxication of Histamin withAscorbic Acid, Biochem. Phormoco. 22:1671-1673,1973.

Morishige. Fukumi. Proceedings of the First IntersectionalCongress of lAMS. Vol. 3-434.1975.

Figure 3:DAILY PRODUCTIO OF ASCORBATE IN ANIMALS

Ascorbale ProduclionMilligrams/Kg Body Wgl/per day

107

2752261901504040o

SnakeTortoiseMouseRabbitGoalRatDogCfllMonkeys. Apes, Man

Texas Reporls on Biology and Medicine. Univ. of Texas. Cal-veston. TX. The Interferon System. A current Review, Vol. 35.\977.

Leibovitz. Brian and Siegal. Benjamin Y.. Ascorbic Acid.Neutrophil Function and the Immune Response. Internat.}. Vit.Nutr. Res. 48. 1978.

Pfeiffer. Cnr! C.. Dr. Carl C. Pfeiffer's Updaled Filet Book onZinc and olher Micro- utrienls. pp 180-181. 1978.

Norsworthy, G.D .. The Feline Leukemia Virus AssociatedDisease. Pari 1 - Lymphosarcoma. Feline Proclice. Vol. 7. No.3. pp 34-36. May 1977.

Hardy. Wm. D.. Jr.. Currenl Status of FeLvDisease, FriskiesResearch Digcsl. Vol. 15. Summer 1979.

Fox. Aldrich. Boylen. Jr.. LC