dietary fats inhealth - athabasca university

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Journal of ,Vutrilioll, Growth and Cancer (1985) 2, 173-.179 DIETARY FATS IN HEALTH NORrvJAN J. TEMPLE Departme/lt uJ Foods alltl f',,'Ulritioll, Facility of} fume EC()/lomic~~ The University (~rA /lJl!r(a,-.l::ctmonto/l. Canada T6G 2:\-18 .~ - This review examines the relationship between dietmy fat intake and health. ,Heal produced by modem farming methods has a high fat content in compddson with irs natural counterpart and, furthermore, the fat is 101-~' in PolyullsaturatiYlfat. The combined result of thi's and dairy food is that our modern diet hasfar mh!'eJar than was consumed by stone-age man, A number of diseases are associated with/he ~'Vestem lifestyle and thus might be caused by a high fat intake. With regard to cofQizafJ' heart disease, there is a better correlation with refined carbohydrates than v.'itltd:ielary Jat. Prospective and case-control studies also indicate that dietary fa! iso/secondary importance. Human and animal studies show that a diet high inJal isa)il"ajor factor in cancer of the breast and, to a lesser extent, in cancer of the colon. hor obesity and diabetes there is contradictory evidence for the im'olvement of dietary fat. A high fat diet reportedly has a deleterious effect on [he immune systerh; therefore possihly constitutes a factor in auioimmlme disease. INTRODUCTION During the vast majority of human evolution man was a hunter-gatherer. The advent of agriculture some 8000-10000 years ago is too recent for any significant degree of further evolution. It is reasonable to presume, therefore, that modern man is adapted to the diet of his stone-age forebear. This diet contained much plant material (I) which, no doubt, was rich in fiber and therefore resembles modern fruit, vegetables and unrefined cereals. In addition, much meat was eaten- from wild animals (2-4). It is often assumed that all meat is similar and that man is therefore well adapted to a diet rich in saturatedfats. Crawford el at. (5,6) compared meat from herbivorous mammals in Uganda with typi-calbutchcr's shop meat purchased in London. Whereas the Ugandan meaLhad a fat content of 2-50/0, in London the figure is around 20-400/0 (before rem()V'aLofvisibleJat)~:Qtherdata for mammalian meat sold in Britain indicates a typica1[atcolltch:tof16-'-3JI}!o(5-11 % in major organs) (7). By comparison Ethiopian meath~.';be~l}repprte<itpc()Jl@it1()nly ] .3070fat (8) (ie even less than Ugandan meat). Inad4itiqnt9tl1es~q\laIi~itati\redifferences the fat of A frican meat is much more rich - inBQl)'ti*ls4t#f~~#4-.fa.nY~~fd~(pUFA): 301170 in Ugandan wild meat (5,6), while the r-eportedyaI4tif()r:L()i~gohl'11;eat is only 2-4% (5,6) or 4.5070 (9-15Irio in major organs) :(9,);Iti~'::tppareriltheraorethat modem farming methods have greatly increased the fat ~9i1:t@:t9JI]:1eata.nclth(ltthis fat has a low ratio of PUF A to saturated fat (P IS).

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Page 1: DIETARY FATS INHEALTH - Athabasca University

Journal of ,Vutrilioll, Growth and Cancer (1985) 2, 173-.179

DIETARY FATS IN HEALTH

NORrvJAN J. TEMPLE

Departme/lt uJ Foods alltl f',,'Ulritioll, Facility of} fume EC()/lomic~~ The University (~rA /lJl!r(a,-.l::ctmonto/l.Canada T6G 2:\-18

.~ -

This review examines the relationship between dietmy fat intake and health. ,Healproduced by modem farming methods has a high fat content in compddson withirs natural counterpart and, furthermore, the fat is 101-~'in PolyullsaturatiYlfat. Thecombined result of thi's and dairy food is that our modern diet hasfar mh!'eJar thanwas consumed by stone-age man, A number of diseases are associated with/he ~'Vestemlifestyle and thus might be caused by a high fat intake. With regard to cofQizafJ' heartdisease, there is a better correlation with refined carbohydrates than v.'itltd:ielary Jat.Prospective and case-control studies also indicate that dietary fa! iso/secondaryimportance. Human and animal studies show that a diet high inJal isa)il"ajor factorin cancer of the breast and, to a lesser extent, in cancer of the colon. hor obesityand diabetes there is contradictory evidence for the im'olvement of dietary fat. Ahigh fat diet reportedly has a deleterious effect on [he immune systerh; thereforepossihly constitutes a factor in auioimmlme disease.

INTRODUCTION

During the vast majority of human evolution man was a hunter-gatherer. The adventof agriculture some 8000-10000 years ago is too recent for any significant degree offurther evolution. It is reasonable to presume, therefore, that modern man is adaptedto the diet of his stone-age forebear. This diet contained much plant material (I) which,no doubt, was rich in fiber and therefore resembles modern fruit, vegetables andunrefined cereals. In addition, much meat was eaten- from wild animals (2-4).

It is often assumed that all meat is similar and that man is therefore well adapted toa diet rich in saturatedfats. Crawford el at. (5,6) compared meat from herbivorousmammals in Uganda with typi-calbutchcr's shop meat purchased in London. Whereasthe Ugandan meaLhad a fat content of 2-50/0, in London the figure is around 20-400/0(before rem()V'aLofvisibleJat)~:Qtherdata for mammalian meat sold in Britain indicatesa typica1[atcolltch:tof16-'-3JI}!o(5-11 % in major organs) (7). By comparison Ethiopianmeath~.';be~l}repprte<itpc()Jl@it1()nly ] .3070fat (8) (ie even less than Ugandan meat).Inad4itiqnt9tl1es~q\laIi~itati\redifferences the fat of A frican meat is much more rich

- inBQl)'ti*ls4t#f~~#4-.fa.nY~~fd~(pUFA): 301170in Ugandan wild meat (5,6), while ther-eportedyaI4tif()r:L()i~gohl'11;eat is only 2-4% (5,6) or 4.5070 (9-15Irio in major organs):(9,);Iti~'::tppareriltheraorethat modem farming methods have greatly increased the fat~9i1:t@:t9JI]:1eata.nclth(ltthis fat has a low ratio of PUF A to saturated fat (P IS).

Page 2: DIETARY FATS INHEALTH - Athabasca University

... . ...

It is only since the advent of agriculture that dairy fOQd~"b~~;.~g~~:":~~~u~i~~:in significant quantities. They are, of course, another rnajOfsgij#4¥:Q(:Ufaf,:Mtlra low PIS ratio. The combined effect of meat and dairy foodC1~a(IYmea11.$tb.Mthe average Western individual now consumes far more fat th<:l.I~qiclb.isdistarJfancestor. .

. . . ... .

: ..

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Evolutionary considerations tell us that because man evolvedCm a low fat diet,this is the typc of diet for which we are most suited. Thus, our modem-day fat-richdiet might possibly be a cause of disease.

The writings of Clcave(W, 11) stand as one of the great pillars, albeitpoorly recognized, of twcntieth century nutrition. He, however, stresses thatman is adapted to a high fat diet as indicated by the a'.@lability of fat-richmeat in bibJical time:,;. However, we would argue that this i$too recent to be ofrelevance.

CORONARY HEART DISEASE

The proposition has been made elsewhere (12) that the role of a high fat diet in coronaryheart disease (CHD) has been much exaggerated. In brief, the cornerstone of the lipid-hypothesis of CHD is the variation, both geographic and temporal, between dietaryfat and CHD. However, there arc numerous exceptions to this relationship whichthrow the whole hypothesis into doubt. Coronary heart disease has, in fact, a strongerrelationship with refined ca,bohydrates. Much of the relationship between dietaryfat and CHO may \vell be due to guilt by association - both being closely correlatedwith refined carbohydrates (12).

Thus, a high fat diet would appear to have a secondary role in CHD. This isconsistent with findings from epidemiological diet and drug intervention studies andevolutionary theory.

Reports from six prospective studies support this conclusion. In each studymiddle-aged men had their diet assessed and this was related to subsequent CHD.\-Vhile there may be some tendency for persons who subsequently suffer ClID toconsume a diet with an above average proportion of calories derived from fat orwith a below average ratio of PIS, this finding is weak and is not consistent(13-19).

Case-control studies of CEO are less reliable than prospective studies since fatalcases are excluded and diet assessment is marc likely to be biased in the first typeof design. A further problem is that data are usually presented as the absolute intakeof dietary components rather than as the nutrient:calorie ratio. This can be misleadingsince CHD cases tend to have a below averagecaloricjnt~l<t)(1~~)p.19).

The results from several case-controlstudiesha\'cindicat~dIJ1iriithaldifferencesin fat intake (20~26).Bassctt ctal.(20),ill~$tlldyjJ1Hi1:WgiiFf(.)J.1p.qtheP/S ratioabout .12WQhight:r.aInQl1g)9ases. ofJap~[l~$~gri~ciR4~mf:~t,ff~retltjncases of.Hawaiian..origill..{v.e.rs~s..respeqtiYe..c()ntr()l~)...~.M9.(ir*#t9{i{&7):g*~~rmtqe9the former

.." .~~hb~;$1i:r.~ii~~ili*ktfie~eskk~jal~ht#i~~t~~~~~[~~~~1~~~1i~~{ii~~~~~~~itL$e~: ~:I~~~~

...I~~~~~!]j~~!~ill'i1iiI1~i;~:{&:~1

Page 3: DIETARY FATS INHEALTH - Athabasca University

CANCER

Cancer of the breast and colon are the two fc.Jrms of the disease most associated witha high fat intake.

Epidemiology proyidcs a major component of the evidence incriminating a highfat diet in the etiology of breast cancer. Strong correlations are seen in bothinternational and intra-national studics (28). However, as with CHD, this might easilybe a case-to a greater or lesser extent-of guilt by association. On the othcthand,case-control investigations support a true role for a high fat diet in breast cancerJ79,30).

Studics of chemically induced and spontaneous mammary tumors in animals areconsistent with human studies in indicating an important role for dietary faCin thegenesis of this disease (28,31). This occurs principally in the promotional rather thanin the initiation phase of carcinogenesis. ~

. Colon cancer studies paral1el those on breast cancer. alihough the evidence is lessstrong. An international correlation between dietary fat intake and cancer of the colonhas been demonstrated (28,32) but suffers, as do lhc CHD correlations, from seriousinconsistencies (33,34). In particular, the finding might reflect a primary rqle for alow intake of dietary fiber (35,36).

Case.control studies tend to support the involvement of a high fat diet in the disease(37,38) but as with the epidemiological data, there is a lack of consistency(39.40).Investigations using animal models of cancer of the colon have mostly (28), but notinvariably (41), reported a positive association of the disease with dietary fat.

OBESITY

There is no doubt of the close association between a Western lifestyle and obesity(42). Unlike the situation with CHD and cancer of the breast and colon, thegeographical distribution of obesity is seldom cited as evidence indicating a majorrole for dietary fat. This almost certainly stems from the lack of reliable quantitativedata concerning the prevalence of obesity. The association with refined carbohydratesis at least as good as that with dietary fat.

Several studies have compared the dietary intake of the obese with that of theirnon-obese counterparts, but no consistent trend emerges in relation to fat intake (eg43-48). Much caution must be observed in interpreting such data since not only isdiet assessment particularly prone to bias but it is also difficult to disentangle causeand effect relationships.

Studies or the effects of an altered dietary fat content on calorie intake also argueagainst obesity being caused by a high fat diet. Altering the dietary fat content fora period of t\ovo weeks was found to leave total calorie intake unchanged (49).

A high fat, low carbohydrate diet has been in vogue for some years as a treatmentfor obesity . More rapid weight loss has often been observed with this approach thanwith diets comaining a more conventional distribution of calories bet\oveen fat andcarbohydrate (50,5l).Bcfore this can be cited as evidence against a role for fat ingbesitY.tWQafeasoLdoubt must be resolved. First, such diets often reduceqgrgpfryqratcititaketpanabnormaUy low level thus inducing ketosis (52), Weight

JMsit;)rid~r>$MC11ij~etabQH<:condilions may possibly have no bearing on the question()fWh~lr.~J;djeta,tYfa{levelis a factor in obesity. Secondly, contradictory results haveb~~:r~:rep9rt;'cLot1theextent to which the extra weight loss is merely a loss of water,(Sh53.);

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Page 4: DIETARY FATS INHEALTH - Athabasca University

Experiments during the ]ast 3°. years have shown that a high fa,t dh::t iuduccs~?,.8~weight gain in rats (54-56), mice ~5~.57,58); (Temple & El-Khatlb, unpubh~li¥(f,:,bservations) and hamst~rs ~59). T~lS IS probably the only area that supportsai()~:tor excess fat consumptIOn In obesIty.

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MATURITY ONSET DIABETES

Diabetes has a close epidemiological relationship to CHD~obesity and a Westernlifestyle (42,60), and the association with refined carbohydrates is cJoser than Withdielary fats (11). For instance, Bang et al. (61) report that, alth6ugh Greenland Eskimoseat a high fat, low carbobydnitc d,iet, diabetes is unknowit. ......

Studies on individuals have, in general, not revealed an assQciation between dietary.fat intake and an impaired ghicose tolerance (44). ......

Solid evidence shows that the most suitable diet for maturity diabetics (type II) is Onerestricted in fat \vith the calories being supplied mainly by fOQ<1srich in carbohydratesand dietary fiber (62,63). If, then, such a diet is an effectivetl.1~rapy, it could be logicalto argue that a high fat diet is a causative agent. Such a conclusion apparently contra.dicts the above mentioned data. Thus, the true role of dktary fat in diabetes is unknown.

THE ItviMUNE SYSTEM

The level of dietary fat affects the functioning of the immune system (64): a depressedresponsiveness after consuming a diet rich in unsalurated fat being the most commonlyreported effect (65,66).

It is possible that autoimmune diseases are related to a high fat diet. They are thoughtto be associated with a Western lifestyle, but the evidence to this effect is meagre(67,68). In an uncontrolled trial, six patients wit.h rheumatoid arthritis experiencedgreatly reduced symptoms on a diet vcry low in fat (69). Similarly, a low (10/0) fatdiet greatly reduced the spontaneous development of one autoimmune disease (immunecomplex nephritis) in a susceptible strain of mice (70).

CONCLUSION

On balance, a high fat diet has a deleterious effect On health. Although this conclusion iis supported not by cJear proof tbat dietary fat is a true cause of specific diseases,there are strong grounds for suspicion in relation to several diseases. Dietary prudencewould, therefore, seem appropriate.

NOTE ADDED IN PROOF

In an excellent article Eaton and Kanner (71)haveatt~rriPtedt\)b~UcililatethcJaLcontentof the paleolilhic (stOne-age) dieLA,~~uJ1lingthatmeatpr()vi<.i~s35r&(by:\veight) of :

.fso~g 0/: hr~e:Ot, °t~ ~llgr~0~~I~~ftf~~mcf~yi~~~~~~h~:¥~t-~~~i~C6Y6iG\~llif..

~he.diet

!.~!~~'L',I. .

T16

Page 5: DIETARY FATS INHEALTH - Athabasca University

Birdsell, J. 13. (1975): [furrum evolution: an introduction to the Ilew physical anthropology. Chicago:Rand McNally Publishing Co.

3 Bunn, H. T. (1981): Archaeological evidence for meat-eating by Plio. Pleistocene hominids fromKoobi Fora and Olduvai Gorge. Nature 291, 574-577.

4 Pott.~, R. & Shipman, P. (1981): Cutmarks made by stone tool.s on !Joues from Olduvai Gorge,Tanzania. Nature 291, 577-5RO.

5 Crawford, M. A. (1968): Fatty acid ratios in free.living and domestic animals, PQssible implicationsfor atheroma. Lam,:et 1, /329-! 333.

6 Crawford, M. A., Gale, M. 1\1., Woodford, 1\1. H. & Casped, N. M. (1970): Comparative studieson fatty acid composit.ion of wild and domestk meats. Int. J. Biochem. 1, 295-305.

7 Paul, A. A. & Southgate., D. A. T. (1978): McCance and ~Viddow:>'OfI's 'The compositiol1of foods'.London: HMSO.

8 Agren, G. & Gibson, R. (1969): Food composition table for llse ill Ethiopia. Uppsala:Almqvistand WiehelL . :.

<}Paul, A. A. & Southgate, D. A. T. (l9S0): AfcCancc and Widdowson's 'The compositioft.hf foods'.Supplemt;nL Landon: HMSO.

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II Cleave, T. L. (1974): The saccharine disease. Bristol: J. Wright. '. .

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Rclationstlip of dietary intake to subsequent coronary heart disease incidence: the Puerto Riu) I-feartHealth Pragram. Am. ./. Clin. NutI'. 33, 1818-]827. . ..:. .'

14 Kromhout. D., Bosschieter, E. B. & Coulander. C. D. (1982): Dietary fibre and 10~ycll.rmortalityfrom coronary heart disease, cancer, and all callses. The Zutphen study, Lallcet2,5~i3-c522.

15 Mcdalic, J. H., Kahn, H. A., Nuefe1d, H. M., Riss. E. & GoJdbourt, U. (1973): Five-ycarn:ryocardialinfarction incidence. 11. Association of single variables to age and birthplace. J. Chron;r,' Dr;,~;'U;"329-349.

16 Morris, J. N., Marr, J. W. & Clayton, D. G. (1977): Diet and heart disease: a postscript,Br. Meel.J.2, 1307-1314.

.

17 ShekelIe, R. B., Shryock, A. M., Paul, 0.. Lepper, )\1.. Stamler, J., Lit!. S. & Raynor, W,J. (1981):Dit:t, serum cholesterol, and death from coronary heart disease. The \Vcstern Electric .~tUcJy,New /lngl.J. Med. 304, 65-70. .

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20 Bassett, D. R., Abe!, M., !'vIoellering, R. C.. Rosenblatt, G. & Stokes, .I. (1969): Coronary heart diseasein Hawaiian and Japanese men. Am. J. Clin. NutI'. '22, J4R3-1503.

21 Fil1(.~gan, A.. Hickey, N., Maurer, B. & iIofulcahy, R. (1968); Diet alld coronary heart disease: dietaryanalysis on 100 male patiems. Am. .l. CUn. NutI', 21, 143-148.

22 LitHe, J. A., Shanoff, H. M. & Csima, A. (1967): Dietary carbohydrate and [at, serum lipoproteins,and human atherosclerosis. Am. ./. Clin. Nut,.. 20, 133-138.

23 Oheycsekere. 1. (1964): Dietary fat, serum cholcsteml, and ischacmic heart disease in Ceylon. Er. HeartJ. 26, 625-630.

24 Obeyesekere, I. (1969); Evaluation of risk [actors in coronary heart disease in Ceylon. l5rael.l. A1ed.Sci. 5, 671-674.

25 Papp, O. A., Padilla, L. & Johnson, A. L. (1965): Dietary intake in patients with and without myocardialinfarction.1.a/lcf!l2, 259-261.

26 Wijeyesd;era, J. G.(J954):J\4yocardialint'arction-a study based on 100 ca~es. Ceylon Afed. J. 2,168-174.

'. .'27 MOore.MoC.i,G1.l7-p'l;l!1,!\'I.A-.,ghilIinf:,J?E,&;Strong, J. P. (1976): .Dietary-at herosclerosis study

on deceasedper$0i1s..l.Aitl.Diei..4$.wj~;.fi.S,216--:m;28 Reddy,B.S.,COllen'!-.A.,r--IcC@',G>p.,IIill/P;,\Veisburgcr, J. H. & Wyndcr, E. L. (1980):

Nutrition andhsieliluoIIS!lip.tQ:\..'<1.ricei;.Adv;Clll'lcer..Res.32; 237 -345..29 Lubin, J.I-J..,m~nJs,g.~.,BI6I.W,J,,7;iegler.K0.;tecs,A. W. & Fraurneni, J. F. (19RI): Dietary

. factors..a'ld...bre<iiit.. canC#'.'.~ioJ>:,.'ltti l;.'.$(lm:e,...28;.'.68?;68.9.30 Nomura.A,HeridersOll, ItfLs.: n;:e, J; (1978): Breastc.aneer and diet among the Japanese in Hawaii.

Arl!. J.C/in,}Vutl'.~1;2&40:,-2!)~!J;... .. . . . .

177

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3(P~lrn~r:S. &. Bakshi, K. (1983): Diet, nutrition. and cancer: inLerim dietary guidelin6s.",t{~fi~.:@#:#.ifInst 70 1151- 1170.

""'..

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32 Arn~stl~nr.. B. ~ Dol.'. R. (1 ~75): Environme~tal factors and cancer incidcncc''ar@)~i§#Yit)iy:different countncs, with specIal reference to dlCtary practlCcs. If/f. J. Cancer 15/fi:t?:H~3J; 1!t

33 Enstrom, J. E. (1975): Colorectal cancer and consumption of beef and f~t. Brit. J.,9'.~H~#~m,A~~!tij::34 1\kMichael, A. J., Potter, J. D. & Hetzel, B. S. (1979): Time trends In colorcctalca~~t::lfiqml~:

~n relation to food. a.nd a~cohol cons~mPtion: United States, United Kingdoll1,.<\.:4Ht#@:::4i;ij:\:f{<li{Zealand. Int. J. EpldemlUl. S, 295 03.

35 Burkitt, D. P. (1971): Epidemiology of cancer of the colon and rectum. CIlf!('(W~;':~@:~~36 Burkitt, D. P. (1978): Colonic-rectal cancer: fiber and other di<:tary factors;:.4i#~+;}Pt(#;:[M~i1.

31, S58-S64." ' ."''''''''''''''''''''''''''''':'.',

37 Dales, L. G., ~ricdl~1an,? D., Ury, H. K., (?rossman, S. & Williams: S. R. og!ZH*:%~~§§.M:~study of rclatwnslups 01 dleL and Qther trailS to colorectal cancer 111Amenc.U~:pla4~>A:fii?1l:"'pidemial.109, 132-144. ,

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38 Miller, A. B., Howe, G. R., Jain, ~1., Craib, K. J. P. & Harrison, L. (19S3)~ FObg:~t~I'h~*ii~J:f~groups as risk factors in a case-control study of diet and cola-rectal cancer. Int. J.q~~~:~~,:JMM6.t

39 Graham, S. & Mcttlin, C. (1979): DieL and cololl cancer. Am. J. EpidemiQI.:lO~;<l+;jJj)'"40 Haenszel, W., Locke, F. B. & Segi, 1"1.(1980): A case-control study of linge bmvcIS~!1F¥)#J~PiiM

.1. Nlltl. Cancer Im..t. 64, 17-22. ,".

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41 Nauss, K. M., Locniskar, IV!. & Newberne, P. M. (1983): Effects of alterati6nS:il))hcqu~1itSr~Mquantity of dietary fat on 1,2-dimeLhylhydrazinc-induced colon tUJIlorigcncsisillratL'R4~WWi,{*'t43, 4083-4090. .'

42 Trowell. H. C. & Burkitt, D. P. (cds) (1981): Westem diseases: their emergel""ed.ttdpJ"et:~ilWm;.London: Edward Arnold.

4~ Bingham, S., McNeil, N. !. & Cummings,.I. H. (1981): The diet of individuals: it stiidyofri,raridQnw;chosen cross section of British auults in a Cambridgeshire village. Brit. J. Nutr.:45,2:}",:3.s:'

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44 Keen, H., Thomas, B. J., Jarrett, R. J. & Fuller, J. H. (1979): Nutrienl intake, adjI':Osjr:ia¥di#I:!.~W~;Hr. Med. J. I, 655.-658. ,

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45 Matter, S., Weltman, A. & Stamford, B. A. (1980): Body fat contenl and serumlihi4.1evcLs/$~Am;:Diet. As~'oc. 77, 149-152. '

116 Nichols, A. B., Ravenscroft, c., Lamphiear, D. E. & Ostrander, L. D. (1976):lJiclcpendC:I1(:#\ifserum lipid levels and dietary habits. The Tecumseh study. J. Am. AIcd. .AsS':2~i'i,lQ4$8i~:t:::

47 Ohlson, ,\Of.A. & Harper, 1.. J. (1976): Longitudinal studic~ of food intake and\veigh((jf:w:<:i#W#:'from ages 18 to 56 years. J. Am. Diet. Assoc. 69, 626-631.

,.." . ", ,

48 Ries, W. (1973): Feeding behaviour in obesity. Proc. Nutr. Soc. 32, 187-193.49 Van Stratum, P., Lussenburg, R. N., Van Wczel. L. A., Vcrgroesen, A. J. & Crctllcr=;:H.:P.'ttrJ.,tI);

The effect of dietary carbohydrate: fat ratio 011 energy intake by adult women. A,ii. fc;/in.jsti4H31, 206-212. .. ,

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50 Rabast, U.. Kasper, H. & Sehonborn, J. (1979): Dietetic treatment of obesity w1ih low aiidJ:i!gl!carbohydrate dicts. Comparativc studies-clinical results. 1m. J. Obes. 3, 201-21 L

51 Rabast. LT., Vornberger, K. H. & Eh!, 1\.1.(198J): Loss of weight, sodium and watei.in obesepers9n~consuming a high-or Jow-carbohydrate diet. A 1/1/. ..'ll/fr. Iv/etab. 25, 341-349.

52 Atkins, R. C. (J9i5): Dr. Atkins diet revolwiof!. New York: Bantam Books.53 Yang, 1\-L-U. & Van Itatlie, T. B. (1976): Composition of weight loss during shorf~terni\veigh~

rednction. J. Clin. bn'est. 58, 722-730..

54 Harman, D. (1971): Free radical theory of aging: effect of the amount and degree o[unsaturaiibiiof dietary fat on mortality rate. J. Geron!. 26, 451-457.

55 Lemonnier, D. (1972): Effect of age, sex, and site on the cellularity of the adipose ti.~stic.i1i:inict".and rats rendered obese by a high-fat diet. J. Cli/!. Invest. 51, 2907-2915... '

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56 :vlickelsen, 0., Takahashi, S. & Craig, C. (1955): Experimental obesity. I. Production ofobesMin rats by feeding high..fat diets. 1. Nutr. 57, 541-554.

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57 Bourgeois. F., Alexiu, A. & Lcmonnier, D. (1983): Dietary-induced obesity: effect of dietary fatson adipose tissue ceUuJarity in mice. Brit. J. {\,'utr. 49, 17-26.'

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.58 Fenton, P. F. & Dowling, M. T. (1953): Studies on obesity. L Nutritional obesity in mice. .1. Nutr.

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