Jump to content
RemedySpot.com

CR optimizes food toxins?

Rate this topic


Guest guest

Recommended Posts

Hi All,

An important it seems to me topic of the group

lies in the area of toxins. The toxins may derive

from pollution-derived chemicals in our fat deposits

that are rapidily released from the deposits during

the introductory phase of CR.

Also, we eat many fruits and vegetables and they

may require more stringent cleaning routines for our

maximum health.

Now the not yet in Medline letter and probably

never in Medline even for an abstract below suggests

to me a completely different scenario.

Maybe, our eating many fruits and vegetables is

a health risk due their toxins. We may overdose

the hormetic effect of the toxins rather than ride

in the saddle of the U-shaped hormetic effect

curve for these toxins.

When animals are subject to CR, they are

supplemented with the vitamins and minerals

that would be in the excess food eaten by ad

lib animals, it seems to me.

So, are multiple pounds of vegetables in

our diets CR-friendly?

I enjoyed the conclusion:

" decreasing the food intake may, from a

toxicological point of view, mean a reduction of the

cumulative exposure to many toxic compounds present

in our diet and produced from it. It may decrease the

energy expenditure for the detoxification processes

allowing for its allocation in other vital processes. This

effect can make also a significant contribution to the

beneficial effects of CR. "

Food toxicity contributes to the beneficial

effects of calorie restriction • CORRESPONDENCE

Journal of Theoretical Biology, In Press,

Corrected Proof, Available online 8 December 2004,

Grzegorz Bartosz

Since 1930s calorie restriction (CR)is known to

ef & #64257;ciently prolong the lifespan of experimental mam-

mals.Further studies have demonstrated that this

treatment is effective on one hand,also for various

non-vertebrates and even yeast and,on the other hand,

for primates and seemingly for man (Heilbronn and

Ravussin,2003;Merry,2002).Various explanations have

been proposed for the bene & #64257;cial effects of CR,the most

popular one consisting in diminution of free radical

production due to decreased metabolic rate including

respiration (Barja,2002;Heilbronn and Ravussin,2003;

Merry,2002).Curiously,an opposite explanation

has been suggested for the yeast:CR consisting in

lowering the glucose level in the medium promotes

earlier diauxic shift increasing respiration which,being a

mild oxidative stress,stimulates antioxidant defense

which proves useful later on (Lin et al.,2002).

Undoubtedly,however,the mechanism of action of

CR is much more complex than only reduction of the

free radical damage and may include the effects of

sirtuins on gene silencing (Lin et al.,2000).Current

theories do not seem to explain the mechanisms of this

phenomenon in full depth.

I would like to draw attention to another aspect of

CR and animal physiology in general which seems

noteworthy.Food supply is a sine qua non-condition for

animals life;however,food is also toxic and the

biological outcome of food consumption,including

longevity,is a net result between these two facets.This

question may be similar,but more general,to that of

advantages of aerobic metabolism and oxygen toxicity

(Halliwell and Gutteridge,1999).

Why food could be toxic?Firstly,because it contains

some toxic component.The presence of secondary

metabolites which are toxic to animals is very common

in plants and diet rich in plant materials (including

vegetables and whole fruits)is rich not only in

antioxidants but also in plant toxins.It has been

estimated that our daily food contains some 1.5 g of

toxic xenobiotics (mostly of plant origin)which is the

main reason for the existence of plethora of mechanisms

for detoxi & #64257;cation and excretion of xenobiotics from the

cells and & #64257;nally from the body,including many

transporters of the ABC superfamily (Dietrich et al.,

2003).Some of the xenobiotics contained in the food

may be subject to redox cycling and contribute to

production of ROS species n the body (Halliwell and

Gutteridge,1999).The whole content of such vital

antioxidants as ascorbic acid,tocopherols and carote-

noids in the human body comes from the food.Toxic

compounds have also a tendency to be absorbed and

distributed in the body,their action being partly but not

totally counteracted by appropriate detoxi & #64257;cation me-

chanisms.Calorie restriction,at least that performed

experimentally (undernutrition but not malnutrition,

involving supplementation of food given in limited

amounts with vitamins and micronutrients)does not

deplete therefore signi & #64257;cantly the tested organisms in

antioxidants but does so in toxins.

Studies of gene transcription pro & #64257;les demonstrated

that calorie restriction decreases the expression genes

involved in stress response,inducible detoxi & #64257;cation

systems and DNA repair systems (Dhahbi et al.,2004;

Sreekumar et al.,2002;Weindruch et al.,2001).It would

be in line with the hypothesis of food toxicity.The stress

response to food components may have a long-

prolonging hormetic effect but perhaps smaller doses

of nutritional toxins,provided under calorie restriction

regime,are closer to optimum for a positive effect on the

life span.

Secondly,excluding direct engulfment of a fresh plant

or animal prey,the food consists of dead biological

material which is subject to autolytic degradation,a

process in which toxic compounds are produced.

Thirdly,the process of digestion produces many

undesired and toxic compounds.The old theory of

Metchnikoff ascribing aging to the toxins released from

bacteria in the intestinal tract (Medvedev,1989)canbe

recalled in this context.A more recent idea along this

line has consisted in ascribing the bene & #64257;cial action of

plant polyphenols to the reduction of toxicity connected

with the process of digestion (Gee and ,2001).

Seemingly the food toxicity argument does not hold

for the yeast where the CR-type procedure consists in

limitation of one well-de & #64257;ned nutrient,i.e.glucose.

However,preparation of yeast medium includes auto-

claving glucose solution (with or without other compo-

nents of the medium);this process leads to formation of

glucose oxidation products (and glycation of other

components of the media)whose toxic action has been

well recognized (Vlassara and Palace,2003).

Taking food as a stressful event for the body leading,i.

a.,to the mobilization of leukocytes,and to oxidative

stress detectable usually as a measurable decrease of the

total antioxidant capacity of blood plasma (Natella

et al.,2002;Ursini et al.,1998).

Therefore,decreasing the food intake may,from a

toxicological point of view,mean a reduction of the

cumulative exposure to many toxic compounds present

in our diet and produced from it.It may decrease the

energy expenditure for the detoxi & #64257;cation processes

allowing for its allocation in other vital processes.This

effect can make also a signi & #64257;cant contribution to the

bene & #64257;cial effects of CR.

References

Barja,G.,2002.Endogenous oxidative stress:relationship to aging,

longevity and calorie restriction.Ageing Res.Rev.1,397 –411.

Dhahbi,J.M.,Kim,H.J.,Mote,P.L.,Beaver,R.J.,Spindler,S.R.,

2004.Temporal linkage between the phenotypic and genomic

responses to calorierestriction.Proc.Natl.Acad.Sci.USA 101,

5524 –5529.

Dietrich,C.G.,Geier,A.,Oude Elferink,R.P.,2003.ABC of oral

bioavailability:transporters as gatekeepers in the gut.Gut 52,

1788 –1795.

Gee,J.M.,,I.T.,2001.Polyphenolic compounds:interactions

with the gut and implications for human health.Curr.Med.Chem.

8,1245 –1255.

Halliwell,B.,Gutteridge,J.M.C.,1999.Free Radicals in Biology and

Medicine.Oxford University Press,Oxford New York.

Heilbronn,L.K.,Ravussin,E.,2003.Calorie restriction and aging,

review of the literature and implications for studies in humans.Am.

J.Clin.Nutr.78,361 –369.

Lin,S.J.,Defossez,P.A.,Guarente,L.,2000.Requirement of NAD

and SIR2 for life-span extension by calorie restriction in

Saccharomyces cerevisiae.Science 289,2126 –2128.

Lin,S.J.,Kaeberlein,M.,Andalis,A.A.,Sturtz,L.A.,Defossez,P.A.,

Culotta,V.C.,Fink,G.R.,Guarente,L.,2002.Calorie restriction

extends Saccharomyces cerevisiae lifespan by increasing respiration.

Nature 418,344 –348.

Medvedev,Z.A.,1989.The past and the future of experimental

gerontology.Arch.Gerontol.Geriatr.9,201 –213.

Merry,B.J.,2002.Molecular mechanisms linking calorie restriction

and longevity.Int.J.Biochem.Cell Biol.34,1340 –1354.

Natella,F.,Belelli,F.,Gentili,V.,Ursini,F.,Scaccini,C.,2002.Grape

seed proanthocyanidins prevent plasma postprandial oxidative

stress in humans.J.Agric.Food Chem.50,7720 –7725.

Sreekumar,R.,Unnikrishnan,J.,Fu,A.,Nygren,J.,Short,K.R.,

Schimke,J.,Barazzoni,R.,Nair,K.S.,2002.Effects of calorier-

estriction on mitochondrial function and gene transcripts in rat

muscle.Am.J.Physiol.Endocrinol.Metab.283,E38 –E43.

Ursini,F.,Zamburlini,A.,Cazzolato,G.,Maiorino,M.,Bon,G.B.,

Sevanian,A.,1998.Postprandial plasma lipid hydroperoxides,a

possible linkbetween diet and atherosclerosis.Free Radic.Biol.

Med.25,250 –252.

Vlassara,H.,Palace,M.R.,2003.Glycoxidation:the menace of

diabetes and aging,Mt.Sinai J.Med.70,232 –241.

Weindruch,R.,Kayo,T.,Lee,C.K.,Prolla,T.A.,2001.Microarray

pro & #64257;ling of gene expression in aging and its alteration by

calorierestriction in mice.J.Nutr.131,918S –923S.

Link to comment
Share on other sites

Join the conversation

You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
×
×
  • Create New...