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life span extension w/methionine limiting diet


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#61 niner

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Posted 14 September 2009 - 09:41 PM

Very disappointing result. Also makes it more strange how methionine restriction actually achieves lifespan extension.

I'm not sure that it's so bad. All this knockout did was eliminate a particular pathway for dealing with oxidized Met. They make it sound like it's some kind of master gene. These mice were more susceptible to certain forms of oxidative stress, but their lifespan was unchanged. That doesn't mean that they were as healthy as other mice that died at the same time; but it does suggest that whatever defects they had were not as lethal as the normal causes of death. What they did didn't alter autophagy, I would think.

#62 niner

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Posted 14 September 2009 - 09:52 PM

Long-term tryptophan restriction and aging in the rat.

Growth-retarded rats fed a tryptophan deficient diet at 21 days for periods of 6-22 months were shown to reach normal body weight when subsequently fed Purina Rat Chow. They demonstrated an increased ability over similar aged controls to recover from hypothermia induced by 3-minute whole-body ice water immersion, were able to bear litters at 17--28 months of age, showed a delay in the age of onset of visible tumors, and indicated an increase in their average lifespan at late ages. Animals fed on this diet from 3 months of age revealed a similar ability to reproduce at advanced ages, but not as marked as those placed on the diet earlier. The average lifespan (in months +/- the standard error of the mean) of the rats recovering from the long-term tryptophan-deficient diets was 36.31 +/- 2.26 while the control rats survived an average of 30.5 +/- 1.90 months. The last of 8 rats surviving the period of tryptophan-deficiency died at 45.50 months (1387 days) while the last of 14 control rats died at 41.75 months (1266 days). It is hypothesized that some kind of subtle mechanism exerts its influence on the rats during the period of tryptophan deficiency which caused an accelerated morbidity and mortality as they approached senescence approximately 1 to 2 years after refeeding. This is parallel to the situation with immature animals subjected to long-term caloric restriction and then fed on normal diets.

I'm not sure I understand what the authors means by accelerated morbidity -- didn't the tryptophan-restricted rats outlive the controls?

I agree, this makes no sense. The only way that I could justify the italicized section is to suppose that they saw some sort of rapid acceleration of senescence (despite their longer lifespans) in the Trp-deprived animals. I hate it when scientists can't communicate. I just went on a tirade about this the other day, with another incomprehesible abstract. Again, the journal provides little or no editorial function, yet holds the text hostage.

Edited by niner, 14 September 2009 - 09:53 PM.


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#63 Blue

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Posted 14 September 2009 - 10:10 PM

A thought about selenomethionine. There is a large cell, animal, and epidemiologic literature suggesting that selenium supplementation should be effective against at least cancer. So the failure of the SELECT trial was strange. Maybe the methionine in the form they used (selenomethionine) has something to be with it?

#64 Blue

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Posted 14 September 2009 - 10:19 PM

What i usually mean by suffering is trying to eat a very low calorie diet (CR) - or heavily restricting carbs. Methionine restriction seems to allow you to consume more calories (to a point) while allowing for a maximal lifespan.

The studies not only limit methionine. They also include 0% cysteine. A diet which is impossible to achieve for humans if you do not pay a laboratory firm to make a special diet.

#65 Blue

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Posted 14 September 2009 - 11:25 PM

There is no lack of theories regarding how MR affects longevity. I think I have seen around ten different theories in this thread and those it links to. Some thoughs. MR is similar to CR in that IGF-I, insulin, and thyroid hormone are lowered. Lowered insulin and IGF-1 seems responsible for many of the effects of CR. These all largely regulated from the hypothalamus. A simple explanation for CR and MR is simply that there are some sort of sensors in the hypothalamus measuring general energy and methionine (+cysteine? sulfur?) levels and change the body's hormonal pattern when long-term starvation is detected. Which then through various pathways, maybe somewhat different for CR and MR, travel down to the cell machinery which is adapted for less food intake which also as a side effect increases longevity.

Low MR -> low homocysteine seems not that likely since intervention studies lowering homocysteine have given disappointing results.

Moderate MR seems not that important since vegetarians do not live much longer.

Edited by Blue, 14 September 2009 - 11:45 PM.


#66 kismet

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Posted 15 September 2009 - 01:39 AM

Moderate MR seems not that important since vegetarians do not live much longer.

Good summary, bad conclusion on this one, though. Just think how many variables such a dietary change involves. While the interventional trials targetting homocysteine and nothing but homocysteine beautifuly refute the Hcy hypothesis. The data on vegetarians, at best, would be suggestive of no protective effect. Small diff. in methionine intake and life span could be easily masked by a. statistical noise, b. other detrimental changes induced by vegetarianism (deficiencies).

BTW, does MR produce exactly the same changes in thyroid and IGF-1 levels as CR?

Edited by kismet, 15 September 2009 - 01:39 AM.


#67 Blue

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Posted 15 September 2009 - 02:11 AM

Moderate MR seems not that important since vegetarians do not live much longer.

Good summary, bad conclusion on this one, though. Just think how many variables such a dietary change involves. While the interventional trials targetting homocysteine and nothing but homocysteine beautifuly refute the Hcy hypothesis. The data on vegetarians, at best, would be suggestive of no protective effect. Small diff. in methionine intake and life span could be easily masked by a. statistical noise, b. other detrimental changes induced by vegetarianism (deficiencies).

BTW, does MR produce exactly the same changes in thyroid and IGF-1 levels as CR?

Agree regarding vegetarian lifespan and MR. Do not know regarding IGF-1 level.

Some prospective studies with methionine. Normal methionine variation do not seem very important.

"Although folic acid has been investigated for its potential to inhibit carcinogenesis, few epidemiologic studies have assessed the effects of intake of thiamin, riboflavin, and niacin, which may reduce cancer risk by acting as cofactors in folate metabolism or by other mechanisms. Using data from a large cohort of Canadian women, we examined the association of dietary intake of these nutrients, as well as intake of folate, methionine, and alcohol, with cancers of the breast, endometrium, ovary, colorectum, and lung ascertained during an average of 16.4 years of follow-up. After exclusions, the following numbers of incident cases were available for analysis: breast, n=2491; endometrium, n=426; ovary, n=264; colorectum, n=617; and lung, n=358. Cox proportional hazard models were used to estimate risk of each cancer with individual nutrients and to explore possible effect modification by combinations of nutrients on cancer risk. Few significant associations of intake of individual B vitamins with the five cancers were observed. Alcohol consumption showed a modest positive association with breast cancer risk but not with risk of the other cancers. There was no evidence of effect modification among the nutrients. This large study provides little support for an association of dietary intake thiamin, riboflavin, niacin, folate, or methionine with five major cancers in women."
http://www.nature.co...l/6604540a.html

"PURPOSE: Components of one-carbon metabolism are believed to influence cancer development with suggested mechanisms, including DNA methylation and DNA repair mechanisms. However, few prospective studies have investigated one-carbon metabolism in relation to prostate cancer risk, and the results have been conflicting. The aim of this study was to do a comprehensive investigation of the components of one-carbon metabolism in relation to prostate cancer risk. A panel of seven circulating B vitamins and related metabolites was selected, most of which have not been studied before. MATERIALS AND METHODS: We analyzed plasma concentrations of betaine, choline, cysteine, methionine, methylmalonic acid (MMA), vitamin B2, and vitamin B6 in 561 cases and 1,034 controls matched for age and recruitment date, nested within the population-based Northern Sweden Health and Disease Cohort. Relative risks of prostate cancer were estimated by conditional logistic regression. RESULTS: Positive associations with prostate cancer risk were observed for choline and vitamin B2, and an inverse association was observed for MMA. The relative risks for a doubling in concentrations were 1.46 [95% confidence interval (95% CI), 1.04-2.05; P(trend) = 0.03] for choline, 1.11 (95% CI, 1.00-1.23; P(trend) = 0.04) for vitamin B2, and 0.78 (95% CI, 0.63-0.97; P(trend) = 0.03) for MMA. Concentrations of betaine, cysteine, methionine, and vitamin B6 were not associated with prostate cancer risk. CONCLUSION: The results of this large prospective study suggest that elevated plasma concentrations of choline and vitamin B2 may be associated with an increased risk of prostate cancer. These novel findings support a role of one-carbon metabolism in prostate cancer etiology and warrant further investigation."
http://www.ncbi.nlm....pubmed/19423531

"Background DNA methylation is an important epigenetic process for transcriptional control of human genome including those genes involved in cancer initiation and progression. Clinical studies have suggested that biological explanation to the protective effect of some nutrients could be linked with the DNA methylation. Folate is a primary methyl donor nutrient; it has been shown to play a key role in DNA methylation, repair and synthesis, by acting as co-factors and/or substrates in this metabolic pathway. Likewise, activity of a key enzyme, the methylenetetrahydrofolate reductase (MTHFR) has also been shown to influence DNA methylation. Overall, these findings support the notion that dietary intake as well as genetic factors play a role in one-carbon metabolism.
Aim of the study This study is to evaluate the dietary intake of nutrients involved in one-carbon metabolism and the genotype of MTHFR 677 C > T with respect to GC risk.
Methods We carried out in January 2004 a population-based case–control study in the metropolitan area of Mexico City. A total of 248 histological confirmed GC patients were recruited from nine tertiary hospitals, along with 478 age and sex-matched controls. Nutrient intake was estimated from food frequency questionnaire; the MTHFR 677C > T genotype was determined by PCR-RFLP analysis.
Results A significant reduction in diffuse GC risk was observed for MTHFR 677 TT genotype among individuals with high consumption of folate (OR = 0.23; 95% CI 0.06–0.84), choline (OR = 0.55; 95% CI 0.33–0.9) and Vitamin B6 (OR = 0.59; 95% CI 0.36–0.96) compared to MTHFR 677 CC + CT carriers. Among subjects with low consumption of methionine, a reduced risk of diffuse GC was also detected (OR = 0.40; 95% CI 0.16–0.97). In contrast, carriers of the MTHFR 677 TT genotype with a low consumption of folate had a significant increased risk of intestinal GC (OR = 1.88 95% CI 1.02–3.47). A folate–MTHFR 677 C > T interaction in the borderline of significance (P = 0.055) was detected.
Conclusions It is probable that GC prevention requires dietary recommendations according to the individual genotype; nevertheless, the available information to this respect is still very limited."
http://www.springerl...3721565743r526/

Dietary B vitamin and methionine intakes and plasma folate are not associated with colorectal cancer risk in Chinese women.
http://www.ncbi.nlm....pubmed/19240230

"Sporadic microsatellite instability (MSI)-high colon cancers are positively associated with MLH1 promoter methylation and inversely with KRAS mutation. One-carbon metabolism is critical for methylation reactions and nucleotide biosynthesis, but the influence of dietary one-carbon nutrients such as folate and B vitamins on molecular changes in colon cancer is not known. Using the database of two independent prospective cohort studies (88,691 women and 47,371 men), we examined the relation between dietary intake of one-carbon nutrients and the incidence of microsatellite instability and KRAS mutation in 669 incident colon cancers. The overall inverse association between folate and colon cancer did not differ significantly according to MSI status [relative ratio (RR), 0.79; 95% confidence interval (95% CI), 0.60-1.03 for microsatellite stable/MSI-low colon cancers; and RR, 0.61, 95% CI, 0.37-1.02 for MSI-high colon cancers; Pheterogeneity = 0.53] or KRAS status (RR, 0.66; 95% CI, 0.49-0.87 for KRAS wild-type colon cancers; and RR, 1.05; 95% CI, 0.68-1.61 for KRAS mutated colon cancers; Pheterogeneity = 0.12), although our analyses had limited power to preclude an effect of folate on KRAS wild-type colon cancers. Similarly, high vitamin B6 or B12 intake was inversely associated with colon cancers, regardless of MSI or KRAS status. No significant effect of methionine intake or alcohol consumption was observed for colon cancers with MSI high or KRAS mutation. In conclusion, the influence of dietary one-carbon nutrient intake on colon cancer risk does not seem to differ according to MSI or KRAS mutational status. (Cancer Epidemiol Biomarkers Prev 2008;17(10):2895–8) "
http://cebp.aacrjour...0/2895.abstract

"Adequate intake of folate, methionine, riboflavin, and vitamin B-6 may prevent aberrant DNA methylation and thereby protect against colorectal cancer (CRC). However, previous epidemiological studies investigating associations between dietary intakes of these nutrients and CRC have been inconsistent. We investigated the associations between intakes of folate, methionine, riboflavin, and vitamin B-6 and CRC risk, accounting for the sublocalization of the tumor. Within the Netherlands Cohort Study on diet and cancer (n = 120,852), 2349 cases and 4168 subcohort members were available for data analyses from a follow-up period of 13.3 y after baseline. Gender-specific adjusted incidence rate ratios (RR) were calculated over quintiles of dietary intake in case-cohort analyses. Folate intake was not associated with CRC risk in either men or women. However, methionine was associated with decreased risk of proximal colon cancer among men (RR = 0.57 for highest vs. lowest quintile of intake; P-trend = 0.03) and rectal cancer among women (highest vs. lowest quintile; RR = 0.45; P-trend = 0.05). Riboflavin tended to be associated with decreased proximal colon cancer risk among women (RR = 0.61; P-trend = 0.07). Conversely, there was a strong positive association between vitamin B-6 and rectal cancer among women (RR = 3.57; P-trend = 0.01). Our findings suggest that relatively high methionine intake may protect against proximal colon cancer in men and rectal cancer in women but that folate may not have a protective effect. This is the 2nd prospective cohort study in which vitamin B-6 intake was associated with increased risk of rectal tumors in women, which might suggest that this vitamin enhances rectal cancer in women."
http://www.ncbi.nlm....pubmed/19022960

"The associations of dietary folate, vitamin B6, vitamin B12, and methionine intakes with risk of stroke subtypes were examined among 26,556 male Finnish smokers, aged 50–69 years, enrolled in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Dietary intake was assessed at baseline by using a validated food frequency questionnaire. During a mean follow-up of 13.6 years, from 1985 through 2004, 2,702 cerebral infarctions, 383 intracerebral hemorrhages, and 196 subarachnoid hemorrhages were identified from national registers. In analyses adjusting for age and cardiovascular risk factors, a high folate intake was associated with a statistically significant lower risk of cerebral infarction but not intracerebral or subarachnoid hemorrhages. The multivariate relative risk of cerebral infarction was 0.80 (95% confidence interval: 0.70, 0.91; ptrend = 0.001) for men in the highest versus lowest quintile of folate intake. Vitamin B6, vitamin B12, and methionine intakes were not significantly associated with any subtype of stroke. These findings in men suggest that a high dietary folate intake may reduce the risk of cerebral infarction."
http://aje.oxfordjou...tract/167/8/954

#68 Blue

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Posted 15 September 2009 - 02:16 AM

The above studies were regarding cancer except the last. Here is another which do find correlation with methionine:

"BACKGROUND AND AIM: Homocysteine, a methionine metabolite, is suggested to be a risk factor for cardiovascular diseases (CVD). To date, the effects of dietary intake of methionine, the key amino acid in homocysteine metabolism, on CVD have not been studied. Our aim was to examine the effects of dietary methionine intake on the risk of acute coronary events. METHODS AND RESULTS: We examined the effects of dietary methionine intake, assessed with 4-d food record, on acute coronary events in a prospective cohort study consisting of 1981 coronary disease free men from eastern Finland, aged 42-60 years at baseline in 1984-89, in the Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study. During an average follow-up time of 14.0 years, 292 subjects experienced an acute coronary event. In a Cox proportional hazards model adjusting for age, examination years, BMI, urinary nicotine metabolites and protein intake (excluding methionine) the relative risks of acute coronary event in the three highest quarters of dietary methionine intake were 1.31 (95% CI: 0.92, 1.86), 1.31 (95% CI: 0.88, 1.96) and 2.08 (95% CI: 1.31, 3.29) as compared with the lowest quarter. Further adjustments did not change the results. However, opposite association was observed with total protein intake, which tended to decrease the risk. CONCLUSIONS: The main finding of this study is that long-term, moderately high dietary methionine intake may increase the risk of acute coronary events in middle-aged Finnish men free of prior CHD. More prospective research is needed to confirm the role of dietary methionine in the development of CVD, and whether its effects are independent of homocysteine."
"http://www.ncbi.nlm....pubmed/16487911

Edited by Blue, 15 September 2009 - 02:30 AM.


#69 stephen_b

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Posted 08 November 2009 - 04:23 PM

I haven't seen this study discussed, The atherogenic effect of excess methionine intake (PMID 14657334, full text here). They found that even when homocysteine was not elevated, a methionine rich diet in mice was atherogenic.

Methionine is the precursor of homocysteine, a sulfur amino acid intermediate in the methylation and transsulfuration pathways. Elevated plasma homocysteine (hyperhomocysteinemia) is associated with occlusive vascular disease. Whether homocysteine per se or a coincident metabolic abnormality causes vascular disease is still an open question. Animals with genetic hyperhomocysteinemia have so far not displayed atheromatous lesions. However, when methionine-rich diets are used to induce hyperhomocysteinemia, vascular pathology is often observed. Such studies have not distinguished the effects of excess dietary methionine from those of hyperhomocysteinemia. We fed apolipoprotein E-deficient mice with experimental diets designed to achieve three conditions: (i) high methionine intake with normal blood homocysteine; (ii) high methionine intake with B vitamin deficiency and hyperhomocysteinemia; and (iii) normal methionine intake with B vitamin deficiency and hyperhomocysteinemia. Mice fed methionine-rich diets had significant atheromatous pathology in the aortic arch even with normal plasma homocysteine levels, whereas mice fed B vitamin-deficient diets developed severe hyperhomocysteinemia without any increase in vascular pathology. Our findings suggest that moderate increases in methionine intake are atherogenic in susceptible mice. Although homocysteine may contribute to the effect of methionine, high plasma homocysteine was not independently atherogenic in this model. Some product of excess methionine metabolism rather than high plasma homocysteine per se may underlie the association of homocysteine with vascular disease.

Another surprise was that a deficiency in dietary B vitamins increased homocysteine but not pathology. The quote "Some product of excess methionine metabolism rather than high plasma homocysteine per se may underlie the association of homocysteine with vascular disease" bears repeating. I wonder what's going on with methionine metabolism.

StephenB

Edited by stephen_b, 08 November 2009 - 05:07 PM.


#70 wolfeye

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Posted 12 November 2009 - 05:32 PM

I haven't seen this study discussed, The atherogenic effect of excess methionine intake (PMID 14657334, full text here). They found that even when homocysteine was not elevated, a methionine rich diet in mice was atherogenic.

Another surprise was that a deficiency in dietary B vitamins increased homocysteine but not pathology. The quote "Some product of excess methionine metabolism rather than high plasma homocysteine per se may underlie the association of homocysteine with vascular disease" bears repeating. I wonder what's going on with methionine metabolism.

StephenB


I've also seen similar conclusions from studies where decreased serum homocysteine from folate intake did not reduce risk of CHD.
Interesting article about methionine intake.

#71 stephen_b

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Posted 12 November 2009 - 06:01 PM

Interesting article about methionine intake.

I've also posted a thread (which hasn't received any lovin' -- <sniff>) about using niacin to deplete methionine. Niacin can deplete methionine, and seems to increase long term all cause mortality.

#72 Blue

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Posted 12 November 2009 - 08:23 PM

Most of the human epidemiologic I cited above found no or little effect of methionine. Also remember that the animal lifespan studies used severe methionine restriction + 0% cysteine. Something not possible to achieve without a completely artificial diet.

Edited by Blue, 12 November 2009 - 08:24 PM.


#73 warner

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Posted 28 November 2009 - 02:41 PM

Most of the human epidemiologic I cited above found no or little effect of methionine. Also remember that the animal lifespan studies used severe methionine restriction + 0% cysteine. Something not possible to achieve without a completely artificial diet.


Also, since high fat diets turned out to be much more damaging to rodents than humans (with those studies causing a great deal of confusion), you have to wonder whether it means much for humans when a study finds that high methionine (or protein or whatever) has a negative effect on a rodent.

#74 TheFountain

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Posted 28 November 2009 - 05:51 PM

Moderate MR seems not that important since vegetarians do not live much longer.

Okinawans are 98% vegetarian. The rest is occasional fish consumption. So your statement is opinionated BS..

#75 TheFountain

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Posted 28 November 2009 - 05:57 PM

Moderate MR seems not that important since vegetarians do not live much longer.

Good summary, bad conclusion on this one, though. Just think how many variables such a dietary change involves. While the interventional trials targetting homocysteine and nothing but homocysteine beautifuly refute the Hcy hypothesis. The data on vegetarians, at best, would be suggestive of no protective effect. Small diff. in methionine intake and life span could be easily masked by a. statistical noise, b. other detrimental changes induced by vegetarianism (deficiencies).

BTW, does MR produce exactly the same changes in thyroid and IGF-1 levels as CR?


It should since both MR and CR entail a degree of protein restriction and there has been lots of correlation pointing to at least animal protein and casein raising IGF-1 levels and dairy effecting thyroid markers.

Edited by TheFountain, 28 November 2009 - 05:58 PM.


#76 Blue

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Posted 28 November 2009 - 06:35 PM

Moderate MR seems not that important since vegetarians do not live much longer.

Okinawans are 98% vegetarian. The rest is occasional fish consumption. So your statement is opinionated BS..

I see no source for your claims. Even if correct says nothing about vegetarians in general.

(Hint. Using foul language just make the speaker look immature.)

#77 TheFountain

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Posted 28 November 2009 - 07:03 PM

Moderate MR seems not that important since vegetarians do not live much longer.

Okinawans are 98% vegetarian. The rest is occasional fish consumption. So your statement is opinionated BS..

I see no source for your claims. Even if correct says nothing about vegetarians in general.

(Hint. Using foul language just make the speaker look immature.)

Being condescending, nitpicking things about specific diets that have been far more proven than the ones you yourself advocate shows ignorance.

#78 kismet

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Posted 28 November 2009 - 07:11 PM

No, CR usually does not entail protein restriction. CRd animals on high protein diets live as long or longer than other animals (a topic we definitely discussed some time ago). Many CRONies from the CR-list present with typical thyroid hormone changes while on a high protein, zone'ish diet.

Edited by kismet, 30 November 2009 - 12:54 AM.


#79 tunt01

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Posted 28 November 2009 - 08:54 PM

http://www.amazon.co.../dp/0609807501/

"aim for 10-20% of diet as protein"

but the food sources are mostly vegetarian, this guy broke down the %s from the book as follows:

http://www.healthboa...ad.php?t=700546


this study (http://www.ncbi.nlm....pubmed/12733696) pegs protein in-take in males at 1.1 g/kg and females at 1.0 g/kg.

assuming each gram of protein converts to 4 calories, that's about 15% of caloric intake coming in the form of protein. this is in-line w/ the okinawa program book.

seems roughly in-line w/ what makes sense in a lower protein/mediterranean diet, where most calories should come from veggies (not cheese/dairy/meat/eggs).

#80 TheFountain

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Posted 29 November 2009 - 11:09 AM

No, CR usually does not entail protein restriction. CRd animals on high protein diets live as long or longer thant other animals (a topic we definitely discussed some time ago). Many CRONies from the CR-list present with typical thyroid hormone changes while on a high protein, zone'ish diet.


I didn't say CR required protein restriction but that it often inadvertently entails it. But whatever, see things as you want to.

#81 stephen_b

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Posted 17 December 2009 - 11:29 PM

Diet high in methionine could increase risk of Alzheimers

A brain sample taken from mice used in the study shows dark spots consistent with amyloid plaque, indicative of the progression of Alzheimer’s disease. Mice fed diets rich in methionine had an increased level of homocysteine and up to 40 percent more amyloid plaque in their brains.

No effort seems to have been made to examine whether methionine increases the level of plaque independent of homocysteine level.

#82 dear mrclock

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Posted 20 November 2012 - 02:40 AM

interesting thread. updates ?

#83 Castiel

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Posted 23 August 2015 - 09:54 PM

No, CR usually does not entail protein restriction. CRd animals on high protein diets live as long or longer than other animals (a topic we definitely discussed some time ago). Many CRONies from the CR-list present with typical thyroid hormone changes while on a high protein, zone'ish diet.

 

But doesn't CR reduce igf-1 in animal models, and fails to do so in humans fed high protein diets?






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