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Al Pater posted the following prospective study [1] (thanks Al!) on the association between nut intake and mortality amongst a group of 20,000 middle aged Italians. It found that compared with people who didn't consume nuts, people who consumed them more than 8 times per month had about a 50% reduction in all-cause mortality risk during the 4 years of followup, largely due to reduced cancer risk. They found the nut eaters also had lower levels of inflammation.

 

Not surprisingly, nut consumption was more beneficial for those who otherwise didn't adhere to a Mediterranean diet.

 

More evidence that nuts are a very healthy food!

 

--Dean

 

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[1] Br J Nutr. 2015 Sep;114(5):804-11. doi: 10.1017/S0007114515002378.

 

Nut consumption is inversely associated with both cancer and total mortality in a

Mediterranean population: prospective results from the Moli-sani study.

 

Bonaccio M(1), Di Castelnuovo A(1), De Curtis A(1), Costanzo S(1), Bracone F(1),

Persichillo M(1), Donati MB(1), de Gaetano G(1), Iacoviello L(1).

 

Author information:

(1)1Department of Epidemiology and Prevention,IRCCS Istituto Neurologico

Mediterraneo,Neuromed,86077 Pozzilli,Isernia,Italy.

 

Nut intake has been associated with reduced inflammatory status and lower risk of

CVD and mortality. The aim of this study was to examine the relationship between

nut consumption and mortality and the role of inflammation. We conducted a

population-based prospective investigation on 19 386 subjects enrolled in the

Moli-sani study. Food intake was recorded by the Italian version of the European

Project Investigation into Cancer and Nutrition FFQ. C-reactive protein,

leucocyte and platelet counts and the neutrophil:lymphocyte ratio were used as

biomarkers of low-grade inflammation. Hazard ratios (HR) were calculated using

multivariable Cox proportional hazard models. During a median follow-up of 4·3

years, 334 all-cause deaths occurred. As compared with subjects who never ate

nuts, rare intake (≤2 times/month) was inversely associated with mortality

(multivariable HR=0·68; 95 % CI 0·54, 0·87). At intake ≥8 times/month, a greater

protection was observed (HR=0·53; 0·32, 0·90). Nut intake (v. no intake) conveyed

a higher protection to individuals poorly adhering to the Mediterranean diet

(MD). A significant reduction in cancer deaths (HR=0·64; 95 % CI 0·44, 0·94) was

also observed, whereas the impact on CVD deaths was limited to an inverse, but

not significant, trend. Biomarkers of low-grade inflammation were reduced in nut

consumers but did not account for the association with mortality. In conclusion,

nut intake was associated with reduced cancer and total mortality. The protection

was stronger in individuals with lower adherence to MD, whereas it was similar in

high-risk groups (diabetics, obese, smokers or those with the metabolic

syndrome), as compared with low-risk subjects. Inflammation did not explain the

observed relationship.

 

PMID: 26313936 [PubMed - in process]

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Al Pater just pointed to another study of nuts and morality [1] - thanks Al!  The authors observed that previous studies (like PMID 26313936 above) that showed benefits of nut consumption on morality rate were conducted mostly among people of European descent and/or high socioeconomic status. They undertook to remedy this by studying people in the rural south of the US, and native Chinese people living in China.

 

They found pretty much the same thing as the previous studies when it came to overall mortality - nut consumption reduced all-cause mortality. Here is the highlight sentence:

 

We found that the highest quartile of nut/peanut consumption vs the lowest nut quintile intake was associated with a 21% and 17% reduction in mortality in the SCCS [Rural US population] and SWHS/SMHS [shanghai women and men study], respectively;

 

Interestingly, unlike PMID 26313936  which found nuts to be protect against cancer but not (significantly) protective again CVD, this study found the opposite. It found no reduction in cancer mortality, but significantly lower CVD mortality among both rural southern US and Chinese populations:

 

When specific types of cardiovascular disease were examined, a significant inverse association was consistently seen for ischemic heart disease in all ethnic groups (HR, 0.62; 95% CI, 0.45-0.85 in blacks; HR, 0.60; 95% CI, 0.39-0.92 in whites; and HR, 0.70; 95% CI, 0.54-0.89 in Asians for the highest vs lowest quintile of nut intake). The associations for ischemic stroke (HR, 0.77; 95% CI, 0.60-1.00 for the highest vs lowest quintile of nut intake) and hemorrhagic stroke (HR, 0.77; 95% CI, 0.60-0.99 for the highest vs lowest quintile of nut intake) were significant only in Asians. 

 

Here is how the authors addressed the non-effect of nut consumption on cancer in their study vs. other studies:

 

The null association for cancer mortality, on the other hand, is in contrast with the finding of the NHS/HPFS,7 which showed reductions in cancer mortality risk of 7% to 11% associated with different frequencies of peanut consumption vs nonconsumption. This inconsistency may be the result of differences in the distribution of the major types of cancer death in our study populations. Smoking-related and upper gastrointestinal cancers accounted for 80% of cancer deaths in the SMHS/SWHS [shanghai] and 60% in the SCCS [southern US], whereas in the NHS/HPFS, which did not include information on the major types of cancer deaths, it can be postulated that many cancer deaths were hormonal and metabolic associated. In addition, the shorter follow-up time in our study (medians: SCCS, 5.4 years; SMHS, 6.5 years; SWHS, 12.2 years vs NHS, 30 years and HPFS, 24 years) may also have contributed to the discrepancy.

 

The other interesting thing to note is that in both populations, the nuts people consumed were mostly to almost exclusively peanuts (>50% in the rural southern US, and almost exclusively peanuts in the Chinese cohort). Although they didn't measure this, it also seems safe to assume that the peanuts were probably mostly roasted, at least for the southern US cohort.

 

--Dean

 

--------------

[1] Prospective evaluation of the association of nut/peanut consumption with total and cause-specific mortality.

 

Luu HN, Blot WJ, Xiang YB, Cai H, Hargreaves MK, Li H, Yang G, Signorello L, Gao YT, Zheng W, Shu XO.
JAMA Intern Med. 2015 May;175(5):755-66. doi: 10.1001/jamainternmed.2014.8347.

PMID: 25730101 Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4474488/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4474488/pdf/nihms698444.pdf

Abstract

IMPORTANCE:

High intake of nuts has been linked to a reduced risk of mortality. Previous studies, however, were primarily conducted among people of European descent, particularly those of high socioeconomic status.

OBJECTIVE:

To examine the association of nut consumption with total and cause-specific mortality in Americans of African and European descent who were predominantly of low socioeconomic status (SES) and in Chinese individuals in Shanghai, China.

DESIGN, SETTING, AND PARTICIPANTS:

Three large cohorts were evaluated in the study. One included 71 764 US residents of African and European descent, primarily of low SES, who were participants in the Southern Community Cohort Study (SCCS) in the southeastern United States (March 2002 to September 2009), and the other 2 cohorts included 134 265 participants in the Shanghai Women's Health Study (SWHS) (December 1996 to May 2000) and the Shanghai Men's Health Study (SMHS) (January 2002 to September 2006) in Shanghai, China. Self-reported nut consumption in the SCCS (approximately 50% were peanuts) and peanut-only consumption in the SMHS/SWHS were assessed using validated food frequency questionnaires.

MAIN OUTCOMES AND MEASURES:

Deaths were ascertained through linkage with the National Death Index and Social Security Administration mortality files in the SCCS and annual linkage with the Shanghai Vital Statistics Registry and by biennial home visits in the SWHS/SMHS. Cox proportional hazards regression models were used to calculate hazard ratios (HRs) and 95% CIs.

RESULTS:

With a median follow-up of 5.4 years in the SCCS, 6.5 years in the SMHS, and 12.2 years in the SWHS, 14,440 deaths were identified. More than half of the women in the SCCS were ever smokers compared with only 2.8% in the SWHS. The ever-smoking rate for men was 77.1% in the SCCS and 69.6% in the SMHS. Nut intake was inversely associated with risk of total mortality in all 3 cohorts (all P<.001 for trend), with adjusted HRs associated with the highest vs lowest quintiles of intake being 0.79 (95% CI, 0.73-0.86) and 0.83 (95% CI, 0.77-0.88), respectively, for the US and Shanghai cohorts. This inverse association was predominantly driven by cardiovascular disease mortality (P<.05 for trend in the US cohort; P<.001 for trend in the Shanghai cohorts). When specific types of cardiovascular disease were examined, a significant inverse association was consistently seen for ischemic heart disease in all ethnic groups (HR, 0.62; 95% CI, 0.45-0.85 in blacks; HR, 0.60; 95% CI, 0.39-0.92 in whites; and HR, 0.70; 95% CI, 0.54-0.89 in Asians for the highest vs lowest quintile of nut intake). The associations for ischemic stroke (HR, 0.77; 95% CI, 0.60-1.00 for the highest vs lowest quintile of nut intake) and hemorrhagic stroke (HR, 0.77; 95% CI, 0.60-0.99 for the highest vs lowest quintile of nut intake) were significant only in Asians. The nut-mortality association was similar for men and women and for blacks, whites, and Asians and was not modified by the presence of metabolic conditions at study enrollment.

CONCLUSIONS AND RELEVANCE:

Nut consumption was associated with decreased overall and cardiovascular disease mortality across different ethnic groups and among individuals from low SES groups. Consumption of nuts, particularly peanuts given their general affordability, may be considered a cost-effective measure to improve cardiovascular health.

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The other interesting thing to note is that in both populations, the nuts people consumed were mostly to almost exclusively peanuts

That is interesting that nuts were associated with lower mortality, yet the study is looking at roasted legumes (peanuts.)  Are seeds associated with lower cardiovascular risk / mortality, or coconuts, rich in saturated fat and palmitic acid?

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The other interesting thing to note is that in both populations, the nuts people consumed were mostly to almost exclusively peanuts

That is interesting that nuts were associated with lower mortality, yet the study is looking at roasted legumes (peanuts.)  Are seeds associated with lower cardiovascular risk / mortality, or coconuts, rich in saturated fat and palmitic acid?

 

Regarding seeds specifically - a quick Pubmed search didn't turn up any studies that broke out "seeds" as its own, separate category (i.e. separate from nuts) for the purpose of all-cause or CVD mortality risk analysis.

 

However, specific seeds, like flax and sesame seeds which are high in lignans, have been shown to reduce CVD risk factors [1]. And of course whole grains, which are the seeds of cereal plants, have been repeatedly shown (e.g. [2]) to reduce all-cause, cancer and CVD mortality - although the effect may be largely mediated by the fiber in whole grains.

 

Regarding coconuts, I couldn't find much. This one study [3] was encouraging for lipids profile, but it was small and as I recall Michael Rae is suspicious of coconuts due to the saturated fat.

 

--Dean

 

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[1] Peterson J, Dwyer J, Adlercreutz H, Scalbert A, Jacques P, McCullough ML. Dietary lignans: physiology and potential for cardiovascular disease risk reduction. Nutrition reviews. 2010;68(10):571-603. doi:10.1111/j.1753-4887.2010.00319.x.

 

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[2] BMC Med. 2015; 13: 59. Published online 2015 Mar 24. doi:  10.1186/s12916-015-0294-7

 
Consumption of whole grains and cereal fiber and total and cause-specific mortality: prospective analysis of 367,442 individuals
 
Tao Huang, Min Xu, Albert Lee, Susan Cho, and Lu Qicorresponding author
 
Abstract
Background
 
Intakes of whole grains and cereal fiber have been inversely associated with the risk of chronic diseases; however, their relation with total and disease-specific mortality remain unclear. We aimed to prospectively assess the association of whole grains and cereal fiber intake with all causes and cause-specific mortality.
 
Methods
 
The study included 367,442 participants from the prospective NIH-AARP Diet and Health Study (enrolled in 1995 and followed through 2009). Participants with cancer, heart disease, stroke, diabetes, and self-reported end-stage renal disease at baseline were excluded.
 
Results
 
Over an average of 14 years of follow-up, a total of 46,067 deaths were documented. Consumption of whole grains were inversely associated with risk of all-cause mortality and death from cancer, cardiovascular disease (CVD), diabetes, respiratory disease, infections, and other causes. In multivariable models, as compared with individuals with the lowest intakes, those in the highest intake of whole grains had a 17% (95% CI, 14–19%) lower risk of all-cause mortality and 11–48% lower risk of disease-specific mortality (all P for trend <0.023); those in the highest intake of cereal fiber had a 19% (95% CI, 16–21%) lower risk of all-cause mortality and 15–34% lower risk of disease-specific mortality (all P for trend <0.005). When cereal fiber was further adjusted, the associations of whole grains with death from CVD, respiratory disease and infections became not significant; the associations with all-cause mortality and death from cancer and diabetes were attenuated but remained significant (P for trend <0.029).
 
Conclusions
 
Consumption of whole grains and cereal fiber was inversely associated with reduced total and cause-specific mortality. Our data suggest cereal fiber is one potentially protective component.
 
PMCID: PMC4371798
 

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[3] J Nutr Metab. 2013; 2013: 481068. Published online 2013 Oct 24. doi:  10.1155/2013/481068

 
Impact of a Traditional Dietary Supplement with Coconut Milk and Soya Milk on the Lipid Profile in Normal Free Living Subjects
 
R. A. I. Ekanayaka, 1 ,* N. K. Ekanayaka, 2 B. Perera, 3 and P. G. S. M. De Silva 2
 
Abstract
 
Background. The effects of coconut fat and soya fat on serum lipids are controversial. This study was designed to investigate the lipid effects of coconut milk and soya milk supplementation on the lipid profile of free living healthy subjects.
 
Methods. Sixty (60) healthy volunteers aged 18–57 years were given coconut milk porridge (CMP) for 5 days of the week for 8 weeks, followed by a 2-week washout period, subsequent to which they received isoenergetic soya milk porridge (SMP) for 8 weeks.
 
Results. The LDL (low density lipoprotein) levels decreased with CMP and reached statistical significance in the total study population and in the >130 baseline LDL group. The HDL (high density lipoprotein) levels rose significantly with CMP supplementation (P = 0.000).
 
Conclusions. We conclude that coconut fat in the form of CM does not cause a detrimental effect on the lipid profile in the general population and in fact is beneficial due to the decrease in LDL and rise in HDL. SMP will be of benefit only in those whose baseline LDL levels are elevated.
 

PMCID: PMC3824402

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On another thread, I was surprised to find that sugar intake wasn't associated with worsened health, where the foods highest in sugars (fruits) seemed to be more protective in many studies than most other plants with regard to cardiovascular disease and all-cause mortality, showing dose-related improvements with greater consumption.  Now, I'm curious about polyunsaturated fats, which I generally avoid for health & longevity reasons.

 

I've read articles / books from nutritionists recommending polyunsaturated fats be limited in the diet to promote longevity / decreased mortality.  Nuts seem to be my biggest source of dietary PUFA.  Are high intakes of PUFA and linoleic acid from natural sources like nuts / seeds benign in the context of calorie restriction when optimizing health and longevity?  What's a safe / optimal lower and upper limit of total PUFA?

 

Macadamia nuts seem like the only exception to the rule, where one could boost MUFA without boosting SFA + PUFA, even more so than olive oil -- I wonder if a large daily serving of macadamia nuts is a wise and beneficial habit, or worth avoiding / cycling for some reason (other than price & variety.)  Randomly, I've read they're poisonous for dogs, and the mechanism is unknown.

Edited by sirtuin

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Are high intakes of PUFA and linoleic acid from natural sources like nuts / seeds benign in the context of calorie restriction when optimizing health and longevity?

 

I'll let others speak to the Macadamia nut question - I avoid them due to their high level of saturated fat. Speaking of which (SFA) and your question about PUFAs, as discussed on this thread, I believe some of the best data comparing the relative health effects of various types of fat and carbs on all-cause and cardiovascular mortality comes from this recent analysis [1] of the Nurses' Health Study and the Health Professionals Study.

 

I won't repeat the detailed findings here since they are covered in the other thread. Suffice it to say that [1] found PUFAs to be the most healthy dietary component to substitute for SFA, trans fats, or refined carbs / added sugar. Compared to replacing those "bad boys" with MUFA or whole grains, PUFAs appeared at least as good, and probably better, at preventing death from all causes and CVD. And [1] is certainly not the first or only study to find PUFAs to be beneficial, at least for the general population.

 

If Michael cares to chime-in on his theory that long-chain fatty acids with multiple double bonds may be bad for CR Practitioners, he's more than welcome to.

 

--Dean

 

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[1] J Am Coll Cardiol. 2015 Oct 6;66(14):1538-48. doi: 10.1016/j.jacc.2015.07.055.

 

Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in

Relation to Risk of Coronary Heart Disease: A Prospective Cohort Study.

 

Li Y(1), Hruby A(1), Bernstein AM(2), Ley SH(1), Wang DD(1), Chiuve SE(3),

Sampson L(1), Rexrode KM(4), Rimm EB(5), Willett WC(5), Hu FB(6).

 

 

BACKGROUND: The associations between dietary saturated fats and the risk of

coronary heart disease (CHD) remain controversial, but few studies have compared

saturated with unsaturated fats and sources of carbohydrates in relation to CHD

risk.

OBJECTIVES: This study sought to investigate associations of saturated fats

compared with unsaturated fats and different sources of carbohydrates in relation

to CHD risk.

METHODS: We followed 84,628 women (Nurses' Health Study, 1980 to 2010), and

42,908 men (Health Professionals Follow-up Study, 1986 to 2010) who were free of

diabetes, cardiovascular disease, and cancer at baseline. Diet was assessed by a

semiquantitative food frequency questionnaire every 4 years.

RESULTS: During 24 to 30 years of follow-up, we documented 7,667 incident cases

of CHD. Higher intakes of polyunsaturated fatty acids (PUFAs) and carbohydrates

from whole grains were significantly associated with a lower risk of CHD

comparing the highest with lowest quintile for PUFAs (hazard ratio

 

: 0.80,

95% confidence interval [CI]: 0.73 to 0.88; p trend <0.0001) and for

carbohydrates from whole grains (HR: 0.90, 95% CI: 0.83 to 0.98; p trend =

0.003). In contrast, carbohydrates from refined starches/added sugars were

positively associated with a risk of CHD (HR: 1.10, 95% CI: 1.00 to 1.21; p

trend = 0.04). Replacing 5% of energy intake from saturated fats with equivalent

energy intake from PUFAs, monounsaturated fatty acids, or carbohydrates from

whole grains was associated with a 25%, 15%, and 9% lower risk of CHD,

respectively (PUFAs, HR: 0.75, 95% CI: 0.67 to 0.84; p < 0.0001; monounsaturated

fatty acids, HR: 0.85, 95% CI: 0.74 to 0.97; p = 0.02; carbohydrates from whole

grains, HR: 0.91, 95% CI: 0.85 to 0.98; p = 0.01). Replacing saturated fats with

carbohydrates from refined starches/added sugars was not significantly associated

with CHD risk (p > 0.10).

CONCLUSIONS: Our findings indicate that unsaturated fats, especially PUFAs,

and/or high-quality carbohydrates can be used to replace saturated fats to reduce

CHD risk.

 

PMID: 26429077

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I'll let others speak to the Macadamia nut question - I avoid them due to their high level of saturated fat.

 

I haven't looked into this very carefully yet (so much else to investigate...), but it's pretty clear that there is a major shortcoming to all the studies cited in this and the other thread about SFA: the category itself, SFA, needs to be broken down into individual fatty acids. There is good reason to believe that 14:0 and 16:0 are the most dangerous SFAs.

 

But it's hard to get good data, since many of the intervention studies looking at individual FAs are industry-financed, and/or not well-conducted. And they look at biomarkers that might be too coarse (postprandial blood lipid changes, not long-term; or LDL, without differentiating different types of LDL). Overall dietary context may also matter more than is generally appreciated, of course.

 

My 50%-educated/-researched view is that it would be wisest to keep SFA-intake low, but that there's a "sour spot" around 14:0 or 16:0 that one REALLY wants to avoid. 18:0 doesn't seem as bad; nor does 12:0.

 

By the way, I uploaded a new version of my nut data file. It's still rough. Added a "B Score" (reflects RDA percentage of a few major B vitamins -- not B12 and folic acid, since those are special cases), and started adding phytochemical data (thanks, Al Pater!).

 

In any event, below is a dump, sorted by 16:0 (the major SFA in nuts and other fatty things we CR practitioners tend to eat). Sorted by SFA, macadamias, cashews, and a few other things look bad. But sorted by 16:0, we see that a lot of that SFA is 18:0, which might not be so bad. And olive oil and avocados don't look so great.

 

(All are 250 calorie-portions.)

 

(Go sunflower seeds and hemp seeds! Thanks again, Dean.)

 

Zeta

 

post-6938-0-24306200-1446895857_thumb.png

Edited by Zeta

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I won't repeat the detailed findings here since they are covered in the other thread. Suffice it to say that [1] found PUFAs to be the most healthy dietary component to substitute for SFA

 

I found these findings when looking into replacing SFA with more PUFA: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4195930/

 

http://www.ncbi.nlm.nih.gov/pubmed/24723079

  • Increased risk of cancer.
  • Increased risk of coronary heart disease, cardiovascular events, death due to heart disease and overall mortality.
  • Increased oxidised LDL-C.
  • Reduction in HDL-C.
  • The benefits of a low-fat diet (particularly a diet replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fatty acids) are severely challenged
  • Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.
I believe SFA is also useful for synthesizing hormones like testosterone?
 
Suppose carbohydrates are best limited to around 400-600 calories (20-30% of 2,000kcal) for promoting longevity: http://perfecthealthdiet.com/category/nutrients/carbohydrates/
 
And suppose polyunsaturated fats are best limited to around 80 calories (4% of 2,000kcal) for promoting longevity: http://perfecthealthdiet.com/notes/#Ch11
 
And, suppose saturated fat is best limited to around 140 calories (7% of 2,000kcal) (AHA guidelines).
 
Just playing with some numbers in cronometer, with beans and olive oil, I would be looking at around 100 net carbs, 62g of protein, 15.5g SFA, and 12.7g PUFA for a 1800kcal day (~10% CR.)
 
Or, by including macadamia nuts, saturated fat increases by less than a gram (barely over goal), while PUFA is then able to drop down by close to 4 grams down from well over 12g to under 9g (within goal) and the omega-3:omega-6 ratio improves from 9.3 to 7.76.  It seems like this would be an improvement and a worthwhile compromise.  A large part of the SFA here (more than the amount over goal) would be replaced with 16:1, which I believe is a beneficial fatty acid that has been shown to increase insulin sensitivity, protect pancreatic beta cells, and supress inflammation, and this would also slightly increase 18:0, which metabolizes to more MUFA.
 
Going with an array of green-highlighted options from Zeta's chart and substituting flax, hemp, chia, & almond in place of olive oil and macadamia nuts, while keeping carbohydrates down around 100 net, PUFA increases to over 40 grams per day while SFA drops down to under 7g (too low?)  This also greatly increases omega-3, which is 200% more peroxidizable than the already highly-peroxidizable omega-6 components.
 
I suppose this is splitting hairs and the dose makes the poison, although this is the sort of optimization game that I enjoy thinking about.
Edited by sirtuin

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I'll let others speak to the Macadamia nut question - I avoid them due to their high level of saturated fat.

 

<snip>

 

There is good reason to believe that 14:0 and 16:0 are the most dangerous SFAs.

 

<snip>

 

My 50%-educated/-researched view is that it would be wisest to keep SFA-intake low, but that there's a "sour spot" around 14:0 or 16:0 that one REALLY wants to avoid. 18:0 doesn't seem as bad; nor does 12:0.

 

In any event, below is a dump [of Zeta's VERY helpful table of nut & seed nutrition - Thanks Zeta!], sorted by 16:0 (the major SFA in nuts and other fatty things we CR practitioners tend to eat). Sorted by SFA, macadamias, cashews, and a few other things look bad. But sorted by 16:0, we see that a lot of that SFA is 18:0, which might not be so bad. And olive oil and avocados don't look so great.

 

On of the "few other things that look bad" is coconut oil - with over 20x the (suspect) 14:0 as any other nut / seed on the list, and over twice has high as (goat) cheese. Seems like support for staying away from coconut oil.

 

The other thing that stands out on your list that we CR Practitioners might consume regularly is baking chocolate - with about 3-5x the (probably) harmful 16:0 (palmitic acid) SFA than any of the nuts/seeds on your list, and even higher than (goat) cheese. This suggests that perhaps it is better to eschew bakers chocolate, and unsweetened dark chocolate (which usual contains some milk), in favor of with cocoa powder which is free of saturated fat.

 

This started me on an investigation of various forms of chocolate products, which has now gotten so long I think it best to start another thread on it, which I'll do - here is the link.

 

--Dean

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I won't repeat the detailed findings here since they are covered in the other thread. Suffice it to say that [1] found PUFAs to be the most healthy dietary component to substitute for SFA

 

I found these findings when looking into replacing SFA with more PUFA: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4195930/

 

http://www.ncbi.nlm.nih.gov/pubmed/24723079

  • Increased risk of cancer.
  • Increased risk of coronary heart disease, cardiovascular events, death due to heart disease and overall mortality.
  • Increased oxidised LDL-C.
  • Reduction in HDL-C.
  • The benefits of a low-fat diet (particularly a diet replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fatty acids) are severely challenged
  • Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.

 

As both I and Michael pointed out in the thread referenced above and which I promised not to repeat  :)xyz, the references you give in favor of SFA have been pretty thoroughly discussed and discounted as methodologically flawed for various reasons, and that well-designed studies (.e.g. PMID: 26429077 which is the [1] I'm referring to in your quote above), show that PUFA, unrefined carbs, and to a lesser extent MUFA, are a better choice than saturated fat. You will get sufficient saturated fat from a diet containing a significant amount of various nuts and/or olive oil. Its even far from clear that a real low fat diet (i.e. < 15% of calories from fat) will be deficient in essential fatty acids, since whole plant foods (particularly vegetables and legumes) have a non-negligible amounts of fat in them, especially Omega-3 and Omega-6 PUFAs sufficient to meet one's essential fatty acid needs.

 

--Dean

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the references you give in favor of SFA have been pretty thoroughly discussed and discounted as methodologically flawed for various reasons, and that well-designed studies (.e.g. PMID: 26429077 which is the [1] I'm referring to in your quote above), show that PUFA, unrefined carbs, and to a lesser extent MUFA, are a better choice than saturated fat.

I'm curious when it's said that PUFA is a better dietary choice than MUFA or SFA, if that applies to the entire dietary intake of SFA into large servings of PUFA, or if this only speaks for the amount of excess SFA ingested after a certain threshold while PUFA is still otherwise limited?  (I apologize if this is getting off the topic of nuts & mortality or has already been discussed in depth elsewhere.)

 

Looking at PMID 26429077, it states higher intakes of PUFA are more optimal than consuming this energy from MUFA or SFA, but it seems like those "higher intakes of polyunsaturated fatty acids" which offer a 25% reduction in heart disease are simply a conversion of 5% of the SFA intake over to PUFA intake.  If SFA is at 140 calories, that's only 7 calories of PUFA (< a half of one walnut).  If one wishes to include more fat in their diet while adhering to this advice, does the recommendation still apply while driving PUFA into 20, 30, 40+ gram zone?

 

If this recommendation of PUFA > MUFA > SFA applies to the entire intake of SFA, then for health and longevity optimization, the current research would point to a low fat diet (although not minimally low), which is high in carbohydrates and high in PUFA (more so than monounsaturated fats) that avoids dietary sources of saturated fat -- Basically, the opposite of a Paleo diet?  In which case, it looks like walnuts would be a better daily addition to the diet than macadamia nuts.  It's confusing when some sources recommend total PUFA intakes down under 5g, or <9g at the most, viewing this as a dangerous fat, while others recommend this as the most optimal protective fat source.

Edited by sirtuin

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I'm curious when it's said that PUFA + Carbohydrates are a better dietary choice than MUFA or SFA, if that applies to the entire dietary intake of SFA, or for the amount of excess SFA ingested after a certain threshold? 

There is no RDA for saturated fat, and as I said two posts ago, you'll get enough SFA from a mix of nuts/olive oil.

 

 

If it applies to the entire intake of SFA, then for health and longevity optimization, the current research would point to a low fat diet (although not minimally low)...

 

Yes, IMO.

 

 which is high in carbohydrates and rich in PUFA (more so than monounsaturated fats) that avoids dietary sources of saturated fat...

 

Yes, with the qualifications that the carbs are mostly whole & unrefined, and the caveat that Michael suspects MUFA is getting a bad rap in many of these studies.

 

 

Basically, the opposite of a Paleo diet?

 

Yes - At least the bastardized, meat-centric version of the paleo diet heavily promoted in the media today.

 

 

 In which case, it looks like walnuts would be a better daily addition to the diet than macadamia nuts.

 

Yes - since Zeta's nut nutrition table above shows macadamia nuts are high in two of the 'suspect' saturated fats (14:0 myristic acid and 16:0 palmitic acid), while walnuts have been directly and repeatedly shown to be associated with improved health and reduced risk of CVD and even cancer. See this Dr. Greger video for a lot more details on the benefits of walnuts and nuts in general as part of a mediterranean-style diet.

 

--Dean

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I'm curious when it's said that PUFA + Carbohydrates are a better dietary choice than MUFA or SFA, if that applies to the entire dietary intake of SFA, or for the amount of excess SFA ingested after a certain threshold? 

There is no RDA for saturated fat, and as I said two posts ago, you'll get enough SFA from a mix of nuts/olive oil.

Got it.  Thanks for the links / studies.  In the video, Greger mentions a beneficial amount of PUFA being something like "less than 4 individual nuts per day added to the diet" -- that's pretty restrictive in terms of PUFA content.  So, it sounds like the healthiest diet under these guidelines would limit olive oil, limit avocados, limit SFA-rich nuts, limit dietary fat, and replace what small amount of SFA would otherwise end up in a vegetarian diet from foods like olive oil / avocados / SFA-rich nuts with PUFA-rich foods like walnuts, and seeds like chia + flax (though not much more than a small handful), while limiting protein, and going all in with carbohydrates from foods like grains, legumes, and fruits while restricting calories (80/10/10 vegan style?)

Edited by sirtuin

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Got it.  Thanks for the links / studies.  In the video, Greger mentions a beneficial amount of PUFA being something like "less than 4 individual nuts per day added to the diet" -- that's pretty restrictive in terms of PUFA content.  So, it sounds like the healthiest diet under these guidelines would limit olive oil, limit avocados, limit SFA-rich nuts, limit dietary fat, and replace what small amount of SFA would otherwise end up in a vegetarian diet from foods like olive oil / avocados / SFA-rich nuts with PUFA-rich foods like walnuts, and seeds like chia + flax (though not much more than a small handful), while limiting protein, and going all in with carbohydrates from foods like grains, legumes, and fruits while restricting calories (80/10/10 vegan style?)

 

Oh now we've done it - bringing up Dr. Greger and his vegan recommendations (which BTW I pretty much agree with). Here comes the wrath of Michael Rae  :)xyz

 

--Dean

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Just a quickie:
 

 

well-designed studies (.e.g. PMID: 26429077 [...]) show that PUFA, unrefined carbs, and to a lesser extent MUFA, are a better choice than saturated fat.


Looking at PMID 26429077, it states higher intakes of PUFA are more optimal than consuming this energy from MUFA or SFA, but it seems like those "higher intakes of polyunsaturated fatty acids" which offer a 25% reduction in heart disease are simply a conversion of 5% of the SFA intake over to PUFA intake.  If SFA is at 140 calories, that's only 7 calories of PUFA (< a half of one walnut).

 


You're misreading this:
 

Replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fatty acids, or carbohydrates from whole grains was associated with a 25%, 15%, and 9% lower risk of CHD, respectively (PUFAs, HR: 0.75, 95% CI: 0.67 to 0.84; p < 0.0001; monounsaturated fatty acids, HR: 0.85, 95% CI: 0.74 to 0.97; p = 0.02; carbohydrates from whole grains, HR: 0.91, 95% CI: 0.85 to 0.98; p = 0.01). Replacing saturated fats with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk (p > 0.10).


That is, if you replace 5% of total energy intake, as taken from SaFA, with the same amount of energy from these various sources, you get the various hazard ratios listed. Thus you get the risk reductions listed if eg, you are consuming a boilerplate 2500  Calorie sedentary male energy-balanced diet, and you replace 5% of energy (125 Cal) from SaFA in your original diet (14 g of SaFA) with equivalent energy (still 125 Cal) from PUFA (14 g PUFA), MUFA (still 14 g), or whole-grain-carb (31 g of available carb, to oversimplify).
 

If one wishes to include more fat in their diet while adhering to this advice, does the recommendation still apply while driving PUFA into 20, 30, 40+ gram zone?


I don't think we can assume a linear relationship here. Even putting the "DHA-accelerated aging hypothesis" aside, much beyond EFA requirements I would recommend filling up with healthy MUFA, which don't have the bioactivity of PUFA and (if from the right source) have benefits beyond their fatty acid profile.
 

If this recommendation of PUFA > MUFA > SFA applies to the entire intake of SFA, then for health and longevity optimization, the current research would point to a low fat diet (although not minimally low), which is high in carbohydrates and high in PUFA (more so than monounsaturated fats) that avoids dietary sources of saturated fat -- Basically, the opposite of a Paleo diet?

 

It wouldn't tell you anything about the %fat in the diet — or if it does, suggests a high-fat diet, since (again) it finds that PUFA and MUFA are both preferable even to healthier carbs for cardiovascular health.

 

Certainly, one should minimize one's SaFA intake, tho' I'm actually not totally convinced that there isn't a small "J" at the very bottom of the SaFA risk curve (<7% of energy) for overall health (not just CVD) if you don't have existing CVD.

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It wouldn't tell you anything about the %fat in the diet — or if it does, suggests a high-fat diet, since (again) it finds that PUFA and MUFA are both preferable even to healthier carbs for cardiovascular health.

 

Certainly, one should minimize one's SaFA intake, tho' I'm actually not totally convinced that there isn't a small "J" at the very bottom of the SaFA risk curve (<7% of energy) for overall health (not just CVD) if you don't have existing CVD.

So, if PUFA and MUFA are healthier to carbs (but come with SFA), and carbs are healthier than SFA (but don't come with PUFA / MUFA), then (in your opinion) for an isocaloric ~2,000kcal diet, would it be best to keep PUFA in the 7-9g range, with SFA in the 18-20g range while consuming more MUFA and less carbs, or keep PUFA in the 12-14gram range with SFA in the <15g range consuming much more MUFA and less carbs, or keep both PUFA in the 7-9g range + SFA in the <15g range consuming much more carbohydrates?  If the charts show that fruits have a lower risk profile than fruits+vegetables or vegetables alone, would the bulk of these carbohydrates be healthiest to consume from sugar?

Edited by sirtuin

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It wouldn't tell you anything about the %fat in the diet — or if it does, suggests a high-fat diet, since (again) it finds that PUFA and MUFA are both preferable even to healthier carbs for cardiovascular health.Certainly, one should minimize one's SaFA intake, tho' I'm actually not totally convinced that there isn't a small "J" at the very bottom of the SaFA risk curve (<7% of energy) for overall health (not just CVD) if you don't have existing CVD.

So, if PUFA and MUFA are healthier to carbs (but come with SFA), and carbs are healthier than SFA (but don't come with PUFA / MUFA), then (in your opinion) for an isocaloric ~2,000kcal diet, would it be best to keep PUFA in the 7-9g range, with SFA in the 18-20g range while consuming more MUFA and less carbs, or keep PUFA in the 12-14gram range with SFA in the <15g range consuming much more MUFA and less carbs, or keep both PUFA in the 7-9g range + SFA in the <15g range consuming much more carbohydrates? If the charts show that fruits have a lower risk profile than fruits+vegetables or vegetables alone, would the bulk of these carbohydrates be healthiest to consume from sugar?

 

"keep PUFA in the 12-14 gram range with SFA in the <15g range consuming much more MUFA and less carbs" is closest to what I practice and think is best, but I'm not sure there's any need to cut SaFA even to 15 g (7% of energy), let alone below it, if you don't have existing CVD, and even have some minor doubts that it's advisable to do so: anywhere from there up to your earlier 18-20 g range is probably still fine, or probably even up to 22 g (10% energy).

 

Ostensibly, you can get the WHO FAO EFA Adequate Intake* (2–3% of energy as LA and >0.5% ALA) on your 7-9 g PUFA range, but I'd hesitate to go that low as a CR person, a veg(etari)an, a person avoiding EPA+DHA, or (in my case) all three, for a couple of reasons. First, the Institute of Medicine's Adequate Intake* of LA is 17 g LA/d for young men and 12 g/d for young women, and 1.6 and 1.1 g (respectively) for ALA; I concluded a while ago that I was comfortable with 12 g LA, for reasons I must confess to not actually recalling, but either way that's significantly more than your suggested range.

 

Second, the human data are overwhelmingly on omnivores, who will have some intake of EPA, DHA, and AA on top of their short-chain EFA intake, and is present as tissue reserves even when short-term studies are done with diets entirely dependent on short-chain EFA sources; for people with little or no long-chain PUFA in their diets I think it makes sense to have a modest buffer for conversion (in)efficiency and lack of long-term studies.

 

There is really no evidence of EFA deficiency in veg(etari)ans not eating extreme low-fat diets, but that doesn't necessarily mean there aren't long-term consequences of low ALA + LA intake that are not being picked up for lack of discriminatory power.

 

Third, while people tend to exaggerate the confidence with which one can adjudicate the best n6:n3 ratio, certainly the conversion of ALA to longer-chain derivatives in rodents is better at or below 4:1, so I'd be reluctant to suggest 12-17 g LA with only 1.6 g ALA, granted the fairly clear importance of omega-3.

 

And finally, people on CR are more likely than ALers to use dietary fat and protein for energy rather than for other metabolic needs, so a buffer is IMO still prudent.

 

Dean, some of your comments above on olive oil seem too narrowly-focused on the fatty acid profile: in addition to the confounding effects of most MUFA in Northern European diets coming from animal sources, which necessarily drag down the overall benefits asociated with MUFA in the meta-analyses, EVOO is a complex food, and a ton of epidemiology and now clinical trials support its benefits. And, again, it's certainly possible to have a high-fat, high-EVOO, low-SaFA diet.

 

If the charts show that fruits have a lower risk profile than fruits+vegetables or vegetables alone, would the bulk of these carbohydrates be healthiest to consume from sugar?

To which charts do you refer? Dean has just reviewed with you some evidence that fruits and vegetables are both good for you, and you're surely aware that sugar is at minimum empty Calories and arguably actively bad for you. Or by "sugar" do you mean "fruits, whose Calories are dominated by sugar"?

 

One thing to note is that potatoes are counted as "vegetables," so the data on the relative healthfulness of "vegetables" are likely dragged down by confounding therewith (especially granted the way most potatoes are consumed in North America and Europe: french fries, chips, baked potatoes with butter and sour cream, scallopped potatoes, potatoes au gratin (as that term is used in the US and Canada), etc. And, of course, the whole "fruit" versus "vegetable" distinction is largely arbitrary and unconnected to the actual biological definition of "fruit."

 

There's plenty of evidence for the benefits of non-starchy vegetables, and much of that is for cancer, so it's not picked up in the CVD discussions that have dominated much of the discussion on the Forums of late.

 

I practice, and gently advise, more non-starchy vegetables than fruit, but I can't say there's a powerful evidence base one way or t'other.

 

* NB: the Adequate Intake is not the minimum you actually physiologically need, but a level that is confidently judged to cover whatever the yet-to-be-determined real physiological requirement is.

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I was referring to those articles Dean reviewed, where the fruit servings (sugar by calories, usually eaten raw and low in fat) had mortality lowering benefits as low as any legume / vegetable serving, if not often lower than carbohydrate calories from starches / non-starchy vegetables (cooked, often with fat.)  I love eating non-starchy vegetables, but there's not much energy there until drizzled with an oil or eaten with another food that provides calories.

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OK - back to the topic of this thread - nuts.

 

A few days ago Al Pater posted this really interesting new meta-analysis [1] of nuts and cardiovascular disease risk factors. It looked at 61 intervention trials (> 2500 subjects total) where subjects either ate nuts or didn't in order to compare the impact of nut consumption on things like cholesterol, ApoB and blood pressure. It should come as no surprise by now that nut consumption improved CVD risk factors. For each 1oz serving of nuts per day, total and LDL cholesterol was reduced by an average of about 5mg/dl, ApoB by 3.7 mg/dl, triglycerides by about 2.2 mg/d.

 

Here is perhaps the most interesting paragraph in the whole full text of the paper:

 

We did not observe significant heterogeneity in outcomes
across different types of tree nuts. In addition, our meta-regression
demonstrated that the major determinant of cholesterol
lowering appears to be the total dose of tree nut consumption
rather than nut type.
 

In other words, it appears its how much nuts you eat, not which type of nuts you eat, that determines the amount of benefit wrt CVD risk factors. More interesting still, the authors observed an apparent non-linear increase in effect with larger nut doses. In other words, rather than the benefits saturating above a certain level of nut consumption, the benefits seemed to get bigger faster as you added more nuts!  Here are the graphs to illustrate this effect, which was seen primarily in total and LDL cholesterol. Notice how the cholesterol-lowering benefits seems really kick in among studies in which subjects consumed more than ~70g of nuts per day:

 

j8umLfY.png

 

The authors speculate in the discussion about potential mechanisms for this improvement, particularly at higher doses, as possibly related to reduced weight gain:

 

Although larger effects on lowering LDL
cholesterol were observed at higher nut doses in our study, we
did not examine the effects of nuts on weight change. A recent
meta-analysis of controlled trials on this topic (11) found that
nut intake had nonsignificant, inverse effects on adiposity, but
doses in most included trials were modest (,56 g/d, or 2 servings,
of nuts). Furthermore, nut intake was associated with
less weight gain over time in US cohorts of male and female
health professionals (89, 90). Taken together, the inverse associations
with weight gain observed in both controlled trials and
free-living populations suggest that nut intake might augment
satiety and displace other, less healthful foods in the diet, potentially
resulting in less weight gain over time.

 

Reduced weight, or less weight gain over time, is definitely associated with improved cholesterol level, so if nuts are satiating and reducing intake of other, unhealthy foods, that might explain the CVD risk factor improvements the authors' observed.

 

--Dean

 

---------

[1] Effects of tree nuts on blood lipids, apolipoproteins, and blood pressure: systematic review, meta-analysis, and dose-response of 61 controlled intervention trials.

Del Gobbo LC, Falk MC, Feldman R, Lewis K, Mozaffarian D.
Am J Clin Nutr. 2015 Dec;102(6):1347-56. doi: 10.3945/ajcn.115.110965. Epub 2015 Nov 11.
PMID: 26561616
 
Abstract
 
BACKGROUND:
 
The effects of nuts on major cardiovascular disease (CVD) risk factors, including dose-responses and potential heterogeneity by nut type or phytosterol content, are not well established.
 
OBJECTIVES:
 
We examined the effects of tree nuts (walnuts, pistachios, macadamia nuts, pecans, cashews, almonds, hazelnuts, and Brazil nuts) on blood lipids [total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein, and triglycerides], lipoproteins [apolipoprotein A1, apolipoprotein B (ApoB), and apolipoprotein B100], blood pressure, and inflammation (C-reactive protein) in adults aged =18 y without prevalent CVD.
 
DESIGN:
 
We conducted a systematic review and meta-analysis following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Two investigators screened 1301 potentially eligible PubMed articles in duplicate. We calculated mean differences between nut intervention and control arms, dose-standardized to one 1-oz (28.4 g) serving/d, by using inverse-variance fixed-effects meta-analysis. Dose-response for nut intake was examined by using linear regression and fractional polynomial modeling. Heterogeneity by age, sex, background diet, baseline risk factors, nut type, disease condition, duration, and quality score was assessed with meta-regression. Publication bias was evaluated by using funnel plots and Egger's and Begg's tests.
 
RESULTS:
 
Sixty-one trials met eligibility criteria (n = 2582). Interventions ranged from 3 to 26 wk. Nut intake (per serving/d) lowered total cholesterol (-4.7 mg/dL; 95% CI: -5.3, -4.0 mg/dL), LDL cholesterol (-4.8 mg/dL; 95% CI: -5.5, -4.2 mg/dL), ApoB (-3.7 mg/dL; 95% CI: -5.2, -2.3 mg/dL), and triglycerides (-2.2 mg/dL; 95% CI: -3.8, -0.5 mg/dL) with no statistically significant effects on other outcomes. The dose-response between nut intake and total cholesterol and LDL cholesterol was nonlinear (P-nonlinearity < 0.001 each); stronger effects were observed for >=60 g nuts/d. Significant heterogeneity was not observed by nut type or other factors. For ApoB, stronger effects were observed in populations with type 2 diabetes (-11.5 mg/dL; 95% CI: -16.2, -6.8 mg/dL) than in healthy populations (-2.5 mg/dL; 95% CI: -4.7, -0.3 mg/dL) (P-heterogeneity = 0.015). Little evidence of publication bias was found.
 
CONCLUSIONS:
 
Tree nut intake lowers total cholesterol, LDL cholesterol, ApoB, and triglycerides. The major determinant of cholesterol lowering appears to be nut dose rather than nut type. Our findings also highlight the need for investigation of possible stronger effects at high nut doses and among diabetic populations.
 
KEYWORDS:
 
apolipoprotein; cardiovascular; cholesterol; lipids; nuts

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All,

 

Here is a new prospective study [1], thanks to Al, on fish vs. all PUFAs vs. nuts for mortality. In a cohort of 2500 older Australians, it found that increased nut consumption and ALA consumption, (but not fish or long-chain omega-3s or 6s), was protective against mortality from inflammatory diseases. Note they excluded cardiovascular disease from their analysis, despite its inflammatory component because there is a lot more to CVD than inflammation. Here are the survival curves for inflammatory disease-related deaths for the three tertiles of nut consumption:

 

twHu4rn.png

 

As you can see, the nut eaters (2nd and 3rd tertile) showed a pretty clear advantage over those who ate few if any nuts (1st tertile) - although interestingly there wasn't a difference between the two upper tertiles, and certainly no dose-response relationship.

 

The quantities for the three nut tertiles were T1: 0.0 - 0.9 g/day ;  T2: 1.4 - 4.5 g/day ; T3: 4.9 - 100 g/day. So it didn't take many nuts to gain the advantage!

 

--Dean

 

---------

[1] Consumption of polyunsaturated fatty acids, fish, and nuts and risk of

inflammatory disease mortality.
Gopinath B, Buyken AE, Flood VM, Empson M, Rochtchina E, Mitchell P.
Am J Clin Nutr. 2011 May;93(5):1073-9. doi: 10.3945/ajcn.110.009977. Epub
2011 Mar 16.
PMID: 21411616 Free Article
 
Abstract
 
BACKGROUND:
 
n-3 (omega-3) Polyunsaturated fatty acids (PUFAs), fish, and nuts can
regulate inflammatory processes and responses.
 
OBJECTIVE:
 
We investigated whether dietary intakes of PUFAs [n-3, n-6 (omega-6), and
Alpha-linolenic acid], fish, and nuts were associated with 15-y mortality
attributed to noncardiovascular, noncancer inflammatory diseases.
 
DESIGN:
 
The analyses involved 2514 participants aged =/>49 y at baseline. Dietary
data were collected by using a semiquantitative food-frequency
questionnaire, and PUFA, fish, and nut intakes were calculated. Inflammatory
disease mortality was confirmed from the Australian National Death Index.
 
RESULTS:
 
Over 15 y, 214 subjects died of inflammatory diseases. Women in the highest
tertiles of total n-3 PUFA intake, compared with those in the lowest tertile
of intake at baseline, had a 44% reduced risk of inflammatory disease
mortality (P for trend = 0.03). This association was not observed in men. In
both men and women, each 1-SD increase in energy-adjusted intake of
Alpha-linolenic acid was inversely associated with inflammatory mortality
(hazard ratio: 0.83; 95% CI: 0.71, 0.98). Subjects in the second and third
tertiles of nut consumption had a 51% and 32% reduced risk of inflammatory
disease mortality, respectively, compared with those in the first tertile
(reference). Dietary intakes of long-chain n-3 and n-6 PUFAs and fish were
not associated with inflammatory disease mortality.
 
CONCLUSIONS:
 
We report on a novel link between dietary intake of total n-3 PUFA and risk
of inflammatory disease mortality in older women. Furthermore, our data
indicate a protective role of nuts, but not fish, against inflammatory
disease mortality.

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Gaaaw T2 is so very few nuts... Just maybe one walnut, one almond, and one hazelnut would about do it for the day haha... General statement of bedazzlement: what's weird about CR is not lack of nutrition due to low calories, but how to healthily increase calories (so I don't wither away into waifdom again) without sending certain vitamins and nutrients into way hyper overboard. Everything I eat is loaded to the teeth with copper, iron, folate, K, C, A, manganese... It's fun.

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[Admin Note: This is a post of mine in response to Mechanism that I moved from Sensible Diet and Lifestyle for Longevity thread to here were it more rightly belongs - Dean]

 

Mechanism,

 

I'm here to learn and crowdsource perspectives... thanks, looking forward to the peer review. 

 

Great attitude! That's what I like to hear. 

 

Nice list though I would remove nuts as the data for benefits is not without controversy: 

 /. https://www.drmcdoug...opic.php?t=6678 & expand the tumeric to include healthy spices & herbs ( maintaing emphasis on turmeric which has some unique potential anti-aging properties ).

 

First off, a couple of mechanical things. Posts are a lot easier to read when you don't embed URLs directly into your text, but instead select an appropriate word of phrase, like Jeff Novick video on nuts, and then use the chain link icon on the toolbar to create a hyperlink to the URL. Here is what the link icon looks like:

 

WhD6BJr.png

 

Simply select your text, click on that icon, and then paste the URL into the box that pops up. Embedding a link is easy to do, and has the added bonus of making you look a lot more like you know what you're talking about- so give it a try! 

 

Having said that, an even better thing to do if you are posting a YouTube video is to embed the video directly into your post, rather than a link to it. Here is a post on how to do that.

 

With those niceties out of the way, now on to the meat of your post:

 

Nice list though I would remove nuts as the data for benefits is not without controversy: 

 /. https://www.drmcdoug...opic.php?t=6678 & expand the tumeric to include healthy spices & herbs ( maintaing emphasis on turmeric which has some unique potential anti-aging properties ).

 

I recommend you not believe everything you hear from Dr. McDougall - he (and Jeff Novick) make a good living off his unique brand of high-starch, low-fat diet - selling his books, running expensive retreats, etc.  While Novick is right to criticize some of the studies showing a Mediterranean diet beats a "low fat" diet, on the grounds that the "low fat" groups are typically not low fat at all. But a lot of new data has come in recently. Here is a flurry of recent meta-analyses [1-5] showing nut consumption in the general population is associated with reduced mortality in prospective studies. Here is a whole thread discussing the benefits of nut for reducing mortality. 

 

Now I'll acknowledge that a cogent argument could possibly be made that an impeccable, really low-fat diet focused on whole plant foods, but without nuts, seeds or oils, could possibly be as healthy as one that includes nuts & seeds, as long as one's essential fatty acid requirements are met. 

 

But such an argument would be irrelevant for the topic of this thread.

 

Remember we're talking about sensible advice for friends and family who aren't about to turn their diet upside down, or crank what they are eating through CRON-O-Meter to see where they may be deficient.

 

Nuts are very satiating and aren't completely digested, so paradoxically, eating them doesn't result in weight gain. In fact, if anything, adding nuts on top of a crappy diet tends to crowd out bad foods. That's why nuts (unlike tumeric - which I wholeheartedly endorse, but not nearly as much as nuts) are so appropriate for this thread. Simply adding nuts to a normal person's crappy diet, without any other dietary advice than to eat a handful or two of nuts per day, significantly improves a person's health and longevity. For example, see the PREDIMED randomized control trial, as featured in this video by Dr. Greger.  

 

But don't trust Dr. Greger either. Instead, check out the references associated with the video (esp. those from the PREDIMED trial) for yourself by clicking on the "Sources Cited" button next to the video and then clicking through the relevant links to read about the studies for yourself.

 

I think in the end you'll find that nuts (and seeds) are indeed one of the healthiest foods around, particularly for friends and family who aren't eating a great diet, and don't plan to.

 

--Dean

 

-----

[1] Br J Nutr. 2016 Jan 28;115(2):212-25. doi: 10.1017/S0007114515004316. Epub 2015
Nov 9.
 
A systematic review and meta-analysis of nut consumption and incident risk of CVD
and all-cause mortality.
 
Mayhew AJ(1), de Souza RJ(1), Meyre D(1), Anand SS(1), Mente A(1).
 
Author information: 
(1)1Department of Clinical Epidemiology and Biostatistics,McMaster
University,Hamilton, ON,Canada, L8N 3Z5.
 
Dietary patterns containing nuts are associated with a lower risk of CVD
mortality, and increased nut consumption has been shown to have beneficial
effects on CVD risk factors including serum lipid levels. Recent studies have
reported on the relationship between nut intake and CVD outcomes and mortality.
Our objective was to systematically review the literature and quantify
associations between nut consumption and CVD outcomes and all-cause mortality.
Five electronic databases (through July 2015), previous reviews and
bibliographies of qualifying articles were searched. In the twenty included
prospective cohort studies (n 467 389), nut consumption was significantly
associated with a lower risk of all-cause mortality (ten studies; risk ratio (RR)
0·81; 95 % CI 0·77, 0·85 for highest v. lowest quantile of intake, P het=0·04, I 
2=43 %), CVD mortality (five studies; RR 0·73; 95 % CI 0·68, 0·78; P het=0·31, I 
2=16 %), all CHD (three studies; RR 0·66; 95 % CI 0·48, 0·91; P het=0·0002, I
2=88 %) and CHD mortality (seven studies; RR 0·70; 95 % CI 0·64, 0·76; P
het=0·65, I 2=0 %), as well as a statistically non-significant reduction in the
risk of non-fatal CHD (three studies; RR 0·71; 95 % CI 0·49, 1·03; P het=0·03, I 
2=72 %) and stroke mortality (three studies; RR 0·83; 95 % CI 0·69, 1·00; P
het=0·54, I 2=0 %). No evidence of association was found for total stroke (two
studies; RR 1·05; 95 % CI 0·69, 1·61; P het=0·04, I 2=77 %). Data on total CVD
and sudden cardiac death were available from one cohort study, and they were
significantly inversely associated with nut consumption. In conclusion, we found 
that higher nut consumption is associated with a lower risk of all-cause
mortality, total CVD, CVD mortality, total CHD, CHD mortality and sudden cardiac 
death.
 
PMID: 26548503  [PubMed - indexed for MEDLINE]
 
-------------
[2] Int J Epidemiol. 2015 Jun;44(3):1038-49. doi: 10.1093/ije/dyv039. Epub 2015 Jun
11.
 
Relationship of tree nut, peanut and peanut butter intake with total and
cause-specific mortality: a cohort study and meta-analysis.
 
van den Brandt PA(1), Schouten LJ(2).
 
Author information: 
(1)Maastricht University Medical Centre, GROW-School for Oncology and
Developmental Biology, Department of Epidemiology, Maastricht, The Netherlands
and Maastricht University Medical Centre, CAPHRI-School for Public Health and
Primary Care, Department of Epidemiology, Maastricht, The Netherlands
PA.vandenBrandt@maastrichtuniversity.nl. (2)Maastricht University Medical Centre,
GROW-School for Oncology and Developmental Biology, Department of Epidemiology,
Maastricht, The Netherlands and.
 
Comment in
    Int J Epidemiol. 2015 Jun;44(3):1049-50.
 
BACKGROUND: Nut intake has been associated with lower mortality, but few studies 
have investigated causes of death other than cardiovascular disease, and
dose-response relationships remain unclear.
METHODS: We investigated the relationship of nut (tree nut, peanut) and peanut
butter intake with overall and cause-specific mortality. In the Netherlands
Cohort Study, 120,852 men and women aged 55-69 years provided information on
dietary and lifestyle habits in 1986. Mortality follow-up until 1996 consisted of
linkage to Statistics Netherlands. Multivariate case-cohort analyses were based
on 8823 deaths and 3202 subcohort members with complete data on nuts and
potential confounders. We also conducted meta-analyses of our results with those 
published from other cohort studies.
RESULTS: Total nut intake was related to lower overall and cause-specific
mortality (cancer, diabetes, cardiovascular, respiratory, neurodegenerative
diseases, other causes) in men and women. When comparing those consuming 0.1-<5, 
5-<10 and 10+ g nuts/day with non-consumers, multivariable hazard ratios for
total mortality were 0.88, 0.74 and 0.77 [95% confidence interval (CI),
0.66-0.89], respectively (Ptrend = 0.003). Cause-specific hazard ratios comparing
10+ vs 0 g/day varied from 0.56 for neurodegenerative to 0.83 for cardiovascular 
disease mortality. Restricted cubic splines showed nonlinear dose-response
relationships with mortality. Peanuts and tree nuts were inversely related to
mortality, whereas peanut butter was not. In meta-analyses, summary hazard ratios
for highest vs lowest nut consumption were 0.85 for cancer, and 0.71 for
respiratory mortality.
CONCLUSIONS: Nut intake was related to lower overall and cause-specific
mortality, with evidence for nonlinear dose-response relationships. Peanut butter
was not related to mortality.
 
© The Author 2015; all rights reserved. Published by Oxford University Press on
behalf of the International Epidemiological Association.
 
PMID: 26066329  [PubMed - indexed for MEDLINE]
 
---------
[3] Am J Clin Nutr. 2015 Apr;101(4):783-93. doi: 10.3945/ajcn.114.099515. Epub 2015
Feb 4.
 
Nut consumption on all-cause, cardiovascular, and cancer mortality risk: a
systematic review and meta-analysis of epidemiologic studies.
 
Grosso G(1), Yang J(1), Marventano S(1), Micek A(1), Galvano F(1), Kales SN(1).
 
Author information: 
(1)From the Department of Clinical and Molecular Biomedicine, Section of
Pharmacology and Biochemistry (GG and FG) and the Department GF Ingrassia,
Section of Hygiene and Public Health (SM), University of Catania, Catania, Italy 
(GG and FG); the Department of Environmental Health, Environmental and
Occupational Medicine and Epidemiology, Harvard School of Public Health, Boston, 
MA (JY and SNK); the Steward St. Elizabeth's Medical Center, Tufts University
School of Medicine, Boston, MA (JY); the Department of Epidemiology and
Population Studies, Jagiellonian University Medical College, Krakow, Poland (AM);
and the Cambridge Health Alliance, Harvard Medical School, Cambridge, MA (SNK).
 
BACKGROUND: Recent pooled analyses supported a beneficial impact of nut
consumption on health, but to our knowledge, whether nuts are associated with
overall decreased mortality has not been previously reviewed.
OBJECTIVES: We aimed to systematically review prospective studies that explored
the effects of nut consumption on all-cause, cardiovascular disease (CVD), and
cancer mortality and quantify the size effect through a meta-analysis. We also
reviewed confounding factors associated with nut consumption to assess potential 
clustering with other covariates.
DESIGN: We searched PubMed and EMBASE for studies published up to June 2014.
Study characteristics, HRs, and 95% CIs were generated on the basis of
quantitative analyses. A dose-response analysis was performed when data were
available.
RESULTS: Seven studies for all-cause mortality, 6 studies for CVD mortality, and 
2 studies for cancer mortality were included in the meta-analysis with a total of
354,933 participants, 44,636 cumulative incident deaths, and 3,746,534 cumulative
person-years. Nut consumption was associated with some baseline characteristics
such as lower body mass index and smoking status as well as increased intakes of 
fruit, vegetables, and alcohol. One-serving of nuts per week and per day resulted
in 4% (RR: 0.96; 95% CI: 0.93, 0.98) and 27% (RR: 0.73; 95% CI: 0.60, 0.88)
decreased risk of all-cause mortality, respectively, and decreased risk of CVD
mortality [RR: 0.93 (95% CI: 0.88, 0.99) and 0.61 (95% CI: 0.42, 0.91),
respectively]. Effects were primarily driven by decreased coronary artery disease
deaths rather than stroke deaths. Nut consumption was also associated with
decreased risk of cancer deaths when highest compared with lowest categories of
intake were compared (RR: 0.86; 95% CI: 0.75, 0.98), but no dose-effect was
shown.
CONCLUSION: Nut consumption is associated with lower risk of all-cause, CVD, and 
cancer mortality, but the presence of confounding factors should be taken into
account when considering such findings.
 
© 2015 American Society for Nutrition.
 
PMID: 25833976  [PubMed - indexed for MEDLINE]
 
----------
[4] Am J Clin Nutr. 2015 Feb;101(2):407-12. doi: 10.3945/ajcn.114.099846. Epub 2014
Dec 17.
 
Nut consumption and risk of mortality in the Physicians' Health Study.
 
Hshieh TT(1), Petrone AB(1), Gaziano JM(1), Djoussé L(1).
 
Author information: 
(1)From the Divisions of Aging (TTH, ABP, JMG, and LD) and Preventive Medicine
(JMG), Brigham and Women's Hospital, Harvard Medical School, Boston, MA; the
Aging Brain Center, Institute for Aging Research, Hebrew SeniorLife, Boston, MA
(TTH); and the Massachusetts Veterans Epidemiology and Research Information
Center (MAVERIC), Geriatric Research (GRECC) and VA Boston Healthcare System,
Boston, MA (JMG and LD).
 
BACKGROUND: Previous studies have suggested that nut consumption is associated
with beneficial cardiovascular outcomes. However, limited data are available on
the association between nut intake and all-cause mortality.
OBJECTIVE: Our aim was to test the hypothesis that nut consumption is inversely
associated with the risk of all-cause mortality.
DESIGN: In this prospective cohort study in 20,742 male physicians, we assessed
nut intake between 1999 and 2002 via a food-frequency questionnaire and
ascertained deaths through an endpoint committee. We used Cox regression to
estimate multivariable-adjusted HRs for death according to nut consumption. In
secondary analyses, we evaluated associations of nut consumption with
cause-specific mortality.
RESULTS: During a mean follow-up of 9.6 y, there were 2732 deaths. The mean (±SD)
age at baseline was 66.6 ± 9.3 y. Median nut consumption was 1 serving/wk.
Multivariable-adjusted HRs (95% CIs) were 1.0 (reference), 0.92 (0.83, 1.01),
0.85 (0.76, 0.96), 0.86 (0.75, 0.98), and 0.74 (0.63, 0.87) for nut consumption
of never or <1 serving/mo, 1-3 servings/mo, 1 serving/wk, 2-4 servings/wk, and ≥5
servings/wk, respectively (P-linear trend < 0.0001), after adjustment for age,
body mass index, alcohol use, smoking, exercise, prevalent diabetes and
hypertension, and intakes of energy, saturated fat, fruit and vegetables, and red
meat. In a secondary analysis, results were consistent for cardiovascular disease
mortality but only suggestive and non-statistically significant for coronary
artery disease and cancer mortality.
CONCLUSION: Our data are consistent with an inverse association between nut
consumption and the risk of all-cause and cardiovascular disease mortality in US 
male physicians.
 
© 2015 American Society for Nutrition.
 
PMCID: PMC4307210
PMID: 25646339  [PubMed - indexed for MEDLINE]
 
--------
[5] Am J Clin Nutr. 2014 Jul;100(1):256-69. doi: 10.3945/ajcn.113.076109. Epub 2014
May 21.
 
Nut consumption and risk of type 2 diabetes, cardiovascular disease, and
all-cause mortality: a systematic review and meta-analysis.
 
Luo C(1), Zhang Y(1), Ding Y(1), Shan Z(1), Chen S(1), Yu M(1), Hu FB(1), Liu
L(1).
 
Author information: 
(1)From the Department of Nutrition and Food Hygiene, Hubei Key Laboratory of
Food Nutrition and Safety, Tongji Medical College, Hua Zhong University of
Science and Technology, Wuhan, China (CL, YZ, YD, ZS, SC, MY, and LL); the
Ministry of Education Key Laboratory of Environment and Health, School of Public 
Health, Tongji Medical College, Wuhan, China (CL, YZ, YD, ZS, SC, MY, and LL);
and the Department of Nutrition and Epidemiology, Harvard School of Public
Health, Boston, MA (FBH).
 
Comment in
    Am J Clin Nutr. 2014 Jul;100(1):8-10.
 
BACKGROUND: Epidemiologic studies have shown inverse associations between nut
consumption and diabetes, cardiovascular disease (CVD), and all-cause mortality, 
but results have not been consistent.
OBJECTIVE: We assessed the relation between nut intake and incidence of type 2
diabetes, CVD, and all-cause mortality.
DESIGN: We searched PubMed and EMBASE for all prospective cohort studies
published up to March 2013 with RRs and 95% CIs for outcomes of interest. A
random-effects model was used to pool risk estimates across studies.
RESULTS: In 31 reports from 18 prospective studies, there were 12,655 type 2
diabetes, 8862 CVD, 6623 ischemic heart disease (IHD), 6487 stroke, and 48,818
mortality cases. The RR for each incremental serving per day of nut intake was
0.80 (95% CI: 0.69, 0.94) for type 2 diabetes without adjustment for body mass
index; with adjustment, the association was attenuated [RR: 1.03; 95% CI: 0.91,
1.16; NS]. In the multivariable-adjusted model, pooled RRs (95% CIs) for each
serving per day of nut consumption were 0.72 (0.64, 0.81) for IHD, 0.71 (0.59,
0.85) for CVD, and 0.83 (0.76, 0.91) for all-cause mortality. Pooled RRs (95%
CIs) for the comparison of extreme quantiles of nut intake were 1.00 (0.84, 1.19;
NS) for type 2 diabetes, 0.66 (0.55, 0.78) for IHD, 0.70 (0.60, 0.81) for CVD,
0.91 (0.81, 1.02; NS) for stroke, and 0.85 (0.79, 0.91) for all-cause mortality.
CONCLUSIONS: Our meta-analysis indicates that nut intake is inversely associated 
with IHD, overall CVD, and all-cause mortality but not significantly associated
with diabetes and stroke. The inverse association between the consumption of nuts
and diabetes was attenuated after adjustment for body mass index. These findings 
support recommendations to include nuts as part of a healthy dietary pattern for 
the prevention of chronic diseases.
 
© 2014 American Society for Nutrition.
 
PMID: 24847854

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More grist for the mill. Most consumption of nuts vs least: risk reduction coronary heart disease 29%, CVD 21%, cancer 15%, respiratory disease 52%, diabetes 39%, infectious disease 79%(?!), premature death 22% - all for one ounce of nuts a day, more not significant.

 

Nut consumption and risk of cardiovascular disease, total cancer, all-cause and cause-specific mortality: a systematic review and dose-response meta-analysis of prospective studies

 

 

  • Dagfinn AuneEmail author,
  • NaNa Keum,
  • Edward Giovannucci,
  • Lars T. Fadnes,
  • Paolo Boffetta,
  • Darren C. Greenwood,
  • Serena Tonstad,
  • Lars J. Vatten,
  • Elio Riboli and
  • Teresa Norat
BMC Medicine201614:207

DOI: 10.1186/s12916-016-0730-3

©  The Author(s). 2016

Received: 28 January 2016

Accepted: 26 October 2016

Published: 5 December 2016

Abstract
Background

Although nut consumption has been associated with a reduced risk of cardiovascular disease and all-cause mortality, data on less common causes of death has not been systematically assessed. Previous reviews missed several studies and additional studies have since been published. We therefore conducted a systematic review and meta-analysis of nut consumption and risk of cardiovascular disease, total cancer, and all-cause and cause-specific mortality.

Methods

PubMed and Embase were searched for prospective studies of nut consumption and risk of cardiovascular disease, total cancer, and all-cause and cause-specific mortality in adult populations published up to July 19, 2016. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random-effects models. The burden of mortality attributable to low nut consumption was calculated for selected regions.

Results

Twenty studies (29 publications) were included in the meta-analysis. The summary RRs per 28 grams/day increase in nut intake was for coronary heart disease, 0.71 (95% CI: 0.63–0.80, I2 = 47%, n = 11), stroke, 0.93 (95% CI: 0.83–1.05, I2 = 14%, n = 11), cardiovascular disease, 0.79 (95% CI: 0.70–0.88, I2 = 60%, n = 12), total cancer, 0.85 (95% CI: 0.76–0.94, I2 = 42%, n = 8), all-cause mortality, 0.78 (95% CI: 0.72–0.84, I2 = 66%, n = 15), and for mortality from respiratory disease, 0.48 (95% CI: 0.26–0.89, I2 = 61%, n = 3), diabetes, 0.61 (95% CI: 0.43–0.88, I2 = 0%, n = 4), neurodegenerative disease, 0.65 (95% CI: 0.40–1.08, I2 = 5.9%, n = 3), infectious disease, 0.25 (95% CI: 0.07–0.85, I2 = 54%, n = 2), and kidney disease, 0.27 (95% CI: 0.04–1.91, I2 = 61%, n = 2). The results were similar for tree nuts and peanuts. If the associations are causal, an estimated 4.4 million premature deaths in the America, Europe, Southeast Asia, and Western Pacific would be attributable to a nut intake below 20 grams per day in 2013.

Conclusions

Higher nut intake is associated with reduced risk of cardiovascular disease, total cancer and all-cause mortality, and mortality from respiratory disease, diabetes, and infections.

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Posted Yesterday, 07:48 PM

AlPater

Nut consumption and risk of cardiovascular disease, total cancer, all-cause and cause-specific mortality: a systematic review and dose-response meta-analysis of prospective studies.

Aune D, Keum N, Giovannucci E, Fadnes LT, Boffetta P, Greenwood DC, Tonstad S, Vatten LJ, Riboli E, Norat T.

BMC Med. 2016 Dec 5;14(1):207.

PMID: 27916000


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