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Greg Scott

hazards and benefits of a fruitarian on CR

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Michael wrote:

As Dean posted in the middle of my composition ;) , substitute! That is the very essence of achieving the "ON" part of "CR." This is all a backpack problem.

Yes Michael. I've been doing CR for over 40 years, but only now learning the "ON" part thanks to CRS members. I've been lucky that my intuitive approach has kept me from catastrophe so far, but it is time to get with the CRON program.

 

I'll be reviewing and repacking my backpack.

 

Michael wrote:

selenium=14%

 

If Brazil nuts are out, selenium is a problem since I don't eat grains or cereals and can't stand any more broccoli (my primary source now).

What about legumes? I was surprised to learn that Dean had an Se problem, too, as I get lots; I see a huge chunk of mine comes from a daily legume stew.

 

I never got started with legumes, having adopted the raw approach since my teen years.

 

My selenium deficiency needs to be attended to, but it might not be so dire as the 14% suggests. Today I added yeast flakes and the value jumped to 47%.

 

Also, I have eaten nuts and intend to resume (mild agoraphobia discouraged a visit to the market that I used for nuts, but now I'm looking at purchasing nuts online).

 

Michael wrote:

BTW, how much sucrose and fructose are you getting? If this isn't already displayed, you can turn it on with the checkboxes in your target preferences.

I'll answer this soon.

 

Thank you.

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Hmm, the label [for Dean's selenium supplementsays it contains gelatin ... :huh:

 

 

My bad. I must admit, that while I'm a vegan for ethical reasons, I've never been a stickler for gelatin in my supplements.  :unsure:

 

Thanks for pointing it out to me. I'll go with this vegan one from Now next time, and take it less frequently, since its 200mcg (286% RDA), rather than 100mcg per capsule.

 

--Dean

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Hmm, the label [for Dean's selenium supplementsays it contains gelatin ... :huh:

 

My bad. I must admit, that while I'm a vegan for ethical reasons, I've never been a stickler for gelatin in my supplements.  :unsure:

 

Thanks for pointing it out to me. I'll go with this vegan one from Now next time, and take it less frequently, since its 200mcg (286% RDA), rather than 100mcg per capsule.

 

--Dean

 

 

Dean,

 

I don't expect those minuscule amounts of gelatin to affect my health, but I prefer to avoid it. I'm not sure whether it's some ethical concern or some irrational motive.

 

In any case, I don't like holier-than-thou attitudes, so you'll never need to defend your choices to me.

 

In case you're interested: of the supplements I checked, the following contained gelatin:

  • Sundown D3
  • Swanson selenium
  • Carlson K2
  • Trunature Lutein
  • Ovega-3 DHA
Finding vegan alternatives on Amazon was easy.

 

Having wasted time on this gelatin distraction, I apologize and want to reaffirm how useful your vegan supplement regime is.

 

Thanks again for the guidance.

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BTW, how much sucrose and fructose are you getting? If this isn't already displayed, you can turn it on with the checkboxes in your target preferences.

Sucrose 21g

Fructose 61g

Glucose 31g

Sugar 139g

 

 

EDIT: updated with the values for a typical day

Edited by Greg Scott

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BTW, how much sucrose and fructose are you getting? If this isn't already displayed, you can turn it on with the checkboxes in your target preferences.

Here are the values for today, the first completely logged day:

Sucrose 11g

Fructose 34g

Glucose 18g

Sugar 78g

 

I hope it's the ratio you were interested in rather than the absolute amounts, since today my calories were subnormal as I was too busy to eat much.

 

My first thoughts here are "wow, I'm often eating more sugar / fructose than a fruitarian?"  I think weekly averages are probably more useful for analysis.  There's a weird effect when calories drop down -- low carb diets can start to look like low fat diets, or high-sugar diets might look low in fructose.  Apparently the average American eats around 82 grams of added sugar per day.

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In case you're interested: of the supplements I checked, the following contained gelatin:

  • Sundown D3
  • Swanson selenium
  • Carlson K2
  • Trunature Lutein
  • Ovega-3 DHA
Finding vegan alternatives on Amazon was easy.Having wasted time on this gelatin distraction, I apologize and want to reaffirm how useful your vegan supplement regime is.Thanks again for the guidance.

Thanks Greg. I too am very doubtful about the health impact of tiny amounts of gelatin. But I'd rather avoid animal derived gelatin (either from bone or wool) for ethical reasons. So thanks for pointing out these to me. I'll change them in future orders, except for the Ovega-3, which is quite clearly vegan per the packaging. It says it's capsules are plant-derived.

 

--Dean

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Have either of you guys had advanced lipids checked while on this sort of diet (NMR Lipoprofile / VAP) ?  (or others on a high fruit diet?)

 

I would be very curious to see where triglycerides / HDL / apoB or LDL particles sit on such a diet.  If A1C is in an optimal range while TGs are low and under HDL, and LDL particles are few and large while eating 30-70% calories as fruit, this would make me feel much more comfortable about a higher fruit diet.

 

It seems like the 'type' of fruit might be important.  Avocados, olives, olive oil, red palm oil, cucumbers, tomatoes, zucchini, bell peppers, etc could all contribute toward a very high fruit diet by calories, while this would be a fairly low fructose diet as compared with one that uses apple sauce / ripe bananas / raisins / date sugar / etc. for a bulk of the calories.

 

I've been following this conversation with interest because I follow a similar diet. I did get an NMR LipoProfile done a few months ago that confirms that a very high-carb low-fat diet, and a relatively high whole-food sugar intake, isn't a problem for me.

 

General diet
70C/14F/11P, 2350kcal (sometimes up to 3000kcal on very active days), whole-food vegan, 80-100g fiber per day; no alcohol; weight stable
 
I've attached a CRON-O-Meter report (actually for the day just prior to the blood draw) to show typical foods, though this is a bit lower in calories than I usually eat, and the high Fitbit activity data is from walking around campus and on my treadmill desk. The amount of fruit and starch (mostly potatoes) may vary but the macro ratios are pretty consistent. I actually have oats in this sample day but that's most often replaced with more fruit.
 
My typical food choices include potatoes (all kinds), fruit (apples, bananas, berries), veggies (lettuce, tomatoes, cauliflower, and carrots raw, otherwise cooked frozen stir fry, broccoli, brussels sprouts and kale), beans or tempeh, flax (rarely other nuts/seeds), pea protein powder, and most of my lunches are a homemade chili with canned tomato paste and tomatoes, brussels sprouts, carrots, beans, lentils, and whatever produce leftovers from the prior week.

 

Body temp--97.0-97.5 F
Blood pressure--105/65
Lipids--Chol (134), HDL-C (38) LDL-C (81), TAG (76), LDL-P (867)
Fasting glucose--77 mg/dL
Fasting insulin--2.9 (range 2.6-24.9 uUI/mL)
HbA1c--5.0
IFG-1--126 (range 98-282 ng/mL)

CRON-O-Meter - 150727.pdf

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In case you're interested: of the supplements I checked, the following contained gelatin:

  • Sundown D3
  • Swanson selenium
  • Carlson K2
  • Trunature Lutein
  • Ovega-3 DHA
Finding vegan alternatives on Amazon was easy.Having wasted time on this gelatin distraction, I apologize and want to reaffirm how useful your vegan supplement regime is.Thanks again for the guidance.

 

I'll change them in future orders, except for the Ovega-3, which is quite clearly vegan per the packaging. It says it's capsules are plant-derived.

 

Dean,

 

Sorry for the error, I should not post when tired. The Ovega-3 is clearly vegan.

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I've been following this conversation with interest because I follow a similar diet. I did get an NMR LipoProfile done a few months ago that confirms that a very high-carb low-fat diet, and a relatively high whole-food sugar intake, isn't a problem for me.

Thanks James,

 

It's good to have someone following a similar diet.

 

I presume you saw Dean's supplement list. I've never taken pills before. Do you?

 

James wrote:

General diet

70C/14F/11P, 2350kcal (sometimes up to 3000kcal on very active days), whole-food vegan, 80-100g fiber per day; no alcohol; weight stable

 

I've attached a CRON-O-Meter report

The only foods on your report I don't eat routinely are oatmeal, pea protein isolate, chili, potato, and tempeh. I don't eat legumes, but only because they need to be cooked. I never cook because I don't want to spend the time. That's why I eat raw foods. Your diet is better.

 

I consumed tempeh until I saw a report that vegans relying on tempeh were B-12 deficient. I don't recall where I read that, and it wouldn't surprise me if it's not a settled question. But anyway I stopped eating tempeh.

 

James wrote:

My typical food choices include potatoes (all kinds), fruit (apples, bananas, berries), veggies (lettuce, tomatoes, cauliflower, and carrots raw, otherwise cooked frozen stir fry, broccoli, brussels sprouts and kale), beans or tempeh, flax (rarely other nuts/seeds), pea protein powder, and most of my lunches are a homemade chili with canned tomato paste and tomatoes, brussels sprouts, carrots, beans, lentils, and whatever produce leftovers from the prior week.

 

Your diet looks exemplary to me.

 

Your CRON-O-Meter breakdown is far superior to mine. You've probably noticed the biggest deficiencies I reported (and I have other less alarming deficiencies).

 

I imagine your intake of legumes and potatoes accounts for much of the superiority.

 

Can you tell me what foods are contributing most to vitamin D, calcium, and selenium on your CRON-O-Meter report?

 

I notice your report doesn't show percentages for omega-3 and omega-6. My report for yesterday had omega-3=128% while omega-6=3%. I wonder how you are getting enough omega-6 to achieve the recommended 3:1 ratio.

 

Thanks for joining this thread. Your data are very interesting.

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I wrote up a long response to this and then lost it before posting, demoralizing a second attempt for a while, but here's round two:
 

I presume you saw Dean's supplement list. I've never taken pills before. Do you?

 
I did see Dean's post, as well as Michael's extensive post on supplements for vegetarians. I take daily 500 mcg B-12, 2000 IU D3 (I don't get out much, and when I do I usually wear UV-blocking clothing or sunscreen), 250 mg calcium citrate (with 175 IU D3), 1/2 tab of a general multivitamin, 3 mg melatonin, and 2.5 g creatine.
 
The melatonin isn't necessary but it noticeably enhances my sleep, and I think the antioxidant value of melatonin (especially for neurons) is motivation enough for me to take it. The multivitamin is mainly for iron, iodine (I usually don't use much salt), and to generally fill in a few potential gaps depending on a day's intake (like zine, vitamin E, selenium). I know some research shows multivitamins may be unhelpful or harmful overall, but I think taking the modest 1/2 tab per day is safe. I started it a while back because my digestion was, and sometime still is, wonky enough that I was concerned with getting adequate micronutrient absorption. I could probably ditch my calcium and maybe even the D3 and B12 since these are covered in the multi at probably adequate levels. The B12 is inexpensive, effective (blood work confirms), and safe, so I'd rather keep the dedicated B12 supplement just to be sure. 
 
I also currently include vitamin K1 and K2 complex (1 capsule per week), CoQ10 with vitamin E spectrum (3-7 capsules per week), and zinc methionine (very infrequently, perhaps every 6-8 weeks, to enhance my sleep when I have insomnia). I think the research on vitamin K2 (from animal products) is promising, showing benefit regardless of adequate K1 (from plant products) levels. I doubt it's at all necessary or beneficial on top of everything else, but for the moment I have a few bottles left over and it lasts a long time taking one capsule each week. The CoQ10 has a noticeable effect on increasing my stress resistance to increased exercise, less sleep, and general stress. I don't always take it but do when I feel I'd like the extra boost. The vitamin E is full-spectrum and is probably accounting for the perceived benefits, and I'm less concerned about this supplement than I would be of overusing a pure dl-alpha tocopherol supplement.
 

The only foods on your report I don't eat routinely are oatmeal, pea protein isolate, chili, potato, and tempeh. I don't eat legumes, but only because they need to be cooked. I never cook because I don't want to spend the time. That's why I eat raw foods. Your diet is better.

I consumed tempeh until I saw a report that vegans relying on tempeh were B-12 deficient. I don't recall where I read that, and it wouldn't surprise me if it's not a settled question. But anyway I stopped eating tempeh.

 

The potatoes provide a lot of nutrients that fill in the gaps of an otherwise vegetable and fruit heavy diet. Cooked potatoes of various varieties are somewhere around .9-1 calorie/gram, and are satiating for me, and are relatively nutrient dense, so they are a staple in my diet. Observations of various cultures like the Andean and Irish people have shown a long-term potato-based diet supports healthy disease-free growth and development, and research trials show a practically potato-only diet (especially when supplemented with a few vegetables) is capable of healthily supporting an adult. The CR community often maligns the potato, but for me I seem to do well with it both subjectively and metabolically. They are also extremely inexpensive.

I'm pretty lazy as a cook and spend a few hours on Sunday baking about 15 points of potatoes and making a big batch of chili. I put these in the fridge to portion out throughout the week. I use canned beans, and often eat just raw veggies or put frozen veggies in the microwave using a glass steamer.

As there is no reliable source of plant-based B12, I consume tempeh mostly because I enjoy it and as a source of probiotics, fiber, protein, and fat.
 

Can you tell me what foods are contributing most to vitamin D, calcium, and selenium on your CRON-O-Meter report?

 
Vitamin D - I get from supplements.

Calcium and Selenium.jpg
 

I notice your report doesn't show percentages for omega-3 and omega-6. My report for yesterday had omega-3=128% while omega-6=3%. I wonder how you are getting enough omega-6 to achieve the recommended 3:1 ratio.

 

I changed a few of the nutrients ranges in Cronometer, and removed them completely for some items for which the data is somewhat meaningless of just serves as noise when looking at the overall report. For me the fatty acid breakdown falls into this category.

 

I've seen the recommended ratio range from 1:1 to 4:1 n-6:n-3, and sometimes a bit higher, depending on which specific tissue or population is being studied. My ratio is 1.042 (6.2 g n-3, 6.5 g n-6), which meets the minimum PUFA requirement and seems to fall within that range. I enjoy the foods that allow me to keep my overall fat intake low and don't feel the need to specifically add more fat unless its out of gastronomic preference. I also consume all of my n-3 as ALA so don't worry when it is sometimes higher than my n-6 intake, and keeping overall PUFA intake quite low enhances ALA conversion into EPA and DHA, evidenced here and here.

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James,

 

Thanks for the very enlightening post.

 

Your response to my question about supplements will take awhile for me to work through, and will result in additions to my supplement regime. Thank you for the great info.

 

I wrote up a long response to this and then lost it before posting, demoralizing a second attempt for a while, but here's round two:

I compose in an editor with frequent saves, and paste into the browser only to preview and post.

 

I imagine a lot of brilliance is forever lost when the post is vaporized. Dean found a way to recover autosaved text, as he explained here.

 

James wrote:

I did see Dean's post, as well as Michael's extensive post on supplements for vegetarians.

I've been working through Michael's document carefully, and have adopted most of Dean's recommendations already.

 

I'm an old hand at CR, but learning about ON from the gurus on the CRS forums (yourself included of course).

 

James wrote:

The potatoes provide a lot of nutrients that fill in the gaps of an otherwise vegetable and fruit heavy diet.

...

The CR community often maligns the potato, but for me I seem to do well with it both subjectively and metabolically. They are also extremely inexpensive.

I've always thought potatoes a great source of nutrients. I simply don't cook and had to forgo their benefits, which is especially regrettable considering their cheapness.

 

I asked:

Can you tell me what foods are contributing most to vitamin D, calcium, and selenium on your CRON-O-Meter report?

James replied:

Vitamin D - I get from supplements.

(A jpg file shows the sources of calcium and selenium.)

That confirms my suspicions. I entered all your foods but the mysterious "Chili 1" and "Stir-fry vegetables, frozen, unprepared" into my CRON-O-Meter. That produced a profile much like my current, slightly deficient profile. So I concluded the mystery ingredients were responsible for the evident superiority of your diet (especially "Chili 1", since I get loads of veggies).

 

I presume the green graphic beside the two mystery items on your CRON-O-Meter report signifies that they are custom foods.

 

I asked:

I notice your report doesn't show percentages for omega-3 and omega-6. My report for yesterday had omega-3=128% while omega-6=3%. I wonder how you are getting enough omega-6 to achieve the recommended 3:1 ratio.

James replied:

I changed a few of the nutrients ranges in Cronometer, and removed them completely for some items for which the data is somewhat meaningless of just serves as noise when looking at the overall report. For me the fatty acid breakdown falls into this category.

That's a relief. I've added walnuts to my daily list, but that only led to omega-6=34% while omega-3=184%. Far from the 3:1 target, but better than the 3%/128% I had before introducing walnuts.

 

Another changed effected by the addition of walnuts is P:F:C went from roughly 10%:10%:80% to 20%:20%:60%, which is moving in the right direction.

 

Well, thank you James. You've given me lots to think on, and I will be making some changes.

Edited by Greg Scott

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I wrote up a long response to this and then lost it before posting, demoralizing a second attempt for a while, but here's round two:

I compose in an editor with frequent saves, and paste into the browser only to preview and post.

 

I imagine a lot of brilliance is forever lost when the post is vaporized. Dean found a way to recover autosaved text, as he explained here.

 

 

Thanks! I used this to recovery my almost-lost post in the coffee thread this morning.

 

I usually copy and paste partially done posts into Word as a sort of "save" but it'd help to have a text editor with coding functions built in.

 

That confirms my suspicions. I entered all your foods but the mysterious "Chili 1" and "Stir-fry vegetables, frozen, unprepared" into my CRON-O-Meter. That produced a profile much like my current, slightly deficient profile. So I concluded the mystery ingredients were responsible for the evident superiority of your diet (especially "Chili 1", since I get loads of veggies).

 

I presume the green graphic beside the two mystery items on your CRON-O-Meter report signifies that they are custom foods.

 

The "Stir-fry vegetables, frozen, unprepared" is a custom recipe entered from weighing the individual components averaged from a few bags of standard frozen stir-fry vegetables. By creating a recipe with the whole foods I get an entry with the micronutrient values included. Most custom foods and packaged foods in the databases only include the information from the nutrition label, so lacks the more detailed breakdown of foods in the USDA database.

 

Here's the "Chili1" recipe:

2 cans (520 g) - Black beans, canned, drained, low sodium

200 g - Lentils, pink or red, raw

2 x 1 lb bags (900 g) - Brussels sprouts, frozen, unprepared

900 g - Mushrooms, portabella, raw

450 g - Kale, raw

2 cans (820 g) - Tomato, canned, low sodium

3 cups - Tap water

 

The Cronometer report for 1/7 of the Chili 1 recipe, which was included in my sample day, is attached.

 

My typical chili recipe is more along the following lines:

Standard ingredients:

2 cans various beans, drained and rinsed, low sodium if possible (most often black, pinto, and kidney)

100-200 g red lentils (I prefer red over brown lentils for flavor and easier digestibility)

2 small cans (170g) tomato paste

2 cans (411 g) diced tomatoes, low sodium

2 x 1 lb bags (900 g) Brussels sprouts, frozen

3-4 cups water

Various spices

 

The most common additional ingredients to fill the 8-quart pot, varies depending on the week:

Frozen pearl onions, peas, and corn

Fresh carrots, cauliflower, and mushrooms

 

1/7 of the various chili recipes ranges from 540-620 g and 290-370 kcal, is pretty high in protein, fiber, and micronutrients.

Chili 1 (0.14 of total recipe).pdf

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James,

 

Thanks for the additional information. It all helps me to work toward the ON part of CRON.

 

I shall add some black beans to my diet, starting today.

 

The CRON-O-Meter report you attached to a previous post was compelling.

 

I found a can of "Black beans, canned, drained, low sodium" at the local H.E.B. supermarket here (coastal TX).

 

Previously I'd avoided beans for flimsy reasons. I don't cook from scratch, and all canned foods seem "dead" to me (irrational impression). Further, when I ate cooked beans from a can, I felt like I had a stomach full of lead shot.

 

Anyway, in the pursuit of ON, I'll be adding some canned black beans, and later on some lentils.

 

Thank you.

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Greg, James, and others: you might want to consider buying dried beans and boiling them yourself (a small hassle, but can be amortated by preparing multi-serving potfulls): canned beans are consistently reported to lead to substantially higher postprandial glucose and insulin (1,3), presumably because a mixture of the high heat conditions during industrial pressure-cooking(2) and time in the can both tend to break down the soluble fiber excessively.

 

Additionally, there is the concern around BPA and many of its substitutes: very few companies use genuinely xenoestrogen-free linings for canned beans, most notably Eden's switch to oleoresin years before BPA became a subject of national headlines. Many manufacturers say their cans are "BPA-free," but use other known or suspected chemical-leaching linings, such as vinyl or bisphenol S — and most won't disclose. (To be clear, however, it really isn't entirely clear that BPA is harmful to humans under real-world exposures — or if it is, if it's meaningfully harmful to adult humans, and I wouldn't consider anyone rash to ignore the issue at this stage in the science).

 

References

1: Traianedes K, O'Dea K. Commercial canning increases the digestibility of beans in vitro and postprandial metabolic responses to them in vivo. Am J Clin Nutr. 1986 Sep;44(3):390-7. PubMed PMID: 3529917.

 

2: Wong S, Traianedes K, O'Dea K. Factors affecting the rate of hydrolysis of starch in legumes. Am J Clin Nutr. 1985 Jul;42(1):38-43. PubMed PMID: 4014066.

 

3: Wolever TM, Jenkins DJ, Thompson LU, Wong GS, Josse RG. Effect of canning on the blood glucose response to beans in patients with type 2 diabetes. Hum Nutr Clin Nutr. 1987 Mar;41(2):135-40. PubMed PMID: 3570870.

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Greg, James, and others: you might want to consider buying dried beans and boiling them yourself (a small hassle, but can be amortated by preparing multi-serving potfulls): canned beans are consistently reported to lead to substantially higher postprandial glucose and insulin (1,3), presumably because a mixture of the high heat conditions during industrial pressure-cooking(2) and time in the can both tend to break down the soluble fiber excessively.

 

Additionally, there is the concern around BPA and many of its substitutes: very few companies use genuinely xenoestrogen-free linings for canned beans, most notably Eden's switch to oleoresin years before BPA became a subject of national headlines. Many manufacturers say their cans are "BPA-free," but use other known or suspected chemical-leaching linings, such as vinyl or bisphenol S — and most won't disclose. (To be clear, however, it really isn't entirely clear that BPA is harmful to humans under real-world exposures — or if it is, if it's meaningfully harmful to adult humans, and I wouldn't consider anyone rash to ignore the issue at this stage in the science).

Thanks Michael,

 

I will look into alternatives, as my distaste for the canned beans makes it unlikely I will continue with canned foods.

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Additionally, there is the concern around BPA and many of its substitutes

Slightly off topic, but I know you have expressed concerns about BPA leaching into food from packaging in the past, and I know you also drink(or at least drank) wine, so I thought this might interest you too:

 

1. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2014;31(9):1605-15.

doi: 10.1080/19440049.2014.941947. Epub 2014 Aug 7.

 

Contamination of wines and spirits by phthalates: types of contaminants present,

contamination sources and means of prevention.

 

Chatonnet P(1), Boutou S, Plana A.

 

Author information:

(1)a Laboratoire Excell , Parc Innolin , 33700 Mérignac , France.

 

This research determines the concentrations of various phthalates in French wines

and grape spirits marketed in Europe or intended for export. Dibutyl phthalate

(DBP), diethylhexyl phthalate (DEHP) and butyl benzyl phthalate (BBP) were the

most frequently detected compounds in the wines analysed. While only 15% of the

samples examined contained quantifiable concentrations (> 0.010 mg kg(-1)) of

DEHP and BBP, 59% of the wines contained significant quantities of DBP, with a

median value as high as 0.0587 mg kg(-1). Only 17% of the samples did not contain

any detectable quantity of at least one of the phthalates and 19% contained only

non-quantifiable traces. In the spirits analysed, DBP (median = 0.105 mg kg(-1))

and DEHP (median = 0.353 mg kg(-1)) were the substances measured at the highest

concentrations, as well as the most frequently detected (90% of samples). BBP was

present in 40% of the samples at an average concentration of 0.026 mg kg(-1).

Di-isobutyl phthalate (DiBP), which is not permitted in contact with food, was

found in 25% of the spirits tested. According to the specific migration limits

(SML) for materials in contact with food, slightly more than 11% of the wines

analysed were non-compliant, as they exceeded the SML for DBP (0.3 mg kg(-1));

just under 4% were close to the SML for DEHP. Concerning spirits, 19% of the

samples analysed were considered non-compliant to the SML for DBP and nearly 7%

were close to the SML for DEHP. The aged grape spirits analysed were often

excessively contaminated with DiBP, which is not permitted to be used in contact

with food (> 0.01 mg kg(-1)). A study of various materials frequently present in

wineries revealed that a relatively large number of polymers sometimes contained

high concentrations of phthalates. However, the epoxy resin coatings used on vats

represented the major source of contamination.

 

PMID: 25099435 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/25099435

A discussion about the study findings and some comments from posters claiming to have in-depth technical knowledge of industrial-scale wine production methods and where and how phthalates might be getting into the wine:

https://www.reddit.com/r/science/comments/2d5pwd/phthalates_a_class_of_environmental_contaminant/

Edited by Brett Black

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This is all very interesting stuff.  Thanks for posting it.  And it is important there be people whose job it is to watch these kinds of things very closely.  But there is a broader perspective:

 

Life expectancy keeps increasing EVERY year.  This is true even in the United States, where life expectancy is already quite high and these chemical contaminants are much more likely to be present because that is where the majority of them are invented, and are introduced first. 

 

And the upward trend in life expectancy seems inexorable. https://www.google.ca/search?q=chart+for+us+life+expectancy&biw=1252&bih=554&tbm=isch&tbo=u&source=univ&sa=X&ved=0ahUKEwjZsP2yibTJAhUQ-GMKHbUdBI4QsAQIGw#imgrc=-yGY8fNhchTjpM%3A  http://www.infoplease.com/ipa/A0005140.html 

 

Of course yer never know if some especially nasty substance may slip in under the radar next year or the year after.  But it does seem we can stop worrying excessively about the ones that have been introduced thus far.  That said, I do agree that during pregnancy and lactation probably-excessive caution is certainly appropriate. 

 

Rodney.

 

=============

 

"The unverified conventional wisdom is almost invariably mistaken."

Edited by nicholson

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Rodney, you seem to be adducing the increase in life-expectancy in the US as evidence that phthalates and the like aren't worth worrying about. Don't follow your logic, unless you're assuming that these substances are the only (or are the major) source of mortality in the US, which, of course they are not.

 

Zeta

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Hi Zeta:

 

No, it was not my point that phthalates are the only cause of death.

 

We all know that everywhere you look there are people fuming about, certainly hundreds, possibly thousands, of newly introduced chemicals, or processes (GMO for example) or other innovations that they claim are seriously undermining our health. 

 

If any single one of these substances was causing very serious problems, or if many of them in combination were causing serious harm, we would not see life expectancy rising every year in a country where obesity rates are huge and rising, dietary habits are on average atrocious and not getting any better, and where these supposedly harmful chemicals are likely to be introduced first.

 

Rising life expectancy suggests we are doing a lot of things right.  When life expectancy flattens out, or when some specific kind of disease suddenly starts seeing rapidly increasing incidence then the causes will need to be ferreted out - as they indeed were in the cases of HIV, and Thalidomide, for example

 

Similarly, the fuss about pesticide residues on food was extensively discussed here several years ago. 

 

Part of the reason people create a fuss without much, if any, evidence is that in some cases the motivations of those who do so are not always apparent.  Not infrequently they are part of a marketing campaign to raise donations, so their 'non-profit' can make no profit by paying out all its revenues to the founder in salary.  There are reasons having nothing to do with the accuracy or relevance of the information supplied, that lie behind many of these claims of damaging health effects.

 

Of course, it is good there are people, mostly in government, whose job it is to watch out for evolving evidence of such harms.  And seeing action is taken when they find it. 

   

Rodney.

 

=============

 

"The unverified conventional wisdom is almost invariably mistaken."

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Back to the original topic of this thread - possible hazards of fruit.

 

As mentioned earlier, fruit is often impuned by nutrition 'experts' like Robert Lustig due to its fructose content. Lustig often (but not always) lets whole fruit "off the hook" (when eaten in moderation) because in addition to fructose it also contains lots of fiber which should slow fructose absorption. I was surprised to see that even Michael Rae seems (or seemed) in this post to suggest caution about eating too much fruit due to fructose and relatively high glycemic index/load, and more specifically to be reluctant to let fruit off the hook due to its fiber, saying:

... the fiber [in fruit] just doesn't seem to impair sugar absorption worth a spit.

 

It seems that (one of) the major concerns Lustig (and Michael) have with fruit is that unlike glucose, fructose (whether from fruit or high fructose corn syrup) is composed of a combination of both glucose and sucrose, which must first be metabolized in the liver. If there is too much fructose in circulation for the liver to handle, it can get converted to lipids and stored in the form of triglycerides, which are a risk factor for cardiovascular disease and metabolic syndrome, not to mention contributing directly to non-alcoholic fatty liver disease (NAFLD) [2]. 

 

So as someone who eats a lot of fruit (but fortunately has low triglycerides), it was with great interest that I read this latest post to the CR email list from our oracle of nutrition research (Al Pater - thanks Al!), which featured study [1], which investigated the association of fruit and vegetable consumption with hypertriglyceridemia (defined as triglycerides > 150 mg/dl) in a population of 8000 Korean adults.

 

It found that higher consumption of fruit was associated with reduced serum triglycerides in study participants in what appears to be a linear, dose-response relationship (see table below). In particular, relative to people in lowest quintile of fruit consumption (less than 3 servings per week), people in the highest quintile of fruit consumption (average of ~3 servings per day) had a 36% lower rate of elevated triglycerides, after controlling for multiple possible confounders, including age, gender, BMI, smoking, alcohol drinking, physical activity, education, income, and waist circumference. Beside the usual factors that directly impact health (BMI, smoking, exercise, etc.) it was good to see the authors controlled for factors that indicate socioeconomic status (education and income), since eating more fruit could otherwise simply be an indication of better education (and therefore overall rational healthy life choices) or wealth (and therefore access to other, health-promoting goods unrelated to fruit, like healthcare). They found in subcategory analysis, that citrus fruits, non-citrus fruits and carotene-rich fruits were about equally associated with lower triglycerides.

 

The really surprising thing was that they found increased vegetable consumption was not associated with lower triglycerides, nor were any of the subcategories of vegetables they analyzed, including green leafy vegetables, cruciferous vegetables or carotene-rich vegetables, with or without controlling for all those possible confounding factors. Going from the lowest vegetable intake quintile (a little over 2 servings per day) to the highest quintile (7 servings per day), was associated with no change in risk of elevated triglycerides (RR = 1.00 (95%CI 0.81–1.24)). In fact, compared with people in the second lowest quintile of vegetable consumption (3.5 servings per day), those in the highest quintile were almost 20% more likely to have elevated triglycerides.

 

Here is the relevant table showing triglyceride levels for each quintile of both total vegetable and fruit consumption, so you can see the details. For risks broken down by fruit and vegetable categories, see the (sci-hub.io) full text.

 

283zSUf.png

 

Now I wouldn't interpret this result as a caution against eating too many vegetables. The authors themselves suggest one possible explanation for their null vegetable result, which seems to contradict previous findings:

 

We found no association of vegetable intake with hypertriglyceridemia,
which is inconsistent with previous studies that
reported an inverse association with serum triglyceride
levels.11,12 One possible explanation for the null association in
our study is that Koreans usually eat steamed, boiled and pickled
vegetable mixed with salt and soy sauce,15 whereas people in
Western countries have a higher intake of raw vegetables.

 

So it sounds like this may be more a recommendation to eat vegetables raw rather than heavily cooked, and to go easy on the sodium. 

 

But the fruit result is more interesting, since fruit (via fructose) has been specifically implicated in the past due to concerns about raising triglycerides. The authors discuss their result in light of all the other previous research showing the health benefits of eating more fruit:

 

In addition to the beneficial effect of fruits on coronary
heart disease [3], stroke [4], and hypertension [5], found in previous
studies, our study adds to the literature that higher consumption
of fruit may have a protective role against elevated blood

triglyceride levels in Asian populations. 

 

Here is what the authors said about the likely mechanism of fruits benefits for triglycerides and other health markers/outcomes:

 

The mechanisms whereby fruit intake may exert effects on
hypertriglyceridemia are not fully understood. First, phytochemicals
are important bioactive compounds found in fruits and
include flavonoids and phenolic acids and so on. The antioxidant
activity and anti-inflammatory potential of those compounds
could reduce systemic inflammation through cellular signaling
processes,27 which have been shown to protect atherosclerosis
and cardiovascular disease.5,28,29 In addition, fruits have low
dietary glycemic load and low energy density,30 which have been
suggested to have a beneficial role in lowering serum triglycerides
levels and increasing HDL-C levels over time, compared with high
glycemic load diets high in refined carbohydrates and sugar.31

 

Strangely, all these explanations should also apply to vegetables, but vegetable intake (not even cruciferous vegetable intake specifically) was not associated with lower triglycerides.

 

Regarding the concern about fructose causing elevated triglycerides, the authors had this to say:

 

Recently, several short-term controlled feeding studies found
that dietary fructose significantly increases postprandial triglyceride
levels;31,32 thus, there may be concerns raised with regard to
the fructose content in fruits. This dietary setting is different from
that of our study because fructose was added to processed food,
and the level of dietary fructose used in those studies was much
higher than the intake from fruits in the general population.

 

So the bottom line appears to be fruit is beneficial, rather than detrimental, when it comes to one of the main concern people have about it, namely that the fructose it contains will raise your triglycerides. Meta-analyses [3-5] also suggest that concerns about other negative health outcomes potentially associated with eating fruit (heart disease, stroke and elevated blood pressure) are unfounded as well - in in fact that fruit is protective against these three killers. 

 

As for all-cause mortality, this recent meta-analysis [6], found that eating more fruit was at least as good as eating more vegetables. Here are the forest plots change in all-cause mortality associated with an extra serving of fruit (left) or vegetables (right) per day:

 

Okq0UoK.png

 

As you can see, the fruit benefits appear more consistent and a bit larger on average than the vegetable benefits, although again their may be some attenuation of the vegetable benefits as a result of preparation methods.

 

Interestingly though, meta-analyses of studies investigating the association of fruit and/or vegetable intake with cancer haven't found much if any effect. From meta-analysis [6]:

 

The hazard ratio for cancer mortality was 0.97 (95% confidence interval 0.90 to 1.03; P=0.31; see fig H, appendix 2) for each additional serving/day of total consumption, 0.99 (0.97 to 1.00; P=0.06; see fig I, appendix 2) for fruit, and 0.99 (0.97 to 1.01; P=0.19; see fig J, appendix 2) for vegetables.

 

However Al did just post a meta-analysis [7] showing a dramatic 50% reduction in risk of oral cancer as a result of an extra serving of fruit or vegetables per day.

 

 

--Dean

 

-----------

[1] Fruit and vegetable consumption and hypertriglyceridemia: Korean National Health and Nutrition Examination Surveys (KNHANES) 2007-2009.
Yuan C, Lee HJ, Shin HJ, Stampfer MJ, Cho E.
Eur J Clin Nutr. 2015 Nov;69(11):1193-9. doi: 10.1038/ejcn.2015.77. Epub 2015 May 27.
PMID: 26014266
 
Abstract
 
Background:
 
Limited research has been conducted on the association between intake of fruits and vegetables and hypertriglyceridemia, especially in Asian populations. This study aimed to investigate the association between total fruit and vegetable intake, as well as subgroups of fruit and vegetable intake, with hypertriglyceridemia among Korean adults.
 
Methods:
 
We conducted a cross-sectional study of 7934 adults aged 19–64 years from the fourth Korean Health and Nutrition Examination Survey. Fruit and vegetable intake was estimated from a food frequency questionnaire. Subgroups of fruits and vegetables included citrus, non-citrus and carotene-rich fruits and cruciferous, green leafy and carotene-rich vegetables. Hypertriglyceridemia (plasma triglyceride 150 mg/dl) was diagnosed using a blood sample drawn after 12+ hours of fasting.
 
Results:
 
There were 2001 (25.2%) cases of hypertriglyceridemia among the participants. Total fruit intake was significantly inversely associated with the prevalence of hypertriglyceridemia; the multivariate odds ratios (95% confidence intervals) of hypertriglyceridemia across increasing quintiles were 1.00 (ref), 0.76 (0.62, 0.92), 0.72 (0.58, 0.90), 0.68 (0.54, 0.85) and 0.64 (0.49, 0.82; Ptrend=0.001) after controlling for survey year, body mass index, waist circumference, smoking, alcohol drinking, physical activity, education and income. Similar inverse associations were found for all fruit subgroups. However, we found no significant association between intakes of total or subgroups of vegetable and hypertriglyceridemia; the odds ratio for top vs bottom quintile was 1.00 (0.81–1.24) for total vegetable intake.
 
Conclusions:
 
Our findings support a potential beneficial role of fruit consumption to reduce blood triglyceride levels in Asian populations.
 
----------
[2] World J Gastroenterol. 2013 Feb 28;19(8):1166-72. doi: 10.3748/wjg.v19.i8.1166.

Fructose as a key player in the development of fatty liver disease.

Basaranoglu M(1), Basaranoglu G, Sabuncu T, Sentürk H.

Author information:
(1)Department of Gastroenterology and Hepatology, Bezmialem Vakif University,
Istanbul 34400, Turkey. metin_basaranoglu@yahoo.com

We aimed to investigate whether increased consumption of fructose is linked to
the increased prevalence of fatty liver. The prevalence of nonalcoholic
steatohepatitis (NASH) is 3% and 20% in nonobese and obese subjects,
respectively. Obesity is a low-grade chronic inflammatory condition and
obesity-related cytokines such as interleukin-6, adiponectin, leptin, and tumor
necrosis factor-α may play important roles in the development of nonalcoholic
fatty liver disease (NAFLD). Additionally, the prevalence of NASH associated with
both cirrhosis and hepatocellular carcinoma was reported to be high among
patients with type 2 diabetes with or without obesity. Our research group
previously showed that consumption of fructose is associated with adverse
alterations of plasma lipid profiles and metabolic changes in mice, the American
Lifestyle-Induced Obesity Syndrome model, which included consumption of a
high-fructose corn syrup in amounts relevant to that consumed by some Americans.
The observation reinforces the concerns about the role of fructose in the obesity
epidemic. Increased availability of fructose (e.g., high-fructose corn syrup)
increases not only abnormal glucose flux but also fructose metabolism in the
hepatocyte. Thus, the anatomic position of the liver places it in a strategic
buffering position for absorbed carbohydrates and amino acids. Fructose was
previously accepted as a beneficial dietary component because it does not
stimulate insulin secretion. However, since insulin signaling plays an important
role in central mechanisms of NAFLD, this property of fructose may be
undesirable. Fructose has a selective hepatic metabolism, and provokes a hepatic
stress response involving activation of c-Jun N-terminal kinases and subsequent
reduced hepatic insulin signaling. As high fat diet alone produces obesity,
insulin resistance, and some degree of fatty liver with minimal inflammation and
no fibrosis, the fast food diet which includes fructose and fats produces a gene
expression signature of increased hepatic fibrosis, inflammation, endoplasmic
reticulum stress and lipoapoptosis. Hepatic de novo lipogenesis (fatty acid and
triglyceride synthesis) is increased in patients with NAFLD. Stable-isotope
studies showed that increased de novo lipogenesis (DNL) in patients with NAFLD
contributed to fat accumulation in the liver and the development of NAFLD.
Specifically, DNL was responsible for 26% of accumulated hepatic triglycerides
and 15%-23% of secreted very low-density lipoprotein triglycerides in patients
with NAFLD compared to an estimated less than 5% DNL in healthy subjects and 10%
DNL in obese people with hyperinsulinemia. In conclusion, understanding the
underlying causes of NAFLD forms the basis for rational preventive and treatment
strategies of this major form of chronic liver disease.

PMCID: PMC3587472
PMID: 23482247

 

--------

[3] Dauchet L, Amouyel P, Hercberg S, Dallongeville J. Fruit, and vegetable consumption and risk of coronary heart disease: a meta-analysis of cohort studies. J Nutr 2006; 136: 2588–2593.

 

[4] 4 He FJ, Nowson CA, MacGregor GA. Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet 2006; 367: 320–326.

 

[5] Appel LJ, Champagne CM, Harsha DW, Cooper LS, Obarzanek E, Elmer PJ et al. Effects of comprehensive lifestyle modification on blood pressure control: main results of the PREMIER clinical trial. JAMA 2003; 289: 2083–2093.

 

-----------

[6] BMJ. 2014 Jul 29;349:g4490. doi: 10.1136/bmj.g4490.

 
Fruit and vegetable consumption and mortality from all causes, cardiovascular
disease, and cancer: systematic review and dose-response meta-analysis of
prospective cohort studies.
 
Wang X(1), Ouyang Y(2), Liu J(2), Zhu M(3), Zhao G(4), Bao W(5), Hu FB(6).
 
 
OBJECTIVE: To examine and quantify the potential dose-response relation between
fruit and vegetable consumption and risk of all cause, cardiovascular, and cancer
mortality.
DATA SOURCES: Medline, Embase, and the Cochrane library searched up to 30 August 
2013 without language restrictions. Reference lists of retrieved articles.
STUDY SELECTION: Prospective cohort studies that reported risk estimates for all 
cause, cardiovascular, and cancer mortality by levels of fruit and vegetable
consumption.
DATA SYNTHESIS: Random effects models were used to calculate pooled hazard ratios
and 95% confidence intervals and to incorporate variation between studies. The
linear and non-linear dose-response relations were evaluated with data from
categories of fruit and vegetable consumption in each study.
RESULTS: Sixteen prospective cohort studies were eligible in this meta-analysis. 
During follow-up periods ranging from 4.6 to 26 years there were 56,423 deaths
(11,512 from cardiovascular disease and 16,817 from cancer) among 833,234
participants. Higher consumption of fruit and vegetables was significantly
associated with a lower risk of all cause mortality. Pooled hazard ratios of all 
cause mortality were 0.95 (95% confidence interval 0.92 to 0.98) for an increment
of one serving a day of fruit and vegetables (P=0.001), 0.94 (0.90 to 0.98) for
fruit (P=0.002), and 0.95 (0.92 to 0.99) for vegetables (P=0.006). There was a
threshold around five servings of fruit and vegetables a day, after which the
risk of all cause mortality did not reduce further. A significant inverse
association was observed for cardiovascular mortality (hazard ratio for each
additional serving a day of fruit and vegetables 0.96, 95% confidence interval
0.92 to 0.99), while higher consumption of fruit and vegetables was not
appreciably associated with risk of cancer mortality.
CONCLUSIONS: This meta-analysis provides further evidence that a higher
consumption of fruit and vegetables is associated with a lower risk of all cause 
mortality, particularly cardiovascular mortality.
 
© Wang et al 2014.
 
PMCID: PMC4115152
PMID: 25073782
 
---------------
[7] Association between fruit and vegetable consumption and oral cancer: a meta-analysis of observational studies.
Pavia M, Pileggi C, Nobile CG, Angelillo IF.
Am J Clin Nutr. 2006 May;83(5):1126-34.
PMID: 16685056 Free Article
 
Abstract
 
BACKGROUND:
 
Oral cancer ranks as the seventh most common form of cancer worldwide. Recent reports have examined the effect of fruit and vegetable intake on the risk of oral cancer, but results are controversial.
 
OBJECTIVE:
 
A meta-analysis was performed to arrive at quantitative conclusions about the contribution of fruit and vegetable intakes to the occurrence of oral cancer.
 
DESIGN:
 
A comprehensive, systematic bibliographic search of medical literature published up to September 2005 was conducted to identify relevant studies. Separate meta-analyses were conducted for fruit and vegetable consumption. The effect of portion or daily intake of fruit or vegetables on the risk of oral cancer was calculated. A multivariate meta-regression analysis was performed to explore heterogeneity. This multivariate meta-regression analysis examined the effect of quality score, the type of cancers included, citrus fruit and green vegetable consumption, and the time interval for dietary recall of the studies on the role of fruit or vegetable consumption in the risk of oral cancer. The presence of publication bias was assessed with a funnel plot for asymmetry.
 
RESULTS:
 
Sixteen studies (15 case-control studies and 1 cohort study) met the inclusion criteria and were included in the meta-analysis. The combined adjusted odds ratio (OR) estimates showed that each portion of fruit consumed per day significantly reduced the risk of oral cancer by 49% (OR: 0.51; 95% CI: 0.40, 0.65). For vegetable consumption, the meta-analysis showed a significant reduction in the overall risk of oral cancer of 50% (OR: 0.50; 95% CI: 0.38, 0.65). The multivariate meta-regression showed that the lower risk of oral cancer associated with fruit consumption was significantly influenced by the type of fruit consumed and by the time interval of dietary recall.
 
CONCLUSION:
The consumption of fruit and vegetables is associated with a reduced risk of oral cancer.

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^^^ Sorry I didn't finish your wall of text because I nearly choked on my mango when I hit

 

... since eating more fruit could otherwise simply be an indication of better education (and therefore overall rational healthy life choices) or wealth (and therefore access to other, health-promoting goods unrelated to fruit, like healthcare)...

And I realized -- whoops -- I'm both stupid and poor, yet I eat a shit ton of sweet delicious fruit. And my triglycerides are insanely low: 17.

 

I could totally renew my status as full on fruitarian (like my orangutan brothers & sisters) but I worry more about my teeth than my blood sugar levels.

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Hi Gerard, and thanks for the useful links. At some point I'm going to do a trial of a low-fat diet, and will need to eat a lot of fruit (I may adopt Dean's "banana approach") to get enough calories. Good to know that, even without exercising all the time, I likely will be able to do it without a disastrous postprandial glucose response.

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All,

 

This may not get male CR practitioners that excited, but it is an interesting new study [1] of the health benefits of fruit nonetheless.

 

Harvard researchers followed doctors participating in the Health Professionals Follow-Up Study for an average of 10 years to see how diet correlated with erectile dysfunction (ED). They found men eating more fruit, especially fruit rich in flavanones, anthocyanins, and flavones had a 14% lower risk of ED. The top five sources of these flavonoids were citrus products, blueberries, strawberries, red wine, and apples/pears, with the first two being the biggest contributors to the association.

 

According to the authors, this amount of ED risk reduction from eating fruit is similar in magnitude to the reduction resulting from 2-5 hours per week of brisk walking. In the free full text they also mention that 2-3 cups of coffee was found to be associated with a 39% reduced risk of ED!  In the previous study it wasn't clear whether it was the caffeine, the flavonoids or a combination of the two that was responsible for the ED benefit from coffee. These authors suggest it was the flavonoids, since their numbers didn't change when when coffee was controlled for.

 

These authors, and this video from Dr. Greger at NutritionFacts.org, discuss how it is likely that ED is a sign of artery dysfunction / hardening / narrowing associated with the onset and progression of cardiovascular disease, which fruit is known to help prevent.

 

So it appears worthwhile to eat more fruit, whether you are interested in your sexual potency or not.

 

Given all our discussions of the upsides (rather than just the hazards) of fruit, I've changed the title of this thread to include "..and benefits..."

 

--Dean

 

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

[1] Am J Clin Nutr. 2016 Jan 13. pii: ajcn122010. [Epub ahead of print]

 
Dietary flavonoid intake and incidence of erectile dysfunction.
 
Cassidy A(1), Franz M(2), Rimm EB(3).
 
 
BACKGROUND: The predominant etiology for erectile dysfunction (ED) is vascular,
but limited data are available on the role of diet. A higher intake of several
flavonoids reduces diabetes and cardiovascular disease risk, but no studies have 
examined associations between flavonoids and erectile function.
OBJECTIVE: This study examined the relation between habitual flavonoid subclass
intakes and incidence of ED.
DESIGN: We conducted a prospective study among 25,096 men from the Health
Professionals Follow-Up Study. Total flavonoid and subclass intakes were
calculated from food-frequency questionnaires collected every 4 y. Participants
rated their erectile function in 2000 (with historical reporting from 1986) and
again in 2004 and 2008.
RESULTS: During 10 y of follow-up, 35.6% reported incident ED. After multivariate
adjustment, including classic cardiovascular disease risk factors, several
subclasses were associated with reduced ED incidence, specifically flavones (RR =
0.91; 95% CI: 0.85, 0.97; P-trend = 0.006), flavanones (RR = 0.89; 95% CI: 0.83, 
0.95; P-trend = 0.0009), and anthocyanins (RR = 0.91; 95% CI: 0.85, 0.98; P-trend
= 0.002) comparing extreme intakes. The results remained statistically
significant after additional adjustment for a composite dietary intake score. In 
analyses stratified by age, a higher intake of flavanones, anthocyanins, and
flavones was significantly associated with a reduction in risk of ED only in men 
<70 y old and not older men (11-16% reduction in risk; P-interaction = 0.002,
0.03, and 0.007 for flavones, flavanones, and anthocyanins, respectively). In
food-based analysis, higher total intake of fruit, a major source of anthocyanins
and flavanones, was associated with a 14% reduction in risk of ED (RR = 0.86; 95%
CI: 0.79, 0.92; P = 0.002).
CONCLUSIONS: These data suggest that a higher habitual intake of specific
flavonoid-rich foods is associated with reduced ED incidence. Intervention trials
are needed to further examine the impact of increasing intakes of commonly
consumed flavonoid-rich foods on men's health.
 
PMID: 26762373
 
------------
[2] Lopez DS, Wang R, Tsilidis KK, Zhu H, Daniel CR, Sinha A. Role of
caffeine intake on erectile dysfunction in US men: results from
NHANES 2001–2004. PLoS One 2014;10:e0123547.

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Yet another study [1] (thanks to Al!) with evidence that eating lots of fruit (or nuts) isn't harmful to one's health, including liver health or triglycerides.

 

In the study researchers recruited 30 you (age ~23) healthy young men and women (avg. BMI 22) and split them into two groups. They were randomly assigned to eat either ~500g of fruit, or ~70g of nuts, per day, in between their regular meals for eight weeks. In the fruit group, this corresponds to about 7 apples per day.  They were told to keep a food diary, and reimbursed for all the extra fruit/nuts they bought during the study. 

 

Results:

  • Compliance in both groups was reported to be high. Everyone reported eating as much fruit or nuts as they were supposed to.
  • Here is the proportions of fruits the fruit group ate: bananas (38.7%), apples (19.4%) citrus fruits (14.8%), pears (8.2%), melons (3.9%), grapes (3.2%) mangos (3.0%), kiwis (2.2%), or persimmons (1.8%) with less than 1% each from pineapples or plums etc.
  • Both groups gained on average about 1.5 lbs over the 8 weeks. Not very much given the potential for something like 400-500 extra kcal/day. They clearly cut down on other foods.
  • In fact, the reported total calorie intake stayed virtually the same in the fruit group, and went up by 250kcal/day in the nut group. Apparently the nuts weren't as filling as all that fruit. But as discussed elsewhere, despite all those apparent extra calories, the mysterious missing calories in nuts meant they didn't cause much weight gain.
  • Fructose intake nearly tripled in the fruit group from (9g -> 25g / day) and halved in the nut group (12g -> 7g / day).
  • Visceral fat (the bad stuff) was close to significantly reduced in the fruit group (P = 0.17), and didn't show any sign of change in the nut group (P = 0.5)
  • LDL cholesterol was close to significantly reduced in both groups, P = 0.13 for fruit group and P = 0.11 for nut group.
  • Systolic BP was significantly reduced in the fruit group (P < 0.001), but not in the nut group.
  • Hepatic (liver) fat was unchanged in both fruit and nut groups (P = 0.44 and 0.99 respectively). This despite all the extra fructose in the fruit group, which some claim to be 'toxic' to the liver even if the source is whole fruit.
  • Triglycerides were unchanged in both fruit and nut groups (P = 0.57 and 0.20 respectively). This is the other problem people say you'll have eating too much fruit - you're triglycerides will go through the roof.
  • Fasting insulin went up some in both groups, numerically more in the nuts group, but it was only significant in the fruit group (P = 0.018 for fruit and 0.14 for nuts).
  • The ApoB/ApoA-1 ratio (a very good predictor of cardiovascular risk [2]) improved in the fruit group only (p = 0.041 vs. p = 0.33).

Admittedly it's a small study, but the most important takeaway message for me is that adding lots of extra fruit to one's diet (and displacing other stuff), doesn't harm the liver or raise triglycerides in healthy people, normal weight people, despite all the extra fructose.

 

--Dean

 

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

[1] PLoS One. 2016 Jan 20;11(1):e0147149. doi: 10.1371/journal.pone.0147149. eCollection 2016.

 

A Randomized Study of the Effects of Additional Fruit and Nuts Consumption on Hepatic Fat Content, Cardiovascular Risk Factors and Basal Metabolic Rate.

 

Agebratt C, Ström E, Romu T, Dahlqvist-Leinhard O, Borga M, Leandersson P, Nystrom FH.

PMID: 26788923

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0147149
http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0147149&representation=PDF

 

Abstract

BACKGROUND:

Fruit has since long been advocated as a healthy source of many nutrients, however, the high content of sugars in fruit might be a concern.

OBJECTIVES:

To study effects of an increased fruit intake compared with similar amount of extra calories from nuts in humans.

METHODS:

Thirty healthy non-obese participants were randomized to either supplement the diet with fruits or nuts, each at +7 kcal/kg bodyweight/day for two months. Major endpoints were change of hepatic fat content (HFC, by magnetic resonance imaging, MRI), basal metabolic rate (BMR, with indirect calorimetry) and cardiovascular risk markers.

RESULTS:

Weight gain was numerically similar in both groups although only statistically significant in the group randomized to nuts (fruit: from 22.15±1.61 kg/m2 to 22.30±1.7 kg/m2, p = 0.24 nuts: from 22.54±2.26 kg/m2 to 22.73±2.28 kg/m2, p = 0.045). On the other hand BMR increased in the nut group only (p = 0.028). Only the nut group reported a net increase of calories (from 2519±721 kcal/day to 2763±595 kcal/day, p = 0.035) according to 3-day food registrations. Despite an almost three-fold reported increased fructose-intake in the fruit group (from 9.1±6.0 gram/day to 25.6±9.6 gram/day, p<0.0001, nuts: from 12.4±5.7 gram/day to 6.5±5.3 gram/day, p = 0.007) there was no change of HFC. The numerical increase in fasting insulin was statistical significant only in the fruit group (from 7.73±3.1 pmol/l to 8.81±2.9 pmol/l, p = 0.018, nuts: from 7.29±2.9 pmol/l to 8.62±3.0 pmol/l, p = 0.14). Levels of vitamin C increased in both groups while Alpha-tocopherol/cholesterol-ratio increased only in the fruit group.

CONCLUSIONS:

Although BMR increased in the nut-group only this was not linked with differences in weight gain between groups which potentially could be explained by the lack of reported net caloric increase in the fruit group. In healthy non-obese individuals an increased fruit intake seems safe from cardiovascular risk perspective, including measurement of HFC by MRI.

 

-----------

[2] Clin Chem Lab Med. 2004;42(12):1355-63.

 

The apoB/apoA-I ratio is better than the cholesterol ratios to estimate the
balance between plasma proatherogenic and antiatherogenic lipoproteins and to
predict coronary risk.

 

Walldius G(1), Jungner I, Aastveit AH, Holme I, Furberg CD, Sniderman AD.

 

Author information:
(1)King Gustaf V Research Institute, Karolinska Institute, Stockholm, Sweden.

 

BACKGROUND: The apolipoprotein B (apoB)/apoA-I ratio represents the balance of
proatherogenic and antiatherogenic lipoproteins. The purpose of this study was to
determine whether the apoB/apoA-I ratio was superior to any of the cholesterol
ratios - total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C),
low-density lipoprotein cholesterol (LDL-C)/HDL-C and non-HDL-C/HDL-C - in
predicting the risk of coronary disease. Moreover, we examined whether any
lipids, lipoproteins or cholesterol ratios add significant predictive information
beyond that provided by the apoB/apoA-I ratio.
METHODS: Plasma lipids, lipoproteins, apoB, and apoA-I were measured in 69,030
men and 57,168 women above 40 years of age. After a mean follow-up of 98 months,
1183 men and 560 women had died from a myocardial infarction in this prospective
apolipoprotein-related mortality risk (AMORIS) study.
RESULTS: High apoB and a high apoB/apoA-I ratio were strongly related to
increased coronary risk, while high apoA-I was inversely related to risk. The
apoB/apoA-I ratio was superior to any of the cholesterol ratios in predicting
risk. This advantage was most pronounced in subjects with LDL-C levels <3.6
mmol/l. Addition of lipids, lipoproteins or any cholesterol ratio to apoB/apoA-I
in risk models did not further improve the strong predictive value of
apoB/apoA-I.
CONCLUSIONS: These results indicate that the apoB/apoA-I ratio is at present the
best single lipoprotein-related variable to quantitate coronary risk. Given the
additional advantages apolipoproteins possess - fasting samples are not required,
apoB/apoA-I is a better index of the adequacy of statin therapy than LDL-C, and
the measurement of apoB and apoA-I are standardized, whereas LDL-C and HDL-C are
not - there would appear to be considerable advantage to integrating
apolipoproteins into clinical practice.

 

PMID: 15576296

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