Tag Archives: Fruit

A 15 minute interview with Bill Faloon and Michael Lustgarten

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On a Paleo Diet? Not if your fiber intake is less than…

Do you think Paleo diets involve eating mostly meat? While how much meat was eaten in that era is debatable, what is known is that they ate a lot of high-fiber fruits and vegetables. Shown below are the estimated daily fiber and energy intake (Eaton et al. 1997). On a 3000 calorie diet it’s estimated that those who lived in the Paleo era consumed 104 g fiber/day. That translates into 3.3 g fiber per 100 calories.

paleo fiber

Do you consider yourself a Paleo eater? If so, do you get that much fiber? For example, I average 2200 calories per day. Based on the estimated Paleo fiber intake of 3.3g fiber/100 calories, I should average 66g or more dietary fiber per day. As shown below, my 7-day average for fiber intake is 94g/day.

myfiber

If you’re interested, please have a look at my book!

Reference:

Eaton SB, Eaton SB 3rd, Konner MJ. Paleolithic nutrition revisited: A twelve-year retrospective on its nature and implications. Eur J Clin Nutr. 1997 Apr;51(4):207-16.

Is Dietary Fiber Associated with Reduced Mortality?

In an earlier I post I hypothesized that gut bacteria may be involved in mechanisms that affect lifespan. Because gut bacteria ferment dietary fiber to make short chain fatty acids such as butyrate, which may be involved in processes that mediate lifespan, investigation of large-scale epidemiological studies about the association between dietary fiber intake with all-cause mortality would be a good way to test this hypothesis. While this post won’t summarize all of the studies that relate fiber intake to mortality risk, in future posts I will sequentially investigate all the studies that have examined this association.

The Dietary National Institutes of Health-AARP Diet and Health Study (Park et al. 2011) included 567,169 men and women, aged 50–71 years who provided dietary intake data for a 9-year period. Dietary intakes were assessed with a self-administered 124 item food frequency questionnaire.

Compared with the lowest dietary fiber intake (13g in men, 11g in women), death from all causes was reduced by 22%, when compared with those with the highest intake (29g in men, 26g in women). So, the answer is to eat more fiber! I should say it’s easy to get 30 grams of fiber/day. That’s pretty close to my breakfast, which includes 100g of flaxseed, 35g yacon and ~90g of medjool dates.

Which dietary component was associated with this reduced risk, fiber from grains, fruits, vegetables or beans? Relative risk (including 95% confidence intervals) for men is shown in Table 1.

Grains Fiber Mortality Table 1

In comparison with the lowest grain fiber intake, those with the highest intake had significantly reduced risk of 23%, 23%, 17%, 52% and 26% death from all causes, cardiovascular disease, cancer, infectious diseases and, respiratory diseases, respectively. In women, fiber from grains significantly reduced mortality risk for each of these categories by 17-28%, with the exception of deaths from infectious disease. So, for the Paleo types who say don’t eat whole grains, the evidence doesn’t support that idea!

In Table 2 we see that fiber from fruits was not significantly associated with reduced mortality risk for any outcome. Does that mean don’t eat fruit? No. Fruit intake is well documented to be associated with improved health, so other components besides fruit fiber are likely involved.

Fruit Fiber Mortality Table 2

What about mortality risk for fiber from vegetables (Table 3)?

Vegetable Fiber Mortality Table 3

In men, compared with the lowest vegetable fiber intake, those with the highest vegetable fiber intake had 5% and 8% significantly reduced all-cause mortality risk and, cancer deaths, respectively. In women, all-cause mortality was significanty reduced by 5%, whereas respiratory disease deaths were reduced by 28%.

The association between fiber from beans with mortality risk is shown in Table 4.

Beans Fiber Mortality Table 4

Fiber from beans was not associated with reduced mortality risk for any outcome in men, but, all-cause, CVD, cancer and infectious disease deaths were significantly reduced by 13%, 17%, 3% and 41%, respectively in women.

The take home message? Eat more fiber!

If you’re interested, please have a look at my book!

References:

Park Y, Subar AF, Hollenbeck A, Schatzkin A. Dietary fiber intake and mortality in the NIH-AARP diet and health study. Arch Intern Med. 2011 Jun 27;171(12):1061-8.

 

High Fructose Corn Syrup, Fruit and Health: A Perspective

Consumption of high fructose corn syrup (HFCS) has been linked to a variety of adverse health conditions, including non-alcoholic fatty liver disease, type II diabetes, increased blood pressure, dislipidemia (i.e. decreased good cholesterol, HDL), and obesity (Nseir et al. 2010).

So, consumption HFCS is not good for health. But, I’d like to add a bit of perspective: the main sugar found in fruit is fructose! Is it possible to suffer from the same adverse metabolic effects by eating too much fruit? How much fruit would one have to consume to reach the levels of fructose found in soda?

One 20 oz. soda contains 240 calories and 65 g sugar. All of this sugar comes from HFCS, which is 55% fructose. To determine the amount of fructose in soda, we multiply 65 grams by 0.55, to obtain 35.75 grams of fructose.

How much fructose is contained within fruit? When normalized to the same amount of calories as a 20 oz. soda, bananas contain 16.4 g of fructose; strawberries, 20.1 g; cherries, 20.8 g; blueberries, 21.2 g; oranges (navels), 21.6 g; peaches, 24.0 g; raisins, 24.0 g; pears 27.4 g; grapes, 28.6 g; apples, 32.0 g. So, we see that most fruits, with the exception of apples contain about 10 grams less fructose than that found in a 20 oz. soda.

If you’re worried about the adverse metabolic effects from eating too much fructose, I suggest, upon your next visit to the doctor to pay close attention to your blood test results. If your triglycerides are higher than 60 mg/dL, if your HDL is low (~40 µM), and if you have liver enzyme (ALT and AST) readings higher than 20 U/L, cutting down fructose containing foods would be a good idea.

If you’re interested, please have a look at my book!

References:

Fructose values determined via http://www.nal.usda.gov/fnic/foodcomp/search/

Nseir W, Nassar F, Assy N. Soft drinks consumption and nonalcoholic fatty liver disease. World J Gastroenterol. 2010 Jun 7;16(21):2579-88.

Raw Vegan vs. Vegan: Which Diet is Best for Optimal for Health?

In a previous article I wrote about how vegans have been shown to have decreased risk of heart disease, cancer, and all-cause mortality. In addition, in 3 separate articles I’ve written about how cooking food at high temperature (above boiling, 212ºF), whether it is roasting, baking, frying or grilling produces molecules that have been shown to shorten lifespan (AGE products), and, that cause cancer in rodents (both acrylamide and furan). Collectively these data indicate that a vegan diet without cooking any of the food at high temperature is optimal for health. However, within the confines of a vegan diet, which is best for health, raw, or raw plus boiled? In this article, I will discuss why a purely raw food diet is not optimal for health.

In short, the reason is because of fructose. Fructose isn’t only found in HFCS, it’s also the main sugar found in fruit. Raw food diets consist of nuts, seeds, fruit and vegetables. However, on a 80-10-10 diet, in which nuts are rarely used, almost all of the calories will come from fruit. For example, bananas contain 27% fructose (http://ndb.nal.usda.gov/ndb/foods/list). In other words, if you eat nothing but bananas in a single day, this would be equivalent to a 27% fructose diet. And, on the fructose scale, bananas are relatively low in fructose. For example, strawberries, cherries, blueberries, oranges, peaches, pears, grapes, watermelon and apples contain 34%, 35%, 35%, 36%, 40%, 46%, 48%, 53%, 53% fructose, respectively. If you ate nothing but watermelon all day you would be on a 46% fructose diet. So, are there any adverse health effects of this amount of dietary fructose?

The answer is yes: both high and low fructose diets have been shown to elevate blood levels of triglycerides, which are a well documented risk factor for cardiovascular disease (Austin et al. 1998). On a 20% fructose diet for 5 weeks, triglycerides (20%), LDL (12%) and total cholesterol (10%) each increased (Reiser et al. 1989). In contrast, although triglycerides were not found to elevated after 4 weeks of a 20% fructose diet (compared with 3% fructose in the controls) in a separate study, both LDL and total cholesterol were significantly elevated (Swanson et. al  1992). However, evidence from 2 additional studies in humans clearly show the positive association between increased fructose intake and elevated triglycerides. Le et. al (2006) found that fructose supplemented at 1.5g/kg body weight for only 1 month was sufficient to raise blood levels of triglycerides by 36% and VLDL-triglycerides by 72%. The amount of fructose supplemented is the Le study is equivalent to 75g and 105g fructose for a 50kg and 70 kg woman and man, respectively, and can easily be obtained by eating 11-15 bananas. In addition, Faeh et. al (2005) showed that fructose supplemented at 3 grams/kg body weight increased triglycerides by 79%. This amount of supplemented fructose is equivalent to eating 22-30 bananas. In addition, these are relatively low-fructose containing diets.

In contrast, rats fed a 67% fructose diet (the control diet contained only starch) more than doubled plasma triglycerides, increased the concentration of triglycerides in liver, increased liver size, and, decreased liver copper content. The importance of copper depletion is illustrated by its role as a cofactor in the enzyme Copper-Zinc superoxide dismutase (CuZnSOD), the first line of defense against superoxide radicals located in the cytosol of all cells. Depletion of liver copper would be expected to reduce CuZnSOD activity, thereby increasing liver oxidative stress. Indeed, the concentration of lipid peroxidation products was shown to be higher in plasma, heart and urine in rats fed the high fructose diet (Busserolles et al. 2003). The good news is that an all fruit diet would never reach the 67% fructose diet found in the Busserolle study, but evidence from relatively low fructose diets (20%) still show elevations in triglycerides.

If on a raw food diet the answer is to not to eat only fruit, what should be substituted? As mentioned earlier, there is no risk of forming AGE products, acrylamide or furan when boiling food. Therefore, substitution of some amount of fruit on a raw food diet, perhaps one third to half of the total calories should come from whole grains. Boiled whole grains (with vegetables, for the added flavor) is a great way to keep your total fructose intake relatively low. To ensure no loss of nutrients during the boiling process, don’t dump the soup, drink it, it’s delicious! The tocotrienols found almost exclusively in whole grains have been shown to reduce cholesterol (Zaiden et. al 2010), to reduce inflammation (Wu et al. 2008), to reduce DNA damage (Chin et al. 2008), to reduce cancer progression (Wada et al. 2005), and are neuroprotective (Khana et al. 2003). Therefore, when substituting fruit for whole grains, you won’t be sacrificing nutrition!

From a personal experience, in 2011 I switched from a Mediterranean diet to almost exclusively raw vegan. However, my triglycerides, which have never been higher than 60 mg/dL jumped from 40 mg/dL in 2011 to 90 in 2012! Nothing else changed in my routine-the supplements that I take, or how often I exercise, my body weight/composition was the same-only my diet changed. Based on this, it seems like raw plus boiled may be the path to optimal health!

If you’re interested, please have a look at my book!

References:
Austin MA, Holkanson JE, Edwards KL. Hypertriglyceridemia as a cardiovascular risk factor. Am J Cardiol 1998;81:7B-12B.

Busserolles J, Gueux E, Rock E, Demigné C, Mazur A, Rayssiguier Y. Oligofructose protects against the hypertriglyceridemic and pro-oxidative effects of a high fructose diet in rats.
J Nutr. 2003 Jun;133(6):1903-8.

Chin SF, Hamid NA, Latiff AA, Zakaria Z, Mazlan M, Yusof YA, Karim AA, Ibahim J, Hamid Z, Ngah WZ. Reduction of DNA damage in older healthy adults by Tri E Tocotrienol supplementation. Nutrition. 2008 Jan;24(1):1-10.

Faeh D, Minehira K, Schwarz J, Periasami R, Seongus P, Tappy L. Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy males. Diabetes 2005;54: 1907-13.

Khanna S, Roy S, Ryu H, Bahadduri P, Swaan PW, Ratan RR, Sen CK. Molecular basis of vitamin E action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced neurodegeneration J Biol Chem. 2003 Oct 31;278(44):43508-15.

Lê KA, Faeh D, Stettler R, Ith M, Kreis R, Vermathen P, Boesch C, Ravussin E, Tappy L. A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans. Am J Clin Nutr. 2006 Dec;84(6):1374-9.

Fructose data in foods provided by http://ndb.nal.usda.gov/ndb/foods/list

Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ. Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch. Am J Clin Nutr. 1989 May;49(5):832-9.

Swanson JE, Laine DC, Thomas W, Bantle JP. Metabolic effects of dietary fructose in healthy subjects. Am J Clin Nutr. 1992 Apr;55(4):851-6.

Wada S, Satomi Y, Murakoshi M, Noguchi N, Yoshikawa T, Nishino H. Tumor suppressive effects of tocotrienol in vivo and in vitro. Cancer Lett. 2005;229:181-91.

Wu SJ, Liu PL, Ng LT. Tocotrienol-rich fraction of palm oil exhibits anti-inflammatory property by suppressing the expression of inflammatory mediators in human monocytic cells. Mol Nutr Food Res. 2008 Aug;52(8):921-9.

Zaiden N, Yap WN, Ong S, Xu CH, Teo VH, Chang CP, Zhang XW, Nesaretnam K, Shiba S, Yap YL. Gamma delta tocotrienols reduce hepatic triglyceride synthesis and VLDL secretion. J Atheroscler Thromb. 2010 Oct 27;17(10):1019-32.