4-ingredient brownies

In an earlier post, I wrote about how easy it is to make 2-ingredient, nutrient-rich chocolate (https://michaellustgarten.com/2014/09/21/homemade-chocolate-in-2-minutes/).

Occasionally (~1x/week), I modify that recipe to make 4-ingredient brownies! The recipe includes 40g of raw, organic cacao beans, 20g oats, 70g Medjool dates, and 1 large egg.

First, I grind/blend the cacao beans and oats into a pine powder. Then, I add the dates and powder into the food processor to mix them. I put this mixture into a small bowl, where I add the egg and thoroughly mix it all together. Last, I put this into the oven at 325F for 35 minutes. After it’s cooked, I wait 15 minutes for it to cool down, then I eat it. It’s soft, and delicious!


PRAL, Mortality Risk, and Lifespan

Within the body, meat, grains, and nuts are generally acid-forming, whereas vegetables and fruits are alkaline-forming. Is the distinction between whether your diet is acid- or alkaline-forming important for optimal health and lifespan? In an earlier post, I discussed the importance of PRAL (potential renal acid load) by correlating it with serum bicarbonate and mortality risk (https://michaellustgarten.com/2016/02/07/using-diet-to-optimize-circulating-biomarkers-serum-bicarbonate/).

More recent data (a 15-year study of 81, 697 older adults; average age ~61y; Xu et al. 2016) has examined the association between PRAL with risk of death from all causes. In women, acidic PRAL values ( > 0) were associated with a significantly increased risk of death from all causes, as were alkaline PRAL values (< -5.6). In addition, very acidic (~40) and very alkaline (-30) PRAL values were associated with the highest risk for all-cause mortality:


Similarly, in men, when compared with a PRAL = 0, both alkaline (PRAl < -5.6) and acidic (> 29.8) values were associated with increased all-cause mortality risk.


While this data suggests that eating too much meat, grains, and/or nuts may not be optimal for health, it also suggests that eating too much alkaline-forming food, including veggies and fruits, may also not be optimal! My high veggie-based diet yields a very negative PRAL, ~-120 (~ -0.05 PRAL units/calorie), which would seem to put me at increased all-cause mortality risk. To further investigate, I decided to look at the PRAL values of long-lived societies.

The PRAL formula, as reported by Remer and Manz (1994) is:

PRAL = (0.49 * protein intake in g/day) + (0.037 * phosphorus intake in mg/day) – (0.02 * potassium intake in mg/day) – (0.013 * calcium intake in mg/day) – (0.027 * magnesium intake in mg/day).

Life expectancy for Seventh-Day Adventist women is 85 years, a value that is the highest in the world (Fraser and Shavlik 2001). What’s the average daily PRAL value for that population?

  • Average daily dietary data in both vegetarian and non-vegetarian Seventh-Day Adventist women (average age, ~72y) has been reported (Nieman et al. 1989). For vegetarians, total calories = 1452; protein = 47g; phosphosphorus = 889 mg; potassium = 2628 mg; calcium = 628 mg; magnesium = 283 mg. These values yield an alkaline PRAL = -33.2. Because higher amounts of these nutrients can result from an increased calorie intake, it’s important to divide PRAL by the average daily calorie value, thereby yielding  PRAL/calorie. For vegetarian Adventists, this value = -0.02.
  • In non-vegetarian Adventists, total calories = 1363; protein = 55g; phosphosphorus = 892 mg; potassium = 2342 mg; calcium = 633 mg; magnesium = 228 mg. These values also yield an alkaline PRAL = -25.5, and PRAL/calorie = -0.019.

Life expectancy for those who live on the island of Okinawa is among the longest in the world (Miyagi et al. 2003). What’s the average daily PRAL value for Okinawan older adults?

  • The average daily dietary data for 75-year old Okinawans  has been reported (Willcok et al. 2007): total calories, 1785; protein, 39g; phosphosphorus, 864 mg; potassium, 5200 mg; calcium, 505 mg; magnesium, 396 mg. These values also yield an  yield a very alkaline PRAL value = -87.4, and PRAL/calorie =  -0.049. Interestingly, these values are very close to my very alkaline PRAL values of -121, and PRAL/calorie = ~-0.05!

My goal is not just to get to 75 in great health, but to live past 100 (and far beyond). What’s the data in centenarians? Unfortunately, I could only find 2 studies that included dietary data for that age group.

  • In a study of 30 Chinese centenarians (average age, 103y), daily dietary values of 1220 calories, 39g protein, 603 mg phosphorus, 1433 mg potassium, 482 mg calcium, and 355 mg magnesium were reported (Cai et al. 2016), thereby yielding an average daily PRAL value = -20.3, and PRAL/calorie = -0.017.
  • Similarly, in a larger study of 104 Japanese centenarians (average age, 100y), daily dietary values of 1137 calories, 44g protein, 676 mg phosphorus, 1695 mg potassium, 414 mg calcium, and 154 mg magnesium were reported (Shimizu et al. 2003), thereby yielding an average daily PRAL value = -16.3, and PRAL/calorie = -0.014.

In contrast to the data of Xu et al. (2016), these data suggest that an alkaline diet may indeed be optimal for lifespan.

So what’s your dietary PRAL value?

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


Cai D, Zhao S, Li D, Chang F, Tian X, Huang G, Zhu Z, Liu D, Dou X, Li S, Zhao M, Li Q.  Nutrient Intake Is Associated with Longevity Characterization by Metabolites and Element Profiles of Healthy Centenarians. Nutrients. 2016 Sep 19;8(9).

Fraser GE, Shavlik DJ. Ten years of life: Is it a matter of choice? Arch Intern Med. 2001 Jul 9;161(13):1645-52.

Miyagi S, Iwama N, Kawabata T, Hasegawa K. Longevity and diet in Okinawa, Japan: the past, present and future. Asia Pac J Public Health. 2003;15 Suppl:S3-9.

Nieman DC, Underwood BC, Sherman KM, Arabatzis K, Barbosa JC, Johnson M, Shultz TD. Dietary status of Seventh-Day Adventist vegetarian and non-vegetarian elderly women. J Am Diet Assoc. 1989 Dec;89(12):1763-9.

Remer T, Manz F. Estimation of the renal net acid excretion by adults consuming diets containing variable amounts of protein. Am J Clin Nutr. 1994;59:1356-1361.

Shimizu K, Takeda S, Noji H, Hirose N, Ebihara Y, Arai Y, Hamamatsu M, Nakazawa S, Gondo Y, Konishi K. Dietary patterns and further survival in Japanese centenarians. J Nutr Sci Vitaminol (Tokyo). 2003 Apr;49(2):133-8.

Willcox BJ, Willcox DC, Todoriki H, Fujiyoshi A, Yano K, He Q, Curb JD, Suzuki M. Caloric restriction, the traditional Okinawan diet, and healthy aging: the diet of the world’s longest-lived people and its potential impact on morbidity and life span. Ann N Y Acad Sci. 2007 Oct;1114:434-55.

Xu H, Åkesson A, Orsini N, Håkansson N, Wolk A, Carrero JJ. Modest U-Shaped Association between Dietary Acid Load and Risk of All-Cause and Cardiovascular Mortality in Adults. J Nutr. 2016 Aug;146(8):1580-5.

Using Diet to Optimize Circulating Biomarkers: Serum Bicarbonate

In an earlier post, I wrote about the association between biomarkers of systemic acid-base balance (serum bicarbonate, the anion gap, urinary pH) with all-cause mortality risk (https://michaellustgarten.com/2015/08/28/serum-bicarbonate-and-anion-gap-whats-optimal/). Based on these data, systemic acidity may not be optimal for health and longevity, when compared with more alkaline values. Can circulating acid-base biomarkers be optimized through diet?

One way to optimize serum bicarbonate is with a low dietary PRAL (potential renal acid load). For a given food, PRAL is a measure of how much acid or base that the kidney will see. In subjects with normal kidney function (or with chronic kidney disease, CKD), a low dietary PRAL (alkaline-forming) is associated with high serum bicarbonate, whereas a high dietary PRAL (acid-forming) is associated with reduced serum bicarbonate (Ikizler et al. 2015):

bicarb pral

So how can we achieve a low dietary acid intake (low PRAL), with the goal of increasing serum bicarbonate? The answer is to abundantly consume foods with a low PRAL (vegetables), while minimizing foods with a high PRAL (animal products, grains). Let’s have a look at the PRAL values for several food groups (Remer and Manz, 1995):

All of the meat and meat products shown below have acid-forming, positive PRAL values:

PRAL meat

Similarly, fish have acid-forming, positive PRAL values:

fish pral

While PRAL values for milk, dairy, and eggs are generally acid-forming, there is a wider range, compared with meat and fish. For example, parmesan and cheddar cheese have high PRAL values (34.2, 26.5, respectively), whereas milk and yogurt have PRAL values ~1:

dairy pral

Grains are similar to animal products in terms of their PRAL values:

grain pral

In contrast, all of the vegetables on the list below have very low, alkaline-forming PRAL values. The All-Star for a low PRAL is spinach (-14):
veg pral

Similarly, most fruits have alkaline forming, low PRAL values. Although raisins seem to be the PRAL All-Star, their data (and all of the other foods on the list) are based on 100g (299 calories for raisins). For an equivalent amount of calories for strawberries, their PRAL equates to -20.6, which is similar to the raisin PRAL. Also included on the list are nuts, which contain a range of PRAL values from negative (hazelnuts) to positive (walnuts, peanuts):

fruit pral

What’s my dietary PRAL? To determine that, it’s first important to define the PRAL equation: PRAL = (0.49 * protein intake in g/day) + (0.037 * phosphorus intake in mg/day) – (0.02 * potassium intake in mg/day) – (0.013 * calcium intake in mg/day) – (0.027 * magnesium intake in mg/day; Remer and Manz, 1994). Using my latest 7-day average dietary data yields a very low, alkaline-forming PRAL, -121.9: (protein, 88g; phosphorus, 2038 mg; potassium, 9868 mg; calcium, 1421 mg; magnesium, 901 mg)! It’s important to note that the major contributor to my very low PRAL value comes from the potassium term. Because of my abundant vegetable intake, my potassium intake is very high, resulting in a highly alkaline PRAL. Considering that PRAL values of -40 were associated with serum bicarbonate values of ~28, my serum bicarbonate value of 31 on my last blood test (8/2015) may in part be explained by my very low dietary PRAL value, -121.9.

Another measure of dietary acid load is NEAP (net endogenous acid production). In subjects with normal (and reduced, CKD) kidney function, a high NEAP diet (acid-forming) is associated with reduced serum bicarbonate, whereas a low NEAP diet (alkaline-forming) is associated with higher serum bicarbonate values (Ikizler et al. 2015):

neap bicarb

NEAP is more easily calculated than PRAL-all you need to know are your dietary protein and potassium intakes: NEAP = (54.5 * protein intake in grams/day)/(potassium intake in mEq/day) -10.2 (Frassetto et al. 1999). To convert your daily potassium intake from mg to mEq, divide by 39.1. Using my 7-day average protein and potassium intake data yields a NEAP = (54.5 * 88)/(9868/39.1) – 10.2 = 8.8. Based on the plot above for NEAP vs. serum bicarbonate, that again puts me on the far left, which is associated with serum bicarbonate values greater than 28.

Collectively, eating more potassium-rich vegetables will reduce PRAL and NEAP, which is associated with systemic alkalinity, as measured by an elevated serum bicarbonate. Because high serum bicarbonate levels are associated with reduced all-cause mortality risk, this may be an important strategy for improving health and longevity!

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


Frassetto LA, Todd KM, Morris RJC, Sebastian A. Estimation of net endogenous noncarbonic acid production in humans from diet potassium and protein contents. Am J Clin Nutr. 1998;68:576-583.

Ikizler HO, Zelnick L, Ruzinski J, Curtin L, Utzschneider KM, Kestenbaum B, Himmelfarb J, de Boer IH. Dietary Acid Load Is Associated With Serum Bicarbonate but not Insulin Sensitivity in Chronic Kidney Disease. J Ren Nutr. 2016 Mar;26(2):93-102.

Remer T, Manz F. Estimation of the renal net acid excretion by adults consuming diets containing variable amounts of protein. Am J Clin Nutr. 1994;59:1356-1361.

Remer, T. and Manz, F. Potential renal acid load of foods and its influence on urine pH. Journal of the American Dietetic Association 1995 ;95(7), 791-797.

Total Cholesterol: What’s Optimal For Longevity?

On my latest blood test (August 2015), my total cholesterol was 127 mg/dL-is that value optimal for health and longevity?

Based on data for 1,104,294 men younger than 60y (median age, 40y) that were followed for up to 14 years (Fulks et al. 2009), my 127 mg/dL value (1 – 2.4%) puts me relatively close to maximally reduced all-cause mortality risk, which occurs at 146-158 mg/dL (5-9% on the graph below):

c hdl mort

But what about the data for men older than 60?

In a 10-year study of 2,277 older adults (average age, ~77y), total cholesterol levels less than 175 mg/dL were associated with ~2-fold higher risk of all-cause mortality, compared with values greater than 226 mg/dL (Schupf et al. 2005):

tc less 175 acm

Similarly, in a 10-year study of even older adults (median age, 89y; 724 subjects), all-cause mortality risk was significantly increased in subjects with total cholesterol values less than 193 mg/dL (dark black line below), compared with values greater than 251 mg/dL (dashed line; Weverling-Rijnsburger et al. 1997). In addition, subjects with cholesterol values greater than 251 mg/dL lived ~2 years longer than those with values less than 191 mg/dL. So higher cholesterol in very old adults…increased lifespan! Does that mean I should alter my dietary approach to increase my circulating cholesterol levels after I reach 60?

chol 89y mort.png

To address that issue, it’s important to understand why cholesterol increases during aging. One possible mechanism involves the role of cholesterol in immune defense against infectious agents (bacteria, viruses, parasites, etc.). Obviously, our immune system is supposed to eliminate these pathogens, but immune function decreases with age (Targonski et al. 2007). As a compensatory mechanism, cholesterol can protect against infectious agents. For example, LDL cholesterol binds to and partially inactivates Staphylococcus aureus (Bhakdi et al. 1983). Staphylococcus aureus infection increases during aging, as its incidence rate is ~3-fold higher in adults older than 60y, when compared with younger subjects (Laupland et al. 2008). In addition, LDL cholesterol inhibits bacterial endotoxin (Weinstock et al. 1992), whose presence in the blood increases during aging (Ghosh et al. 2015). In support of the link between circulating cholesterol with infectious agents, in the older adults of Weverling-Rijnsburger et al. (1997), cholesterol values greater than 251 mg/dL (solid black line) were associated with significantly decreased infectious disease-related mortality, when compared with values less than 193 mg/dL:

infect mort

So if we’re better able to keep infectious agents out of our blood, that would be expected to reduce the need for elevated circulating cholesterol during aging. How can we do that?

One approach involves increased dietary fiber. Fermentation of dietary fiber by gut bacteria produces short-chain fatty acids, which improve gut barrier function (Chen et al. 2013), and decrease cholesterol synthesis (Wright et al. 1990). However, older adults do not eat high-fiber diets, as values of only ~19g/day have been reported (Lustgarten et al. 2014). In contrast, dietary fiber intakes greater than only 29g/day are associated with less infectious disease (and all-cause mortality) risk (Park et al. 2011). So definitely eating at least 29g fiber/day is important, but is that amount optimal to minimize the need for elevated cholesterol during aging?

In a 2-week study of the role of dietary fiber on circulating cholesterol, subjects that ate only 10g fiber/1000 calories did not significantly reduce their baseline total cholesterol values from ~182 mg/dL (Jenkins et al. 2001). In contrast, a dietary fiber intake of 19g/1000 calories reduced baseline total cholesterol from 185 to 150 mg/dL, and subjects that ate even more fiber than that, 55g/1000 calories reduced their total cholesterol values from ~182 to 142 mg/dL, a drop that was also significantly different compared with the 19g fiber/1000 calorie group.

Collectively, these data suggest that to maximally boost gut barrier function, thereby minimizing circulating infectious agents and the need for elevated circulating cholesterol during aging, a very-high fiber-diet may be important. Accordingly, my average daily fiber intake is ~100 g/day on a 2300 calorie diet, resulting in ~43g fiber/1000 calories. Based on this, I don’t expect for my total cholesterol values to change during aging, as my gut barrier function will be optimal, and infectious agents in my blood will be minimized.

To add some specificity to this approach, 2 additional measurements may be important: serum albumin and HDL cholesterol. In agreement with the studies of Weverling-Rijnsburger et al. and Schupf et al., in a 5-year study of 4,128 older adults (average age, ~79y), those with total cholesterol values less than 160 mg/dL had significantly higher all-cause mortality risk, compared with values greater than 240 mg/dL (Volpato et al. 2001):

low tc mortl

However, when considering subjects’ albumin and HDL cholesterol levels, the differential mortality risk was abolished. Subjects that had low total cholesterol but also high (within-range) albumin and HDL had improved survival compared to the higher cholesterol groups:

adj tc mort for alb hdl

If your total cholesterol values are less than 160 mg/dL, what serum albumin and HDL values should you shoot for? As shown below, albumin levels greater than 38 g/L and HDL values greater than 47 mg/dL were associated with maximally reduced all-cause mortality risk in subjects with total cholesterol values less than 160 mg/dL (Volpato et al. 2001):


My albumin values are consistently between 46-48 g/L, but during recent measurements my HDL levels have been lower than optimal (35 mg/dL on 8/2015). The good news is that I was able to increase my HDL from 28 (7/2013 measurement) to 35 mg/dL by adding ~4 oz of fish every day! To further increase my HDL, I’ve doubled my fish oil intake (~3.3 g of combined EPA + DHA per day, from 5-9 g of cod liver oil). I’ll test the effect of this on my circulating biomarkers in a couple of months, so stay tuned!

3/23/2016 Update: Because of concerns that the pre-formed Vitamin A (that is found in cod liver oil) may negate the potential health-promoting effects of optimal Vitamin D levels (Schmutz et al. 2016), I stopped taking cod liver oil during the 3-month period that preceded my latest blood test (3/23/2016). However, I was able to increase my HDL from 35 to 53 mg/dL! I attribute this increase to the daily inclusion of ~60g/walnuts per day. In doing that, although I only replaced ~200 calories from carbohydrates with fat, lower carbohydrate diets have been shown to increase HDL (Manor et al. 2016).

Nonetheless, in terms of the all-cause mortality data that includes total cholesterol (137 mg/dL), albumin (51 g/L), and HDL (53 mg/dL), based on my latest blood test results, my risk is now maximally low!

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


Bhakdi S, Tranum-Jensen J, Utermann G, Füssle R. Binding and partial inactivation of Staphylococcus aureus alpha-toxin by human plasma low density lipoprotein. J Biol Chem. 1983 May 10;258(9):5899-904.

Chen H, Mao X, He J, Yu B, Huang Z, Yu J, Zheng P, Chen D. Dietary fibre affects intestinal mucosal barrier function and regulates intestinal bacteria in weaning piglets. Br J Nutr. 2013 Nov;110(10):1837-48.

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.

Fulks M, Stout RL, Dolan VF. Association of cholesterol, LDL, HDL, cholesterol/ HDL and triglyceride with all-cause mortality in life insurance applicants. J Insur Med. 2009;41(4):244-53.

Ghosh S, Lertwattanarak R, Garduño Jde J, Galeana JJ, Li J, Zamarripa F, Lancaster JL, Mohan S, Hussey S, Musi N. Elevated muscle TLR4 expression and metabolic endotoxemia in human agingJ Gerontol A Biol Sci Med Sci. 2015 Feb;70(2):232-46.

Jenkins DJ, Kendall CW, Popovich DG, Vidgen E, Mehling CC, Vuksan V, Ransom TP, Rao AV, Rosenberg-Zand R, Tariq N, Corey P, Jones PJ, Raeini M, Story JA, Furumoto EJ, Illingworth DR, Pappu AS, Connelly PW. Effect of a very-high-fiber vegetable, fruit, and nut diet on serum lipids and colonic function. Metabolism. 2001 Apr;50(4):494-503.

Laupland KBRoss TGregson DBStaphylococcus aureus bloodstream infections: risk factors, outcomes, and the influence of methicillin resistance in Calgary, Canada, 2000-2006. J Infect Dis. 2008 Aug 1;198(3):336-43.

Lustgarten MS, Price LL, Chalé A, Fielding RA. Metabolites related to gut bacterial metabolism, peroxisome proliferator-activated receptor-alpha activation, and insulin sensitivity are associated with physical function in functionally-limited older adults. Aging Cell. 2014 Oct;13(5):918-25.

Mansoor N, Vinknes KJ, Veierød MB, Retterstøl K. Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials. Br J Nutr. 2016 Feb;115(3):466-79.

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.

Schmutz EA, Zimmermann MB, Rohrmann S. The inverse association between serum 25-hydroxyvitamin D and mortality may be modified by vitamin A status and use of vitamin A supplements. Eur J Nutr. 2016 Feb;55(1):393-402.

Schupf N, Costa R, Luchsinger J, Tang MX, Lee JH, Mayeux R. Relationship Between Plasma Lipids and All-Cause Mortality in Nondemented Elderly. J Am Geriatr Soc. 2005 Feb;53(2):219-26.

Targonski PV, Jacobson RM, Poland GA. Immunosenescence: role and measurement in influenza vaccine response among the elderly. Vaccine. 2007 Apr 20;25(16):3066-9.

Vasto S, Scapagnini G, Rizzo C, Monastero R, Marchese A, Caruso C. Mediterranean diet and longevity in Sicily: survey in a Sicani Mountains population. Rejuvenation Res. 2012 Apr;15(2):184-8.

Volpato S, Leveille SG, Corti MC, Harris TB, Guralnik JM. The value of serum albumin and high-density lipoprotein cholesterol in defining mortality risk in older persons with low serum cholesterolJ Am Geriatr Soc. 2001 Sep;49(9):1142-7.

Weinstock C, Ullrich H, Hohe R, Berg A, Baumstark MW, Frey I, Northoff H, Flegel WA. Low density lipoproteins inhibit endotoxin activation of monocytes. Arterioscler Thromb. 1992 Mar;12(3):341-7.

Weverling-Rijnsburger AW, Blauw GJ, Lagaay AM, Knook DL, Meinders AE, Westendorp RG. Total cholesterol and risk of mortality in the oldest old. Lancet. 1997 Oct 18;350(9085):1119-23.

Wright RS, Anderson JW, Bridges SR. Propionate inhibits hepatocyte lipid synthesis. Proc Soc Exp Biol Med. 1990 Oct;195(1):26-9.

130 grams of fiber, 2400 calories

How do I eat ~100 grams of fiber, on average, every day? Here’s my full dietary breakdown from December 30, 2015:

my diet 12-30.png

Green tea is associated with reduced all-cause mortality risk (https://michaellustgarten.com/2015/10/20/drink-green-tea-reduce-and-all-cause-mortality-risk/), so I start every day with  green tea + lemon.

Then, I ate a giant salad (https://michaellustgarten.com/2015/10/09/what-i-eat-giant-salad/), consisting of pickles, lettuce, tomato, purple cabbage and corn, and topped with a blended dressing of fresh lemon, sesame seeds, cumin, jalapeño, and raw garlic.

Also on the list were sardines, which I eat every day. Snacks in between bigger meals were carrots, 1 whole red pepper, mushrooms, and a Brazil nut.

Then I ate a big bowl of broccoli topped with cherry tomatoes. I added mustard powder after the broccoli and tomatoes were done cooking (~10 minutes), because broccoli’s sulfurophane content decreases with cooking time (https://michaellustgarten.com/2014/08/13/restoring-boiling-induced-sulfurophane-depletion-in-broccoli-with-mustard-powder/).

At some point after that I had cod liver oil, to get my daily dose of Vitamin D and the fish oil fatty acids, EPA and DHA. I just (last week) sent my blood for analysis of my circulating Vitamin D, so I may need to increase my vitamin D intake based on what the result shows.

Next I had my beet-berry smoothie (https://michaellustgarten.com/2015/08/09/beet-berry-smoothie/).

For dinner I had my barley-veggie mix (https://michaellustgarten.com/2015/10/08/what-i-eat-barley-cauliflower-collard-tomato-celery-onion-corn-mix/), including barley, cauliflower, celery, tomato, corn, collards, onions and olive oil. Also, with an orange for dessert!

In sum, 2400 calories, 130 grams of dietary fiber, and maximal nutrition!

fiber 130

7/2017 Update: When considering the link between linoleic acid and all-cause mortality (https://michaellustgarten.com/2015/12/20/the-essential-fatty-acid-linoleic-acid-dietary-intake-and-circulating-values-whats-optimal-for-health/), Ive increased my intake of omega-6 fats, almost exclusively from walnuts, while cutting my carbohydrate intake to try to stay calorie neutral. In doing so, this change increased my HDL from 28 to ~50, while keeping my total cholesterol < 150, and LDL < 70.

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

The Essential Fatty Acid, Linoleic Acid: Dietary Intake And Circulating Values, What’s Optimal For Health?

Linoleic acid (C18:2, n-6) is an essential fatty acid that must be obtained from the diet, because  our body can’t make it. How much linoleic acid should we eat every day for optimal health? To answer this question, I’ll investigate the association between circulating levels of linoleic acid with all-cause mortality risk, followed by identification of a corresponding dietary intake. Let’s have a look!

First, are circulating levels of linoleic acid associated with all-cause mortality risk? 4 studies have investigated this issue:

  • In a 15-year study of 1,551 middle-aged men (average age, 52y), increased circulating linoleic acid was associated with significantly reduced all-cause mortality risk in 3 of the 4 multivariable-adjusted models (Laaksonen et al. 2005).
  • In a 15-year study of 4,232 older adults (60y) elevated circulating linoleic acid was associated with significantly reduced all-cause mortality risk in men, but not women (Marklund et al. 2015).
  • In a 34-year study of 2,009 middle-aged men (average age, 50y) increased circulating linoleic acid was associated with significantly decreased risk of all-cause mortality (Warensjö et al. 2008). For example, shown below is the association between the risk of death from cardiovascular-related disease with the circulating linoleic acid concentration. At both 20 and 30 years after study onset, subjects that had circulating linoleic values above the median had approximately half of the mortality risk from CVD, when compared with below-median values for linoleic acid.

LA CVD mortality

  • In a 13-year study that included both older men and women (average age, 74y), and, more subjects (2,792) than the studies of Laaksonen and Warensjöet combined, plasma phospholipid percentages of linoleic acid greater than ~21-24% were associated with significantly reduced all-cause mortality risk:

LA total mort

Colectively, these 4 studies show that increased circulating levels of linoleic acid are associated with reduced all-cause mortality risk. How much linoleic acid should we eat to achieve optimal circulating values? In other words, what dietary intake of linoleic acid corresponds to 21%+ of plasma phospholipid linoleic acid? Based on the data below, dietary intakes of linoleic acid that are greater than 14% of total calories are associated with circulating linoleic acid values of 21% (Wu et al. 2014).

LA dietary in PL

On my ~2300 calorie diet, that translates into 322 calories (36g) from linoleic acid. I get a significant amount of dietary linoleic acid from one of the best linoleic acid food sources, walnuts, which contain 5.8 grams of linoleic acid per 100 calories (see Lipids, C18:2, http://ndb.nal.usda.gov/ndb/foods/show/3690?fg=&man=&lfacet=&count=&max=&qlookup=&offset=&sort=&format=Full&reportfmt=other&rptfrm=&ndbno=&nutrient1=&nutrient2=&nutrient3=&subset=&totCount=&measureby=&_action_show=Apply+Changes&Qv=.152&Q6919=1&Q6920=1&Q6921=1&Q6922=1&Q6923=1&Q6924=1).

Just using walnuts alone, I’d need ~700 calories per day to reach 14% dietary linoleic acid! Although I’m always interested in dietary strategies that may reduce all-cause mortality risk, allocating ~30% of my daily calories to only walnuts is not ideal for my high-fiber approach to health (https://michaellustgarten.com/2015/07/17/on-a-paleo-diet-not-if-you-fiber-intake-is-less-than/), nor would it satiate me, as high-volume vegetable meals are best for that. A more reasonable dietary linoleic acid target (for now) is ~8%, the point at which plasma linoleic acid mostly plateaus (see the plot above). 8% on my 2300 calorie diet translates into 20 grams of linoleic acid per day. I should note that I also get a good amount of linoleic acid (6.4 grams) from the 30 grams of sesame seeds that goes into my giant salad’s dressing, which I eat 2-3x per week. When combined with ~300 calories from walnuts/day, that gets me to at least 8% of my daily calories from linoleic acid.

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


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