Thursday, August 15, 2019

The Nutri-Dex!

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Nutrient Density Scoring: The essential nutrient yields of over 700 foods are ranked and adjusted for bioavailability, nutrient absorption capacity, and metabolic conversion capacity.

Specialized Nutrition Scoring: Figure out the right foods for you with 30 different nutrition scores that stratify foods by a number of different dietary goals (low carb, low FODMAP, etc).

Custom Nutrition Scoring: Use the included Custom Score tab to help create your own personal nutrition score to plan your own ideal diet.

Diverse Nutrition Data: Custom-tailor your diet with in-depth nutrition data, including oxalates, phytates, glycemic index, glycemic load, satiety, FODMAPs, PCDAAS, price, shelf life, and over 500 polyphenolic compounds.

Food Toxicity Profiles: Avoid toxicities from nutrients and other compounds with the included toxicity profile data.

Vegan-Friendly Categorization: Use the included vegan-friendly categorization to help you navigate through the best vegan options.

Keto-Friendly Categorization: Use the included keto-friendly categorization to help you navigate through the best keto options.

Nutrient Ratio Data: Keep everything in balance with seven different nutrient ratio scores, including omega-3/omega-6, vitamin E/PUFA, and more.

Grocery List: Keep expenses in check with an interactive grocery list that can intelligently estimate the cost of your grocery trip.

Nutrition Analyser: Use the included nutrition analyser to quantify the nutrient content of your food selection, and minimize anti-nutrients, hunger, calories, sugar, and more!

Meal Schedule: Schedule your meals and workouts, as well as calculate your calorie and macro requirements based on your goals and body composition!
Regular Updates: The Nutri-Dex is also regularly updated with new foods and nutrition data!

*Disclaimer: The information contained herein does not constitute medical advice and is for educational purposes only. Please consult with your physician before starting any new dietary protocol.

The Backstory!

It all started when I lost my job in May, 2019. I had to figure out how I could continue to target nutrient density (ND), but also integrate a cost-saving approach to my diet. Initially, while searching for a resource that could answer my question, I was directed to Efficiency Is Everything. They take some nutrition data and stratify foods by rank divided by cost. However, their approach lacks the nuance and personalization that I would have preferred. For example, their analyzes routinely suggest that white flour, breads, and pastries come out on the top of almost every score. While it may be true that these foods provide the most nutrition for the least money, these aren't healthy foods in my estimation. They're not healthy for reasons unrelated to their nutrient content. A healthy diet has a place for those foods, absolutely. But a healthy diet is not characterized by those foods. I just didn't find their resource terribly useful for my goals.

Essentially, I wanted to stratify my most preferred foods by ND, divide it by prices relevant to my region, dust my hands off, and call it a day. Partially inspired by Mat Lalonde's AHS12 talk Nutrient Density: Sticking to the EssentialsI started by making a short list of foods that I typically eat, and sort of eyeballed their nutritional content in a nutrition-tracking tool called Cronometer. I had about 75 foods on the original list, if I recall correctly. Using a really clumsy point-system that wasn't super accurate, I assigned a score to each food on my list. The approach wasn't very sophisticated, but it didn't need to be⁠—the spreadsheet was just going to be for my own personal use, so I didn't care if the numbers weren't arrived at using the most objective methods possible.

For price data, I took some time to go through the online inventories of several large grocery stores here in Winnipeg. My primary sources were Real Canadian Superstore, Save-On-Foods, FreshCoWalmart, and Bulk Barn. Some price data was unavailable online, and I was actually required to take a few trips to a couple of different specialty stores. Weirder things like beef tongue and rabbit aren't commonly sold at big-box grocery stores (though I did find some cow aorta at FreshCo). So it took a while to compile this data, and it is likely most applicable to people living in my region. I don't suspect that the price of salmon is the same in Seattle, for example.

I essentially got what I wanted. In the end I had a list of foods, some rough approximation of their nutritional content, a list of prices, and a column that divided one by the other. But I wasn't quite ready to dust my hands off just yet. It had come to my attention that there was an entire community on Reddit who live for this sort of thing. Their subreddit is called EatHealthyAndCheap. I figured someone might get something out of it, so I posted it. It exploded. It was one of the most heavily upvoted and heavily discussed subjects in the history of that entire subreddit. People had no shortage of questions and suggestions. I was inspired, and I listened to every suggestion and criticism.

I realized that there is massive demand for a resource like this, and people want to be able to personalize it. People want to be able to organize foods based on their own values and goals. I decided I was going to expand the spreadsheet to include more foods, more nutrition data, and more scores.
⁠ I wanted to turn this clunky piece of crap into something people could use in a very personal and practical way. I included more nutrition data, and I decided that I was actually going to generate ND scores using the most objective methods I could. I rolled my sleeves up, and I went straight to the USDA's SR28 database. This is a gigantic inventory of foods with astoundingly granular nutritional content data. 

I chopped the database down to a handful of common foods (approximately 700). I then used the database to calculate my ND scores. The scores are calculated by assigning points to foods based on how many multiples of each essential nutrient a food provides relative to each individual nutrient’s DRI. This method standardizes points across all nutrients. For example, the adult DRI for calcium is 1000mg per day. If a food provides 500mg, calcium would contribute 0.5 points to the food’s score. The results for every essential nutrient in a food are summed to generate the final score. The scores are then normalized from 0 to 100, and a stratification of foods by ND is generated. At the top of the list we have veal liver, at a score of 100. At the bottom of the list we have coconut oil, at a score of 0. Left out of the scores were all non-essential nutrients and sodium. Added salt would unacceptably confound the data by creating artificially high scores for certain processed foods. 

The scores are also calculated to be non-linear. If a nutrient exceeds one multiple of the RDA, that nutrient's score is calculated to the power of 0.33. This favours the overall distribution of nutrients rather than allowing one single nutrient to inflate the score. For example, brazil nuts are extremely high in selenium relative to other nutrients. If the scores are calculated exactly linearly, the sheer amount of selenium inflates brazil nuts' score unreasonably high. Applying this non-linear formula dampens this effect without applying a hard cap. This way foods can still be stratified based on absolute amounts of individual nutrients, but a much larger emphasis is placed on nutrient distribution. Basically, this formula allows the score to favour the breadth of the nutrient content of a food rather than merely the height.

Nutrient Density Score Adjustments:
  • No adjustments are made to vitamin B1, vitamin B2, vitamin B3manganese, phosphorus, and potassium, due to their DRIs only representing total daily intake, or due to the nutrient having close to 100% bioavailability [1][2][3][4][5][6][7].
  • The DRI for vitamin B5 is multiplied by 2 in order to accommodate its average 50% bioavailability from food [8].
  • The DRI for plant-derived vitamin B6 is multiplied by 1.74 in order to accommodate the average ~42.5% reduction in bioavailability of pyridoxine glucoside [9].
  • The DRI for animal-derived vitamin B6 is multiplied by 1.33 in order to accommodate the average ~25% reduction in bioavailability of as a result of cooking [10].
  • The contribution of vitamin B12 is capped at 1.5mcg in order to account for the average absorption cap of ~1.5mcg per serving in healthy people [11].
  • The DRI for folate has been multiplied by 2 in order to accommodate its average 50% bioavailbility from food [12].
  • The contribution of plant-derived vitamin A (as retinol activity equivalents) is capped at 900mcg. This is to accommodate the fact that it is unlikely that the body can convert more than the DRI of vitamin A from carotenoids [13].
  • The DRI for plant-derived vitamin K, phylloquinone, is multiplied by 10 in order to accommodate its 10% bioavailability from plant foods [14].
  • The DRI for vitamin C has been multiplied by 1.25 in order to accommodate its average ~80% bioavailability [15].
  • The DRI for vitamin E has been multiplied by 4.65 in order to accommodate its average 21.5% bioavailability [16].
Essential Fatty Acids:
  • The DRIs for omega-3 and omega-6 have been recalculated to 250mg/day and 500mg/day, respectively. This better reflects our actual physiological requirements for these fatty acids as provided by their pre-elongated, animal-derived varieties [17][18].
  • The DRIs for plant-derived omega-3 and omega-6 have been multiplied by 6.66 in order to reflect their maximal ~15% conversion rate [19].
  • The contributions of plant-derived omega-3 and omega-6 are capped at 4.4444g before conversion rates are factored, in order to accommodate their conversion rate cap of 2% of calories per day [20].
  • The DRI for calcium has been adjusted dynamically based on the oxalate-to-calcium ratio of each food.
  • The DRI for plant-derived copper has been multiplied by 2.94 in order to accommodate its average ~34% bioavailability from plant foods [21].
  • The DRI for animal-derived copper has been multiplied by 2.43 in order to accommodate its average ~41% bioavailability from animal foods [21].
  • The DRI for magnesium has been multiplied by 2.85 in order to accommodate its 35% bioavailability [22].
  • The DRI for iron has been adjusted dynamically based on the phytate-to-iron ratio of each food.
  • The DRI for selenium has been multiplied by 1.11 in order to accommodate its 90% bioavailability [23].
  • The contribution of zinc is capped at 7mg in order to account for the average absorption cap of 7mg per serving in healthy people [24].
  • The DRI for zinc has been adjusted dynamically based on the phytate-to-zinc ratio of each food.
Essential Amino Acids:
  • The DRIs for all essential amino acids from non-animal sources have been multiplied by 1.492 in order to accommodate their average PDCAAS score of .67 [25].
  • All scores reflecting total protein yield of non-animal foods have been multiplied by .67 in order to accommodate the average 67% bioavailability of protein from non-animal sources [25].
In my estimation, this is a more accurate reflection of how these foods contribute their nutrition to the diet. If any errors or oversights can be found, please feel free to drop me a line and I'll work to correct the issues as quickly as possible!

In addition to nutritional content, ND, and price, the spreadsheet also includes data for phytate, oxalate, FODMAPs, satiety, protein digestibility, glycemic index, glycemic load, and resistant starch. Phytate and oxalate data were pulled from various sources, but mostly the FAO’s "PhyFoodComp" Phytate Database and an independent Oxalate Database I found on Google. FODMAP data was mostly collected from a freely available crowd-sourced version of the Monash FODMAP Database. Satiety data was calculated by applying a modified version of Nutrition Data’s “Fullness Factor” equation to the nutrient data in the spreadsheet. Glycemic Index information was pulled from a variety of sources, but primarily from the University of Sydney's GI Database. Data relating to polyphenols was sourced from Phenol Explorer, a freely available polyphenol database. Resistant starch data is still under construction, but data is being gathered from multiple sources on PubMed until a comprehensive resource becomes available. Protein digestibility data is also still under construction, and will likely be under construction until the FAO accepts the DIAAS as their standard protein digestibility metric and collects comprehensive data.
That sums up what I have so far. I hope you find the Nutri-Dex useful!

I'm continuing to be open to suggestions and criticisms. Any such comments can be forwarded to my email at, or directed to my twitter, @The_Nutrivore. The more people suggest, the more useful the Cheat Sheet becomes, the more value people can get out of it. As long as there is sufficient data to be integrated, I will do my best to get it done. I will be taking a little break from working on the spreadsheet, but I promise that I will do my best to implement any suggestions that can be implemented.

PS. If you like what you've read and want me to continue writing, consider supporting me on Patreon. Every little bit helps! Thank you for reading!


[1] Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Thiamine. National Academies Press. 1998.

[2] Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Riboflavin. National Academies Press. 1998.

[3] Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Niacin. National Academies Press. 1998.

[4] Institute of Medicine. Dietary Reference Intakes for Calcium and Vitamin D. National Academies Press. 2011.

[5] Institute of Medicine. Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. Manganese. Chapter 39, page 352. 2006.

[6] Institute of Medicine. Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. Phosphorus. Chapter 41, page 364. 2006.

[7] Institute of Medicine. Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. Potassium. Chapter 41, page 372. 2006

[8] Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Panthotheic Acid. National Academies Press. 1998.

[9] Reynolds RD. Bioavailability of vitamin B-6 from plant foods. Am J Clin Nutr. September 1988.

[10] Shibata, Keiko, Yasuyo Yasuhara, and Kazuto Yasuda. Effects of Cooking Methods on the Retention of Vitamin B6 in Foods, and the Approximate Cooking Loss in Daily Meals. J. Home Econ. Jpn. 2001.

[11] Carmel R. How I treat cobalamin (vitamin B12) deficiency. Blood. September 2008.

[12] Veronica E Ohrvik and Cornelia M Witthoft. Human Folate Bioavailability. Nutrients. April 2011.

[13] Janet A Novotny, et al. β-Carotene Conversion to Vitamin A Decreases As the Dietary Dose Increases in Humans. J Nutr. May 2010.

[14] Gijsbers BL, Jie KS, and Vermeer C. Effect of food composition on vitamin K absorption in human volunteers. Br J Nutr. August 1996.

[15] Jacob RA and Sotoudeh G. Vitamin C function and status in chronic disease. Nutr Clin Care. March 2002.

[16] Emmanuelle Reboul. Vitamin E Bioavailability: Mechanisms of Intestinal Absorption in the Spotlight. Antioxidants (Basel). December 2017.

[17] Zhiying Zhang, et al. Dietary Intakes of EPA and DHA Omega-3 Fatty Acids among US Childbearing-Age and Pregnant Women: An Analysis of NHANES 2001–2014. Nutrients. April 2018.

[18] Isabelle Sioen, et al. Systematic Review on N-3 and N-6 Polyunsaturated Fatty Acid Intake in European Countries in Light of the Current Recommendations – Focus on Specific Population Groups. Ann Nutr Metab. April 2017.

[19] Burdge GC and Wootton SA. Conversion of alpha-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Br J Nutr. October 2002.

[20] Brian S Rett and Jay Whelan. Increasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic review. Nutr Metab (Lond). June 2011.

[21] Lönnerdal B. Bioavailability of copper. Am J Clin Nutr. May 1996.

[22] Fine KD, et al. Intestinal absorption of magnesium from food and supplements. J Clin Invest. August 1991.

[23] Fairweather-Tait SJ, Collings R, and Hurst R. Selenium bioavailability: current knowledge and future research requirements. Am J Clin Nutr. May 2010.

[24] Lönnerdal B. Dietary factors influencing zinc absorption. J Nutr. May 2000.

[25] PDCAAS Wikipedia article

Tuesday, June 11, 2019

Plant Nutrients, Part 1: Vitamin C

If you’ve been anywhere near the nutrition-oriented corner of Twitter or if you follow certain public figures like Jordan Peterson or Joe Rogan, surely you’ve heard of the carnivore diet. The diet is characterized by a strict abstinence from all plant foods, with approaches ranging from diets consisting only of muscle meats to diets including any and all animal foods as they are tolerated. Needless to say, much like an approach such as veganism, certain nutrients are typically scarce on such a restrictive diet. With vitamin C being the most obvious of the lot. However, many advocates of the carnivore diet propose that an all-meat diet lowers one’s vitamin C requirements.

Essentially, this is how the argument goes—the recommended dietary allowance (RDA) for Vitamin C was established using subjects who were eating ostensibly high carbohydrate diets. Vitamin C and glucose are so structurally similar that they share the same transporters across cell membranes. This creates a competition between glucose and vitamin C for uptake into cells from the bloodstream. Therefore, eating a high carbohydrate diet will artificially inflate our vitamin C requirements because glucose will be inhibiting vitamin C’s entry into cells. Sounds pretty persuasive. But, is it true?

First, let’s talk about what vitamin C does in the body. Very broadly speaking vitamin C has two very important jobs [1]. Vitamin C’s first job is to act as a co-factor for collagen synthesis [2]. When this system fails due to insufficient vitamin C intake, a life-threatening condition known as scurvy quickly develops. Scurvy is a condition of poor connective tissue functioning, leading to bruising, bleeding gums, loose teeth, and stunted growth. 

Vitamin C’s second job is to act as an antioxidant [3]. In this capacity vitamin C acts as a single cog in a large network of antioxidant molecules. These molecules pass electrons between each other so that free radicals can be neutralized as cleanly as possible.

First, α-tocopherol (vitamin E) becomes oxidized by free radicals and becomes α-tocopheroxyl radical (vitamin E radical). From there, vitamin E radical accepts electrons from vitamin C, oxidizing vitamin C and turning it into dehydroascorbic acid (DHAA). DHAA then accepts electrons from glutathione (GSH), turning two GSH molecules into a single glutathione disulfide (GSSG). The end of this chain involves reduced nicotinamide adenine dinucleotide phosphate (NADPH) donating its electrons to GSSG. This creates two GSH molecules and one nicotinamide adenine dinucleotide phosphate (NADP+) molecule. NADP+ is a form of co-enzyme vitamin B3 (niacin).

Now that we understand the basics of vitamin C’s roles in the body, we can now address a number of carnivore talking points related to vitamin C:

1) Glucose inhibits the cellular uptake of vitamin C.

As the story goes, vitamin C and glucose share the same transporters on cell membranes. Therefore, an excessive amount of glucose in the bloodstream creates a competition between glucose and vitamin C for cellular uptake. This artificially increases our need for vitamin C. As such, diets that aim to reduce glucose intake as low as possible (such as an all-meat diet) should lower our vitamin C requirement. Again, this sounds persuasive. But, it’s only a half-truth. Maybe even a quarter-truth.

Generally speaking, vitamin C comes in two forms (seen below). One form is ascorbic acid (AA), and the other form is dehydroascorbic acid (DHAA). AA is the reduced (or “active”) form of vitamin C, while DHAA is the oxidized (or “inactive”) form of vitamin C.

As it turns out, both types of vitamin C use different transporters to cross cell membranes. AA uses specialized transporters called sodium-dependent vitamin C transporter 1 (SVCT1) and sodium-dependent vitamin C transporter 2 (SVCT2) [4]. However, DHAA actually does rely on the same transporters as glucose. DHAA uses glucose transporter type 1 (GLUT1), glucose transporter type 3 (GLUT3), and glucose transporter type 4 (GLUT4) [5]. GLUT1 and GLUT3 transporters are virtually always present on eukaryotic cell membranes for passive glucose uptake. However, GLUT4 is an insulin-dependent glucose transporter. It is responsible for transporting the majority of glucose across cell membranes after a high carbohydrate meal [6].

Despite the fact that dietary DHAA does contribute to a cell’s total pool of AA, we probably should not be terribly concerned with DHAA as a significant source of vitamin C. We’re primarily concerned with AA’s transport into cells, because the lion’s share of AA inside of a given cell got there as active AA from the diet, not by having large amounts of dietary DHAA reduced back to AA inside the cell [7][8]. The point is, AA and glucose do not share transporters. DHAA and glucose do share transporters, but DHAA is less much, much less relevant to the argument. Very, very little of our bodies' stores of AA got there first as DHAA [9]. On the basis of this alone, I’m going to assume carnivores are not talking about DHAA when they are referring to vitamin C uptake into cells.

But, does glucose still somehow inhibit the active transport of AA into cells? Actually, yes it does! Glucose does compete with AA for access to the sodium ions needed to properly transport AA via SVCT1 and SVCT2. Despite the fact that glucose does not actually use this transporter itself for its own entry into the cell [10].

It sounds like the carnivore proponents might be right! Well, not so fast. While it is true that glucose inhibits AA’s uptake into cells, it isn’t relevant in my estimation. This is because the rate of competition largely remains constant at physiologically normal concentrations of blood glucose. There are also wide swings in variation between tests.

Here, researchers measured the uptake of AA by human enterocytes in varying concentrations of glucose. As we can see, AA uptake into the cells is superb when there is no glucose present. However, nobody is walking around with no blood glucose. For this reason, we absolutely should not care about this fact. It’s not physiologically relevant. AA uptake decreases steadily as glucose concentrations increase until about 4 mmol/L of glucose. Which is the bottom of the reference range for healthy blood glucose levels. The rate of AA uptake stays relatively constant until around 10 mmol/L of glucose, which is analagous to the blood glucose of a type II diabetic after a high carbohydrate meal. So yes, glucose inhibits AA uptake into cells, but not in any way we should care about if we are non-diabetic. Based on these data, the rate of competition would be the same regardless of whether or not we’re eating an all-meat diet, because even someone eating an all-meat diet has blood glucose that is well within the reference range.

Also, as an added painful irony, even though DHAA shares transporters with glucose, glucose does not meaningfully inhibit DHAA absorption at any concentration. DHAA uptake into cells with no glucose present is virtually identical to DHAA uptake when glucose is at its highest recorded concentration. It's a surprising yet hilarious twist of fate that the type of vitamin C that actually does share transporters with glucose seems to be completely uninhibited by glucose. So, even if the lion's share of vitamin C did enter the body first as DHAA, uptake would still be fantastic.

But just to hammer the point home, let’s stratify the in vitro glucose concentrations in the graph above by what each concentration represents physiologically.

Based on the above graph, we see that there is a ~37.5% reduction in AA uptake into cells from 4 mmol/L of glucose to 8 mmol/L of glucose. Mind you that this means that we'd have to go from the best fasting blood glucose to the worst non-diabetic postprandial blood glucose to even get an effect that large. This should not adequately justify reducing the RDA of vitamin C by 88.9-91.6%, going from 90-120 mg/day down into the neighborhood of 10mg/day. How does a 37.5% decrease in AA availability end up translating to an eightfold to elevenfold increase in AA requirements? Do we just piss AA out that fast? Not according to this study, which found that AA bioavailability and retention was better when AA was taken in a solution containing glucose as opposed to merely being dissolved in water [11].

Personally, I would like to see some AA and glucose-titration kinetics data in humans to look at the area under the curve for excretion and blood concentration over time. That should settle the question definitively, in my opinion. If anybody knows of such data, let me know. 

Above, we see that pretty much the exact same findings were replicated by another group studying human neutrophils [12]. AA uptake into the neutrophil is excellent when no glucose is present, but the rate of AA inhibition by glucose remains relatively constant at physiologically analogous concentrations of glucose. Again, if competition is such that the presence of glucose creates an artificially higher need for vitamin C, as some carnivores claim, it applies to carnivores too. AA uptake into cells is virtually the same regardless of whether our blood glucose is 4 mmol/L as fasting, fat-burning carnivores or 8 mmol/L as well-fed, carb-burning couch potatoes.

But for the sake of argument, let’s actually just pretend that AA can utilize the glucose transporters as well. It can't, but let’s pretend it can. In normal people, blood glucose is always accompanied by the hormone insulin. So, even if it were true that AA and glucose shared transporters, the rate of competition would still be roughly the same regardless of the glucose concentration. This is because the representation of GLUT4 on cell membranes is modulated by insulin. More glucose, more insulin, more GLUT4, and thus more AA transport into cells. No matter which way we cut it, the argument that high carbohydrate diets increases vitamin C requirements doesn’t make any sense.

Not to mention that nearly all of the plant foods highest in AA are typically low-carbohydrate plant foods, and typically contain low-to-negligible DHAA [8]. Virtually none of the food selections listed as the richest sources of AA would even m
ove the needle on blood glucose. So, even if it were true that glucose artificially inflates our vitamin C requirements, a food like broccoli should still be a viable option for vitamin C. But hey, who cares about these sorts of details, right?

2) All-meat diets do not cause scurvy.

At this point in the discussion, someone proposing the first argument is usually keen to eventually propose this second argument. The idea is that a diet consisting of only meat does not reliably produce scurvy, if at all. Therefore, it must be the case that an all-meat diet does indeed lower our vitamin C requirement, at the very least through some unknown mechanism. This is a common rebuttal. But in my opinion it is very weak, as it demonstrates a failure to understand precisely what vitamin C does in the body and how it does what it does.

Remember when I stated that vitamin C has two primary functions in the body? One function is preventing scurvy through promoting healthy collagen synthesis. The other function is supporting the antioxidant defense system. Well, those two different functions require two different amounts of vitamin C. It has been documented in depletion-repletion experiments that the amount of vitamin C needed to support collagen synthesis (and thus prevent scurvy) is around 10mg of vitamin C per day [13]. It was also discovered that for some individuals, body vitamin C stores required to prevent scurvy could be maintained with less than 6.5mg of vitamin C per day. 

Subjects H and P were given 6.5mg of vitamin C per day for the entirety of phase IV (in red) of the experiment. Vitamin C status gradually improved with an indication of a plateau that was broken by complete repletion in phase V.

The RDA for vitamin C is mostly set to accommodate its turnover in relation to its use as an antioxidant [14]. The RDA for vitamin C is not specifically set to accommodate its turnover as it relates to its use as a co-factor for collagen synthesis, because the body requires so little for that particular function (300mg of a total body pool of 2000mg).

When it is proposed that an all-meat diet must reduce absolute vitamin C requirements, I ask: "which requirement?" Remember, vitamin C demands two different requirements for two different functions. One requirement is huge, but there are no obvious symptoms related to deficiency (because oxidative stress is a chronic long term issue). One requirement is very tiny, and the deficiency symptom is, well, scurvy.

This is actually an excellent example of Bruce Ames’ triage theory [15]. Which in my opinion is closer to being a principle rather than a theory or hypothesis at this point. The theory proposes that the body will direct the use of nutrients toward functions that maximize short term survival and away from functions that maximize long term health under conditions of scarcity. For example, say we’re running low on folate. Folate has a few functions, one of which is participating in the production of certain neurotransmitters, creatine, red blood cells, and all sorts of acutely important things. Another function of folate is preventing DNA damage and regulating gene expression. Under conditions of scarcity, the body will actually direct folate to functions that maximize short term survival, and sacrifice functions that maximize long term health [16]

We can observe that sub-optimal folate status causes DNA damage, but acutely important functions are presumably defended first. If they weren't, the subject would be either dead or gravely ill. The same is probably true of vitamin C. Under conditions of scarcity it is likely that collagen synthesis is defended before antioxidant support. We can't feel or see oxidative stress the way we can feel or see bleeding gums or bruising. We also can't feel or see DNA damage the way we can feel or see exercise intolerance or anemia.

Unless the individuals making the argument for reduced vitamin C requirements on all-meat diets are actually having their antioxidant capacity measured, they can’t know for certain. It is entirely possible to get ~6.5mg/day of vitamin C on an all-meat diet. There is absolutely no question about that. Even a diet of pure muscle meats could potentially supply enough vitamin C to prevent scurvy.

But there is another side to this as well. There is an added detail to consider from the depletion-repletion studies. For some of the subjects, it took over 100 days on a zero vitamin C diet to maximally deplete their body’s total pool of vitamin C [13]

People eating a carnivore diet were, at least ostensibly, eating a vitamin C sufficient diet long before they decided to abstain from eating plant foods. Let's say for the sake of argument that an all-meat diet doesn't provide much vitamin C at all. If we were to provide the body with merely less than 6.5mg of vitamin C per day instead of just zero (starting with total body stores that are potentially maximally replete), how long would it take to get scurvy? Who knows. My guess is that it would take longer than 100 days. Maybe it would take years? A decade? Maybe it wouldn't happen at all. It’s uncertain. But, I wouldn’t personally take the absence of scurvy in the short term as an indication that vitamin C needs are actually being met.

3) Vitamin C’s role as an antioxidant is merely theoretical.

The idea sounds cute, and I will admit the justification for the RDA of vitamin C being as high as it is might appear a bit wishy-washy in the official DRI report [14]. However, vitamin C’s usage and turnover in the antioxidant defense system has been well documented, and it is well understood [17][18][19][20][21][22]. There are perfectly legitimate reasons to conclude that the RDA of vitamin C is a reasonable recommendation. Personally, I feel there is ample justification to increase the RDA of vitamin C beyond 200mg/day. As there is no obvious downside, and it is virtually guaranteed to capture all documented variation in vitamin C turnover in humans. Not to mention it has been associated with lower morbidity and mortality in epidemiological studies [23].

Here we see that the total body turnover of vitamin C in 14 non-smoking subjects ranges from 14.4mg/day all the way to 142mg/day [24]. This means that there can be a whole order of magnitude difference in vitamin C turnover from person to person. Given that the turnover of vitamin C in the support collagen synthesis leaves us requiring somewhere south of 10mg/day as a baseline, the above turnover rates give us a picture of just how much vitamin C is required each day to fulfill the rest of its functions outside of collagen synthesis. The average of these turnover rates is around 65.74mg/day. If we minus 10mg/day for collagen synthesis, this leaves us with an average of ~56mg/day worth of vitamin C turnover that probably can’t be adequately explained by collagen synthesis alone. The body is presumably using that vitamin C. It's probably a fair bet that vitamin C is being used by the body in amounts that sometimes exceed what would be satisfied by the RDA alone.

There is an additional complication to measuring turnover accurately, however. One of the primary ways to measure vitamin C turnover since the early 1900s is to measure 2,3-diketogulonic acid (
2,3-DKG) in urine or plasma. This is a metabolite of vitamin C that occurs when vitamin C's carbon ring spontaneously ruptures. Typically, this rupture occurs when vitamin C has exceeded the number of redox cycles it can support. This means we can actually directly measure just how much vitamin C the body is using.

Here we see that 2,3-DKG (DKA in this paper) is maintained at approximately 10-15% of total vitamin C excretion in human subjects on low-plant diets [25]. Free AA excretion only increased with 75mg of vitamin C per day. Interestingly, in one subject 2,3-DKG excretion increased with supplementation while the other subject's 2,3-DKG excretion decreased. 

In an odd contrast, another paper measured plasma 2,3-DKG and found that up to half of human plasma vitamin C could consist of 2,3-DKG [26]. Sometimes up to 15mg or 25mg of plasma vitamin C was 2,3-DKG. This could indicate that urinary excretion is not the most accurate way to measure turnover. But without data to measure the flux of 2,3-DKG generated and excreted, this number doesn't mean much. But, it could mean that vitamin C turns over at a rate that far exceeds what you could reliably get from meat.

I would be super interested to see complex flux or kinetics data on 2,3-DKG, considering that the body tends to retain more 2,3-DKG than it excretes. As we can see below, urinary excretion of 2,3-DKG pretty much never exceeds intake from the diet. This is puzzling to me and I want to understand more about this. I'm guessing that some proportion of the 2,3-DKG in the blood gets converted to another metabolite like oxalate and is excreted that way.

Nevertheless, all of the subjects in the study were excreting far more AA than 2,3-DKG. One might respond to this by saying: "a-ha! See, those fuckers are pissing way more ascorbic acid than they're using!" Right. But remember those depletion-repletion graphs above? We urinate a relatively steady amount of free AA all the way to scurvy, regardless of how depleted or repleted we are. Even after months with an AA intake of zero. So, don't get excited.

Additionally, we have direct evidence of vitamin C supplementation upwards of 1000mg/day reducing levels of oxidative stress relative to placebo [20]. We have other research indicating that 500mg/day can lower markers of oxidative stress in humans when compared to 50mg/day over five years. In fact, the group receiving a mere 50mg/day had net increases in average oxidative stress [27]. Implying that their needs were probably higher than a mere 50mg/day.

Think about it. The body has a maximum storage capacity of 2000mg of vitamin C. Scurvy symptoms only present when total body pool drop below 300mg. We know from the above experiments that certain people who are asymptomatic for scurvy (meaning they have a total body pool of >300mg of vitamin C), can reduce markers oxidative stress with vitamin supplementation ranging from 500-1000mg per day. This implies to me that you need a total body pool of 300mg of vitamin C to prevent scurvy, and that the bulk of your storage capacity (~1700mg) is likely to support other functions, like the antioxidant defense system. 
The exercise data referenced above paints a very important picture that is critical for understanding human vitamin C requirements—you can exercise your way to a higher vitamin C requirement, but you cannot exercise your way to scurvy. 

Some could argue that studies on vitamin C supplementation aren’t always consistent. Some studies show no significant effect of vitamin C supplementation on oxidative stress [28]. I would agree. However, remember that vitamin C doesn’t act alone. Vitamin C requires good vitamin E status, riboflavin status, niacin status, and adequate protein intake in order to properly fulfill its role as an antioxidant. To illustrate this, whether in humans or in animals, effects of vitamin C supplementation are more pronounced when it is complimented with vitamin E supplementation [29][30][31][32].

It is possible that the few vitamin C supplementation studies that have yielded null or near-null results may have been confounded by poorer nutritional status in the subjects. It’s hard to say for sure. Even when we randomize subjects, we're still randomizing subjects belonging to a single population. So, it's possible for population-specific variables to confound a study. I realize this is speculative on my part, but it's not at all impossible. 

Nevertheless, what we do know is that we need enough vitamin E to accept electrons from vitamin C once vitamin E is oxidized. We also need to take in enough protein to make the GSH to pass electrons to vitamin C once it is oxidized by vitamin E radical. We then need adequate riboflavin to oxidize NADPH to NADP+. But before that, we need adequate niacin status to provide the nicotinamide adenine dinucleotide (NAD) to make the NADPH. What I’m saying is that a lot can go wrong here, and merely dosing vitamin C is not a guarantee that we will see a result at all. Null results in vitamin C dosing trials shouldn’t automatically be taken as an indication that vitamin C doesn’t matter.

4) Glutathione can replace vitamin C as an antioxidant.

This is probably the most outlandish claim of the lot, but I’ve heard it many times from many different individuals. I have no idea where this claim comes from or who first proposed it. Naturally, my knee-jerk response is to simply remind those making this claim that it just doesn’t work that way. For reasons I’ve already described vitamin C is an integral part of the antioxidant defense system. We can’t just hotswap reducing agents at our leisure. They all depend on each other because they all require their own unique enzymes to facilitate each reduction-oxidation (redox) reaction [33]. For example, we simply cannot pass electrons from two GSH molecules to DHAA without dehydroascorbate reductase (DHAR). Without this enzyme, there is a break in the chain of redox reactions that carry electrons all the way from NADPH to vitamin E radical.

In fact, at least one group of researchers have attempted to answer this exact question [34]. What happens when the antioxidant defense system within a cell is deprived of vitamin C, and that vitamin C is replaced by GSH? Spoiler alert! The cell straight up dies. Without vitamin C present to pass and accept electrons between the other two reducing agents, GSH and vitamin E, the cell cannot withstand oxidative stress at all. GSH cannot act as a stand-in for vitamin C. Period. When vitamin C status is lower than would be required for optimal antioxidant capacity within a given cell, the cell suffers. If we remove vitamin C entirely, the cell dies. Simple.

5) Dietary collagen can spare vitamin C.

In the body, vitamin C is responsible for the hydroxylation reactions that convert proline and lysine into hydroxyproline and hydroxylysine. It has been proposed that perhaps consuming dietary collagen could spare vitamin C by providing these two pre-hydroxylated amino acids. However, researchers have suggested that they are not very likely to survive digestion [35]. At least two studies have discovered that hydroxyproline peptides are detectable in human blood after ingestion [36][37]. But, these are not the free hydroxylated amino acids necessary for the production of new collagen. However, ingestion of collagen peptides does seem to have an effect on pre-existing collagen structures in humans [38][39]

It is unlikely that the ingestion of collagen peptides turns down the body's production of its own collagen. In fact, one group discovered that ingesting collagen peptides was most effective at augmenting the body's collagen when vitamin C was provided, and that the supplement they provided actually stimulated collagen synthesis [40]

In an interview, researcher Keith Baar remarked that one unpublished experiment failed to yield results because the vitamin C content of the collagen supplement was lost due to overcooking. This is likely because vitamin C is also responsible for activating the enzymes that cross-link collagen [41]. Meaning that upon ingestion of collagen peptides, the effects are most robust when vitamin C status is optimal. It is possible that ingesting collagen for the purpose of augmenting the body's collagen actually taxes our vitamin C rather than sparing it.

But for the sake of argument, let's be generous and pretend that ingesting collagen peptides spares all of the vitamin C necessary for collagen synthesis. At most, we'd be expected to spare less than 10mg/day. This does not leave enough to cover even a fraction of recorded vitamin C turnover in some humans. Again, vitamin C has two primary functions. The requirement for one function is very large, and the other is very small. Collagen synthesis requires very little vitamin C. Antioxidant support requires an enormous amount of vitamin C by comparison. 

6) The guinea pigs.

There is a lot of love in the carnivore community for a vitamin C depletion study performed on guinea pigs [42]. Like us, guinea pigs do not synthesize their own vitamin C, so they are a reasonable choice for designing rodent models of vitamin C deficiency. Essentially, researchers deprived the guinea pigs of vitamin C and administered a form of bioavailable GSH (remember GSH is also an important part of the antioxidant defense system). Doing this, the researchers were able to slow the progression of scurvy. Some in the carnivore community have claimed that this is a vitamin C-sparing effect of GSH that could explain the absence of scurvy on all-meat diets. I can see the logic—diets higher in protein would probably best support GSH status.

However, I look at this a little bit differently. Again, we know that vitamin E is recycled by vitamin C, vitamin C is recycled by GSH, and GSH is recycled by NADPH. It's a system, and the system has many cogs that all need to function together. If you dose GSH and delay the onset of scurvy, this isn't an effect of GSH sparing vitamin C so much as it is just an example of what happens when everything works properly. If there is not enough GSH to reduce DHAA back to AA, a steady supply of AA is required to make up for it. Not only that but you will have more vitamin C wasting due to DHAA spontaneously converting to 2,3-DKG. 

In this context, insufficient GSH creates a higher-than-normal need for AA. When you delay the onset of scurvy by administering GSH to the AA-deprived guinea pigs, what you're seeing is the guinea pigs just needing more GSH. You are not seeing the guinea pigs requiring less vitamin C per se. The guinea pigs are made artificially deficient in vitamin C as a consequence of sub-optimal GSH status. You're just seeing what happens when you correct a GSH deficiency.

  • Ascorbic acid does not share transporters with glucose. Dehydroascorbic acid does share transporters with glucose, but it doesn’t matter.
  • Glucose does inhibit cellular uptake of ascorbic acid, but it is not meaningful at physiologically relevant concentrations of glucose.
  • Less than 10mg of vitamin C per day is required to prevent scurvy.
  • Vitamin C turnover in healthy people far exceeds 10mg per day, presumably as a consequence of its use as an antioxidant.
  • Vitamin C requires a number of other nutrients to do its job correctly, and could explain why vitamin C supplementation has inconsistent effects on markers of oxidative stress.
  • The antioxidant effects of vitamin C are more robust when coupled with either glutathione or vitamin E.
  • Vitamin C is an integral part of the body’s antioxidant defense system, and complete vitamin C deprivation triggers cell death.
  • Consuming collagen is unlikely to spare vitamin C and could perhaps even increase the body's demand for vitamin C.
  • Vitamin E, vitamin C, and glutathione all cooperate together to support the antioxidant defense system. Reducing any of them increases the need for the other two.
  • There is no persuasive reason to believe that an all-meat diet modulates our vitamin C requirements such that the RDA should be reduced from 90-120 mg/day to any amount one could reasonably expect to obtain from eating only animal foods.
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