Protein Basics

On January 15, 2010, in Protein, by Andrea


As important as it is, protein is perhaps one of the most confusing topics in the WLS world – even though there is a ton of research and information available about it out there.

Protein is an important macronutrient required to help maintain and build muscle mass within the human body.  Without protein, the body will not have the requisite materials to keep the heart beating, legs walking, or arms moving.

Protein, during digestion, is broken down into it’s components to provide amino acids.  Amino acids are building blocks of proteins and are critical in various biochemical reactions throughout the body on the molecular level – without them, our mood, energy, brain function, ability to move, EVERYTHING is affected.  Some of these amino acids can be synthesized by the body using other amino acids as building blocs, but there are nine according to one accepted classification (eight by another, even ten by even another) that must be provided by the diet called Indispensible Amino Acids (IAA’s) or essential amino acids.  The IAA’s are:

  • Isoleucine
  • Leucine
  • Valine
  • Histadine
  • Lysine
  • Methionine
  • Phenylalnine
  • Threonine
  • Tryptophane

Additionally, there are three conditionally indispensable amino acids, so-termed depending on the body’s ability to synthesize them.  They are:

  • Arginine
  • Cysteine
  • Tyrusine

Lastly are the dispensable amino acids.  These are amino acids the body can synthesize given that it has enough of the basic building blocks to create them.  These are also found in food and supplements — the body does not have to create these if we consume enough in dietary or supplemental sources.  The DAA’s are:

  • Alanine
  • Aspartic Acid
  • Cystene
  • Glutamic Acid
  • Glutamine
  • Glycene
  • Ornithine
  • Proline
  • Serine
  • Taurine

The content and ratio of these amino acids in your foods and protein supplements are the things that control the quality of the food or supplement that you are ingesting.

Bioavailability of protein has been measured in a number of ways for years.  Rats have been fed various diets and their fur growth has been measured as a way to determine digestibility of protein – this especially rings true as the standard test for protein in foods and supplements actually looks for nitrogen, not protein.

Depending on the industry, you are likely to see any number of protein quality measurements – of course using the one that makes their particular product look best.

PER (Protein Efficiency Ratio) — Basically, various combinations of proteins were given to young rats; their growth was then measured.  A PER above 2.5 was considered excellent.  This method gave too much weight to the importance of methionine, which is more important to developing rat hair than it is in human nutrition.

NPU (Net Protein Utilization) — Outdated and seldom used, egg protein given a score of 94; 100 would indicate that every bit of protein eaten would be used to produce lean tissue

BV (Biological Value) — Also generally considered outdated; evaluates protein based on amount of nitrogen retained in body after absorption of a protein food; egg is the standard and highest value possible is 100 (despite some products selling tactics)

PDCAAS (Protein Digestibility Corrected Amino Acid Score) — In 1991, the World Health Organization adopted the PDCAAS method of protein scoring.  In this method, the amino acid profile of the food or supplement in question is compared against a standard amino acid profile.  PDCAAS looks at the limiting amino acid – meaning that if a food is completely missing one of the IAA’s, it has a score of 0.  Rather than score the protein on what it has, the PDCAAS scores on the lowest common denominator – on what it does not have.
While PDCAAS is the preferred scoring method supported by the NIA and WHO, it is not the end-all to protein scoring.  While many see it as the most reliable, it does have it’s criticisms as well.  If a food product is missing just one IAA, it has a PDCAAS score of 0; however the same food item paired with another item that has that missing amino acid will work together to create a complete protein, raising the PDCAAS score – potentially even to the max score of 1.  The question, of course becomes how soon do the two food products have to be consumed to be of benefit to one another?  There’s some speculation and the answer, typically depends on the industry involved.  For example, the collagen protein industry would like for you to believe that the IAA’s they are missing can be made up through the diet.  There are two flaws with this argument:  first, the IAA’s collagen is missing are the ones many diets are typically low in, thus the shortfall still exists; second,  there is a time frame, albeit it’s one of those wishy washy mythical numbers that tends to get turned into rules of law when said too many times sorta deal for you to consume the missing IAAs so we really don’t know what the number is deal.  Sometimes, it’s just easier not to have to plan your protein supplements that much.

Beyond the basics (I know, I know — THAT was basic?), the next question invariably comes into type of protein supplements.  The typical supplements are made from whey (milk product), soy, and egg.  Beyond the type of protein, which simply states where it came from, you have classifications of concentrate and isolate.

Concentrates are proteins that are typically concentrated through dehydration to remove the moisture.  The process will leave some things like lactose in whey, fat, and sugars behind and are only about 60-70% protein by dry weight.

Soy and whey isolates, however, have been further filtered to remove additional impurities.  It is this process that leaves whey protein isolate lactose-free as this is one of the molecules removed through filtration.  In the end, isolates are 90-95% pure protein, and have less taste due to fewer contaminates within the protein itself.  Additionally, within the isolate market, there are grades of isolates — depending on the company purchasing and marketing the product, you may get “A” grade isolate or “B” grade.  The quality is typically a taste difference — although there are a few small differences as well.

Typical protein supplements will have combinations of protein types.  The more expensive proteins will be the isolates due to the expensive filtration process.  It is said that isolates will absorb better, but in many cases it is thought that blends will absorb just as well.

A special note about collagen bullets: Collagen, in of itself, has a PDCAAS score of 0.08 and a PER of 0.  Knowing this, the companies marketing these products have added just enough whey protein to give a minor amino acid profile, but not enough of one to benefit unless you drank several gallons worth.  Additionally, these proteins will deflect their inferior amino acid profile by highlighting their “hydrolyzed” content.  Hydrolyzation, which is the process of breaking up protein molecules, is actually how collagen protein is created.  This process of hydrolyzation is how the collagen is rendered from the carcasses of the animals it once came from.  So while hydrolyzed protein is neither good nor bad — the fact that collagen is using it as a selling point is a bit under-handed here.  Along the same vein, if we absolutely needed our food to be hydrolyzed, then we would waste away — because the chicken in our sandwich hasn’t been pre-digested for us, and neither has that steak you ate last week.

There is much controversy when it comes to protein amounts needed by adults.  The current reccomendation is 0.8g/k or 0.37g/lb of body weight, which works out to a nice 59.2g for a 160lb person.  Looking at this number, it’s not hard to believe why some groups feel this number is severely understated.

However, if you were to plug in the same numbers for an obese individual — say someone weighing 350lbs — the same formula has the need at 129.50g per day, which seems a bit high.

If we really want to get fun and interesting, let’s look at WLS concerns.  What about the malabsorption component?  How much protein should we factor in for that?  Current recommendations for normies is that no more than 35% of their daily calories come from protein, but with such strictly restricted carbohydrate diets, many post-0ps have protein amounts in the 40-50% range.  How does this measure up with recommendations?

So while there is plenty of research on the amount people should eat, there are still no hard and fast rules — yet.  So that means there are even fewer rules when it comes to US.

PDCAAS and PER scores for common foods and supplements.  PDCAAS scores out of 1; PER above 2.5 considered good

PDCAAS:  0.08
PER:  0

PDCAAS:  0.8 – 0.92
PER:  2.0-2.3

PDCAAS:  1.0
PER:  1.8 – 2.3

Egg White
PDCAAS:  1.0
PER:  2.8

Milk Protein
PDCAAS:  1.0
PER:  2.8

PDCAAS:  1.0
PER:  2.9

Whey Protein
PER:  3.0-3.2

Special thanks to Jerome at Unjury for going over some of this info with me.

Information compiled from National Academies Press: Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients)

Vitamins A-Zinc — Vitamin B1

On January 9, 2010, in Vitamins, by Andrea

Whole Grains

What is it?

Thiamin (sometimes spelled thiamine) was once called aneurine.  It was isolated and characterized in the 1930′s and was one of the first organic chemicals to be recognized as a vitamin.  Since it was the first B vitamin to be recognized, it was given the moniker of vitamin B1.

Thiamin occurs in the human body as free thiamin, and in several phosphorylated forms: thiamin monophosphate (TMP), thiamin triphosphate (TTP), and thiamin pyrophosphate (TTP), which is also known as thiamin diphosphate.

What is it good for?

Thiamin pyrophosphate (TPP) is a required enzyme for a small number of very important enzymes.  Additionally, all forms of thiamin play critical roles in the production of energy from food.

Cataracts – there is some limited evidence that thiamin will help prevent cataracts

Alzheimer’s – there is slight and inconsistent evidence that thiamin supplements are of benefit to those with Alzheimer’s

Congestive Heart Failure – diuretics used in the treatment of CHG, notably Lasix, have been found to increase thiamin excretion, potentially leading to marginal thiamin deficiency; however, studies have shown that CHF patients have a low incidence of thiamin deficiency, although older patients are at greater risk than their younger counterparts — thus thiamin supplementation in CHF patients is currently still very controversial

Cancer – thiamin deficiency has been observed in some cancer patients with rapidly growing tumors; studies have shown that some of these rapid cell-dividing tumors have a high requirement for thiamin;  thiamin supplementation is common in cancer patients to prevent deficiency due to frequent vomiting, but given these findings, perhaps supplementation should be given only to those who have a definitive need versus as a prophylaxis

Where do I get it?

Thiamin is mainly absorbed in the jejunum and is transported in the blood via the red blood cells (erythrocytes) and plasma.  Only a small percentage of a high dose of supplemental thiamin is actually absorbed and elevated serum values will result in active urinary excretion.  After an oral dose, peak excretion occurs in about 2 hours, and is nearly complete after 4 hours.

For all of that information, we still know very little about the bioavailability of this critical water-soluble vitamin.

Food Sources

Median intake of thiamin from food in the US by young men was approximately 2mg and young women 1.2mg.

Food Serving Thiamin (mg)
Lentils (cooked) 1/2 cup 0.17
Peas (cooked) 1/2 cup 0.21
Long grain brown rice (cooked) 1 cup 0.19
Long grain white rice, enriched (cooked) 1 cup 0.26
Long grain white rice, unenriched (cooked) 1 cup 0.04
Whole wheat bread 1 slice 0.10
White bread, enriched 1 slice 0.11
Fortified breakfast cereal 1 cup 0.5-2.0
Wheat germ breakfast cereal 1 cup 4.47
Pork, lean (cooked) 3 ounces* 0.72
Brazil nuts 1 ounce 0.18
Pecans 1 ounce 0.19
Spinach (cooked) 1/2 cup 0.09
Orange 1 fruit 0.10
Cantaloupe 1/2 fruit 0.11
Milk 1 cup 0.10
Egg (cooked) 1 large 0.03

Vitamin Sources

Thiamin can be purchased by itself, or in a package with other B-vitamins as a B-complex.

Recommended Dietary Allowance (RDA) for Thiamin
Life Stage Age Males (mg/day) Females (mg/day)
Infants 0-6 months 0.2 (AI) 0.2 (AI)
Infants 7-12 months 0.3 (AI) 0.3 (AI)
Children 1-3 years 0.5 0.5
Children 4-8 years 0.6 0.6
Children 9-13 years 0.9 0.9
Adolescents 14-18 years 1.2 1.0
Adults 19 years and older 1.2 1.1
Pregnancy all ages - 1.4
Breastfeeding all ages - 1.4

There is not sufficient data concerning adverse effects to set a Tolerable Upper Intake Level (UL).  There are no reports available of adverse effects from consumption of excess thiamin from food or supplements, and there have been no studies done for high-dose thiamin supplementation.  However, it should be noted that although there have been no adverse reactions associated with excess thiamin intake from food or supplements, this does not mean that there is no potential for adverse effects resulting from high intakes — just that there have been none associated with high-dose thiamin supplementation.

There have been occasional reports of severe adverse reactions and even death in relation to injected supplementation therapy of thiamin.  Sympotms of anaphylaxis include anxiety, respitory distress, nausea, abdominal pain, shock, and sometimes death.


Thiamin deficiency has severe implications.  A B1 deficiency alters mitochondrial function, impairs oxidative metabolism, and causes selective neuronal death by diminishing vitamin B1-dependant enzymes.  It affects the cardiovascular, nervous, muscular, and gastrointestinal systems, resulting in peripheral neuropathy, ataxia, encephalopathy, and may even lead to permanent impairment of recent memory.  It is important to note that the encephalopathy and neuropathy of a B1 deficiency may occur despite supplementation of thiamin because vomitting may preclude effective absorption.

Beriberi, the disease resulting from severe thiamin deficiency was described in Chinese literature as early as 2600 B.C. and has four distinct types:

Dry (paralytic or nervous) beriberi is peripheral neuropathy.  Early in the course of the neuropathy, “burning feet syndrome” may occur.  Other symptoms are:

  • abnormal or exaggerated reflexes
  • diminished sensation
  • weakness in the legs and arms
  • muscle wasting
  • muscle pain and tenderness
  • difficulty rising from a squatting position
  • may have seizures

Wet (cardiac) beriberi is characterized by cardiovascular manifestations of thiamin deficiency

  • rapid heart rate
  • enlargement of heart
  • severe swelling (edema)
  • difficulty breathing
  • ultimately congestive heart failure

Cerebral beriberi may lead to Wernicke’s encephalopathy and Korsakoff’s psychosis, especially in people who abuse alcohol

  • Diagnosis of Wernicke’s based on a triad of signs in addition to the thiamin deficiency:
    - abnormal eye movements
    - stance & gait abnormalities
    - abnormalities in mental function that may include a confused, apathetic state or a profound memory disorder termed Korsakoff’s psychosis
  • without amnesiac state, only Wernicke’s disease
  • most WKS sufferers are alcoholics, but cases have been seen in other disorders of gross malnutrition including stomach cancer, AIDS, and bariatric surgery
  • administration of IV thiamin to WKS patients generally results in prompt improvement of the eye symptoms but motor coordination and memory may take longer or may have less recovery depending on how long symptoms were present before treatment began
  • classic presentation of Wernicke’s only happens in 20% of patients

Infantile beriberi is possible in breast-fed infants whose mothers are thiamin-deficient.
Beriberi may progress for years if left untreated, but has been known to progress as quickly as 3 days.  Substantial recovery typically occurs within 3-6 months of the initiation of therapy; however, neurological recovery may never be complete if left untreated for a long period of time.

Biochemical changes in thiamin status occur well before the appearance of overt signs of deficiency.  Because erythrocyte transketolase activity decreases early in thiamin deficiency, measurement of its activity in red blood cells has been used to assess thiamin nutritional status; however it has some limitations so additional indicators should be considered as well in testing for a possible deficiency.

Deficiency may result from inadequate intake, an increased requirement for thiamin, excessive thiamin loss from the body, consumption of foods high in anti-thiamin factors, or a combo of the above.

Inadequate Intake

Deficiency is common in low-income populations whose diets are high in carbohydrates and low in thiamin (ie milled or polished rice).  Alcoholism, which is associated with low intake of thiamin, among other nutrients, is the primary cause of thiamin deficiency in industrialized countries.

Increased Requirement

Those with an increased requirement include those who have strenuous physical exertion, high fever, pregnancy, breast-feeding, and adolescent growth.  Such conditions place individuals with marginal thiamin intake at risk for developing symptomatic thiamin deficiency.  Recently, malaria and HIV patients were found to be in increased need of thiamin as well.  Those being treated with hemodialysis or peritoneal dialysis and individuals with a malabsorption syndrome are also in need for additional thiamin.

Reduced blood levels of thiamin have been reported in individuals with seizure disorders (epilepsy) taking the anticonvulsent medication Phenytoin for long periods of time.  Lasix may increase risk of thiamin deficiency in individuals with marginal thiamin intake due to increased urinary excretion of thianmin, and chronic alcohol abuse is associated with thiamin deficiency so these individuals have an increased requirement.

Excessive Loss

By increasing urinary flow, diuretics may prevent reabsorption of thiamin by the kidneys and increase it’s excretion in the urine, although this point still remains quite controversial.  Women experiencing excessive vomiting during pregnancy are at additional risk for thiamin deficiency and should be monitored closely.

Anti-Thiamin Factors (ATF)

The presence of anti-thiamin factors in foods also contribute to the risk of thiamin deficiency.  Certain plants contain ATF which react with thiamin to form an oxidized, inactive product — rendering the thiamin useless.  Consuming large amounts of tea and coffee (including decaffeinated versions) has been associated with thiamin depletion.  Thiaminases are enzymes that break down thiamin in food and are found in raw freshwater fish, raw shellfish, and certain ferns.  When cooked, these enzymes are destroyed and the thiamin-eating enzymes are destroyed.


No well-established toxic effects from the consumption of excess thiamin in food or through long-term oral supplementation (up to 200mg / day) have been notated.  However, there have not been any studies into this, so that is not to say that there are no toxic effects to high-dose thiamin supplementation, or to long-term over-supplementation of thiamin.

WLS Concerns

We know that thiamin absorbs in the jejunum, which is partially bypassed in RNY folk.  It’s also completely bypassed in DS folk.  This is something that needs to be watched in both surgeries to make sure a deficiency does not arise.  Deficiencies in B1 are common enough after bariatric surgery that a new term has been coined — either “bariatric beriberi” or even the cuter and shorter “bariberi.”

Beyond the fact that we know it is a water-soluble vitamin that absorbs in the jejunum, we know that the body only absorbs a small portion of high-dose supplementation.  When we give the body a huge dose at once, it causes the body to excrete extra through the urine.

And that’s what we know about the bioavailability.  Which isn’t much in the grand scheme of things.  We don’t know if there is a maximum we can absorb at a time, or how often we should take it for max absorption.  There simply have not been enough studies to tell us this.  That’s why our labwork is so critical to tell us where we stand — and if you think there could possibly be a problem, it’s time to get it checked immediately, not in a week, or next month when you get your labs anyway.

Another concern comes from intractable vomiting.  Oral supplementation may not be enough if you are losing thiamin through vomiting.

Looking through medical database sites, I found multiple papers about the neurological complications after bariatric surgery.  There were two about thiamin alone — and another that also discussed B12, E and copper.  The point is that B1 needs to be on your labslip, and if it is not, there is a problem.

Information compiled from:

Linus Pauling Institute
The National Acadamies Press: Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline
The Neurological Complications of Bariatric Surgery
Thiamine Deficiency May Complicate Gastric Bypass

Vitamins A-Zinc — B-vitamin Primer

On January 7, 2010, in Vitamins, Water Solubles, by Andrea

The B vitamins are a complex of vitamins that play an important role in many body systems.  Once thought to be a single vitamin and referred to as such (such as vitamins C and D), we now know there are eight separate water-soluble vitamins, each with a different structure and purpose.

B vitamins are necessary for metabolism, neurological health, maintaining healthy skin and muscle tone, immune system health, and promoting cell growth and division — including the red blood cells making them crucial in the role of anemia status.

All B vitamins are water-soluble and most must be replenished regularly as the body excretes excess through the urine.  There are a few exceptions (such as B12) in which the body holds a store that can last even years.

The eight B vitamins are:

B1 – Thiamin(e)
B2 – Riboflavin
B3 – Niacin
B5 – Pantothenic Acid
B7 – Biotin
B9 – Folic Acid
B12 – Cobalamin

Individual B vitamins can be supplemented individually, or in a group as a “B-complex.”

There are additional compounds that were once believed to be vitamins and have similar structure, and thus given names to fill in the gaps of the B vitamin series.  Some are not essential to humans but are to other organisms; others have no nutritional value.

Vitamins from A-Zinc — Vitamin A

On January 2, 2010, in Fat Solubles, Vitamins, by Andrea

Vitamin A

Vitamin A — What is it?

Vitamin A is a generic term that refers to compounds with the biological activity of retinol.  These compounds include the precursor, or provitamin A carotenoids – principally beta-carotene, alpha-carotene, and beta-cryptoxanthin, which are provided in the diet by green, yellow, or orange vegetables and by some fruits, and preformed vitamin A, namely retinyl esthers (such as retinyl palmitate and retinyl acetate) and retinol itself which are present in foods of animal origin – mainly in organ meats such as liver, other meats, eggs, and dairy products.

Rarely in research, you may come across connotations of vitamins A1 and A2.  Vitamin A1 is retinol as mentioned above, while vitamin A2 is dehydroretinol, an oily yellow alcohol found in some fish that is 40% less active in mammals.  These differentiations are rare in common usage – retinol is typically called as such rather than vitamin A1 and the other vitamin A analogues such as beta-carotene do not have such distinctions as they are not technically vitamin A – just precursors to the vitamin.

What is it good for?


Regulation of gene expression

Immunity – commonly known as the anti-infective vitamin, it is required for normal function of the immune system; plays a central role in development and differentiation of white blood cells

Growth and Development – essential for embryonic development; during fetal development, retinonic acid (RA) functions in limb development and formation of heart, eyes and ears; RA has been found to regulate expression of the gene for growth hormone

Red Blood Cell Production – stem cells are dependant on retinoids for differentiation into red blood cells; vitamin A appears to facilitate mobilization of iron from storage to developing red blood cells for incorporation into hemoglobin

Where do I get it?

As a fat-soluble compound, beta-carotene’s absorption in the GI tract depends on the fat content of the meal with which it is eaten.  It is less easily absorbed than retinol and must be converted to retinol and retinal by the body.  For this reason, a conversion factor has been created to represent this.  The most recent international standard of measure for vitamin A is Retinol Activity Equivalents (RAE) which represent vitamin A activity as retinol.

2 micrograms (mcg) of supplemental beta-carotene can be converted by the body into 1mcg of retinol, giving it an RAE ratio of 2:1.

1 mcg of dietary vitamin A     =     1mcg retinol     =     1:1 RAE ratio
1 mcg supplemental vitamin A     =     1mcg retinol     =     1:1 RAE ratio
2mcg supplemental beta-carotene     =     1mcg retinol     =     2:1 RAE ratio
12mcg dietary beta-carotene     =     1mcg retinol     =     12:1 RAE ratio
24 mcg dietary alpha-carotene     =     1mcg retinol     =     24:1 RAE ratio
24mcg dietary beta-crytoxanthin     =     1mcg retinol     =     24:1 RAE ratio

1 IU = 0.3mcg of retinol

Food Sources

Food Vitamin A (IU)* %DV**
Liver, beef, cooked, 3 ounces 27,185 545
Liver, chicken, cooked, 3 ounces 12,325 245
Milk, fortified skim, 1 cup 500 10
Cheese, cheddar, 1 ounce 284 6
Milk, whole (3.25% fat), 1 cup 249 5
Egg substitute, ¼ cup 226 5
Food Vitamin A (IU)* %DV**
Carrot juice, canned, ½ cup 22,567 450
Carrots, boiled, ½ cup slices 13,418 270
Spinach, frozen, boiled, ½ cup 11,458 230
Kale, frozen, boiled, ½ cup 9,558 190
Carrots, 1 raw (7½ inches) 8,666 175
Vegetable soup, canned, chunky, ready-to-serve, 1 cup 5,820 115
Cantaloupe, 1 cup cubes 5,411 110
Spinach, raw, 1 cup 2,813 55
Apricots with skin, juice pack, ½ cup 2,063 40
Apricot nectar, canned, ½ cup 1,651 35
Papaya, 1 cup cubes 1,532 30
Mango, 1 cup sliced 1,262 25
Oatmeal, instant, fortified, plain, prepared with water, 1 cup 1,252 25
Peas, frozen, boiled, ½ cup 1,050 20
Tomato juice, canned, 6 ounces 819 15
Peaches, canned, juice pack, ½ cup halves or slices 473 10
Peach, 1 medium 319 6
Pepper, sweet, red, raw, 1 ring (3 inches diameter by ¼ inch thick) 313 6

Vitamin Sources

Most multivitamins contain vitamin A as a combination of a retinyl esther and beta-carotene.  There have been some studies showing a higher risk of osteoporsis in older adults taking more than 5,000 IU of retinol per day, which has led many companies to reduce the retinol content in their multivitamin supplements to 750mcg (2,500 IU).  Additionally, there have been some studies showing supplemental beta-carotene as a pro-oxident, meaning it helps grow free radicals in the body rather than reduce them.  However, there has not been a push to reduce or limit beta-carotene from multivitamin supplements as of yet.  In fact, there are some experts that still believe a separate RDA should be set specifically for beta-carotene should be set — one that is set approximately 6x the current RDA for the entire vitamin A RDA is today.

The current RDA for vitamin A is:

(mcg RAE)
(mcg RAE)
(mcg RAE)
(mcg RAE)
(mcg RAE)
1-3 300
(1,000 IU)
4-8 400
(1,320 IU)
9-13 600
(2,000 IU)
14-18 900
(3,000 IU)
(2,310 IU)
(2,500 IU)
(4,000 IU)
19+ 900
(3,000 IU)
(2,310 IU)
(2,565 IU)
(4,300 IU)

Keep in mind that the RDA is the amount needed to avoid deficiency symptoms – not to achieve an optimum level.  Unfortunately, there have been no studies conducted to determine what the optimum vitamin A level is as of now.


Severe zinc deficiency often accompanies vitamin A deficiency.  Zinc is required to make retinol binding protein (RBP), which transports vitamin A, so a zinc deficiency limits the body’s ability to move vitamin A stores from the liver to body tissues where they are needed.  Zinc also helps to protect against potential toxicity of retinol.  Additionally, a zinc deficiency results in decreased activity of the enzyme that releases retinol from it’s storage form, retinyl palmitate, in the liver.  Zinc is also required for the enzyme that converts retinol into retinal.  Despite these well-documented associations between zinc and vitamin A, the health consequences of zinc deficiency on vitamin A nutrition status in humans is still unclear as of now.

Vitamin A deficiency may exacerbate iron deficiency anemia.  Vitamin A supplementation has beneficial effects on iron deficiency anemia and has been show to improve iron nutritional stores status among children and pregnant women.  A combination of supplemental vitamin A and iron seems to reduce anemia more effectively than supplemental iron or supplemental vitamin A alone.  Additionally, there have been some studies in which iron deficient anemia has been helped by supplemental vitamin A, even in the absence of a vitamin A deficiency.

Night blindness is one of the first symptoms of vitamin A deficiency.  Vitamin A deficiency contributes to blindness by making the cornea very dry, which damages it and the retina.

Deficiency in A also diminishes the body’s ability to fight infections.  In vitamin A deficient individuals, the cells lining the lungs lose the ability to remove disease-causing microorganisms.  This may contribute to a larger amount of pneumonia cases seen in vitamin A deficient individuals.

Keep in mind that a subclinical deficiency does not exhibit the signs and symptoms of a deficiency, but still may have the adverse effects of the deficiency.  A mild form of deficiency may increase the risk of developing respitory or diarrheal infections, decrease growth rate and slow bone development in children, and decrease the liklihood to survive a serious illness.

A vitamin A deficiency early in life could have adverse effects on neurologic and behavioral development and function later in life.  Some researchers even believe that schizophrenia may result from vitamin A deficiency.


Hypervitaminosis A refers to a high storage level of vitamin A in the body that can lead to toxic symptoms.  Severe cases may result in liver damage, hemmorrhage, and coma, and may generally only occur in individuals with long-term consumption in excess of 8,000-10,000 mcg/day or 25,000-33,000 IU/day.

Acute toxicity is relatively rare.  Symptoms include nausea, vomiting, headache, fatigue, loss of appetite, dizziness, dry skin, desquamation, cerebral edema, bone and joint pain, blurred vision, lack of muscular function, and abnormal liver function.

It is important to note a few things about vitamin A toxicity.  First, the Upper Limit (UL) does not apply to malnourished individuals receiving vitamin A either periodically or through fortification programs as a measure of preventing a vitamin A deficiency.  Additionally, beta-carotene and other carotenoids in foods, even when consumed in high levels have not produced toxicity; therefore, the UL does not include the carotenoids.

0-1 600
(2,000 IU)
1-3 600
(2,000 IU)
4-8 900
(3,000 IU)
9-13 1,700 (5610 IU)
14-18 2,800 (9,240 IU) 2,800 (9,240 IU) 2,800 (9,240 IU) 2,800 (9,240 IU)
19+ 3,000 (10,000 IU) 3,000 (10,000 IU) 3,000 (10,000 IU) 3,000 (10,000 IU)

There are some troubling concerns with the two major forms of vitamin A found in supplements today.

Intakes of retinol not far above the RDA, but well under the UL may reduce bone mineral density and increase the risk of osteoporatic disease and breaks.  It is speculated that perhaps retinol increases the bone resorption response or perhaps interferes with vitamin D in the maintenance of calcium within the bones.  This problem has only been found with the retinol form of vitamin A and not with beta-carotene, which has caused some multivitamin manufacturers to limit the amount of retinol in their product to 750mcg (2,500 IU).  In fact, my bottle of Centrum has a warning about taking too much vitamin A in the form of retinol on the label.

My bottle of Centrum...

The picture for beta-carotene isn’t a bed of roses, either.  Believing beta-carotene to be a powerful anti-oxidant, researchers gave patients supplements of both retinol and beta-carotene supplements to ascertain exactly how good it really was.  The findings of the Beta-Carotene and Retinol Efficacy Trial (CARET) shocked everyone.  Results suggest that high-dose supplementation of vitamin A and beta-carotene should be avoided in people at high risk of lung cancer.  One hypothesis had to do with the high amount of oxidation in the lung tissue – but there were no definative conclusions reached except the spike of lung cancers in high risk individuals who received the extra supplementation.  Despite this higher risk, there has been no push to remove or reduce beta-carotene from multivitamins.  However, a quick Google search will find a few tailor-made vitamins without beta-carotene for smokers, at a premium price of course.


Under conditions of vitamin A adequacy, most mammals, including humans, store more than 90% of their total vitamin A in their liver.

The safety of vitamin A is frequently questioned during pregnancy.  With vitamin A, there is such a thing as “too little” as well as “too much.”  Vitamin A is important in fetal development during cellular and tissue differentiation.  Excess retinol during pregnancy is known to cause birth defects.  There have been no birth defects observed at doses of preformed A from supplements below 3,000mcg (10,000 IU/day), but since foods are commonly supplemented, it is advised to stay under 5,000 IU/day.  It should be noted that vitamin A from beta-carotene is not known to increase the risk of birth defects.

WLS Concerns

Beta-carotene is a poor supplement of vitamin A for those who have had RNY, DS, and VSG.

To begin with, beta-carotene requires an acidic environment to absorb properly.  A study was conducted to measure the absorption of retinol, retinyl palmitate, and beta-carotene in an achlorhydriac, or low gastric acidic environment.  To test the supplements, subjects were given a proton pump inhibitor (PPI) to neutralize gastric acidity over a period of time, then tested with a gastric probe to ensure the pH level.  Once a low gastric level was reached, individuals were given supplements, then serum levels were checked.  Serum concentrations of beta-carotene were significantly greater at a low gastric pH (ie normal) than those at a high gastric pH (ie achlorhydria, or low gastric acid environment).  Serum concentrations of retinol and retinyl palmitate were not significantly different between the low gastric pH and high gastric pH.  Those with a lower acid content will not absorb beta-carotene fully, if at all.  It is also important to note that as we age, even those of normal stomachs will begin to neutralize their gastric acidity.  This was confirmed by a study published in the New England Journal of Medicine in reference to the breakdown of calcium citrate versus carbonate — but the problem of acidity remains the same.

Additionally, beta-carotene is absorbed in the duodenum, which is bypassed in the RNY and DS procedures.  Since this absorption site is bypassed completely, beta-carotene does little-to-no good to patients with either surgery – especially coupled with the lower gastric-acid component present in both surgeries as well.

Those with Adjustable Gastric Bands (AGB’s) should take note as well – beta-carotene absorbs better when eaten with some fat.  Those who have been extreme in removing fat from their diets should note this key interaction.

For post-WLS patients who become deficient in vitamin A, one can find dry-form, or water-miscible forms of the vitamin.  It should be noted that labs should be watched carefully, as always, when supplementing.  There is some evidence that water-miscible forms of retinol vitamins can be more toxic than their oil-based counterparts – but the study conducted was on non-bypassed individuals who had no level of malabsorption.  There are many rules in the nutrition world that simply do not apply to us – but I’m not going to be the one to say which ones are which.  Labs are really your only guide to know where you stand nutritionally and you should follow them accordingly.

Information compiled from:

Handbook of Vitamins, 4th Edition
Linus Pauling Institute
Advanced Health and Life

Office of Dietary Supplements
Gastric acidity influences the blood response to a beta-carotene dose in humans
Water-miscible, emulsified, and solid forms of retinol supplements are more toxic than oil-based preparations
NEJM — Calcium absorption and achlorhydria