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Health news:
 
June 2010 - Dec 2013

Minimizing breast cancer risk

May 2010

Time to move beyond salt ?

Salt hypothesis vs. reality

Is sodium bad?

April 2010

Salt studies: the latest score

From Dahl to INTERSALT

Salt hypothesis' story

March 2010

Salt war

Do bone drugs work?

Diabetes vs. drugs, 3:0?

February 2010

The MMR vaccine war: Wakefield vs. ?

Wakefield proceedings: an exception?

Who's afraid of a littl' 1998 study?
 

January 2010

Antibiotic children

Physical activity benefits late-life health

Healthier life for New Year's resolution

 

December 2009

Autism epidemic worsening: CDC report

Rosuvastatin indication broadened

High-protein diet effects

 

November 2009

Folic acid cancer risk

Folic acid studies: message in a bottle?

Sweet, short life on a sugary diet

 

October 2009

Smoking health hazards: no dose-response

C. difficile warning

Asthma risk and waist size in women

 

September 2009

Antioxidants' melanoma risk: 4-fold or none?

Murky waters of vitamin D status

Is vitamin D deficiency hurting you?

 

August 2009

Pill-crushing children

New gut test for children and adults

Unhealthy habits - whistling past the graveyard?

 

July 2009

Asthma solution - between two opposites that don't attract

Light wave therapy - how does it actually work?

Hodgkin's lymphoma in children: better alternatives

 

June 2009

Hodgkin's, kids, and the abuse of power

Efficacy and safety of the conventional treatment for Hodgkin's:
behind the hype

Long-term mortality and morbidity after conventional treatments for pediatric Hodgkin's

 

May 2009

Late health effects of the toxicity of the conventional treatment for Hodgkin's

Daniel's true 5-year chances with the conventional treatment for Hodgkin's

Daniel Hauser Hodgkin's case: child protection or medical oppression?

April 2009

Protection from EMF: you're on your own

EMF pollution battle: same old...

EMF health threat and the politics of status quo
 

March 2009

Electromagnetic danger? No such thing, in our view...

EMF safety standards: are they safe?

Power-frequency field exposure
 

February 2009

Electricity and health

Electromagnetic spectrum: health connection

Is power pollution making you sick?

January 2009

Pneumococcal vaccine for adults useless?

DHA in brain development study - why not boys?

HRT shrinks brains

NEWS ARCHIVE
2009
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            6 

Vitamin A and your health

Vitamin A is fat soluble vitamin, which means that: (1) needs either dietary fat or bile in order to be absorbed, and (2) is more likely to be stored by the body (mostly in the liver). Since body stores vitamin A that it doesn't need immediately, you don't need to consume it daily, assuming that your total intake over several days covers your average daily needs.

In general, vitamins stored by the body can easier build up to a toxic level, thus more careful supplementation (or therapeutic use) is advised.

Vitamin A comes either from animal sources, as retinol, or from plant sources, as beta-carotene. Unlike retinol, beta-carotene is an inactive vitamin A form (provitamin A), which body converts to the active form on "as needed" basis. Thus beta-carotene has low toxicity potential, which makes it preferred vitamin A supplemental form. More so considering that vitamin A excess suppresses absorption and use of vitamin D. On the flip side, diabetics may have lowered ability to convert beta-carotene into usable vitamin A form.

In the typical American diet, nearly half of the vitamin A intake comes from animal sources (retinol), with the other half coming from beta-carotene.

Average dietary intake of vitamin A in the U.S. is estimated to be below the DRI, but not significantly. Its body levels can be further compromised by inefficient absorption which, among other factors, can result from gastrointestinal disorders or excessive alcohol intake. Also, since the body needs zinc in order to use vitamin A, zinc deficiency can cause vitamin A deficiency, not correctable with vitamin A supplementation alone.

Most important functions of vitamin A are in assisting vision, immune system support and cell differentiation (multiplying). Vitamin A deficiency brings on "night blindness" in adults as an early symptom, and further deterioration of vision with prolonged deficiency. In children, prolonged severe deficiency can cause permanent blindness; an estimated 1/3 million of children, mostly in poor countries, become blind every year as a result of prolonged vitamin A deficiency.

Disturbances in cell differentiation caused by vitamin A deficiency cause deterioration in the appearance and function of the skin, lung and intestinal tissue, with a number of related symptoms possible. Vitamin A also protects and stimulates thymus gland, and enhances white blood cells activity. Hence, deficiency results in lowered resistance to infectious diseases - especially viral infections - and cancer.

Vitamin A toxicity is, as mentioned, limited to retinol. Acute intake of over 200mg can cause nausea, vomiting and other acute symptoms (this is an average response; toxic dose for retinol, as for any other compound, varies significantly individually). Longer-term excessive intake of 10 times DRI, or more, can cause hair loss, muscle and bone pain, liver damage and birth defects.

Vitamin A DRI (Dietary Reference Intakes, the most recent set of dietary recommendations set by the government) for an average healthy adult female is 0.7mg (700μg) and 0.9mg (900μg) of retinol activity equivalents (RAE) for male. Retinol activity equivalent equals:

1μg (microgram) of retinol,
12μg of beta-carotene (it takes 12 times as much of beta-carotene to produce similar effect), and
24μg for other carotenoids.

This is relatively new standard, introduced by the U.S. Institute of Medicine in 2001. It is based on empirical observations, and applies to the population of developed countries (for instance, in Indonesia and Vietnam - perhaps due to their diets lower in fats - 1 RAE for beta carotene is 21μg).

The older standard, set by FAO (Food and Agriculture Organization of the United Nations) in 1965, uses retinol equivalent (RE) as a unit measure, with 1 RE equaling:

  1μg of retinol
  6mcg of beta carotene (2μg for oil-based supplemental form), and
  12μg of other carotenoids.

This standard is based on an estimated 50% lower activity of beta carotene (mainly established in experiments on rats) combined with estimated 33% absorption in humans (rough average, since experiments showed wide 1-88% variations in the rate of absorption).

Yet another standard, so called International Unit (IU) System, applies the 50% lower activity for beta carotene, but not the 33% absorption factor. With 1 international unit set as:

1 IU = 0.3μg of retinol = 0.6μg of beta carotene = 1.2μg of other carotenoids

conversion from the FAO RE standard to IU is as follows:

1 RE = 3.33 IU = 10 IU of beta carotene = 20 IU of other carotenoids

(1RE = 10IU comes from 1RE = 6μg of beta carotene, hence tenfold the content of a single International Unit of 0.6μg for it).

To translate all this into DRI for vitamin A, recommended intake for an adult female of 700μg of RAE equals 700μg, or 700x3.33=2,333 IU of retinol, while 700x12=8,400μg (8.4mg), or 8,400/0.6=14,000 IU of beta carotene.

Likewise, for adult male they are 900μg/3000IU of retinol, or 10,800μg/18,000IU of beta carotene.

While the presence of lipid is important for absorption of vitamin A in general, it is particularly important for absorption of beta carotene. A 2004 study (White and Brown) found no absorption of beta carotene from green salad w/o lipid in any form, and good absorption when lipid (canola oil) was added. This means that you might be having little use of of a carrot or carrot juice, if consumed without lipids.

To further complicate the matter, absorption rate for beta carotene  - as well as nutrients in general - also varies with its meal content. It is established that average absorption for a meal containing up to 1,000μg (1mg) beta carotene is about 50%, dropping to 33% for 1 to 4mg meal content, and to 20% for beta carotene meal content over 4mg.

With respect to supplemental beta carotene, natural form is preferred to synthetic. The latter has been associated with increased risk of developing lung cancer in smokers. While no factual link has been established, some mechanisms leading to such outcome are possible. One is that higher supplemental doses of synthetic beta carotene may interfere with absorption of antioxidants, with synthetic beta carotene itself being rather weak protection from oxidative damage. It may also interact with fluoride and chlorine, increasing their level in the body17. In addition, as studies on animals indicate, high level of antioxidants colud interfere with anti-cancer activity of natural killer lymphocytes.

Best natural food sources of retinol are fish liver oils, liver and eggs. Best food sources of beta-carotene are yellow fruits and vegetables and green leafy vegetables. R

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