67 replies to this topic

[FunkOdyssey]

Read the following, and after you are done, stay on the extra safe side by instead of a 10:1 ratio of A to D, stick to a 6:1 ratio of D to A. 6000IU of vitamin D3 to 1000IU of natural vitamin A (retinol).

How did you arrive at this 6:1 D to A ratio, especially if you subscribe to Weston Price views on the function and dietary requirements of these two Vitamins? Why wouldn't the ratio favor a higher intake of Vitamin A?

Edited by FunkOdyssey, 07 January 2009 - 12:24 AM.

[stephen_b]

Read the following, and after you are done, stay on the extra safe side by instead of a 10:1 ratio of A to D, stick to a 6:1 ratio of D to A. 6000IU of vitamin D3 to 1000IU of natural vitamin A (retinol).

How did you arrive at this 6:1 D to A ratio, especially if you subscribe to Weston Price views on the function and dietary requirements of these two Vitamins? Why wouldn't the ratio favor a higher intake of Vitamin A?

In the editorial to the Annals of
Otology, Rhinology, and Laryngology late this year, Cannell et al wrote:

Our main concern with the previous work of Linday et al is the cod liver
oil. They gave their children approximately 3,500 to 5,000 IU/d of
preformed retinol, although none of their children had low serum retinol
levels. However, they only administered 700 IU/d of vitamin D.
(International units of vitamin A and vitamin D ar not comparable.) We
believe, first, that the ratio of the vitamins should be reversed ...

Reversing the ratio would give a D:A ratio of roughly 6 to 1 (in IU/IU).

The commentary is titled "Cod Liver Oil, Vitamin A Toxicity, Frequent
Respiratory Infections, and the Vitamin D Deficiency Epidemic",
available here for $20 US.

Edited by stephen_b, 07 January 2009 - 04:15 AM.

[FunkOdyssey]

Rebuttal to Cannell (please digest this and comment): http://www.greenpasture.org/node/115

[FunkOdyssey]

Here's the reason for my recent interest in Vitamin A:

J Infect Dis. 1996 Oct;174(4):747-51.
Vitamin A deficiency exacerbates murine Lyme arthritis.
Cantorna MT, Hayes CE.

Department of Biochemistry, University of Wisconsin-Madison 53706, USA.

Vitamin A deficiency predisposes the host for a strong inflammatory response, suggesting that it may foster susceptibility to diseases, such as Lyme arthritis, in which activated macrophage and inflammatory cytokine production are pathogenic. Infected mice had a rapid serum retinal decline that correlated with the onset of arthritis. The mice with the least retinol developed acute arthritis earlier and more severely than those with the highest retinol. Earlier and stronger interleukin (IL)-12, interferon-gamma (IFN)-gamma, and tumor necrosis factor responses were found in Borrelia burgdorferi-infected, vitamin A-deficient mice compared with controls. The spirochetes induced IFN-gamma secretion from unprimed cells, and retinoid addition in vitro inhibited IFN-gamma synthesis. Vitamin A deficiency may exacerbate acute Lyme arthritis by enhancing an acute arthritogenic inflammatory response initiated by spirochete-driven IFN-gamma secretion. Conversely, vitamin A may lessen acute Lyme arthritis pathology by blocking IFN-gamma and IL-12 synthesis.

Przegl Epidemiol. 2005;59(1):35-41.
[Vitamin A, E and C serum concentration in patients with Borrelia burgdorferi antibodies--non-symptomatic carriers]
[Article in Polish]

Pancewicz SA, Skrzydlewska E, Hermanowska-Szpakowicz T, Stankiewicz A, Sniecińska A, Kondrusik M, Zajkowska J, Swierzbińska R.

Klinika Chorób Zakaznych i Neuroinfekcji AMB.

To estimate vitamin A, E and C serum concentrations among forestry workers showing antibodies against Borrelia burgdorferi presence. Vitamins A, E and C concentrations were evaluated in 117 sera of forestry workers. 78 persons aged 18-63 (x=43.07) showed antibodies against Borrelia burgdorferi presence. In this group 13 persons showed presence of IgM, 42 persons with IgG and 23 with IgM and IgG. Control group consisted of 39 persons aged 18-56 years (x=40,97), with no detectable anti-Borrelia burgdorferi antibodies in serum. Serologic diagnosis was performed with use of ELISA kit - Borrelia recombinant IgM, IgG (Biomedica, Austria). Vitamins A and E serum concentrations were detected by RP-HPLC method with spectrophotometric detection (De Leenheet and co.). Vitamin C was detected by RP-HPLS method with spectrophotometric method (Ivanovic and co). Obtains results were statistically analysed. Significantly lower of vitamin A and E serum concentration of persons with anti-borrelia antibodies presence. The lowest concentration was observed in group showing presence of IgM and IgG. No significant difference in vitamin C serum concentration in examined groups was observed. These results may suggest that low serum concentrations of vitamin A and E may have influence on Borrelia burgdorferi infection development.

PMID: 16013408

Edited by FunkOdyssey, 07 January 2009 - 05:07 PM.

[stephen_b]

Funk, I found these products interesting, and I'm going to try the capsules for myself. I'm going to continue with 7500 IU of Jarrow D3 too. The butter oil itself is high in K2-MK4 (though I do wish that exact levels were specified), and the unprocessed cod liver oil is high in A and D.

I was unaware that most cod liver oils remove much of vitamin A and most of vitamin D in their processing and then add back synthetic vitamin A (retinol palmitate). I'm somewhat reassured about vitamin A toxicity after reading some of the links you provided and some whole health source blog postings here and here.

StephenB

[FunkOdyssey]

I don't like the unknown quantity of K2 either (dislike it enough that I would not use the product). I don't really see any advantage of these products over what is typically available elsewhere, you can get natural vitamin A from fish liver oil on iherb, cholecalciferol is cholecalciferol, and measured quantities of K2 are preferable. Also, I hope you have been or are planning to be tested for 25OHD in the near future because that is a very high level of supplementation.

[TheLion]

Our main concern with the previous work of Linday et al is the cod liver oil. They gave their children approximately 3,500 to 5,000 IU/d of preformed retinol, although none of their children had low serum retinol levels. However, they only administered 700 IU/d of vitamin D. (International units of vitamin A and vitamin D ar not comparable.) We believe, first, that the ratio of the vitamins should be reversed ...

I don't have an immediate source to back up my claim here, but I have read information from Krispin Sullivan, a woman knowledgeable on the subject of vitamin D, fat-soluble vitamins, and nutrition, that serum tests for retinol are not indicative of tissue - skin, liver, and organ levels of vitamin A. With that said, it is arguable that formulating suggestions to avoid natural food sources providing pre-formed retinol based partly on normal serum vitamin A test results is flawed.

Additionally, in the response to the Cannell study citing 'toxicity of cod liver oil' that FunkOdyssey previously linked to a few posts back, I just wanted to call out this specific excerpt from Sally Fallon:

WAPF Cod Liver Oil Update Dec 2008

In order for vitamin D to activate the expression of its target genes, it must bind to the vitamin D receptor (VDR) and then combine with the retinoid X receptor (RXR), which is activated by a particular form of vitamin A called 9-cis retinoic acid. RESEARCHERS FROM SPAIN RECENTLY SHOWED THAT VITAMIN D CAN ONLY EFFECTIVELY ACTIVATE TARGET GENES WHEN ITS PARTNER RECEPTOR IS ACTIVATED BY VITAMIN A. In the ABSENCE OF VITAMIN A, molecules called "corepressors" bind to the VDR/RXR complex and PREVENT vitamin D from functioning.

I have a hard time swallowing the blanket recommendations from the D council to avoid natural sources of pre-formed retinols from otherwise our most nutrient-dense foods (liver, cod liver oil, etc.)

It their claims of vitamin A blocking the effects of or inhibitively competing with vitamin D were true, then how was Weston Price able to record the resolution of bone loss and unhealed fractures in nutritionally malnourished children and other unhealthy subjects after providing them with nutrient dense foods and super-food supplements like high-vitamin cod liver oil and high-vitamin butter oil?

The cod liver oil supplied vitamin D to facilitate calcium absorption, but it also most likely contained significant amounts of natural vitamin A complex. Additionally, the butter oil also provided an excellent source of vitamin A and K2 (activator X), which have been proposed to play a synergistic role in the proper utilization of vitamin D and minerals from the diet.

I would guess that the vitamin A content of the meals and supplements provided to his subjects was higher than the vitamin D content, yet he consistently observed the same beneficial effects when providing the nutrition. If the blanket, isolated argument that vitamin A from animal sources is toxic and counteractive of the vitamin D provided by such nutrition, and causative of bone loss, then how was he able to measure increases in skeletal mineralization (and in certain cases complete mending of unset fractures) after applying such nutrition?

I remain completely open minded to the idea of an excess of vitamin A causing problems in the presence of vitamin D deficiency, but I must admit that it is difficult to take recommendations about avoiding all preformed retinols, especially those found in natural, otherwise very nutrient dense foods, from someone who clearly doesn't share my views (and many other individuals) on human evolution and diet.

[stephen_b]

On the subject of synthetic retinal palmitate, is it a different molecule from the vitamin A found in cod liver (before processing)?

StephenB

[krillin]

Also, it's mixed natural beta carotene along with the others such as cryptoaxanthin. So no smoker-synthetic beta carotene concern.

I think the only difference between synthetic and natural beta carotene is that the synthetic is absorbed better. The body can convert cis to trans and vice versa. In the first abstract below, with equal doses of synthetic and natural, the synthetic group actually ended up with higher cis levels than the natural group. In the second abstract, a dose of nearly all cis ended up as nearly all trans in plasma.

Lipids. 1995 Jun;30(6):493-8.
9-cis beta-carotene in human plasma and blood cells after ingestion of beta-carotene.
Tamai H, Morinobu T, Murata T, Manago M, Mino M.
Department of Pediatrics, Osaka Medical College, Japan.

For 44 wk, thirty male volunteers were given daily either 60 mg of synthesized all-trans beta-carotene, a naturally-occurring beta-carotene derived from Dunaliella bardawil, or a placebo. Basal levels of 9-cis beta-carotene in plasma, platelets, and mononuclear cells were 10, 20, and 25% of those of the all-trans form, respectively. The plasma levels reached a maximum after two weeks of administration and plateaued thereafter in the subjects who took the beta-carotene preparations. The all-trans beta-carotene level in the subjects given the synthesized all-trans form was almost twice that for the Dunaliella preparation. The plasma 9-cis level was found to be higher in the all-trans beta-carotene group than in the Dunaliella group, despite no intake of the 9-cis form in the all-trans group and the higher intake of the 9-cis form in the Dunaliella group. This finding suggests that isomerization of the all-trans form to the 9-cis form may occur in the body either during or after absorption.

PMID: 7651075

Am J Clin Nutr. 1996 Aug;64(2):177-83.
Evidence of cis-trans isomerization of 9-cis-beta-carotene during absorption in humans.
You CS, Parker RS, Goodman KJ, Swanson JE, Corso TN.
Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.

Absorption and metabolism of [13C]9-cis-beta-carotene ([13C]9c beta C) was studied in three subjects after a single oral dose. Subjects given 1.0 mg [13C]beta-carotene (mean: 99.4% 9-cis-beta-carotene, 0.6% all-trans-beta-carotene; dose A) had substantial concentrations of [13C]all-trans-beta-carotene ([13C]tr beta C) and [13C]all-trans retinol ([13C]retinol) but very low concentrations of [13C]cis-beta-carotene ([13C]cis beta C) in saponified plasma 5 h after dosing, as determined by HPLC and isotope-ratio mass spectrometry. There was no evidence of appreciable absorption of [13C]9-cis retinol. To determine the proportion of [13C]tr beta C and [13C]retinol derived from [13C]9c beta C, a second set of studies in the same subjects was performed with the same isomeric composition except with 13C labeling only in all-trans-beta-carotene (dose B). The results indicated that > 95% of plasma [13C]tr beta C and [13C]retinol observed after dose A was derived from [13C]9c beta C. The concentrations of [13C]tr beta C observed, in excess of that derived from the trace amounts of [13C]tr beta C in the dose, indicated that a significant proportion of the [13C]9c beta C dose was isomerized to [13C]tr beta C before entering the bloodstream. Although precise quantitative estimates of the extent of isomerization of 9-cis-beta-carotene could not be made, it is apparent that cis-trans isomerization of 9-cis-beta-carotene to all-trans-beta-carotene contributed to the near absence of postprandial plasma 9-cis-beta-carotene after its oral administration in humans. The observation of different ratios of beta-carotene to retinol between the two dosing protocols suggests that isomerization did not occur exclusively before uptake by the intestinal mucosa. These results indicate that isomerization of ingested 9-cis-beta-carotene before its secretion into the bloodstream limits the potential supply of 9-cis retinoids to tissues, and increases the vitamin A value of 9-cis-beta-carotene.

PMID: 8694017

Edited by krillin, 14 March 2009 - 04:49 AM.

[krillin]

Let's see what we can dig up about an optimal A intake. The RDA is more than covered by my vegetable intake, but I take 10,000 IU preformed A once per week because of that genomic stability study. I'm not taking any more without a good reason, because all the vitamin A supplement studies I've found are depressing. I'm also not encouraged by the butter data. (Besides, olive oil was used by the 300, and look at how awesome they were.)

Br J Cancer. 2001 Mar 2;84(5):728-35.
Diet, smoking and lung cancer: a case-control study of 1000 cases and 1500 controls in South-West England.
Darby S, Whitley E, Doll R, Key T, Silcocks P.
ICRF/MRC/BHF Clinical Trial Service Unit & Epidemiological Studies Unit, Radcliffe Infirmary, Harkness Building, Oxford, OX2 6HE, UK.

We have examined the relationship between diet and lung cancer in a case-control study of 982 cases of lung cancer and 1486 population controls in south-west England in which subjects were interviewed personally about their smoking habits and their consumption of foods and supplements rich in retinol or carotene. Analyses were performed for 15 dietary variables, including intake of pre-formed retinol and carotene. There were significant associations (P< 0.01) with lung cancer risk for 13 of the variables, eight of which remained after adjustment for smoking. When the 15 variables were considered simultaneously, independent significant associations remained for 5: pre-formed retinol (increased risk), and fish liver oil, vitamin pills, carrots and tomato sauce (decreased risk). It is unlikely that all five associations represent biological effects, or that they can all be explained by residual confounding by smoking, or by biases. We conclude that there is at least one as yet unidentified factor that is causally related to lung cancer risk and of considerable importance in terms of attributable risk in this population. Copyright 2001 Cancer Research Campaign.

PMID: 11237398

Int J Cancer. 2000 Jun 1;86(5):626-31.
Role of macronutrients, vitamins and minerals in the aetiology of squamous-cell carcinoma of the oesophagus.
Franceschi S, Bidoli E, Negri E, Zambon P, Talamini R, Ruol A, Parpinel M, Levi F, Simonato L, La Vecchia C.
Servizio di Epidemiologia, Centro di Riferimento Oncologico, Aviano, Italy. epidemiology@ets.it

Between 1992 and 1997 we conducted a case-control study of oesophageal cancer in 3 areas of northern Italy. Cases were 304 patients (29 women), ages 39-77 years (median age 60 years), with a first incident squamous-cell carcinoma (SCC) of the oesophagus. Controls were 743 patients (150 women), ages 35-77 years (median age 60 years), admitted for acute illnesses, unrelated to tobacco and alcohol, to major hospitals of the areas under surveillance. We derived estimates of daily dietary intake of 6 macronutrients, cholesterol, and 20 micronutrients or minerals from a validated food-frequency questionnaire, including 78 food groups and recipes and 15 questions on individual eating patterns. After allowance for age, gender, area of residence, education, body mass index, physical activity, smoking habit, alcohol consumption and energy intake, most micronutrients were inversely associated with oesophageal SCC risk. Highly significant associations emerged for monounsaturated fatty acids [odds ratio (OR) in highest vs. lowest intake quintile = 0.5]; carotene (OR = 0.3); lutein + zeaxanthin (OR = 0.4); vitamin C (OR = 0.4); and niacin (OR = 0.5). Only retinol appeared to be positively related to risk (OR = 1.9). The effect of the above nutrients, expressed as ORs, appeared to be similar in non-smokers and smokers, and non/light drinkers and heavy drinkers. Copyright 2000 Wiley-Liss, Inc.

PMID: 10797282

Cochrane Database Syst Rev. 2008 Apr 16;(2):CD007176.
Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases.
Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C.
Copenhagen University Hospital, Rigshospitalet, Department 3344,Copenhagen Trial Unit, Centre for Clinical Intervention Research, Blegdamsvej 9, Copenhagen, Denmark, DK-2100. goranb@junis.ni.ac.yu

BACKGROUND: Animal and physiological research as well as observational studies suggest that antioxidant supplements may improve survival. OBJECTIVES: To assess the effect of antioxidant supplements on mortality in primary or secondary prevention randomised clinical trials. SEARCH STRATEGY: We searched The Cochrane Library (Issue 3, 2005), MEDLINE (1966 to October 2005), EMBASE (1985 to October 2005), and the Science Citation Index Expanded (1945 to October 2005). We scanned bibliographies of relevant publications and wrote to pharmaceutical companies for additional trials. SELECTION CRITERIA: We included all primary and secondary prevention randomised clinical trials on antioxidant supplements (beta-carotene, vitamin A, vitamin C, vitamin E, and selenium) versus placebo or no intervention. Included participants were either healthy (primary prevention trials) or had any disease (secondary prevention trials). DATA COLLECTION AND ANALYSIS: Three authors extracted data. Trials with adequate randomisation, blinding, and follow-up were classified as having a low risk of bias. Random-effects and fixed-effect meta-analyses were performed. Random-effects meta-regression analyses were performed to assess sources of intertrial heterogeneity. MAIN RESULTS: Sixty-seven randomised trials with 232,550 participants were included. Forty-seven trials including 180,938 participants had low risk of bias. Twenty-one trials included 164,439 healthy participants. Forty-six trials included 68111 participants with various diseases (gastrointestinal, cardiovascular, neurological, ocular, dermatological, rheumatoid, renal, endocrinological, or unspecified). Overall, the antioxidant supplements had no significant effect on mortality in a random-effects meta-analysis (relative risk [RR] 1.02, 95% confidence interval [CI] 0.99 to 1.06), but significantly increased mortality in a fixed-effect model (RR 1.04, 95% CI 1.02 to 1.06). In meta-regression analysis, the risk of bias and type of antioxidant supplement were the only significant predictors of intertrial heterogeneity. In the trials with a low risk of bias, the antioxidant supplements significantly increased mortality (RR 1.05, 95% CI 1.02 to 1.08). When the different antioxidants were assessed separately, analyses including trials with a low risk of bias and excluding selenium trials found significantly increased mortality by vitamin A (RR 1.16, 95% CI 1.10 to 1.24), beta-carotene (RR 1.07, 95% CI 1.02 to 1.11), and vitamin E (RR 1.04, 95% CI 1.01 to 1.07), but no significant detrimental effect of vitamin C (RR 1.06, 95% CI 0.94 to 1.20). Low-bias risk trials on selenium found no significant effect on mortality (RR 0.91, 95% CI 0.76 to 1.09). AUTHORS' CONCLUSIONS: We found no evidence to support antioxidant supplements for primary or secondary prevention. Vitamin A, beta-carotene, and vitamin E may increase mortality. Future randomised trials could evaluate the potential effects of vitamin C and selenium for primary and secondary prevention. Such trials should be closely monitored for potential harmful effects. Antioxidant supplements need to be considered medicinal products and should undergo sufficient evaluation before marketing.

PMID: 18425980

Int J Cancer. 2000 Jul 15;87(2):289-94.
Food groups and risk of squamous cell esophageal cancer in northern Italy.
Bosetti C, La Vecchia C, Talamini R, Simonato L, Zambon P, Negri E, Trichopoulos D, Lagiou P, Bardini R, Franceschi S.
Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy. bosetti@irfmn.mnegri.it

To better understand the nutritional etiology of squamous cell esophageal cancer, we conducted a case-control study in 3 areas of northern Italy. A total of 304 incident, histologically confirmed cases of squamous cell carcinoma of the esophagus (275 men, 29 women) and 743 hospital controls (593 men, 150 women) with acute, non-neoplastic conditions, not related to smoking, alcohol consumption or long-term diet modification, were interviewed during 1992 to 1997. The validated food-frequency questionnaire included 78 questions on food items or recipes, which were then categorized into 19 main food groups, and 10 questions on fat intake pattern. After allowance for age, sex, education, area of residence, tobacco smoking, alcohol drinking and non-alcohol energy, a significant increased risk emerged for high consumption of soups (OR=2.1 for the highest vs. lowest quintile), whereas inverse associations with esophageal cancer risk were observed for pasta and rice (OR=0.7), poultry (OR=0.4), raw vegetables (OR=0.3), citrus fruit (OR=0.4) and other fruit (OR=0.5). The associations with dietary habits were consistent in different strata of tobacco smoking and alcohol drinking. Among added lipids, olive oil intake showed a significant reduction of esophageal cancer risk, even after allowance for total vegetable consumption (OR=0.4), while butter consumption was directly associated with this risk (OR=2.2). Our results thus provide further support to the evidence that raw vegetables and citrus fruit are inversely related to the risk of squamous cell esophageal cancer and suggest that olive oil may also reduce this risk. Copyright 2000 Wiley-Liss, Inc.

PMID: 10861489

Int J Cancer. 1998 Mar 30;76(1):7-12.
Diet and squamous-cell cancer of the oesophagus: a French multicentre case-control study.
Launoy G, Milan C, Day NE, Pienkowski MP, Gignoux M, Faivre J.
Registre des cancers digestifs du Calvados (CJF INSERM 9603), Caen, France.

An increasing number of reports suggest that diet has an impact on oesophageal cancer risk in Western countries, where alcohol and tobacco are held to be the major determinants of the risk. The aim of our study was to identify dietary factors influencing the risk of oesophageal cancer in France and to determine whether certain of these could explain some of the geographical variations. We conducted a multicentre case-control study in 3 regions expected to have different diet and drinking habits (Normandy, Burgundy and Midi Pyrénées). Two hundred eight cases and 399 controls, all males, were interviewed about their eating, drinking and smoking habits. After proper adjustment for drinking and smoking, high consumption of butter and low consumption of fresh fish, vegetables and fruits were associated strongly and independently with an increase in oesophageal-cancer risk. Consistently, cholesterol appeared as a risk factor and vitamin E, vitamin D and phosphorus as independent protective factors. The protective effect of citrus and other fresh fruits (vitamin C) was confined strictly to heavy drinkers. Our findings suggest that more than one-third of the high incidence of oesophageal cancer in northwest France could be explained by the local excess in butter consumption, whereas geographical variations in consumption of dietary protective factors could explain no more than 10% of it. Overall, a large proportion (57%) of the excess incidence of oesophageal cancer in northwest France could be explained by local dietary habits, e.g., drinking hot Calvados liquor and excessive consumption of butter.

PMID: 9533754

Cancer Causes Control. 2007 Dec;18(10):1153-67.
Pancreatic cancer, animal protein and dietary fat in a population-based study, San Francisco Bay Area, California.
Chan JM, Wang F, Holly EA.
Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA 94118-1944, USA.

OBJECTIVE: The associations between animal protein or fat and risk of pancreatic cancer have been reported previously with inconsistent results. A population-based case-control study of pancreatic cancer was conducted in the San Francisco Bay Area to examine these associations. METHODS: A semi-quantitative food-frequency questionnaire was administered to 532 cases and 1,701 controls between 1995 and 1999. Odds ratios (OR) and 95% confidence intervals (CI) were computed as estimates of the relative risk of pancreatic cancer. RESULTS: When comparing highest versus lowest levels of intake in multivariable adjusted models, positive associations were observed for several beef/lamb and individual animal protein items, including beef/lamb as a main dish (OR = 2.2, 95% CI: 1.0-4.5), regular hamburger (OR = 1.7, 95% CI: 1.2-2.4), whole eggs (OR = 1.6, 95% CI: 1.0-2.4), butter (OR = 2.4, 95% CI: 1.6-3.5), and total dairy not including butter (OR = 2.6, 95% CI: 1.8-3.7). Some high-fat/processed-meat products (i.e., sausage, salami, bacon), but not all (i.e., beef, pork, or poultry hot dogs), also were positively associated with risk. An inverse association was noted for greater chicken/turkey consumption (OR = 0.7, 95% CI: 0.5-1.0). The risk comparing the highest versus lowest quartiles for fats and cholesterol consumption were: total fat (OR = 1.6, 95% CI: 1.2-2.1); animal fat (OR = 1.9, 95% CI: 1.4-2.5); saturated fat (OR = 1.9, 95% CI: 1.4-2.6); monounsaturated fat (OR = 1.3, 95% CI: 1.0-1.8); and dietary cholesterol (OR = 1.5, 95% CI: 1.1-2.0, all p-trends < or = 0.02). CONCLUSIONS: These data provide some evidence that beef or lamb, eggs, dairy, fat, or cholesterol may increase the risk of pancreatic cancer.

PMID: 17805983

J Egypt Public Health Assoc. 2006;81(3-4):143-63.
Risk factors of Cancer Prostate A case control study.
Kamel NM, Tayel ES, El Abbady AA, Khashab SS.
Department of Community Medicine, Faculty of Medicine, Alexandria University, Alexandria, Egypt. nahidmkamel@yahoo.com.

The purpose of this study is to reveal the different risk factors related to this cancer particularly that there is no agreement about which factors affect the risk. A fishing expedition hospital based case control study was carried out. Cases and controls were identified from the Urology Department of Alexandria Main University Hospital, 2004. All cases diagnosed as having the tumor were included in the case series. For each case the second subject proved to have a negative pathological examination was included in the control group (50).Data collection was carried out blindly using a structured interview schedule. Analysis was applied using Chi-square test, Fisher exact and Student's t-test. Odds Ratios and 95% Confidence Intervals were calculated. Results indicated that regular consumption of sausages was greater among cases than controls (X(2)= 10.19, p= 0.001 and an odds ratio of 5.92 (CI: 1.69-25.99). Also more cases claimed consuming regularly butter and natural ghee than controls (X(2)= 5.47, p= 0.019). The estimate risk was as high as 2.79 (Cl: 1.07-7.33). However regular consumption of vegetables was more encountered among controls than cases (X(2) = 5.005, p= 0.025 where the odds ratio was 0.19 (Cl: 0.02-1.01). Moreover the multiple regression analysis confirmed the results obtained from univariate analysis. The consistency of results of current work as regards sausages and butter with several other research works can support the identification of these specific possible risk factors. Also other research workers pointed out to the protective effect of vegetables. However further research is needed to address other risk factors.

PMID: 17382058

[VespeneGas]

hmmm. The first abstract you posted indicates that fish liver oil consumption is inversely correlated with lung cancer risk. Yet fish liver oil is high in "pre-formed retinol", which was associated with increased risk. Well, I'm glad I get my extra A from fish liver oil anyway, but that still puzzles me.

I'm a bit wary of any study of A or D that doesn't take into account the other and K2 status, because (seemingly) healthy vitamin A intake in a vitamin D insufficient state has led to epidemic osteoporosis among the elderly in the US. Healthy D levels without K2 can cause soft-tissue calcification (yikes). Ergo, I'm not sure how applicable vitamin A consumption data is to us, who have higher 25(OH)D and K2 status than the average citizen.

Makes my head spin sometimes.

[TheLion]

I'm a bit wary of any study of A or D that doesn't take into account the other and K2 status, because (seemingly) healthy vitamin A intake in a vitamin D insufficient state has led to epidemic osteoporosis among the elderly in the US. Healthy D levels without K2 can cause soft-tissue calcification (yikes). Ergo, I'm not sure how applicable vitamin A consumption data is to us, who have higher 25(OH)D and K2 status than the average citizen.

Agreed.

Edited by TheLion, 14 March 2009 - 04:42 PM.

[krillin]

hmmm. The first abstract you posted indicates that fish liver oil consumption is inversely correlated with lung cancer risk. Yet fish liver oil is high in "pre-formed retinol", which was associated with increased risk.

Omega-3 compensated, most likely. Here's something I dug up for First Immortal last July.

Nutr Cancer. 2005;52(2):121-9.
Nutritional intervention with omega-3 Fatty acids in a case of malignant fibrous histiocytoma of the lungs.
Pardini RS, Wilson D, Schiff S, Bajo SA, Pierce R.
Department of Biochemistry, College of Agriculture, Biotechnology and Natural Resources, University of Navada, Reno, NV 89557, USA. ronp@cabnr.unr.edu

We present a case of a 78-yr-old man with malignant fibrous histiocytoma with multiple lesions in both lungs. Following diagnosis, he declined conventional chemotherapy and elected nutritional intervention by increasing intake of omega-3 fatty acids and lowering intake of omega-6 fatty acids. We estimated that he consumed 15 g of the long-chain omega-3 fatty acids eicosapentaenoic (EPA) and docosahexaenoic acid (DHA) per day, and the ratio of linoleic acid/long-chain omega-3 fatty acids in his diet was 0.81. Serial computed tomography scans and pulmonary x-rays revealed remarkably a slow and steady decrease in the size and number of bilateral nodules. He has no apparent side effects from consuming large quantities of fish and algae oils rich in DHA and EPA and he remains asymptomatic.

PMID: 16201843

I'm a bit wary of any study of A or D that doesn't take into account the other and K2 status, because (seemingly) healthy vitamin A intake in a vitamin D insufficient state has led to epidemic osteoporosis among the elderly in the US. Healthy D levels without K2 can cause soft-tissue calcification (yikes). Ergo, I'm not sure how applicable vitamin A consumption data is to us, who have higher 25(OH)D and K2 status than the average citizen.

If thousands of A IU per day is seemingly healthy, then it should be pretty easy to come up with data to support long-term use at that level. I couldn't find any, but the A literature is so vast I could easily have missed it. Hence my request for input.

[TheLion]

If thousands of A IU per day is seemingly healthy, then it should be pretty easy to come up with data to support long-term use at that level. I couldn't find any, but the A literature is so vast I could easily have missed it. Hence my request for input.

Krillin, perhaps I can offer something. Administration of high-dose vitamin A (in most cases synthetic retinyl palmitate) has been used, at least as an adjunct, to address cancer. This approach is more common in the alternative health field. The study I cite below illustrates this use and also concludes that administration of extremely high doses is concluded to be reasonably safe for time-frames of up to 2 years.

Laboratory evaluation during high-dose vitamin A administration: a randomized study on lung cancer patients after surgical resection.

Summary The laboratory findings in patients receiving high-dose vitamin A as adjuvant treatment for stage I lung cancer are here reported. A group of 283 patients were randomized to either treatment with retinyl palmitate (300 000 IU daily for 12 months) or standard followup, and are now evaluable after a median observation period of 28 months. At regular intervals, all the patients underwent a physical examination, chest roentgenogram, blood chemistries, haematological assays, hepatic and renal function tests and determinations of serum triglycerides and cholesterol. Serum transaminase abnormalities were of similar magnitude in cases and controls, while-glutamyltransferase levels were abnormally elevated in 69% of the treated patients compared to 39% of controls (mean values 149 vs 57 IU/l at 24 months,P<0.05). Serum triglyceride concentrations over 150 mg/dl were seen in 74% of treated patients compared to 43% of controls at 12 months, the average concentration was 283 mg/dl compared to 179 mg/dl (P<0.05). Cholesterol levels showed a modest, non-significant rise with time in both groups, and there was no other laboratory evidence of toxicity attributable to vitamin A. Serum retinol and retinol-binding protein, assessed on a limited sample of patients, were higher in the treatment arm (P<0.05) at 12 months. In our experience 300 000 IU/day of retinyl palmitate can be administered as a possible chemopreventive agent with reasonable safety for up to 2 years.

Keep in mind that this was performed with a (most likely) synthetic palmitate supplement, and obviously not accompanied by any D3 or K2.

Additionally...

Adjuvant treatment of stage I lung cancer with high-dose vitamin A.

U Pastorino, M Infante, M Maioli, G Chiesa, M Buyse, P Firket, N Rosmentz, M Clerici, E Soresi and M Valente
Istituto Nazionale Tumori, Ospedale Niguarda, Milan, Italy.

PURPOSE: Vitamin A and retinoids are strong inhibitors of epithelial cancer promotion and progression in experimental carcinogenesis. This study examined whether they may prevent the occurrence of upper aerodigestive cancer in subjects heavily exposed to tobacco smoking, such as patients already cured of an early-stage lung cancer. PATIENTS AND METHODS: The adjuvant effect of high-dose vitamin A was tested on 307 patients with stage I non-small-cell lung cancer. After curative surgery, patients were randomly assigned to either a group prescribed retinol palmitate administration (orally 300,000 IU daily for 12 months) or a control group prescribed no treatment. RESULTS: After a median follow-up of 46 months, the number of patients with either recurrence or new primary tumors was 56 (37%) in the treated arm and 75 (48%) in the control arm. Eighteen patients in the treated group developed a second primary tumor, and 29 patients in the control group developed 33 second primary tumors. A statistically significant difference in favor of treatment was observed concerning time to new primary tumors in the field of prevention (P = .045, log-rank test). The treatment difference in terms of disease-free interval was close to statistical significance (P = .054, log-rank test) and just significant when adjusted for primary tumor classification (P = .038, Cox regression model). CONCLUSION: Daily oral administration of high-dose vitamin A is effective in reducing the number of new primary tumors related to tobacco consumption and may improve the disease-free interval in patients curatively resected for stage I lung cancer. The impact of such a treatment on survival needs to be further explored.

Again, using synthetic retinyl palmitate. So, based on these two studies, you can see that not only is high dose vitamin A supplementation typically not as toxic as is commonly claimed, but it also shows statistical significance as a chemopreventive agent at least in one type of cancer.

[FunkOdyssey]

hmmm. The first abstract you posted indicates that fish liver oil consumption is inversely correlated with lung cancer risk. Yet fish liver oil is high in "pre-formed retinol", which was associated with increased risk.

Omega-3 compensated, most likely. Here's something I dug up for First Immortal last July.

That's a a pretty bold assumption and IMHO an example of trying to interpret data to fit preconceived notions. Vitamin A promotes cell differentiation and apoptosis of cancerous cells and is huge in all kinds of cancer fighting protocols.

Edited by FunkOdyssey, 17 March 2009 - 04:55 PM.

[FunkOdyssey]

This looks to be an important paper to review if we want to get to the bottom of the confusion with lung cancer (they claim to have it figured out):

J Exp Clin Cancer Res. 2008 Jul 14;27:18.
Role of retinoic receptors in lung carcinogenesis.
Bogos K, Renyi-Vamos F, Kovacs G, Tovari J, Dome B.

Tumor Biology, Budapest, Hungary. bogosa@freemail.hu

Several in vitro and in vivo studies have examined the positive and negative effects of retinoids (vitamin A analogs) in premalignant and malignant lesions. Retinoids have been used as chemopreventive and anticancer agents because of their pleiotropic regulator function in cell differentiation, growth, proliferation and apoptosis through interaction with two types of nuclear receptors: retinoic acid receptors and retinoid X receptors. Recent investigations have gradually elucidated the function of retinoids and their signaling pathways and may explain the failure of earlier chemopreventive studies. In this review we have compiled basic and recent knowledge regarding the role of retinoid receptors in lung carcinogenesis. Sensitive and appropriate biological tools are necessary for screening the risk population and monitoring the efficacy of chemoprevention. Investigation of retinoid receptors is important and may contribute to the establishment of new strategies in chemoprevention for high-risk patients and in the treatment of lung cancer.

[krillin]

hmmm. The first abstract you posted indicates that fish liver oil consumption is inversely correlated with lung cancer risk. Yet fish liver oil is high in "pre-formed retinol", which was associated with increased risk.

Omega-3 compensated, most likely. Here's something I dug up for First Immortal last July.

That's a a pretty bold assumption and IMHO an example of trying to interpret data to fit preconceived notions. Vitamin A promotes cell differentiation and apoptosis of cancerous cells and is huge in all kinds of cancer fighting protocols.

I don't have any preconceived notions about vitamin A. My opinion originates from my list of case-control and prevention studies showing that higher A intake is worse, a U-curve for bone health with a sweet spot at 2000 IU/day, and evidence that high vitamin A concentrations can cause oxidative damage (see below). We have a choice of either taking the studies seriously, or being like Bill Faloon and dismissing the ones we don't like the results of.

Cancer-fighting protocols include all sorts of nasty things like radiation that are not useful for prevention. I need some epidemiology or prevention trials to convince me that I should consume more than 2000 IU/day.

Neurochem Res. 2009 Mar 3. [Epub ahead of print]
Increased Receptor for Advanced Glycation Endproducts Immunocontent in the Cerebral Cortex of Vitamin A-Treated Rats.
de Oliveira MR, Oliveira MW, Behr GA, de Bittencourt Pasquali MA, Moreira JC.
Centro de Estudos em Estresse Oxidativo (Lab. 32), Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, rua Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, CEP 90035-003, Brazil, mrobioq@yahoo.com.br.

Vitamin A, beyond its biological role, is an alternative choice in treating some life threatening pathologies, for instance leukemia and immunodeficiency. On the other hand, vitamin A therapy at moderate to high doses has caused concern among public health researchers due to the toxicological aspect resulting from such habit. It has been described hepatotoxicity, cognitive disturbances and increased mortality rates among subjects ingesting increased levels of vitamin A daily. Then, based on the previously reported data, we investigated here receptor for advanced glycation endproducts (RAGE) immunocontent and oxidative damage levels in cerebral cortex of vitamin A-treated rats at clinical doses (1,000-9,000 IU/kg day(-1)). RAGE immunocontent, as well as oxidative damage levels, were observed increased in cerebral cortex of vitamin A-treated rats. Whether increased RAGE levels exert negative effects during vitamin A supplementation it remains to be investigated, but it is very likely that deleterious consequences may arise from such alteration.

PMID: 19255841

Toxicol In Vitro. 2008 Aug;22(5):1123-7.
Retinol up-regulates the receptor for advanced glycation endproducts (RAGE) by increasing intracellular reactive species.
Gelain DP, de Bittencourt Pasquali MA, Caregnato FF, Zanotto-Filho A, Moreira JC.
Centro de Estudos em Estresse Oxidativo, Departamento de Bioquímica, Universidade Federal do Rio Grande do Sul, Laboratório 32, Rua Ramiro Barcelos 2600 anexo, CEP 90035-003, Porto Alegre, RS, Brazil. dgelain@yahoo.com.br

Retinol (vitamin A) and other retinoids have been suggested to exert an important antioxidant function in biological systems, besides their more established role as regulators of cell growth and differentiation. On the other hand, many authors have recently observed pro-oxidant activities of vitamin A and other retinoids in vitro and in vivo, resulting in cell death and/or transformation associated to increased oxidative damage. However, the mechanisms by which retinol causes oxidative stress are still not fully understood. Receptors for advanced glycation endproducts (RAGE) have been recently implied as promoters and/or amplifiers of oxidant-mediated cell death induced by diverse agents, and increased RAGE expression is observed in conditions related to unbalanced production of reactive species, such as in atherosclerosis and neurodegeneration. In the present work, we observed that retinol supplementation increases RAGE protein expression in cultured Sertoli cells, and antioxidant co-treatment reversed this effect. Retinol-increased RAGE expression was observed only at concentrations that induce intracellular reactive species production, as assessed by the DCFH assay. These results indicate that retinol is able to increase RAGE expression by an oxidant-dependent mechanism, and suggest that RAGE signaling may be involved in some of the deleterious effects observed in some retinol-supplementation therapies.

PMID: 18396385

Prog Neuropsychopharmacol Biol Psychiatry. 2009 Mar 17;33(2):353-62.
Evaluation of the effects of vitamin A supplementation on adult rat substantia nigra and striatum redox and bioenergetic states: Mitochondrial impairment, increased 3-nitrotyrosine and alpha-synuclein, but decreased D2 receptor contents.
de Oliveira MR, Oliveira MW, Behr GA, Hoff ML, da Rocha RF, Moreira JC.
Centro de Estudos em Estresse Oxidativo (Lab. 32), Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, rua Ramiro Barcelos, 2600-Anexo, CEP 90035-003, Porto Alegre, RS, Brazil.

Vitamin A at moderate to high doses is applied in the treatment of some life threatening pathological conditions, for instance cancers. Additionally, vitamin A at low concentrations is a known antioxidant molecule. However, by increasing vitamin A (or its derivatives) concentrations, there is an increase in the levels of oxidative stress markers in several experimental models. Furthermore, it was reported that vitamin A therapy at high doses might induce cognitive decline among the patients, which may become anxious or depressive, for example, depending on vitamin A levels intake. We have previously reported increased levels of oxidative stress markers in rat substantia nigra and striatum. However, the mechanism by which this vitamin altered the redox environment in such rat brain regions remains to be elucidated. In the herein presented work, we have investigated the effects of vitamin A supplementation at clinical doses (1000-9000 IU/kg day(-1)) for 28 days on rat substantia nigra and striatum mitochondrial electron transfer chain (METC) activity, which may produce superoxide anion radical (O(2)(-*)) when impaired. Additionally, the levels of non-enzymatic antioxidant defenses were evaluated, as well as 3-nitrotyrosine, alpha- and beta-synucleins and TNF-alpha levels through ELISA assay. We observed impaired METC in both rat brain regions. Moreover, we found increased O(2)(-*) production and nitrotyrosine content in the nigrostriatal axis of vitamin A-treated rats, suggesting that the use of vitamin A at therapeutic doses may be rethought due to this toxic effects found here.

PMID: 19166897

[krillin]

This looks to be an important paper to review if we want to get to the bottom of the confusion with lung cancer (they claim to have it figured out):

http://www.jeccr.com/content/27/1/18

They say that A is ineffective because tumors become resistant to it. They propose that synthetic retinoids that are selective for a certain receptor(s) might work better.

[k10]

Would taking a mega dose of Vitamin A once a week be just as effective as taking it daily?

ie. 100,000 IU once a week.

[krillin]

Would taking a mega dose of Vitamin A once a week be just as effective as taking it daily?

ie. 100,000 IU once a week.

I believe so. The half-life is very long and absorption shouldn't drop off much since single-dose toxicity is possible.

[krillin]

I now believe that 5000 IU (coincidentally the 1968 RDA) is a good target. For gastric cancer prevention, 4th quartile (median 5933 IU/day) was better than 3rd quartile (median 3810 IU/day). Optimal D and K2 intakes will probably prevent any bone loss at 5000 IU. Retinol increases mortality at 25,000 IU (PMID 18425980) and lung cancer at >5120 IU (PMID 11237398).

Am J Clin Nutr. 2007 Feb;85(2):497-503.
Vitamin A, retinol, and carotenoids and the risk of gastric cancer: a prospective cohort study.
Larsson SC, Bergkvist L, Näslund I, Rutegård J, Wolk A.
Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden. susanna.larsson@ki.se

BACKGROUND: Vitamin A may influence gastric carcinogenesis through its essential role in controlling cell proliferation and differentiation. However, epidemiologic studies of vitamin A, retinol (preformed vitamin A), and provitamin A carotenoids in relation to the risk of gastric cancer have documented inconsistent results. OBJECTIVE: The objective of the study was to examine the associations between intakes of vitamin A, retinol, and specific carotenoids and the risk of gastric cancer in a prospective population-based cohort study of Swedish adults. DESIGN: The study cohort consisted of 82 002 Swedish adults aged 45-83 y who had completed a food-frequency questionnaire in 1997. The participants were followed through June 2005. RESULTS: During a mean 7.2-y follow-up, 139 incident cases of gastric cancer were diagnosed. High intakes of vitamin A and retinol from foods only (dietary intake) and from foods and supplements combined (total intake) and of dietary alpha-carotene and beta-carotene were associated with a lower risk of gastric cancer. The multivariate relative risks for the highest versus lowest quartiles of intake were 0.53 (95% CI: 0.32, 0.89; P for trend = 0.02) for total vitamin A, 0.56 (95% CI: 0.33, 0.95; P for trend = 0.05) for total retinol, 0.50 (95% CI: 0.30, 0.83; P for trend = 0.03) for alpha-carotene, and 0.55 (95% CI: 0.32, 0.94; P for trend = 0.07) for beta-carotene. No significant associations were found for beta-cryptoxanthin, lutein and zeaxanthin, or lycopene intake. CONCLUSION: High intakes of vitamin A, retinol, and provitamin A carotenoids may reduce the risk of gastric cancer.

PMID: 17284749

[hamishm00]

My diet is pretty good. But I recently (3 weeks ago) decided to take a product called "Visual Eyes" by Source Naturals, which contains 25,000 IUs of Beta Carotene and 7,500 IUs of palmitate. I also added 300-400mcg of MK7 to the mix, and upped my Vitamin d3 from 2000IUs to 5000 IUs per day.

MASSIVE increase in visual accuity noticed (brighter colours, sharper shapes, increased peripheral vision), especially indoors, and at night.

Whilst this is all anecdotal, and I can't say for sure it's all due to Vitamin A, this was one of the most significant benefits I have felt from taking supplements in the last 5 or so years.

Edited by hamishm00, 10 April 2009 - 05:05 PM.

[stephen_b]

I now believe that 5000 IU (coincidentally the 1968 RDA) is a good target.

I'm wondering lately how much value to place in studies that don't control for levels of the other fat soluble vitamins, especially D. Perhaps these studies have more to say about what happens when A is supplemented to people that are D and K deficient.

Stephen

[Dmitri]

I now believe that 5000 IU (coincidentally the 1968 RDA) is a good target.

I'm wondering lately how much value to place in studies that don't control for levels of the other fat soluble vitamins, especially D. Perhaps these studies have more to say about what happens when A is supplemented to people that are D and K deficient.

Stephen

Seems like no one is in agreement about how much Vitamin A we should be taking. Another problem is that many companies sell Vitamin A in massive dosages (10,000-25,000 IU), it appears like only Solgar and GNC sell a lower dose of natural A (5,000 IU of fish liver oil).

[Jay]

I now believe that 5000 IU (coincidentally the 1968 RDA) is a good target. For gastric cancer prevention, 4th quartile (median 5933 IU/day) was better than 3rd quartile (median 3810 IU/day). Optimal D and K2 intakes will probably prevent any bone loss at 5000 IU. Retinol increases mortality at 25,000 IU (PMID 18425980) and lung cancer at >5120 IU (PMID 11237398).

Am J Clin Nutr. 2007 Feb;85(2):497-503.
Vitamin A, retinol, and carotenoids and the risk of gastric cancer: a prospective cohort study.
Larsson SC, Bergkvist L, Näslund I, Rutegård J, Wolk A.
Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden. susanna.larsson@ki.se

BACKGROUND: Vitamin A may influence gastric carcinogenesis through its essential role in controlling cell proliferation and differentiation. However, epidemiologic studies of vitamin A, retinol (preformed vitamin A), and provitamin A carotenoids in relation to the risk of gastric cancer have documented inconsistent results. OBJECTIVE: The objective of the study was to examine the associations between intakes of vitamin A, retinol, and specific carotenoids and the risk of gastric cancer in a prospective population-based cohort study of Swedish adults. DESIGN: The study cohort consisted of 82 002 Swedish adults aged 45-83 y who had completed a food-frequency questionnaire in 1997. The participants were followed through June 2005. RESULTS: During a mean 7.2-y follow-up, 139 incident cases of gastric cancer were diagnosed. High intakes of vitamin A and retinol from foods only (dietary intake) and from foods and supplements combined (total intake) and of dietary alpha-carotene and beta-carotene were associated with a lower risk of gastric cancer. The multivariate relative risks for the highest versus lowest quartiles of intake were 0.53 (95% CI: 0.32, 0.89; P for trend = 0.02) for total vitamin A, 0.56 (95% CI: 0.33, 0.95; P for trend = 0.05) for total retinol, 0.50 (95% CI: 0.30, 0.83; P for trend = 0.03) for alpha-carotene, and 0.55 (95% CI: 0.32, 0.94; P for trend = 0.07) for beta-carotene. No significant associations were found for beta-cryptoxanthin, lutein and zeaxanthin, or lycopene intake. CONCLUSION: High intakes of vitamin A, retinol, and provitamin A carotenoids may reduce the risk of gastric cancer.

PMID: 17284749

After reading the recent vit D council newsletter (will provide link as soon as they put it up on their website) and considering the issue further, I think 5000IU is too much retinol. The vit D council states that cod liver oil is commonly consumed in many Scandinavian countries, with the result that many of the people with the highest vitamin D levels in these countries also have high retinol intakes. The vitamin D council postulates that retinol thwarts some of the protective effect of vit D and the correlation between high intakes of vitamin D and retinol accounts for the relatively narrow U shaped curve for vit D in these countries.

However, the correlation between retinol and vitamin D may also have implications for the gastric cancer study cited above by Krillin. That study is important because it is the most positive vit A study of which I am aware. It found that those in the 4th quartile (median 5933 IU/day) fared better than those in the 3rd quartile (median 3810 IU/day). The study was, however, conducted in Sweden, so if we interprete it in light of the postulated correlation between high intakes of retinol and vit D in Scandinavia, the study could wrongly suggest that high retinol intakes are protective when, in fact, it might just be that high vit D intakes are protective and, in Sweden, those with high retinol intakes, on average, also have high vit D intakes. (That said, people can consume supplemental retinol without consuming much vit D by taking certain multi-vitamins, with the result that the correlation may not work as well in reverse; i.e., high D => high retinol in Scandinavia but high retinol may not imply high vit D in Scandinavia, at least not as strongly)

I am starting to think that Cannell may be correct about the thwarting effect of retinol, as it is a better explanantion for some of the findings than Vieth's declining level theory. I have been getting about 1500-2000IU per day of retinol from dairy fat and fish oil, and I think I am going to cut try to cut that in half. I get enough carotenes to cover the RDA for vit A anyway.

Edited by Jay, 28 February 2010 - 05:08 AM.

[pro-d]

We will ever get rid of vitamin A containing foods, and the worry so far about vitamin A is supplementing when it's not very hard to find in the average Western diet in the first place. My own advice is to only supplement if you know you're not getting any of it.

Think paleolithic, eat paleolitihic.

[Jay]

We will ever get rid of vitamin A containing foods, and the worry so far about vitamin A is supplementing when it's not very hard to find in the average Western diet in the first place. My own advice is to only supplement if you know you're not getting any of it.

Think paleolithic, eat paleolitihic.

Some suggests that early humans ate a lot of retinol from liver. While I have no doubt that early humans would have eaten the liver of animals they hunted, there is only 1 liver per animal so the percentage of their food that was so retinol enriched may have been small. Early humans did not consume dairy fat and eggs were probably somewhat seasonal and don't contain that much retinol anyway. If anybody (think WAPF) suggests that early humans got 5000IU per day, or more, from retinol, they must be smoking some pretty strong cod liver oil.

Also, dieatery retinol can be an issue for those lipophiles that have a very high dairy fat diet. I used to be one of them, but the amount of CLA/ruminent trans fat and retinol I was getting scared me off. I liked dairy because it is a low-PUFA source of fat. Without over-consuming dairy, I don't think it's possible, or at least at all convenient, to restrict PUFAs on a low-carb diet. Coconut oil is great but I don't see it as a source of more than a few hundred calories per day. For that reason, I gave up on low-carb a few months ago. I eat about 50% of my calories from starchy vegetables now.

Edited by Jay, 28 February 2010 - 03:48 PM.

[rwac]

I have been getting about 1500-2000IU per day of retinol from dairy fat and fish oil, and I think I am going to cut try to cut that in half. I get enough carotenes to cover the RDA for vit A anyway.

Just keep in mind that some people are bad (about half the population?) at converting carotenes to retinol, so carotenes aren't always useful.

[Jay]

I have been getting about 1500-2000IU per day of retinol from dairy fat and fish oil, and I think I am going to cut try to cut that in half. I get enough carotenes to cover the RDA for vit A anyway.

Just keep in mind that some people are bad (about half the population?) at converting carotenes to retinol, so carotenes aren't always useful.

Agreed, but it isn't clear to me that it is a genetic weakness. Many things affect carotene conversion to retinol. Being well nourished goes a long way to making sure you can convert carotenes. It was discoverd recently that retinol, vitamin D, and vitamin E all affect the conversion rate of K1 to K2. I suspect the fat soluble vitamins, among othr factors, all play a role in conversion carotenes to retinol as well.

Edited by Jay, 28 February 2010 - 04:28 PM.

[rwac]

Agreed, but it isn't clear to me that it is a genetic weakness. Many things affect carotene conversion to retinol. Being well nourished goes a long way to making sure you can convert carotenes. It is known that retinol, vitamin D, and vitamin E all affect the conversion rate of K1 to K2. I suspect the fat soluble vitamins, among othr factors, all play a role in conversion carotenes to retinol as well.

Genetic or not, you better get some retinol if your body can't convert. And your suspicion is just a suspicion.

I know for a fact that retinol works way better on me than carotenes.