Update on Vitamins A and D

[Guest guest]

About a year ago or so, I seem to remember a few people here discussing

vitamin D and how much they were taking. I have been reading today about a

fermented cod liver oil recommended by the Weston A Price Foundation and

came across this and thought that some here would be interested.

blessings

Shan

excerpts from .........

Update on Vitamins A and D

_http://www.westonaprice.org/cod-liver-oil/1954-update-on-vitamins-a-and-d.h

tml_

(http://www.westonaprice.org/cod-liver-oil/1954-update-on-vitamins-a-and-d.html)

June 24, 2010

THE IDEAL RATIO

But now to the exciting part.

The authors devoted a section of their paper to the ideal ratio of vitamin

A to D. **In the responses to [Cannell and colleagues] from the on-line

supplement and nutrition newsletter communities,** they wrote, **the issue of

the proper ratio of vitamin A to vitamin D emerged as a major concern.**

They gave three references, including one to the Weston A. Price Foundation’

s **Cod Liver Oil Update** from December, 2008.

In fact, the importance of balance between vitamins A and D was raised in

the pages of Wise Traditions even earlier than 2008. In the spring of 2006,

I discussed the issue in my article **Vitamin A on Trial: Does Vitamin A

Cause Osteoporosis?** when I argued that vitamin A only contributes to

osteoporosis when vitamin D levels are deficient or when the ratio of vitamin A

to D is massively out of balance. The following fall, I raised the issue

again in my article **From Seafood to Sunshine: A New Understanding of

Vitamin D Toxicity,** wherein I presented research showing that vitamin A

protects against vitamin D toxicity and introduced the possibility that

vitamins

A, D, and K2 may be cooperative factors that should all be consumed in

proper balance. I more fully developed this concept in my spring 2007 article

on

vitamin K2, **On the Trail of the Elusive X-Factor: A Sixty-Two-Year- Old

Mystery Finally Solved.**

As a result of this research, in December of 2007, I published a

hypothesis on the molecular mechanism of vitamin D toxicity in the journal

Medical

Hypotheses entitled **Vitamin D toxicity redefined: vitamin K and the

molecular mechanism,** which emphasized interactions between vitamins A, D, and

K2. The following year, researchers from Tufts University published a paper

in the Journal of Nutrition supporting this hypothesis, showing that

vitamin A protects against vitamin D toxicity in part by helping to properly

regulate the production of vitamin K-dependent proteins.

One question I have never been able to answer in any of these articles is

the one everyone wants an answer to: what, precisely, is the proper ratio

of vitamins A and D?

Dr. y and her colleagues offer a suggestion: poultry studies suggest

optimal A-to-D ratios between four and eight. Similarly, in her own studies

showing that cod liver oil protects against upper respiratory tract

infections, y supplied her patients with A-to-D ratios between five and

eight.

They also point out that rat studies showing that vitamin A is toxic and

antagonizes the effects of vitamin D used much higher ratios, ranging from

5,000 to 55,000!

It is refreshing to see a powerful defense of cod liver oil in the

scientific literature, and especially refreshing to see the work of the Weston

A.

Price Foundation cited therein.

We owe a big thank you to Dr. y (MD) of St. Luke’s-Roosevelt

Hospital Center in NY, NY, Dr. C. Umhau (MD, MPH) of NIH in Bethesda,

MD, D. Shindledecker of New York Downtown Hospital in NY, NY, Dr. Jay

N. Dolitsky (MD) of New York Eye and Ear Infirmary in NY, NY and

F. Holick (PhD, MD) of Boston University Medical Center in Boston, MA for

helping to sort out these important questions about the fat-soluble vitamins.

OPTIMAL VITAMIN D LEVELS

Are some people pushing their vitamin D levels too high? Has science

proven that the minimal acceptable blood level of vitamin D, in the form of

25(OH)D, is above 50 ng/mL (125 nmol/L)?

The answer is **No.** If you’ve been trying to maintain your levels this

high because you thought this was the case, I’m sorry to break the news.

There is, on the contrary, good evidence that 25(OH)D levels should be at

least 30-35 ng/ mL (75-88 nmol/L). Much higher levels may be better, or they

could start causing harm, especially in the absence of adequate vitamins A and

K2. Once we leave the land of 30-35 ng/mL, however, we enter the land of

speculation.

The idea that science has proven we need to maintain 50 ng/mL as a minimum

comes from Dr. Cannell of the Vitamin D Council. In his article **Am

I Vitamin D Deficient?** he writes the following: **Thanks to Bruce Hollis,

Heaney, Neil Binkley, and others, we now know the minimal

acceptable level. It is 50 ng/ ml (125 nmol/L). In a recent study, Heaney, et

al

expanded on Bruce Hollis’s seminal work by analyzing five studies in which

both the parent compound (cholecalciferol) and 25(OH)D levels were measured.

They found that the body does not reliably begin storing cholecalciferol in

fat and muscle tissue until 25(OH)D levels get above 50 ng/ml (125 nmol/L).

The average person starts to store cholecalciferol at 40 ng/ml (100

nmol/L), but at 50 ng/ml (125 nmol/L) virtually everyone begins to store it for

future use. That is, at levels below 50 ng/ml (125 nmol/L), the body uses up

vitamin D as fast as you can make it, or take it, indicating chronic

substrate starvation—not a good thing. 25(OH)D levels should be between

50–80

ng/ml (125–200 nmol/L), year-round.**

DIFFERENT CONCLUSIONS

There are a few problems with this argument. To begin with, Drs. Hollis,

Heaney, Binkley, and the other authors of this study rightly made very

different conclusions from their own data. In the report they wrote for the

American Journal of Clinical Nutrition, they wrote the following: **One could

plausibly postulate that the point at which hepatic 25(OH)D production

becomes zero-order [this is the point at which the enzymes converting vitamin D

to 25(OH) D are saturated with vitamin D] constitutes the definition of the

low end of normal status. This value, as suggested in an equation shown in

the article, is at a serum 25(OH)D concentration of 88 nmol/L (35.2 ng/mL).

It is interesting that this estimate is very close to that produced by

previous attempts to define the lower end of the normal range from the

relations of serum 25(OH) D to calcium absorption and to serum parathyroid

hormone

concentration (ie, 75–85 nmol/L, or 30–34 ng/mL).**

According to the authors of this study, then, the point at which the

vitamin D enzymes are saturated and vitamin D **accumulates within the body,

both in serum and probably in body fat** is not 40 or 50 ng/mL (100 or 125

nmol/L) but rather 35 ng/mL (88 nmol/L).

The authors used a statistical approach that pooled together data from

several studies. They presented most of their data in Figure 4, and the data

from one other study in Figure 5 (see below). They did not determine the

point at which vitamin D starts getting stored in body fat in particular

individuals. On the contrary, they used a statistical approach to infer the

point at which this occurs in their entire study population. Now, if you

compare Figures 4 and 5, looking for the point at which the slope of the line

dramatically changes, you will see that it changes at a higher level of

25(OH)D in Figure 5. Dr. Cannell seems to have used the data from Figure 5 to

say

when vitamin D gets stored in body fat in **virtually everyone** as opposed

to **the average person,** but in fact the authors stated that they did

not use the data from Figure 5 to determine this point because a different

and apparently inferior method of measuring vitamin D levels was used in

that data set.

So, we are back to the authors’ original conclusions, that vitamin D

saturates its activation enzymes and starts getting stored in body fat when

25(OH)D levels reach 35 ng/mL (88 nmol/L).

The second problem is that this study does not **prove** or **show** or

**demonstrate** what the optimal or minimal blood level of vitamin D is. The

authors state that one could plausibly postulate that the minimum

acceptable blood level is the point at which the enzymes are saturated and

vitamin D

is stored in body fat, but they never state that “we now know the minimal

acceptable level.â€

The most definitive way to determine the ideal 25(OH)D level would be to

conduct a randomized, controlled trial with different levels of vitamin D

supplementation targeted at reaching specific blood levels of 25(OH)D and to

test the effects of the different levels of supplementation on clinical

outcomes, such as bone mineral density, fracture rate, insulin resistance,

glucose tolerance, cancer or heart disease.

We do not yet have this type of data. We do, however, have some strong

support for raising 25(OH)D levels to at least 35 ng/mL (88 nmol/L). For

example, as the authors of the study we have been looking at pointed out,

similar attempts to use statistical approaches to define the 25(OH)D level that

maximizes calcium absorption, maximally suppresses parathyroid hormone (which

leaches calcium from bone), or maximizes bone mineral density have

suggested similar results. A recent randomized, placebocontrolled trial showed

that supplementing insulin-resistant women with 4,000 IU of vitamin D per day

for six months reduced insulin resistance and had the most powerful effect

in women whose 25(OH)D level was raised to over 32 ng/mL (80 nmol/L).

POSSIBLE HARM

What about higher levels? The evidence is conflicting, and some of it

indicates possible harm. For example, a study in the American Journal of

Medicine published in 2004 found that in Americans aged over fifty, the maximal

bone mineral density (BMD) occurs around 32-40 ng/mL (80- 100 nmol/L). Among

Mexican Americans, BMD continues to rise a little after this point, but for

whites it plateaus and begins dropping off around 45 ng/mL (110 nmol/L)

and for blacks it begins dropping off even before 40 ng/mL (100 nmol/L).

If 50 ng/mL (125 nmol/L) is our minimal acceptable level, this study would

seem to suggest that those of us who have “acceptable†levels of 25(OH)D

would have lower bone mineral density than those of us who are moderately

deficient. And that premise just doesn’t make sense.

Another study published in the European Journal of Epidemiology in 2001

found that South Indians with 25(OH)D levels higher than 89 ng/mL (223

nmol/L) were three times more likely to have suffered from ischemic heart

disease

than those with lower levels—and of course with such a dramatic elevation

of heart disease risk, the risk may have begun increasing at levels

substantially lower than 89 ng/mL.

Neither of these studies was designed to show that high levels of 25(OH)D

cause decreases in bone mineral density or increases in heart disease risk,

but it is possible. As I especially emphasized in my Wise Traditions and

Medical Hypotheses articles on vitamin K2, bone resorption and blood vessel

calcification are prominent symptoms of vitamin D toxicity in animal

experiments. I also emphasized the role of vitamins A and K2 in protecting

against vitamin D toxicity. So, even if these levels are in fact harmful, they

may only be harmful or may be primarily harmful in the absence of adequate

vitamins A and K2. The presence of the other fat-soluble vitamins could even

turn these levels from harmful to beneficial.

STILL NEEDED

Nevertheless, what we need in order to show that levels higher than 50

ng/mL are helpful or harmful are vitamin D supplementation trials comparing

the effect of different doses resulting in different blood levels on clinical

health outcomes, and similar studies examining the interactions between

vitamin D and the other fat-soluble vitamins.

Lifeguards in the tropics can reach blood levels in the 50s and 60s

naturally from sun exposure, suggesting these levels are **natural,** although

lifeguards in Israel have twenty times the rate of kidney stones as the

general population.

Kidney stones may be the most sensitive indicator of vitamin D toxicity

and are a symptom of vitamin A and K2 deficiency. Thus, I suspect these

levels are healthful in the context of a diet rich in vitamins A and K2, and if

my levels were to reach this high in the summer sun while I was eating such

a diet, I certainly would not worry.

But if you are trying desperately to maintain year-round 25(OH)D status

between 50-80 ng/ mL using vitamin D supplements, you have entered the land

of speculation. Enter at your own risk.

SIDEBARS

THE FAT SOLUBLE ACTIVATORS

The key finding of Dr. Weston Price was very high levels of **fat-soluble

activators** in traditional diets. No matter what the particulars of the

diet—whether in the frozen north, the Alpine highlands or the tropical South

Seas—traditional peoples consumed plentiful amounts of vitamins A, D and

what Dr. Price referred to as Activator X—now determined to be vitamin K2—

from seafood, organ meats and the fat of grass-fed animals. It is difficult

to obtain adequate amounts of these activators in Western diets, partly

because government agencies have demonized the foods that contain these

vitamins, and also because the industrializaton of agriculture has taken most

livestock off pasture.

Properly processed cod liver oil is an excellent source of vitamins A and

D, and this is why we recommend it for westerners, especially in

preparation for conception, during pregnancy and lactation, and for growing

children.

Unfortunately, while the need for vitamin D has received considerable

recognition in recent years, many researchers have spoken out against vitamin A

and especially cod liver oil. Chief among the detractors are Dr.

Cannell of the Vitamin D Council, and Dr. ph Mercola of mercola.com. This

article, which is necessarily technical in parts, serves as part of the

ongoing debate on this subject.

For background and more information, see

_www.westonaprice.org/cod-liver-oil/1622.html_

(http://www.westonaprice.org/cod-liver-oil/1622.html) . This

article combines two recent blog postings by Masterjohn. Visit his blog

at _www.westonaprice.org/blogs.html_

(http://www.westonaprice.org/blogs.html) .

2 GRAPHS ....

FIGURE 4. Plot of the relation between serum concentrations of vitamin D3

and 25-hydroxyvitamin D after 18–20 weeks of treatment with various doses

of vitamin D3. Triangles represent subjects from study B; circles subjects

from study C; squares subjects from study F. The regression line is a

least-squares fit of the data to a combination exponential and linear function.

FIGURE 5. Plot of the relation between serum vitamin D3 and

25-hydroxyvitamin D in study D only. As in Figure 4, the regression line is a

least-squares fit of the data to a combination exponential and linear function.

From the American Journal of Clinical Nutrition, Vol. 87, No. 6,

1738-1742, June 2008. Used with permission.