Re: Re: osteoporosis and D hypervitaminosis

[Guest guest]

----- Original Message -----

From: " penny " <pennyhoule@...>

SNIP

" Based on the latest research,

people supplementing with D and calcium for osteoporosis is probably

the worst thing people can be doing. "

Penny,

The last time we exchanged views on this, I said that I hoped you were not

assuming that groups of non-sarcoidosis patients were suffering from the

inflammatory-immune problem that the Marshall protocol addresses. You

assured me that this was not the case, and gently chided me for making an

assumption myself.

I think the sentence of yours above bears out my apprehension. The

research on D is by no means as conclusively in favour of Trevor's

position as he claims. When I asked him to tell me what D actually does in

muscles, he referred me to PubMed, but none of the papers really tackles

the question -- certainly not for skeletal muscle as opposed to smooth

muscle in blood vessel walls. Furthermore, D receptors are found in a long

list of different types of tissues and the functions of D in those tissues

is similarly poorly understood.

I have left the Marshal group because I regard the discussion as

unbalanced and I fear that some people are going to get hurt. The

tradition of this group is to try to be objective as various enthusiasms

come and go, and I think the need here is to bear in mind that there are

numerous subgroups in these illnesses. I do not question that some might

benefit from reducing D intake, but others are likely to suffer.

Because of soft-tissue calphos deposits fifteen years ago, I avoided D

supplementation until recently. Having read research showing the

prevalence of D deficiency in FMS and other musculoskeletal pain

conditions, I have been re-evaluating the position for about the last nine

months. Below are two documents that I would ask interested members to

read. The first is my own (just revised) notes on the subject in which I

go through the arguments for and against. The second is a relevant paper

on PubMed.

Rob

Cholecalciferol, or vitamin D, is either ingested in the diet, or

synthesized in the skin from 7-dehydrocholesterol in the presence of

ultraviolet light. It is hydroxylated mostly in the liver to form

25-hydroxycholecalciferol and converted as required mostly in the kidneys

to the active hormonal form 1,25-dihydroxycholecalciferol, also known as

calcitriol. In addition to its function in calcium homeostasis (q v), D

receptors and activities have been found in tissues such as those of the

brain, pancreas, pituitary, skin and muscle and in immune cells.

Vitamin D receptors are found in significant concentrations in the T

lymphocytes and macrophages. D seems to act as an immune regulator,

reducing excessive responses. Adequate levels are therefore important in

autoimmune diseases like MS, which is more prevalent in cool climates. D

at physiological concentration has also been found to protect cell

proteins and membranes against oxidative stress by inhibiting peroxidative

attack on membrane lipids. D is now thought to have wide-ranging

neuroprotective functions, including an anti-inflammatory effect on the

CNS. It is also required for sulphur homeostasis; deficiency results in

increased excretion of sulphates and low serum levels, which is

significant in view of the well-established benefits to rheumatic

patients, including myself, of sulphate supplementation. A study of

patients with peripheral arterial disease found that severity increased

with D deficiency, though exposure to sunlight will diminish with disease

progression. Too much A without corresponding D can lead to what is known

as relative D deficiency.

A study has found that of patients suffering from persistent, non-specific

musculoskeletal pain, over 90% had low or very low levels of D. Another

study of D deficient women found that muscle performance was significantly

worse than controls on all measured parameters. In both studies, only

25-hydroxy levels were measured. However, Dr Trevor Marshall, a

researcher, says that high serum levels of 1,25 dihydroxy can worsen

immune inflammatory conditions. This stems from his work on sarcoidosis,

with the characteristic granuloma. He says high 1,25 dihydroxy levels

assist the process whereby cell wall-deficient (CWD) bacteria parasitise

immune cells, which are then stimulated to convert 25-hydroxy to 1,25

dihydroxy in a vicious circle, thus creating hypervitaminosis and a high

ratio of 1,25 dihydroxy to 25-hydroxy. Tests of both D levels on sufferers

from a number of inflammatory conditions, including some with CFS, have

revealed this state, which would mean a Th1 shift as opposed to the

usually presumed Th2 shift. Granuloma are said often to develop first in

the lungs or lymph nodes and it is not clear whether hidden granuloma are

envisaged or a state where macrophages are parasitised without going on to

form them.

I have difficulty in absorbing and utilising calcium and magnesium and D

might help but what are the risks here? Calcitriol is formed in response

to parathyroid hormone or low blood levels of calcium or phosphates, and

is said to increase renal resorption of both and to increase the uptake of

calcium, magnesium and phosphates from the gastrointestinal tract, but it

is hard to judge the balance of advantage regarding increased phosphate

uptake. Soft tissue calphos deposition and resulting atherosclerosis from

excessive phosphates are recognised signs of overconsumption of D. On the

other hand, reduced calcitriol production in renal failure is said to lead

to hyperparathyroidism, hypocalcaemia and hyperphosphataemia and the

treatment includes calcium and D supplementation. This could indicate that

the net result of taking D as well as calcium and magnesium might be to

favour these two minerals over phosphates.

Testing for 1,25 dihydroxy levels is fairly recent, rarely used, not

cheap, requires the blood sample to be frozen and in the UK to be sent to

Manchester Royal Infirmary. What can I deduce about my D status from my

experience? If modest amounts of cod liver oil could be followed by a hard

lump on my left wrist, my D levels cannot have been very low, which would

be associated with phosphaturia and hypophosphataemia, in those days. On

the other hand the deposits went immediately with magnesium, so my D

levels are unlikely to have been excessively high either. Today, I have

some symptoms, like fatigue, paraesthesias, musculoskeletal pains,

tinnitus, sinus congestion, abdominal discomfort and photosensitivity,

that are possible indicators of D hypervitaminosis, but all of these are

also common in FMS. The usual indicators of frank hypervitaminosis,

nausea, poor appetite, constipation and weight loss, I definitely do not

have and in fact my appetite for D-rich foods, like oily fish, liver

(pate) and (fortified) dairy products, is strong. Non-bone indicators of

hypovitaminosis have not yet been detailed but also include

musculoskeletal pains and there must be many more, given the numerous

tissues that have D receptors.

In November 03, I re-started taking daily a halibut oil capsule containing

85 iu D (42% RDA). At first, aching in my leg muscles reduced my walking

range but after a few months, it started to improve. In May 04, I added

morning and evening a tablet containing 400 iu. For the first 48 hours,

there were lots of small, warm pains in my lower legs. There was also some

immune response - left sinus constriction and tinnitus followed by

increased nasal (initially, some of it thick) and bronchial mucus. For the

first week, there would be an antioxidant-type response 90 minutes after

each dose of red eyes and eyelids from stinging tears, and also the effect

of other antioxidants was noticeably increased. Aching and pains on

exercise in my legs and feet (including my right big toe joint and the

ends of several toes, where there would be transitory burning pains) were

strong and there was a rash in my groin. After 10 days, I suspended all D

supplementation: within 48 hours, the rash disappeared.

I then spent 15 minutes in a pair of shorts in the midsummer sun, said to

synthesise at least 10,000 iu. There were stinging tears and red eyes and

eyelids, followed by fatigue and increased bronchial and nasal mucus that

lasted for much of the next 24 hours. There were clearance pains at

numerous sites from my knees down to my toes and darker urine with a

chemical odour. My need for sleep increased and after a few days, my

immune system seemed to normalise, with mucus from time to time but

otherwise clearer sinuses and without the sharp swings in response. More

pains in my legs were followed by an increased walking range. I repeated

the exercise several times and managed one or two unusually long walks,

though there were very strong, active pains and tenderness one to five

hours afterwards at numerous sites in muscles from my knees down. So far,

nothing has simultaneously addressed so many seemingly unrelated problems

as improving my D status. Sub-optimal levels could account for most if not

all of my symptoms, my strong appetite for certain foods and the

improvement in symptoms following substantial meals. It is a pity that I

was misled by calphos deposition that was probably caused by excessive

phosphates coupled with lack of magnesium.

Hypovitaminosis D myopathy without biochemical signs of osteomalacic bone

involvement.

Glerup H, Mikkelsen K, Poulsen L, Hass E, Overbeck S, Andersen H,

P, sen EF.

Department of Endocrinology and Metabolism C, Aarhus Amtssygehus,

University Hospital of Aarhus, Tage Hansensgade 2, DK-8000 Aarhus C,

Denmark.

The aims of this study were to investigate myopathy in relation to vitamin

D status, and to study the muscular effects of vitamin D treatment on

vitamin D-deficient individuals. Further, hypovitaminosis D myopathy was

investigated in relation to alkaline phosphatase (ALP), the most commonly

used marker for hypovitaminosis D osteopathy. Eight patients with

osteomalacia had an isokinetic dynamometer test of all major muscle groups

before and after 3 months of vitamin D treatment. The most pronounced

improvements in muscle power were seen in the weight-bearing antigravity

muscles of the lower limbs. A cross-sectional study was performed among 55

vitamin D-deficient veiled Arab women living in Denmark and 22 Danish

controls. An isometric dynamometer model was used for determination of

quadriceps muscle power. Both maximal voluntary contraction (MVC) and

electrically stimulated values (single twitch, maximal production rate

(MPR), and maximal relaxation rate (MRR)) were determined. The women

underwent high-dose vitamin D treatment and were retested after 3 and 6

months. Prior to vitamin D treatment all parameters of muscle function in

the group of vitamin D-deficient Arab women were significantly reduced

compared with Danish controls. MVC: 259.4 +/- 11.0 N (Newton) versus 392.6

+/- 11. 4 N (P < 10(-6)), single twitch: 47.0 +/- 1.8 N versus 74.6 +/-

2.2 N (P < 10(-5)), MPR 8.9 +/- 0.3 N/10 ms versus 14.3 +/- 0.4 N/10 ms (P

< 10(-6)), MRR 4.5 +/- 0.2 N/10 ms versus 6.2 +/- 0.2 N/10 ms (P <

10(-6)). Muscle function was affected to a similar degree in women with

and without bone involvement (as indicated by elevated ALP). After 3

months of vitamin D treatment all muscle-related parameters improved

significantly. After 6 months only MVC was reduced compared with Danish

controls (320.7 +/- 14.3 N (P < 0.02)), whereas all other measurements

were normalized. Hypovitaminosis D myopathy is a prominent symptom of

vitamin D deficiency, and severely impaired muscle function may be present

even before biochemical signs of bone disease develop. Full normalization

of hypovitaminosis D myopathy demands high-dose vitamin D treatment for 6

months or more. Our findings indicate that serum levels of ALP cannot be

used in the screening for hypovitaminosis D myopathy. Assessment of

s-25OHD is the only reliable test.

PMID: 10821877 [PubMed - indexed for MEDLINE]

[Guest guest]

Bob,

If people are having success with MP and it turns out to be lasting, I

shall be genuinely pleased for them. I am having remarkable success with D

supplementation and I would welcome similar encouragement but no one has

so far offered it. Surely MP enthusiasts could extend the same courtesy to

me?

The question of subsets is something that anyone who has been working on

treatments as long as I have has come up against time and again, usually

to our great frustration. Whatever you recommend works for some but not

others.

However, it has nowhere been better demonstrated than with vitamin D.

After the second world war, the UK government decided on medical advice to

prevent he scourge of bone deformation in children through D deficiency.

All parents were issued with cod liver oil and required to give their

child a spoonful every day. I remember it well because cod liver oil drunk

off a spoon is not a pleasant experience. After a few years, however, this

had to be abandoned because some children were developing problems of D

hypervitaminosis. We'd swapped one problem for another.

If you become really photophobic, perhaps because of toxification and the

inability to deal with the free radicals that sunshine generates, not

getting enough sunshine is very easy -- believe me, I've done that for

years.

I note that no one has yet commented on the many other points that I

raised.

Rob

----- Original Message -----

From: " Bob H " <blue74730@...>

Rob,

I could not ignore the success PWC's were having using the MP. It is

the first protocol I know of that has had this kind of success. My

vitamin D tests were way too high. After researching how we get

vitamin D from sunshine, in fact just 10 minutes in the sunshine

gives us out daily need, I do not understand how many, if any, can

be deficient in vitamin D. If they are, it has to from a result of

living in a closed up house and never getting out or something is

wrong with their processing of sunshine. I will probably try the MP

as it is a relatively safe program (I have tried many things in my

29 years and I will continue my quest)and I usually try most things.

I do have to take issue with your statement that there are subsets

of us. This has not been proven, though this is a popular theory. I

hope this does not come across as confrontational as it is not meant

to be.

Bob H.

This list is intended for patients to share personal experiences with each

other, not to give medical advice. If you are interested in any treatment

discussed here, please consult your doctor.

[Guest guest]

Hi all,

It was strange for me to note about a week ago that my muscles have gotten much

stronger. I was surprised to see that. There was no difference at my activity

level. The only difference is that I have been using Ca -2 aep for some time.

This is very important for me as I need strong muscles to support my weak

bones.Lately I have been taking about 400 i.u. of vit D every other day for

about a month or so but I suppose this is too little to have an effect.

So I am thinking that the cause was probably Ca 2 aep.Could that be true?

Just wanted to share this strange finding with you and also get your opinion.

Thanks.

Re: osteoporosis and D hypervitaminosis

Hi Rob,

> If people are having success with MP and it turns out to be lasting, I shall

> be genuinely pleased for them. I am having remarkable success