As soon as our brain is sure that we’re in a safe place to get paralyzed (lying down) we enter Stage III sleep. ( Stage III and what was Stage IV are now grouped together as just Stage III )
Stage III is called “Slow Wave Sleep” (SWS) because the brain wave pattern becomes slow and synchronized.
During Stage III sleep our body becomes paralyzed.
Growth hormone (GH) is released from the brain in a pulsatile fashion in SWS , if you don’t get and stay in SWS you don’t get this GH.
Growth Hormone in Slow Wave Sleep may help us heal
Growth Hormone (GH) is the same hormone that makes kids grow during sleep. In children it is a sustained release during SWS, they grow while paralyzed .
I believe that nightly GH in adults may act analogously, as a repair hormone; the “boss hormone” that calls out all of the individual muscle, bone, tendon, artery, nerve, repair factors. In adults paralysis for repair.
People with PLMS often wake in the morning with leg or back pain.
This may suggest that if your SWS is frequently interrupted or shortened by apnea or PLMS, your repair phase doesn’t happen normally and you may wake up with pain in the morning.
Stumpf WE, Sar M, Reid FA, Tanaka Y, DeLuca HF. Target cells for 1,25-dihydroxyvitamin D3 in intestinal tract, stomach, kidney, skin, pituitary, and parathyroid . Science. 1979 Dec 7;206(4423):1188-90.
Stumpf, WE and O'Brien, LP. 1,25 (OH)2 Vitamin D3 sites of action in the brain: an autoradiographic study . Histochem.87:393-406, 1987.
Stumpf, WE, Clark, SA, O'Brien, LP and Reid, FA. 1,25 (OH)2 vitamin D3 sites of action in spinal cord and sensory ganglion . Anat. Embriol. 177:307-310, 1988.
Stumpf WE, Denny ME . Vitamin D ( soltriol ), light, and reproduction. Am J Obstet Gynecol. 1989 Nov;161(5):1375-84.
Stumpf WE, Privette TH. Light, vitamin D and psychiatry. Role of 1,25 dihydroxyvitamin D3 (soltriol) in etiology and therapy of seasonal affective disorder and other mental processes. Psychopharmacology (Berl). 1989;97(3):285-94
Bidmon HJ, Gutkowska J, Murakami R, Stumpf WE. Vitamin D receptors in heart: effects on atrial natriuretic factor . Experientia. 1991 Sep 15;47(9):958-62.
(This is a small sample of many, many articles.)
Why would we have a hormone made by UVB that bosses the pituitary and hypothalamus?
UVB is the only wavelength present in summer not in winter.
D hormone adjusts metabolism to the two, very different, states of weather and food availability.
In the summer we eat lots of perishable food, plow the soil, gather food, build things, sleep little.
In the winter there is no food .
We hibernate, we sleep more, channel more of the calories we eat into fat.
Any animal that can eat very little and still put on a little fat in the winter has a survival advantage.
Where are the D Receptors? (Where they are may suggest what they do.)
When the statin lowers the cholesterol does that mean that 7 dehydrocholesterol, the raw material that makes vitamin D, is lower on the skin too? If so does that imply that I won’t be able to make vitamin D now when I go out in the sun?
There is conflicting literature on this as well.
Might this also mean that my sun exposed areas are now exposed without the protective effects of vitamin D producing more wrinkling, color changes, and bruising?
We have the enzyme that makes active D 1,25 OH on our skin, it keeps the skin cells in line, keeps them from turning cancerous or reproducing inappropriately. Keeps the fibroblasts healthy repairing our skin.
25 hydroxyvitamin D, IGF-1 and metabolic syndrome at 45 years of age: a cross sectional study in the 1958 British Birth Cohort. Diabetes 2008 Feb 57(2) 298-305. Serum 25 (OH) D is inversely associated with metabolic syndrome. Metabolic syndrome prevalence is lowest when both 25(OH) D and IGF-1 are high.
25 Hydroxyvitamin D deficiency is independently associated with cardiovascular disease in the Third National Health and Nutrition Examination Survey. Atherosclerosis . 2009 205 (1) 255-260. Strong independent relationship of 25 (OH) deficiency with prevalence CVD in a large sample.
Vitamin D, race and cardiovascular mortality: findings from a national US sample. Ann Fam Med 2010 Jan-Feb 8(1) 11-18. Black white differences in 25(OH) D levels may contribute to excess cardiovascular mortality in blacks.
Adiposity, cardiometabolic risk, and vitamin D status: the Framingham Heart Study. Diabetes . 2010 Jan 59 (1) 242-248 . Vitamin D status is strongly associated with variation in subcutaneous and especially visceral adiposity.
Vitamin D status and Cardiometabolic Risk Factors in the United State Adolescent Population. Pediatrics 2009 Aug 3. Low serum vitamin D in US adolescents is strongly associated with hypertension, hyperglycemia and metabolic syndrome independent of adiposity.
Vitamin D in relation to metabolic risk factors, insulin sensitivity and adiponectin in a young Middle-Eastern population . Eur J Endocrinol 2009 160(6) 965-71. In non obese young subjects we observe new relationships between 25 (OH) D and several metabolic risk factors and adiponectin.
Association of leptin, 25 hydroxyvitamin D and parthyroid hormone in women. Nutr Cancer 2009 61(2) 225-31. Leptin was highly correlated with the BMI/25 OH Vit D ratio consistent with a model in which BMI and 25 (OH) Vit D are the primary determinants of circulating leptin and PTH levels.
Effect of vitamin D deficiency and replacement on endothelial function in asymptomatic subjects. J Clin Endo Metab 2009 Oct 94(10) 4023-30. 25 (OH) D deficiency is associated with endothelial dysfunction and increased lipid peroxidation. Hypoviaminosis D associated endothelial dysfunction may predisopose to higher rates of cardiovascular disease.
Vitamin D receptors in heart: Effects on atrial naturetic factor. Experimentia 1991 47 958-962. In rats vitamin D receptors concentrated in the right atrium, colocalizing with atrial naturetic peptide. Changes in ANF tissue and blood levels under dietary deficiency and treatment with 1,25 D3 suggest direct genomic action of vitamin D on myoendocrine cells of the atrium for the regulation of ANF manufacture and secretion.
Epidemiology is fine. What about treatment trials?
OK so they’re seen together. Lets see the vitamin D cure the disease.
VITAMIN: What’s the right dose?
HORMONE: What’s the right level?
What’s the dose to get to the right level? This is the hard part.
Why is the sleep observation so pivotal?
Restorative sleep is the cure for cardiovascular disease
We know that correcting the sleep has profound effects on disease.
The cure is the sleep, not the D . CPAP is one way, D perhaps another.
If it’s a deficiency state why not try treat that first?
The curative effect is not D, it’s a perfect D level .
Too high D makes the sleep disorder return .
60-80 ng/ml appears to be the range for no pills, no pain normal, restorative sleep.
Normal sleep, night after night, is what cures the body.
D Lower than 50 appears to bring on the sleep disorder.
How to replace the D to fix the sleep and why all the controversy about dosing?
From 8/2010 - 12/2010 I had given FDA recommended 1000 IU of vitamin D3 . (Contrary to popular rumor I am not really a vitamin nut.)
The two guys wearing the CPAP were the only ones who got better probably because their D levels were higher, in the 40’s, before supplementing and CPAP definitely helps.
In January 2010, after learning about D, I came back expecting all my headache patients to be cured, but none were better, they still couldn’t sleep and had a headache every day. So I checked their levels again.
On 1000 IU/day their D levels were all 10 points lower . They were 28 in August, 18 in January. So 1000 IU per day is just fine if you start with a level of 80 in August, but it won’t get you normal sleep in the winter if you’re starting below 30.
This is a hormone with a narrow band of normal. The level changes in each person from month to month and year to year based on sun exposure and skin type.
How could the FDA possibly recommend a single dose for all Americans living from Florida to Alaska with very divergent skin colors and lifestyles without screwing everyone up?
They wisely chose to recommend a tiny, tiny dose, i.e., not enough to screw anyone up.
This chemical should never be supplemented by the government, it’s as odd as putting testosterone or estrogen in the milk.
It should never have been over the counter so that we’re not sure how much is in the non regulated pills we’re taking.
The FDA recommended dose has absolutely nothing to do with the blood level that should be achieved in a clinical trial to produce normal sleep and cure disease. It also has nothing to do with the dose you want for your sleep to be normal so you don’t have to take those pills.
The sleep study experts have already documented that every American with hypertension needs a sleep study. Why don’t we do it? Because we don’t want them to have to use that stupid CPAP device, and they all have sleep disorders they just don’t all have severe sleep apnea.
Hypertension = sleep disorder. Just measure the D get it up to 60 and watch the hypertension resolve.
This is especially true in your patients with “hard to control” hypertension. If they sleep well one night the BP’s too low the next day, sleep badly and it’s too high despite the 4 medications
Your African American and Mexican American patients have the lowest D levels you will see. They are made for high sun environments and may need 8 hours of sun a day to make 20K D.
Gallbladder disease; gallstones and dysmotility always has D deficiency in the background. After D is made it goes to the liver. Cholesterol and D make up the liquid part of bile, bile acids the solid. No D bile acids come out of solution.
The entire GI tract nervous system, motility of the esophagus, stomach, gall bladder and upper and lower GI tract are linked to D
If gallbladder surgery is anticipated try to get the D level up for a month or so before surgery to prevent post surgical complications: DVT, infection, poor healing. Maybe their GB disease will resolve. Short course 10,000 IU/day.
All of your patients with atrial fibrillation have low D in the background. Remember the level moves monthly so do your patients’ levels in March-May and you’ll find out just how terrible they really are every spring. Remember it’s the non restorative sleep that causes the heart disease.
Most of the patients with heart failure have vitamin D deficiency, especially those with right heart failure and leg swelling.
“ Arthritis” is the name we have applied to “My__________ hurts when I wake up in the morning, I take a shower and limber up and it goes away”.
Each one of these people have low D and a sleep disorder. The parts that are moving or tensing in sleep don’t get repaired properly and hurt in the morning.
We make D less efficiently as we get into our 70-80’s so normal aging is made up of: “rheumatism”, don’t sleep as well, bowel’s don’t work and a runny nose. It’s true that older people have “arthritis” but now so do younger people. All from low D.
In young people we call this “allergies” “irritable bowel” “arthritis” and “insomnia” they’re caused by the same thing, just in a younger population.
American Academy of Pediatrics recommends all babies receive 400 IU of D per day. It is not in the breast milk, even if mom takes supplement. Formula fed babies have it in formula, breast fed babies need it daily in dropper form.
www.vitamindcouncil.org has pediatric dosing recommendations by weight for children. Always watch their sleep. Always follow their levels every 3 months for the first 1-2 years until you’re sure of the dosing for each child.
The D level for children should be the same as for adults 60-80. When they wake up before you do and are happy and playful and interested and want to learn their sleep is normal.
When asked, all children say their sleep is “fine”, ask the mom if she has to wake her up several times in the morning for school.
All children who can’t fall asleep have very low D’s.
Medicare pays for it 4 times per year: ICD 9 268.9
D2 and D3 are not really the same. Wallmart, and Sam’s Club carry 5,000 IU D3 pills. Sam’s is the cheapest and most dependable. You don’t need D2 to get a big dose.
Start yourself and your patients on whatever dose you feel comfortable with, then measure a level again in 2-3 months. Pay attention to whether it’s winter or summer! Once your level doesn’t budge, go up a little on the dose, teach yourself what I learned but don’t go above 80.
Get the level to 60-80 ng/ml. Sleep does not get better until then.
If the recognized “normal” is 30-100 it can’t hurt to get the level to 60-80. See how you and your patients feel there instead of 15-20.