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Scott Gets His Blood Checked

10 Feb

After a discussion with my mother concerning my family’s health history and heart disease, I did some investigating into heart healthy diets.  I was influenced by the low-carbohydrate research referenced in Good Calories, Bad Calories by Gary Taubes, and the Paleo Diet by Loren Cordain.  According to these books, and a recent review published in the American Journal of Clinical Nutrition in March, 2010, in order to decrease cardiovascular risk we should reduce excess body fat and limit refined carbohydrates in our diet, such as processed starches (i.e. crackers, pastas, breads) and sugar.  That sounded like an interesting proposition to test for myself.  In addition, I wanted to challenge the notions that 1) dietary fat does not raise LDL cholesterol (the “bad” cholesterol), 2) that sugar and refined carbohydrates do raise LDL cholesterol, and 3) a high saturated fat diet would actually increase HDL (the “good” cholesterol) .

I have followed the guidelines of a low-carbohydrate diet for approximately two years that kept overall carbohydrate intake (including fruit and vegetables) to approximately  100 grams per day, ate little to no bread, and consumed a higher-fat diet, especially saturated fat.  While I am at work, with poor meal-preparation and needing to eat between clients, I have two Muscle Milk shakes and/or a protein bar(s) per day.  During the week, I eat an assortment of meat, seafood, nuts, fish and whole eggs.  As for vegetables, I eat primarily dark green veggies, such as broccoli, spinach, arugula and asparagus, but I also include cauliflower and watercress. Additionally, I exercise 4-5 times per week with at least 3 intense Crossfit routines ranging from 8-30+ minutes and 2-3 heavy lifting exercise routines.  I am 35 years old, with two children (4 & 7 years old).  My current body fat is around 10%, I average six hours of sleep six days per week, and I sleep in on Sundays.

There has been an extensive amount of research concerning the benefits and consequences of a deficiency in vitamin D.  With the importance of an adequate vitamin D level in mind, and because I go to work and return home in the dark during the winter (vitamin D is called the “sunlight vitamin” because our bodies make it from sunlight), I inconsistently supplement with 5,000-10,000 IU of vitamin D3.  Unfortunately, a specific test needs to be ordered to determine an individual’s vitamin D level – it is not a part of a regular physical exam blood profile.  So, I was looking forward to seeing my lipid profile and vitamin D level in order to determine how healthy my blood might suggest I am.  Otherwise, exercising regularly and eating a specific diet is not worth missing the lounging around, consuming pies and doughnuts, and watching television. ☺

Here are the results of my lipid profile:

Component                            My Value                        Standard Range*
CHOLESTEROL                        144                                      < 200-  mg/dL
TRIGLYCERIDE                        79                                        < 150-  mg/dL
HDL                                              69                                        > 55-65-  mg/dL
LDL CALCULATED                  59                                        <100-129-  mg/dL
VITAMIN D, 25-HYDROXY    34                                        30-100 ng/mL

*Standard range based on desirable or optimal ranges

My physician said my laboratory tests all look great.  At one time, the cholesterol ratio was considered better for physicians to assess a patient’s risk of heart disease, but it appears times have changed.  Physicians are more interested in the raw numbers.  However, my lipid profile is unique in that my HDL cholesterol is actually higher than my LDL cholesterol.  I attribute this aspect of my lipid profile to my higher-fat diet.  Short-term and long-term low-carbohydrate studies consistently show to increase in HDL cholesterol with increased saturated fat intake.

As for the vitamin D results, although I am in the “normal range”, I am alarmed that I am in the low normal range after supplementing with vitamin D3.  The conversion of vitamin D3 in the body is dependent on the concentration of a certain enzyme, and the concentration varies among people.  Although controversial on the optimal level, evidence suggests vitamin D3 level should be above 50 – 80 ng/dL.  Therefore, either I need to increase my vitamin D3 supplementation, get more sun, or a little bit of both.  Either way, I need to have another vitamin D3 test in another three months to see if I am increasing my levels effectively.

In conclusion, I am happy with my results, but the vitamin D test was a novel piece of health knowledge. Everybody should have a yearly physical to record personal markers of health, and identify detrimental changes.

So, when is the last time you had your blood tested?

Vitamin D: Can it Prevent Everything from Certain Cancers, the Common Cold, Diabetes, Multiple Sclerosis or Even Autism?

28 Jan

I usually do not like to write about a single vitamin or supplement. It seems too boring for me to have to research and for you to have to read. Usually, something like a general vitamin description would be easily accessible on the Internet and I see no reason for me to regurgitate what you could easily find elsewhere.

However, there is some very interesting research regarding vitamin D that can benefit our society on an assortment of levels. Unfortunately, the research into vitamin D’s potential is in its infancy: spurring many questions and theories with few answers thus far, and spurring controversy in the realms of the RDA’s recommendations. What’s all of the fuss about? Lets see…

The Sun Vitamin

It is summer time again, and that means barbecues, beaches, gardening and/or just spending more time outside. Many people are aware that with our increasing sun exposure comes an increase in the production of vitamin D in our skin. This is very beneficial for us as this is the optimal way our bodies can utilize vitamin D.

However, the media reminds us during this time of year that with an increase in sun exposure comes an increase in diagnoses of skin cancer because many do not protect ourselves enough from UV exposure of the sun. Recent research is now starting to suggest that although skin melanomas are certainly a danger with increasing unprotected-ultraviolet B exposure, the lack of vitamin D we would normally produce is just as dangerous. For example, since the 1980s, scientists have recognized that the risk of developing and dying of breast, colon, prostate, ovarian, and many other cancers is increased in relation to living at higher latitudes and being more prone to developing vitamin D deficiency.

Biologic Function

Before we dive in any deeper to what vitamin can do, lets understand what it is. The primary function of vitamin D in humans is to maintain intracellular and extracellular calcium and phosphorus. Vitamin D refers to two biologically inactive precursors – D3, also known as cholecalciferol, and D2, also known as ergocalciferol. The former, produced in the skin on exposure to UVB radiation (290 to 320 nm), is said to be more bioactive. The latter is derived from plants and only enters the body via the diet, from consumption of foods such as oily fish, egg yolk and liver.

Vitamin D made in the skin or ingested in the diet, however, is biologically inactive and requires obligate hydroxylations first in the liver to 25-hydroxyvitamin D (25(OH)D), and then in the kidney to 1,25-dihydroxyvitamin D (1,25(OH)2D). 25-Hydroxyvitamin D is the major circulating form of vitamin D that is the best indicator of vitamin D status. 1,25-dihydroxyvitamin D is the biologically active form of vitamin D.

Regulation of Vitamin D

Ever heard of somebody dieing from vitamin D toxicity because of too much sun exposure? No. That is because the production of vitamin D and its metabolism are tightly regulated by the body. Once vitamin D enters the circulation, it can be stored in fat cells for later use or metabolized in the liver to 25(OH)D. This hydroxylation step is feedback regulated, meaning that if there is too much 25(OH)D present, our body will store the vitamin D. If there is not enough, more 25(OH)D will be produced.

This fat-soluble hormone interacts with its specific nuclear receptor in the intestine and bone to regulate calcium metabolism. It is now recognized that the vitamin D receptor is also present in most tissues and cells in the body. 1,25-dihydroxyvitamin D, by interacting with its receptor in non-calcemic tissues, is able to elicit a wide variety of biologic responses. 1,25-dihydroxyvitamin D regulates cellular growth and influences the modulation of the immune system.

There is compelling epidemiologic observations that suggest that living at higher latitudes is associated with increased risk of many common deadly cancers. Both prospective and retrospective studies help support the concept that it is vitamin D deficiency that is the driving force for increased risk of common cancers in people living at higher latitudes.

Most tissues and cells not only have a vitamin D receptor, but also have the ability to make 1,25-dihydroxyvitamin D. It has been suggested that increasing vitamin D intake or sun exposure increases circulating concentrations of 25-hydroxyvitamin D, which in turn, is metabolized to 1,25-dihydroxyvitamin D(3) in prostate, colon, breast, etc. The local cellular production of 1,25-dihydroxyvitamin D acts in an autocrine fashion to regulate cell growth and decrease the risk of the cells becoming malignant. Therefore, measurement of 25-hydroxyvitamin D is important not only to monitor vitamin D status for bone health, but also for cancer prevention.

Vitamin D and gene expression

25 Aug

Blood concentrations of vitamin D has a major role in gene expression for several diseases according to a new study.

From the Vitamin D Council

19 Mar
The Vitamin D Newsletter
More Vitamin D Studies of Interest
March 14, 2010
This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you are not subscribed, you can do so on the Vitamin D Council’s website. If you want to unsubscribe, go to the end of this newsletter.
This newsletter is now copyrighted but you may reproduce it for non-economic reasons without prior permission as long as you properly attribute its source.
The mainstream American press is ignoring much of the recent Vitamin D scientific literature. I suspect newspaper editors have decided that too many favorable Vitamin D stories run the risk of repeating the folic acid, beta-carotene and vitamin E affairs, when early epidemiological research was not routinely substantiated by later randomized controlled trials. If the press has made that decision, then this newsletter is your best source of information on new Vitamin D science.
Genetics, as well as dose, determine response to vitamin D supplements.
Your vitamin D blood level depends entirely on how much you take or how often you sunbathe, right? Wrong. Prior studies of identical twins show that about 25 -50% of the variation of Vitamin D levels depends on genetics. In July, researchers at the University of Toronto discovered the heritability of 25(OH)D is probably mediated through the Vitamin D binding protein (VDBP).
One of the common emails I get (and I’m sorry I can’t answer individual emails) is “I am taking 5,000 IU per day but my blood level is only 35 ng/ml.” What should I do? This study helps answer such questions. You probably inherited a tendency to not respond to higher doses of Vitamin D. Simply take a little more and get your blood tested again in 3-4 months.
Also, don’t forget your weight. Does it make sense that if you weigh 300 pounds, you need more vitamin D than a 3 pound baby? If that makes sense to you, congratulations, it has not made sense to any of the five Food and Nutrition Boards (FNB) that have convened and issued recommendations to Americans over the last 60 years; they have all recommended the same 200 IU/day dose for infants and young adults, no matter how much the adults weigh.

More researchers actually recommend that people take Vitamin D and not just give more money to scientists.
Researchers from Austria concluded their review paper on vitamin D and high blood pressure by stating: “In view of the multiple health benefits of vitamin D and the high prevalence of vitamin D deficiency, as well as the easy, safe, and inexpensive ways in which vitamin D can be supplemented, we believe that the implementation of public health strategies for maintaining a sufficient vitamin D status of the general population is warranted.” 
Good for Austria! By the way, while vitamin D may improve hypertension, it is not the be all and end all of hypertensive disease. If your doctor can stop your high blood pressure medication after you start taking vitamin D, great, but I doubt that will happen. Most people will have to continue taking their antihypertensive medication even after adequate vitamin D supplementation, albeit sometimes at a lower dose.
While I am on the subject, remember, that vitamin D will not prevent all cancer or heart disease or respiratory infections. True, evidence is accumulating that it will help, but you can still develop cancer, heart disease and respiratory infections with adequate blood levels of vitamin D. That’s why I believe in complimentary, not alternative, medicine.
Professor Michael Holick keeps increasing the amount of vitamin D he recommends.
As readers know, Professor Holick is one of the world’s foremost authorities on vitamin D. However, after being on the 1997 Food and Nutrition Board (FNB), he stuck with the FNB’s 200 IU/day recommendation well into the next century. Then he slowly went to 400 IU, then 800 IU, then 1,000 IU and now he is at 2,000 IU/day. Professor Holick is going in the right direction and is almost there.
Professor Robert Heaney of Creighton University just discovered that if you take 2,200 IU of vitamin D every day, you only have about 12 days supply of vitamin D in your body.
I love Robert Heaney’s papers. In a previous paper, Dr. Heaney discovered that at blood levels of 35 ng/ml, 50% of people are using up their vitamin D as quickly as they take it, that is, they are not storing any for future use and suffer from chronic substrate starvation. Obviously, one wants to take enough so the body has all it can use, which is why I recommend 25(OH)D levels of at least 50 ng/ml. At that level, no one should have chronic substrate starvation.
In the paper below, Dr. Heaney collaborated with two other Creighton scientists, Dr. Diane Cullen and Dr. Laura Armas, as well as one of the premier experts in measuring vitamin D in the world, Dr. Ron Horst of Heartland Assays. Ron runs tens of thousands of vitamin D samples a year as Heartland Assays performs vitamin D testing for most of the big studies and Dr. Horst is one of the few people in the world who can accurately measure cholecalciferol, and not just 25(OH)D.
Anyway, in his latest paper, Dr. Heaney found that if you regularly take 2,200 IU per day, you have about 12 days supply of vitamin D in your body. He explained, “What this indicates is that fat reserves of the vitamin are essentially running on empty and that . . . additional vitamin D inputs are [converted to 25(OH)D] almost immediately.” . . “The currently recommended intake of vitamin D needs to be revised upward by at least an order of magnitude.”
What is not known, at least by me, is what happens when cholecalciferol intake far exceeds the body’s requirement. We know it is stored in the body, mainly in fat and muscle, but what does the body do to control excess cholecalciferol from building up in the body? Professor Reinhold Vieth has written that much of it will simply be excreted unchanged in the bile, but how does that system work exactly, to get rid of excess cholecalciferol? We know it works because the few patients with vitamin D toxicity reported in the literature – almost always due to industrial errors – reduce their vitamin D levels rather quickly by simply stopping the vitamin D and staying out of the sun.
Zocor has no effect on vitamin D levels.
I know several studies have found statins raise vitamin D levels but different scientists report different findings. This paper found Zocor had no effect of vitamin D levels while a previous paper found Crestor almost tripled vitamin D levels. What’s the truth? I don’t know. The above study did find that higher vitamin D levels were strongly associated with better triglycerides and weakly associated with higher HDL (the good cholesterol) levels.
Vitamin D lowers statin blood levels
This study makes the point that things are often more complex than they first appear. Almost nothing is known of vitamin D’s drug-drug interactions. That is, how does vitamin D affect the blood level of other drugs? The below study measured the effects of vitamin D on Lipitor levels and cholesterol levels hours after Lipitor was given to patients taking vitamin D. The authors were looking for drug-drug interactions and found them.
The above study found vitamin D not only lowered Lipitor levels, but vitamin D lowered bad cholesterol levels as well. That is, the lowest bad cholesterol levels were found in patients on vitamin D with the lowest Lipitor levels, just the opposite of what one would think. I mean, wouldn’t higher Lipitor levels result in lower cholesterol levels? Not when vitamin D was taken into account. If you think my explanation of this study is confusing, you should read the study.
Intensive treatment with vitamin D, statins, and omega-3 fish oil reverses coronary calcium scores.
The below open study by Dr. William Davis and colleagues studied 45 adults with evidence of calcified coronary arteries, treating them with high dose statins, niacin, fish oil (not cod liver oil) capsules, and enough vitamin D (average of about 4,000 IU/day) to obtain 25(OH)D levels of 50 ng/ml. They found that regimen reduced coronary calcium scores in 20 patients and slowed progression in 22 additional patients. That is, it reversed the coronary calcification process in about half of patients and slowed its progression in most of the rest.
Most studies have shown high dose statins on their own do not reverse coronary arthrosclerosis, so we know it was not the statins alone. What would vitamin D levels of 70 ng/ml do? So, if you have coronary artery disease: ask your cardiologist about statins and niacin, take 5-10 fish oil capsules per day, and at least 5,000 IU of vitamin D3 per day.
A word about fish oil is in order. Fish oil means fish body oil, not fish liver oil. And, four or five capsules of omega-3 fish oil a day will do very little if you do not limit your intake of omega-6 oils. Your ratio of omega-6 to omega-3 is the crucial number, your want that ratio at 2 or below, which means no chips, no French fries and no processed foods, a difficult diet. Omega-6 oils are vegetable oils such as corn oil, safflower oil, soybean oil, sunflower oil and cottonseed oil. Read the packages to see what is in them and if they contain the above oils do not eat them. In additions to taking fish oil capsules, try to eat wild-caught salmon three times a week.
Our group’s second paper on influenza is now the most accessed paper in the history of Virology Journal.
I was asked to write the paper by the editor of another journal, who then refused it! I almost decided to scrap the paper but, in the end, submitted it to Virology Journal. I’m glad I did.
I was glad to see that six other experts recently recommended that the diagnosis and treatment of vitamin D deficiency be part of our national preparedness for the H1N1 pandemic.
In addition, I hear through the grapevine that the CDC has discovered that, of the 329 American children who have died so far from H1N1, vitamin D levels in the dead children were lower than in children who survived the swine flu. Maybe something can be done to save our children by next winter? Not to mention the 16,000 adult Americans the CDC thinks died from H1N1.
Low vitamin D levels mean higher death rates in patients with kidney disease.
The below study is the first of its kind; Dr. Rajnish Mehrota and his eight colleagues studied 3,000 of the 28 million U.S. adults who have chronic kidney disease, finding those with vitamin D levels below 15 ng/ml had a 50% increased risk of death compared to those with levels above 30 ng/ml over the nine years of the study. These researchers from UCLA, Harvard, the Los Angeles Biomedical Research Institute, and other institutions concluded: “The broad public health implications of our findings cannot be overemphasized given the high prevalence of vitamin D deficiency among individuals with chronic kidney disease, and the ease, safety, and low cost of maintaining replete vitamin D levels.”
These words are music to my ears; these words are strong words, urgent words, and, better yet, they are not my words. This is the first large study looking at a representative group of Americans with kidney disease, before dialysis, finding about 1/3 of them died over the 9 years of the study. Those with low vitamin D levels were more likely to die; in fact, they were more likely to have about every chronic disease you can think of before they died. The average age of those with kidney disease was only 55. This is a very important study, well written and well-conducted.
However, there is a scandal in medicine, a scandal not openly discussed in scientific papers, one not yet reported by the mainstream press. The scandal is this: if you are on dialysis, the chances are very high that your kidney doctor thinks he is giving you vitamin D when he is doing no such thing and some drug companies encourage such ignorance.
Drug companies market very lucrative activated vitamin D drugs to nephrologists as “vitamin D.” The kidney doctors, in turn, think they are giving vitamin D to their dialysis patients when they are doing no such thing. If anything, the activated vitamin D analogs nephrologists use in kidney disease will lower 25(OH)D levels by turning on the enzyme that gets rid of vitamin D.
The ugly secret is that plain old dirt-cheap vitamin D would lower the amount of activated vitamin D analogs needed to treat kidney disease. We used to think it was all or none, the kidneys would either make activated vitamin D to maintain blood calcium or the kidneys would not, as in renal failure. However, it is not all or none; the more vitamin D building blocks available to the diseased kidneys, the more activated vitamin D diseased kidneys can make. And, tissues other than the kidney, such as the skin, pancreas, adrenal medulla, and certain white blood cells, can contribute to serum activated vitamin D levels, and probably would if they had enough of the building block (plain old, dirt-cheap old, regular old, vitamin D).
Just out: Vitamin D administration (plain old vitamin D) to renal dialysis patients reduces the need for expensive vitamin D analogues, reduces inflammation, reduces the need for medication that increases red blood count, and improves cardiac function.
As I was about to finish this tirade about vitamin D and kidney failure, the below open study was published on March 4, 2010 and I ordered it. (By the way, the Council has to pay $11.00 for every paper I get and only one paper in ten is worth reporting on). The study below confirms what the above authors predicted; plain old cheap vitamin D helps patients with kidney disease.
Dr. Patricia Matias and colleagues in Portugal gave vitamin D3 to 158 patients on renal dialysis, using a sliding scale of vitamin D3 administration dependent on baseline 25(OH)D levels. Some patients got 50,000 IU per week, some got 10,000 IU per week, etc. Their dosing regimen increased 25(OH)D levels from a mean of 22 ng/ml at the beginning of the study to a mean of 42 ng/ml during treatment, indicating half of patients still had levels lower than 42 ng/ml after treatment. Interestingly, most of the patients who did not increase their 25(OH)D very much had diabetes, suggesting the metabolic clearance (how quickly it is used up) of vitamin D is increased in diabetes. By the way, we know the patients took the vitamin D; the doctors gave it to them when they came in for dialysis.
The results of this study were amazing. After vitamin D administration, parathyroid hormone, albumin, CRP (a measure of inflammation), brain natriuretic peptide (a measure of heart failure), and left ventricular mass index (a measure of heart function) all improved significantly. The dose of activated vitamin D (Zemplar in this case) was reduced, and some patients were able to stop it all together. Also, the dose of two other drugs used in kidney failure, one to bind phosphorus and the other to raise hemoglobin, was reduced.
It is a tragedy that drug companies sell more expensive vitamin D analogs by having their drug salesman assure kidney doctors that the expensive vitamin D analogues are vitamin D, even if it kills their clients. But, with the brand new knowledge that kidney failure patients live much longer on vitamin D, the drug companies might want to do some simple math. They might make even more money if they kept their patients alive longer. True, they will need less vitamin D analogues and other expensive kidney drugs every day, but the patients may live many more days.
John Cannell, MD
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