Low Carb Diet After Bariatric Surgery

Low Carb Diet After Bariatric Surgery

1. What is diabetes?
2. About blood sugar
3. Food & diabetes
4. Improving blood sugar
5. Science of diabetes reversal
6. A message of hope

Do you have type 2 diabetes, or are you at risk for diabetes? If so, then you've come to the right place.

This guide gives you an overview of what you need to know about treating and reversing type 2 diabetes. Our other guides can teach you more about the symptoms of diabetes, as well as provide specific information about type 2 diabetes and type 1 diabetes.

Many people with diabetes or prediabetes have improved their health with dietary changes. You can too! Making these changes may allow you to reduce or eliminate diabetes medication, and help you lose weight as well.¹

Keep reading to see if this could work for you!

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1. What is diabetes?

Simply put, diabetes is a disorder of blood sugar (glucose) and insulin.  In diabetes, something is wrong with the way a person makes and/or uses insulin, a pancreatic hormone that lowers blood sugar by moving it out of the bloodstream and into the body's cells.

Type 1 diabetes results when, for autoimmune or other rare reasons, the pancreas becomes damaged and fails to produce insulin. This form of diabetes is most often diagnosed in childhood but can occur in adults.

In type 2 diabetes, there are defects in both the production of insulin by the pancreas (insulin deficiency) and the use of insulin by the body (insulin resistance). When damage to the pancreas' insulin-producing cells progresses to the point where the pancreas can no longer spontaneously release enough insulin to overcome the body's resistance to it, blood sugar levels rise.

Excess glucose in the blood is a problem because it can damage blood vessels. What's more, the body's tissues can't effectively use glucose for energy because too much of it stays in the bloodstream instead of entering the cells.

It is important to recognize that high glucose levels are a consequence of an underlying process that has been going on for years before blood sugar becomes high.

The good news is that diet and exercise can help decrease insulin resistance and its associated weight gain, which may help prevent or even reverse diabetes.²

To learn more about diabetes, click here:

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2. Testing blood sugar

Our guide on what you need to know about blood sugar can help you learn more about both high and low blood sugar. This guide focuses specifically on the high blood sugar levels that occur in diabetes.

How do you know if you have too much sugar in your blood? If you don't know already, it's simple to test in a few seconds, either in your doctor's office or with your own inexpensive blood glucose meter.⁷

Compare your own blood sugar reading with the ranges below: ⁸

• Normal blood sugar: Less than 100 mg/dL (5.6 mmol/L ) after fasting overnight, and up to 140 mg/dL (7.8 mmol/L ) two hours after a meal
• Prediabetes: Between 100-125 mg/dL (5.6-7.0 mmol/L) after fasting overnight
• Diabetes: 126 mg/dL (7.0 mmol/L) or higher after fasting overnight, or higher than 200 mg/dL (11.1 mmol/L) at any time

Keep in mind that you should not use glucometer readings alone to make a diagnosis of diabetes or prediabetes. If your blood sugar is high on a glucometer, ask your doctor to run a blood test to confirm the diagnosis. Also, most guidelines state that a single abnormal blood sugar reading is not sufficient to secure a diagnosis of diabetes; at least two are needed.

If you are already on a low-carbohydrate diet and you are concerned about the measurements you're getting, find out how a low-carb diet affects blood sugar measurements.

Learn more about how to test your blood sugar

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3. Food & diabetes

People with diabetes have difficulty keeping blood sugar levels in a normal range. The blood turns "too sweet" as glucose levels rise.⁹

Sugar in your blood comes from two places: your liver and the food that you eat. You can't do much to control the amount of sugar your liver makes, but you can control the foods you eat.

Foods are made up of three broad categories known as macronutrients (major nutrients): carbohydrate, protein, and fat. Many foods are a combination of two or all three macronutrients, but we often group foods according to whether they are mostly carbohydrate, protein, or fat.

Carbohydrates and blood sugar

Carbohydrates, or carbs, usually come from starches or sugars and turn into glucose when they are digested. When glucose enters the bloodstream, it's called blood glucose, or blood sugar.

Carbohydrates

The more carbohydrate eaten in a meal, the more sugar is absorbed into the bloodstream and usually the higher the blood sugar will be.

Although very few people would agree that sugary foods are good for you, some foods that we think of as "healthy" — such as fruit — can have a lot of sugar. And many people don't know that starchy foods — such as bread, rice, pasta, and potatoes — quickly turn to sugar when you digest them.¹⁰

For some people, eating a potato could raise blood sugar as much as eating 9 teaspoons of sugar! It can be hard to predict exactly how someone's blood sugar will respond, as this will likely vary based on genetics and baseline insulin sensitivity.¹¹ By testing your blood sugar before eating and every 30-minutes after eating for up to two hours, you can quickly learn how different foods affect your blood glucose level. The results may surprise you!

Protein

Protein containing foods include eggs, poultry, meat, seafood and tofu. Although individuals have different responses to these foods, consuming moderate amounts of protein at a meal generally has a mild to no effect on blood sugar.¹²

Fat

Dietary fat by itself has practically no effect on blood sugar. However, we seldom eat fat all by itself. Some foods, like cheese, are made up of mostly protein and fat. These foods probably won't raise your blood sugar very much.¹³

But other foods, like doughnuts and French fries, are made up mostly of carbohydrate and fat. Because they're high in carbs and fat together, these foods are likely to significantly raise your blood sugar.

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4. How to lower blood sugar with diet

What happens if you remove foods that raise your blood sugar from your diet? Is there anything good left to eat? We think so. In fact, we have a whole guide on the best foods to control diabetes.

But a picture is worth a thousand words. These are just a few of the delicious foods that don't raise blood sugar for just about everyone:

Many people with type 2 diabetes are now choosing a diet based primarily on low-carb foods, and many clinicians are catching on as well.¹⁴

A person with type 2 diabete will often notice that, starting with the first meal, their blood sugar improves. The need for medications, especially insulin, is usually dramatically reduced. Substantial weight loss and health marker improvements often follow.¹⁵ Finally, people usually feel better and have more energy and alertness. ¹⁶

Choosing foods low in carbs is an effective way to help you control your blood sugar and is safe for most people. However, if you are taking medications for your diabetes, you must work with your healthcare provider to adjust your medications when you change your diet since the need for medications, especially insulin, may be greatly reduced.¹⁷

If you are looking for a doctor who will work with you to control your diabetes with a change in diet, our map may help you find one.

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5. The science of diabetes reversal

In 2019, the American Diabetes Association (ADA) stated that reducing carbohydrate intake was the most effective nutritional strategy for improving blood sugar control in those with diabetes.¹⁸

Research shows that low-carb diets are a safe and effective option for treating type 2 diabetes. This body of evidence includes systematic reviews and meta-analyses of randomized controlled trials (the highest quality of evidence by our ratings.).¹⁹

A meta-analysis from 2017 found that low-carb diets reduced the need for diabetes medication and also improved certain bio-markers in people with type 2 diabetes. This included reductions in hemoglobin A1c (HbA1c), triglycerides, and blood pressure; and increases in high-density lipoprotein (HDL) cholesterol, sometimes called the "good" cholesterol.²⁰

Additionally, in a non-randomized trial from Virta Health, the intervention group of subjects with type 2 diabetes followed a very low-carb diet and received remote monitoring by physicians and health coaches. After one year, 94% of those in the low-carb group had reduced or stopped their insulin use. Furthermore, 25% had an HgbA1c in the normal range without needing any medications, suggesting their disease was in remission, and an additional 35% did the same with only metformin.²¹

At the two-year mark, a high proportion of subjects continued to demonstrate sustained improvements in glycemic control.²²

Other interventions have also demonstrated efficacy for inducing remission of type 2 diabetes, although there is a lack of consistency with how different trials define "remission."²³ The DiRECT trial reported severe caloric restriction (eating around 850 calories per day) resulted in 46% remission at one-year.²⁴ And bariatric surgery demonstrates between 25% and 50% diabetes remission up to ten-years post surgery.²⁵

This evidence suggests that type 2 diabetes does not have to be a progressive and irreversible disease. It is clearly a treatable disease.

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6. A message of hope

As recently as 50 years ago, type 2 diabetes was extremely rare. Now, around the world, the number of people with diabetes is increasing rapidly and is heading towards 500 million. This is a worldwide epidemic.

In the past, type 2 diabetes was thought to be a progressive disease with no hope for reversal or remission. People were — and sometimes still are — taught to "manage" type 2 diabetes, rather than to try to reverse the underlying process.

But now people with type 2 diabetes can hope to regain their health! Today we know that the hallmarks of type 2 diabetes — high blood sugar and high insulin — can often be reversed with a very low-carb diet, severe caloric restriction, or weight loss surgery.

People don't just have to "manage" their diabetes as it progresses. Instead, they can often lower their blood sugar to normal levels with diet alone, and may be able to avoid or discontinue most medications.

Normal blood sugar levels and fewer or no medications likely means no progression of disease, and no progression of complications. People with a diagnosis of type 2 diabetes may be able to live long, healthy lives, with toes, eyesight, and kidneys intact!

If you are not on any medications, you can start your journey back to health today. If you are on medications for diabetes or for other conditions, consult your doctor before beginning any lifestyle change, such as a low-carb diet, so your medications are adjusted safely as your blood sugars improve.

When you're ready, here's where to start: A low-carbohydrate diet for beginners. During your own journey, you might be inspired by some spectacular diabetes success stories.

If you want to learn more about how you can improve your health and the health of your family, start here by keeping up with the latest news from Diet Doctor.

Low Carb Diet After Bariatric Surgery

Source: https://www.dietdoctor.com/diabetes

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Cherries On Low Carb Diet

Cherries On Low Carb Diet

Low-Carb Fruits Ranked from Lowest to Highest Carbs

All fruits are good for you and nutrient-rich. But if you're watching your carbs, some are lower than others.

Fruit often gets a bad rap because it's sweet and not low in carbs. But nature's candy delivers more than just carbs in the form of natural sugar. Fruits are packed with important vitamins and minerals, plus fiber. Fiber helps slow the absorption of sugar into your bloodstream so you're less likely to experience spikes and lows. Plus, eating fruit is actually associated with a lower risk of diabetes. If you're watching your carb intake, you may be wondering which fruits are lowest in carbs. Here we rank fruit based on how many carbs you'll get.

How Many Carbs Are in Your Fruit?

Carbs Graphic

We've ranked these common fruits based on a recommended serving size, but also provide information about how many carbs per 100 grams of fruit (about 3.5 ounces) to give you a better understanding when you're (literally) comparing apples to oranges. Here they are ranked from lowest-carb fruit to highest-carb fruit.

1. Watermelon

Watermelon Fruit Pizza

1 cup chopped watermelon: 11 grams carbs, 46 calories.

100 grams: 8 grams carbs, 30 calories.

2. Strawberries

Strawberry-Chocolate Greek Yogurt Bark

1 cup sliced strawberries: 13 grams carbs, 53 calories.

100 grams: 8 grams carbs, 32 calories.

3. Cantaloupe

Triple Melon Smoothie

1 cup cubed cantaloupe: 13 grams carbs, 54 calories.

100 grams: 8 grams carbs, 34 calories.

4. Peach

Peach & Roasted Beet Salad

1 medium peach: 14 grams carbs, 58 calories.

100 grams: 9 grams carbs, 37 calories.

5. Raspberries

Cocoa-Chia Pudding with Raspberries

1 cup raspberries: 15 grams carbs, 64 calories.

100 grams: 12 grams carbs, 52 calories.

6. Orange

Orange-Walnut Salad with Chicken

1 medium orange: 15 grams carbs, 62 calories.

100 grams: 12 grams carbs, 47 calories.

7. Blueberries

Purple Fruit Salad

1 cup blueberries: 21 grams carbs, 84 calories.

100 grams: 14 grams carbs, 57 calories.

8. Pineapple

Pineapple & Avocado Salad

1 cup cubed pineapple: 22 grams carbs, 82 calories.

100 grams: 13 grams carbs, 50 calories.

9. Mango

100+ Kid-Friendly Snack Ideas

1 cup chopped mango: 25 grams carbs, 99 calories.

100 grams: 15 grams carbs, 60 calories.

10. Cherries

Cherry-Berry Oatmeal Smoothie

1 cup cherries: 25 grams carbs, 97 calories.

100 grams: 16 grams carbs, 63 calories.

11. Apple

Apple Mini Fruit Pizzas

1 medium apple: 25 grams carbs, 95 calories.

100 grams: 12 grams carbs, 47 calories.

12. Banana

Sprouted-Grain Toast with Peanut Butter & Banana

1 medium banana: 27 grams carbs, 105 calories.

100 grams: 15 grams carbs, 57 calories.

13. Grapes

Chicken, Fennel & Grape Quinoa Salad

32 grapes: 28 grams carbs, 108 calories.

100 grams: 18 grams carbs, 69 calories.

Bottom Line

It's recommended that you eat two cups of fruit per day as part of a healthy diet. And variety is important to get the health benefits of each fruit. Certain colors provide certain benefits-orange for eyesight and purple for brain health for example-so choose your favorite fruits but mix it up. Fruit is a good carb and the kind you should be eating. And skip fruit juice if you're worried about carbs. Just one cup has 25-plus grams of carbohydrates and none of the beneficial fiber.

• Best & Worst Fruits for Diabetes
• Low-Carb Meal Plans
• What Does a Serving of Carbs Look Like?

Cherries On Low Carb Diet

Source: https://www.eatingwell.com/article/290638/low-carb-fruits-ranked-from-lowest-to-highest-carbs/

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Low Vitamin B And D

Low Vitamin B And D

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Vitamin B-12 is an essential nutrient that keeps the body functioning properly. Symptoms of vitamin B-12 deficiency include fatigue, low mood, and nerve problems.

The human body does not create vitamin B-12, so people must get this nutrient from their diet. It is crucial for making DNA and red blood cells, and it helps support the nervous system.

Vitamin B-12 plays a vital role in the production of blood cells.

Many of the symptoms of vitamin B-12 deficiency arise because it causes a lack of healthy blood cells. The body needs plenty of these cells to get oxygen around the body and keep the organs in good health.

A vitamin B-12 deficiency can lead to both physical and psychological problems. In this article, we explore 11 symptoms of vitamin B-12 deficiency and explain why they occur.

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Vitamin B-12 deficiency can cause symptoms that impact a person's mental and physical health.

Vitamin B-12 deficiency may affect between 1.5 and 15.0 percent of people.

This deficiency can cause a wide range of symptoms that affect a person's mental and physical health.

It is important to consume foods that contain vitamin B-12 on a regular basis. Adults need around 2.4 micrograms (mcg) of vitamin B-12 each day.

Vitamin B-12 is a water-soluble vitamin that is present in animal-based foods, such as:

• red meat
• poultry
• eggs
• dairy
• fish

If a person does not eat animal products, they will need to add vegetarian and vegan sources of vitamin B-12 to their diet. These include fortified cereals, plant milks, bread, and nutritional yeast.

As vitamin B-12 deficiency shares many symptoms with other nutritional deficiencies and health conditions, it is possible that people may neither notice it nor get a diagnosis.

Being aware of all of the signs can help people identify the deficiency and seek treatment.

Below, we look at the symptoms of vitamin B-12 deficiency and their causes.

Vitamin B-12 deficiency may cause "pins and needles" in the hands or feet. This symptom occurs because the vitamin plays a crucial role in the nervous system, and its absence can cause people to develop nerve conduction problems or nerve damage.

In the nervous system, vitamin B-12 helps produce a substance called myelin. Myelin is a protective coating that shields the nerves and helps them transmit sensations.

People who are vitamin B-12 deficient may not produce enough myelin to coat their nerves. Without this coating, nerves can become damaged.

Problems are more common in the nerves in the hands and feet, which are called peripheral nerves. Peripheral nerve damage may lead to tingling in these parts of the body.

Over time, peripheral nerve damage resulting from vitamin B-12 deficiency can lead to movement problems.

Numbness in the feet and limbs may make it hard for a person to walk without support. They may also experience muscle weakness and diminished reflexes.

Pale or yellow skin, called jaundice, may be a symptom of vitamin B-12 deficiency.

Jaundice develops when a person's body is not able to produce enough red blood cells. Red blood cells circulating under the skin provide it with its normal color. Without enough of these cells, the skin may look pale.

Vitamin B-12 plays a role in the production of red blood cells. A vitamin B-12 deficiency can cause a lack of red blood cells, or megaloblastic anemia, which has an association with jaundice.

This type of anemia can also weaken the red blood cells, which the body then breaks down more quickly. When the liver breaks down red blood cells, it releases bilirubin. Bilirubin is a brownish substance that gives the skin the yellowish tone that is characteristic of jaundice.

Megaloblastic anemia due to vitamin B-12 deficiency may lead to a person feeling fatigued.

Without enough red blood cells to carry oxygen around their body, a person can feel extremely tired.

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A fast heart rate and shortness of breath may be symptoms of vitamin B-12 deficiency.

A fast heart rate may be a symptom of vitamin B-12 deficiency.

The heart may start to beat faster to make up for the reduced number of red blood cells in the body.

Anemia puts pressure on the heart to push a higher volume of blood around the body and to do it more quickly. This response is the body's way of trying to ensure that enough oxygen circulates through all of the body's systems and reaches all the organs.

Anemia that results from vitamin B-12 deficiency may cause a person to feel a little short of breath. It is possible to link this to a lack of red blood cells and a fast heartbeat.

Anyone who is experiencing real difficulty breathing should see a doctor straight away.

Vitamin B-12 affects oral health. As a result, being deficient in vitamin B-12 may cause the following mouth problems:

• glossitis, which causes a swollen, smooth, red tongue
• mouth ulcers
• a burning sensation in the mouth

These symptoms occur because vitamin B-12 deficiency causes a reduction in red blood cell production, which results in less oxygen reaching the tongue.

Vitamin B-12 deficiency may cause problems with thinking, which doctors refer to as cognitive impairment. These issues include difficulty thinking or reasoning and memory loss.

One study even linked low vitamin B-12 levels to an increased risk of Alzheimer's disease, vascular dementia, and Parkinson's disease.

The reduced amount of oxygen reaching the brain might be to blame for the thinking and reasoning problems.

Being deficient in vitamin B-12 can affect a person's mood, potentially causing irritability or depression.

There is a need for more research into the link between vitamin B-12 and mental health. One theory is that vitamin B-12 helps break down a brain chemical called homocysteine. Having too much homocysteine in the brain may cause mental health problems.

Vitamin B-12 deficiency can affect the digestive tract.

A lack of red blood cells means that not enough oxygen reaches the gut. Insufficient oxygen here may lead to a person both feeling and being sick. It may also cause diarrhea.

As a result of digestive problems, such as nausea, people with vitamin B-12 deficiency may lose their appetite. A decreased appetite can lead to weight loss in the long term.

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Eating a vegan diet increases the risk of vitamin B-12 deficiency.

Even if a person gets enough vitamin B-12 in their diet, some underlying health conditions can affect the absorption of vitamin B-12 in the gut.

These conditions include:

• Crohn's disease
• celiac disease
• atrophic gastritis
• pernicious anemia

The following factors make a person more likely to have a vitamin B-12 deficiency:

• being older, because a person becomes less able to absorb B-12 as they age
• eating a vegetarian or vegan diet
• taking anti-acid medication for an extended period
• weight loss surgery or other stomach surgery, which can affect how the digestive system absorbs vitamin B-12

Most people can get enough vitamin B-12 from dietary sources. For those who cannot, a doctor may prescribe or recommend B-12 supplements. People can also get B-12 supplements from drug stores or choose between brands online.

Most multivitamins contain vitamin B-12. People can take B-12 supplements in the form of oral tablets, sublingual tablets that dissolve under the tongue, or injections. A doctor can provide advice on the correct dosage of this vitamin.

People who have trouble absorbing vitamin B-12 may need shots of the vitamin to treat their deficiency.

A doctor can advise people on the best way to prevent vitamin B-12 deficiency, depending on their dietary choices and health.

The body needs vitamin B-12 for a range of bodily functions, which include making red blood cells. Being deficient in vitamin B-12 causes physical and psychological symptoms, including nerve problems, fatigue, and difficulty thinking.

Most vitamin B-12 deficiency symptoms occur due to a lack of red blood cells, which means that the body does not get enough oxygen. The body's oxygen supply is crucial for many aspects of health.

As with other nutrients, the best way for most people to get vitamin B-12 is in the diet. If a person cannot get enough from their usual diet, fortified foods and other dietary supplements may help.

In most cases, doctors can treat vitamin B-12 deficiency. However, people with long-term deficiency may have long-lasting effects, such as nerve damage.

Spotting the signs of vitamin B-12 deficiency early on and getting the right treatment can improve a person's outlook.

Low Vitamin B And D

Source: https://www.medicalnewstoday.com/articles/324265

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Is Vitamin D Derived From Cholesterol

Is Vitamin D Derived From Cholesterol

Vitamin D was discovered in 1920, culminating the long search for a way to cure rickets, a painful childhood bone disease. Within a decade, the fortification of foods with vitamin D was under way, and rickets became rare in the United States. But solving the problem of rickets was only the beginning of research into vitamin D. Research results suggest that vitamin D may have a role in  other aspects of human health.

Breaking the old rules

Vitamin D is one of the 13 vitamins discovered in the early 20th century by doctors studying nutritional deficiency diseases. Ever since, scientists have defined vitamins as organic (carbon-containing) chemicals that must be obtained from dietary sources because they are not produced by the body's tissues. Vitamins play a crucial role in our body's metabolism, but only tiny amounts are needed to fill that role.

Although vitamin D is firmly enshrined as one of the four fat-soluble vitamins, it is not technically a vitamin. True, it's essential for health, and only minuscule amounts are required. But it breaks the other rules for vitamins because it's produced in the human body, it's absent from all natural foods except fish and egg yolks, and even when it's obtained from foods, it must be transformed by the body before it can do any good.

As our habits change, most of us cannot rely on our bodies to produce vitamin D the old-fashioned way. Instead, we increasingly depend on artificially fortified foods and pills to provide this vital nutrient. Coming full circle in the modern world, this substance may actually come to fit the technical definition of a vitamin.

What is vitamin D?

Vitamin D is not one chemical but many. The natural type is produced in the skin from a universally present form of cholesterol, 7-dehydrocholesterol. Sunlight is the key: Its ultraviolet B (UVB) energy converts the precursor to vitamin D₃. In contrast, most dietary supplements are manufactured by exposing a plant sterol to ultraviolet energy, thus producing vitamin D₂. Because their function is almost identical, D₂ and D₃ are lumped together under the name vitamin D — but neither will function until the body works its magic (see figure).

How your body makes vitamin D

The sun's energy turns a chemical in your skin into vitamin D₃, which is carried to your liver and then your kidneys to transform it to active vitamin D.

The first stop is in the liver, where vitamin D picks up extra oxygen and hydrogen molecules to become 25-hydroxyvitamin D, or 25(OH)D. This is the chemical that doctors usually measure to diagnose vitamin D deficiencies. But although 25(OH)D is used for diagnosis, it can't function until it travels to the kidney. There it acquires a final pair of oxygen and hydrogen molecules to become 1,25 dihydroxy vitamin D; scientists know this active form of the vitamin as 1,25(OH)₂D, or calcitriol, but for ordinary folks the name vitamin D is accurate enough.

How it works

Vitamin D's best-known role is to keep bones healthy by increasing the intestinal absorption of calcium. Without enough vitamin D, the body can only absorb 10% to 15% of dietary calcium, but 30% to 40% absorption is the rule when vitamin reserves are normal. A lack of vitamin D in children causes rickets; in adults, it causes osteomalacia. Both bone diseases are now rare in the United States, but another is on the rise — osteoporosis, the "thin bone" disease that leads to fractures and spinal deformities.

Low levels of vitamin D lead to low bone calcium stores, increasing the risk of fractures. If vitamin D did nothing more than protect bones, it would still be essential. But researchers have begun to accumulate evidence that it may do much more. In fact, many of the body's tissues contain vitamin D receptors, proteins that bind to vitamin D. In the intestines, the receptors capture vitamin D, enabling efficient calcium absorption. But similar receptors are also present in many other organs, from the prostate to the heart, blood vessels, muscles, and endocrine glands. And work in progress suggests that good things happen when vitamin D binds to these receptors. The main requirement is to have enough vitamin D, but many Americans don't.

Vitamin D deficiencies

Vitamin D deficiencies were rare when most men rolled up their sleeves to work in sunny fields. But as work shifted from farms to offices, that changed. Because pigmentation can reduce vitamin D production in the skin by over 90%, nonwhite populations are at particular risk. Deficiencies are also common in patients with intestinal disorders that limit absorption of fat and those with kidney or liver diseases that reduce the conversion of vitamin D to its active form, calcitriol (1,25(OH)2D). In addition, certain medications reduce the availability or activity of vitamin D. And even in healthy people, advancing age is linked to an increased risk of vitamin D deficiency.

Although standards vary, most experts agree that levels of 25(OH)D below 20 ng/ml (nanograms per milliliter) reflect clear-cut vitamin D inadequacy, while levels between 20 and 30 ng/ml are borderline.

A number of factors can play a role. Limited exposure to sunlight heads the list. Except during the short summer months, people who live at latitudes above 37 degrees north or below 37 degrees south of the equator don't get enough UVB energy from the sun to make all the vitamin D they need. The same is true for people who spend most of their time indoors and for those of us who avoid sunshine and use sunscreens to protect our skin from the harmful effects of ultraviolet radiation (see box below). It's an example of an unforeseen consequence of wise behavior, but you can enjoy sun protection and strong bones, too, by taking vitamin supplements.

Sunscreens

Like politicians, doctors often have to compromise; when it comes to sunshine, most pols promise blue skies, while most docs turn out to be the shady guys — or, at least, sunscreen advocates.

Sunlight contains two forms of radiant energy, ultraviolet A (UVA) and ultraviolet B (UVB). UVB provides the energy your skin needs to make vitamin D, but that energy can burn the skin and increase the cell damage that leads to cancer. UVA also contributes to skin damage and premature aging.

To protect yourself, avoid the summer sunshine, especially between 10 a.m. and 2 p.m. Whenever possible, wear a large-brimmed hat and a tightly woven, dark-colored long-sleeve shirt and long pants when you go out in the sun.

But summer garb is usually lightweight and exposes a lot of skin. That's where a sunscreen comes in. Look for a product with an SPF of 30 or higher. Look for a "broad spectrum" sunscreen that also protects against both UVA and UVB. Apply your sunscreen early, often, and liberally.

These many factors explain why vitamin D deficiencies are shockingly common in the United States. Although standards vary, most experts agree that levels of 25(OH)D below 20 ng/ml (nanograms per milliliter) reflect clear-cut vitamin D inadequacy, while levels between 20 and 30 ng/ml are borderline. Using similar criteria, American researchers have reported deficiencies in 42% of African American women aged 15 to 49, in 41% of non-hospitalized patients aged 49 to 83, and in up to 57% of hospitalized patients. And low levels of vitamin D are common even in apparently healthy young adults; in one study, more than a third of people between the ages of 18 and 29 were deficient.

Numbers can never tell the whole story, but in this case, "D-ficiencies" add up to a wide range of health concerns.

Osteoporosis and fractures

It's a paradox: Skeletal health is the best-known contribution of vitamin D, but it has also become the most controversial. Although doctors agree that vitamin D deficiency increases the risk of osteoporosis and fractures, they disagree about the benefits and optimal dosage of supplements.

Without enough vitamin D, the intestines cannot efficiently absorb calcium. But because blood calcium is critical for neuromuscular and cardiac function, the body does not allow levels to fall. Instead, it pours out parathyroid hormone, which mobilizes calcium from bone. Blood calcium levels remain normal, so your heart and nerves keep working nicely. But your bones bear the brunt: As bone calcium density falls, bones become weak and fracture-prone.

Most studies show that a lack of vitamin D increases the risk of osteoporosis and the likelihood of hip and other non-spinal fractures. But there is considerable disagreement about how much supplements reduce the risk of fractures. Some studies include only women, others both men and women; some include only frail, elderly, or institutionalized subjects, others physically active people; some use vitamin D alone, others a combination of D and varying doses of calcium; and some administer 400 international units (IU) of vitamin D a day, others up to 800 IU a day.

Prostate cancer

Some men mistakenly dismiss osteoporosis as a women's worry, but none fail to recognize the importance of prostate cancer.

Vitamin D has an important role in regulating cell growth. Laboratory experiments suggest that it helps prevent the unrestrained cell multiplication that characterizes cancer by reducing cell division, restricting tumor blood supply (angiogenesis), increasing the death of cancer cells (apoptosis), and limiting the spread of cancer cells (metastasis). Like many human tissues, the prostate has an abundant supply of vitamin D receptors. And, like some other tissues, it also contains enzymes that convert biologically inactive 25(OH)D into the active form of the vitamin, 1,25(OH)2D. These enzymes are much more active in normal prostate cells than in prostate cancer cells.

Do the results from these experiments translate into clinically important effects? Possibly.

In 1998, Harvard's Health Professionals Follow-up Study of 47,781 men reported that a high consumption of calcium supplements was associated with an increased risk of advanced prostate cancer. The risk was greatest in men getting more than 2,000 mg of calcium a day from a combination of supplements and food. Since then, other studies have confirmed a link between very high levels of calcium intake and increased risk, but they have exonerated dietary calcium consumption. The Harvard scientists speculate that the problem is not calcium itself but a relative lack of active vitamin D.

Other malignancies

The risk of colon cancer, breast cancer, and other malignancies appears to rise in populations at latitudes far from the equator. Sun exposure and vitamin D levels may be part of the explanation. A recent clinical trial looking at a daily 1,000 IU vitamin D supplement did not show a decreased risk of cancer, but it was associated with a decreased risk of cancer death.

"D" right amount

The most widely used recommended dietary allowance (RDA) for vitamin D is 600 IU daily for adults up to age 69 and 800 IU daily for people older than 70.

Is more better? We don't know yet, but you definitely can get too much of a good thing. Like the other fat-soluble vitamins, vitamin D is stored in the body's adipose (fat) tissue. That means your body can mobilize its own reserves if your daily intake falters temporarily — but it also means that excessive doses of vitamin D can build up to toxic levels. At those extremes, vitamin D can raise blood calcium to levels that can cause grogginess, constipation, and even death. But it takes massive overdosing to produce toxicity.

How to get vitamin D

You can make your vitamin D the old-fashioned way, by exposing your skin to UVB radiation in sunlight. It doesn't take much, but people living north of the 37-degree-latitude line — roughly the imaginary line between Philadelphia and San Francisco — can't get enough UVB in winter to do the trick. And many others will find it all too easy to overdose on UVB, increasing their risk of malignant melanomas and other skin cancers, as well as wrinkles and premature skin aging. All in all, most doctors recommend avoiding sunlight (see box) and getting vitamin D by mouth.

Diet can help, but it's very hard to approach the new goals with food alone. Fish and shellfish provide natural vitamin D (oily fish are best), but you'll have to eat about 5 ounces of salmon, 7 ounces of halibut, 30 ounces of cod, or nearly two 8-ounce cans of tuna to get just 400 IU. An egg yolk will provide about 20 IU, but since it also contains nearly a day's quota of cholesterol, you can't very well use eggs to fill your tank with D. Other foods have even less D, which is why manufacturers fortify milk, some yogurt, some orange juice, and many cereals with vitamin D. In general, a serving will provide about 100 IU; that means drinking a quart of fortified milk to get 400 IU.

Most people require supplements to get the vitamin D they need. It's the main benefit of a daily multivitamin; most provide 400 IU. Remember to read the labels carefully so you won't get too little or too much. And although cod liver oil is rich in vitamin D, it has too much vitamin A for regular use.

New light on the sunshine vitamin

It used to be simple: just get a "healthy" tan and your body will make all the vitamin D it needs. Desk jobs and sunscreen have changed all that, just as research is underlining the importance of vitamin D and suggesting its possible role in preventing many health problems. That makes vitamin D a dilemma of modern life that has a modern solution: eating fish and drinking some low-fat fortified milk, along with judicious doses of vitamin D supplements.

As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

Is Vitamin D Derived From Cholesterol

Source: https://www.health.harvard.edu/staying-healthy/vitamin-d-and-your-health-breaking-old-rules-raising-new-hopes

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How To Read Vitamin D Lab Results

How To Read Vitamin D Lab Results

Mayo Clin Proc. 2010 Aug; 85(8): 752–758.

Vitamin D Deficiency in Adults: When to Test and How to Treat

This article has been cited by other articles in PMC.

Abstract

Recent evidence for the nonskeletal effects of vitamin D, coupled with recognition that vitamin D deficiency is common, has revived interest in this hormone. Vitamin D is produced by skin exposed to ultraviolet B radiation or obtained from dietary sources, including supplements. Persons commonly at risk for vitamin D deficiency include those with inadequate sun exposure, limited oral intake, or impaired intestinal absorption. Vitamin D adequacy is best determined by measurement of the 25-hydroxyvitamin D concentration in the blood. Average daily vitamin D intake in the population at large and current dietary reference intake values are often inadequate to maintain optimal vitamin D levels. Clinicians may recommend supplementation but be unsure how to choose the optimal dose and type of vitamin D and how to use testing to monitor therapy. This review outlines strategies to prevent, diagnose, and treat vitamin D deficiency in adults.

AI = adequate intake; CKD = chronic kidney disease; D2 = vitamin D₂; D3 = vitamin D₃; 1,25(OH)2D = 1,25-dihydroxyvitamin D; HPT = hyperparathyroidism; 25(OH)D = 25-hydroxyvitamin D; PTH = parathyroid hormone; UVB = ultraviolet B

Vitamin D has been appreciated for its role in calcium homeostasis and bone health since its identification in 1921.¹ Even so, 25% to 50% or more of patients commonly encountered in clinical practice are deficient in vitamin D. Recent advances in biochemical assessment, therapeutic goals for vitamin D nutrition for optimal bone health, and the association of vitamin D deficiency with nonskeletal disease have revived interest in this hormone.

Vitamin D consists of 2 bioequivalent forms. Vitamin D₂ (D₂), also known as ergocalciferol, is obtained from dietary vegetable sources and oral supplements. Vitamin D₃ (D₃), also known as cholecalciferol, is obtained primarily from skin exposure to ultraviolet B (UVB) radiation in sunlight, ingestion of food sources such as oily fish and variably fortified foods (milk, juices, margarines, yogurts, cereals, and soy), and oral supplements. Aside from rich sources such as oily fish, the vitamin D content of most foods is between 50 and 200 IU per serving. This value varies greatly by region of the world because fortification markedly improves the availability of vitamin D through diet. Both D₂ and D₃ are biologically inert. Once absorbed from the intestine, they are metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], composed of 25(OH)D₂ and 25(OH)D₃; 25(OH)D (also called calcidiol) is subsequently converted to 1,25-dihydroxyvitamin D [1,25(OH)₂D], also known as calcitriol, in the kidney and select other tissues by the action of the 1α-hydroxylase enzyme. The predominant effects of vitamin D are exerted through the endocrine and autocrine actions of calcitriol via activation of the vitamin D receptor in cells.

TESTING AND INTERPRETING VITAMIN D STATUS

How Prevalent Is Vitamin D Deficiency And Who Is At Risk?

Worldwide, naturally occurring dietary sources of vitamin D are limited, and food fortification is optional, inconsistent, inadequate, or nonexistent. Therefore, for most people, vitamin D is primarily obtained by cutaneous production from sun exposure. However, many variables influence the amount of UVB from sunlight that reaches the skin and its effectiveness. These include time of day, season, latitude, altitude, clothing, sunscreen use, pigmentation, and age. In Minnesota in 2008, less than half of days provided enough solar UVB radiation at noon to effect cutaneous vitamin D production.² Even those who normally reside in sunny climates are commonly found to be deficient in vitamin D, probably due to cultural habits and/or dress.³ Even if regularly exposed to sunlight, elderly people produce 75% less cutaneous D₃ than young adults.⁴ Further barriers to cutaneous vitamin D production are ongoing public health campaigns promoting sunscreen use, as advocated by the American Academy of Dermatology (http://www.aad.org/forms/policies/ps.aspx, accessed December 24, 2009). Unfortunately, commonly recommended daily intakes of vitamin D are known to be insufficient if sunlight exposure is limited.⁵

Vitamin D deficiency is more common than previously thought. The Centers for Disease Control and Prevention has reported that the percentage of adults achieving vitamin D sufficiency as defined by 25(OH)D of at least 30 ng/mL (to convert to nmol/L, multiply by 2.496) has declined from about 60% in 1988-1994 to approximately 30% in 2001-2004 in whites and from about 10% to approximately 5% in African Americans during this same time. Furthermore, more people have been found to be severely deficient in vitamin D [25(OH)D <10 ng/mL].⁶ Even when using a conservative definition of vitamin D deficiency, many patients routinely encountered in clinical practice will be deficient in vitamin D, as shown in Table 1.

TABLE 1.

Prevalence of Vitamin D Deficiency in Commonly Encountered Clinical Patient Populations

Who Should Be Tested For Vitamin D Deficiency?

Although vitamin D deficiency is prevalent, measurement of serum 25(OH)D levels is expensive, and universal screening is not supported. However, vitamin D testing may benefit those at risk for severe deficiency (Table 2) or those with laboratory or radiographic findings commonly associated with vitamin D deficiency (Table 3). In these patients, knowledge of the 25(OH)D blood level provides an accurate assessment of vitamin D body stores, helps identify the need for vitamin D therapy, and may help to determine an effective dose. Alternatively, empiric vitamin D supplementation without testing can be justified for patients who have no overt risk factors or evidence of deficiency but are thought to have inadequate sun exposure or dietary intake.

TABLE 2.

Clinical Risk Factors for Vitamin D Deficiency

TABLE 3.

Laboratory and Radiographic Findings That suggest Possible Vitamin D Deficiency

Vitamin D deficiency can contribute to bone loss from decreased vitamin D–mediated intestinal calcium absorption and resultant secondary hyperparathyroidism (HPT). Vitamin D supplementation can improve muscle strength and reduce fall frequency by approximately 50%.⁷ Thus, patients who have low bone mineral density or a prior low-impact (fragility) skeletal fracture and those at risk of falling should be evaluated for vitamin D deficiency to reduce the risk of all types of skeletal fractures.^8,9

Patients with chronic kidney disease (CKD) have decreased conversion of 25(OH)D to 1,25(OH)₂D as a result of impaired renal 1-α hydroxylase activity. This contributes to secondary HPT and metabolic bone disease. Superimposed nutritional deficiency may aggravate secondary HPT both directly (as a result of low vitamin D levels) and indirectly (as a result of impaired vitamin D–mediated intestinal calcium absorption). Patients with stage I to III CKD should be tested and supplemented with vitamin D as needed to achieve optimal levels of 25(OH)D in addition to modifying calcium and phosphate intake. Emerging evidence is challenging our understanding of bone and vascular health in stage IV to V CKD, such that vitamin D, calcitriol, or vitamin D analogs should be used according to current CKD guidelines and under the guidance of a nephrologist.

It has been suggested that clinicians should routinely test for hypovitaminosis D in patients with musculoskeletal symptoms, such as bone pain, myalgias, and generalized weakness, because these symptoms are often associated with hypovitaminosis D and might be misdiagnosed as fibromyalgia, chronic fatigue, age-related weakness, or even depression.¹⁰ Some studies and numerous anecdotal observations report vitamin D deficiency in 80% to 90% of children and adults with pain, myalgias, and weakness.¹¹ However, few high-quality interventional studies support a causal relationship between vitamin D deficiency and pain. Furthermore, vitamin D status can be a surrogate marker of poor nutritional status such that the high prevalence of vitamin D deficiency in these populations may reflect suboptimal nutrition and lack of outdoor activity associated with chronic illness. Indeed, a recent randomized, blinded, placebo-controlled trial showed no benefit of vitamin D supplementation for such symptoms.¹² The role of vitamin D testing in pregnant or lactating women may be refined by data from ongoing interventional trials.

Which Test Best Measures Vitamin D Status?

Ingested and cutaneously produced vitamin D is rapidly converted to 25(OH)D, but in serum only a fraction of 25(OH)D is converted to its active metabolite 1,25(OH)₂D. Thus, measurement of the total 25(OH)D level is the best test to assess body stores of vitamin D. The total 25(OH)D level allows for the diagnosis and monitoring of vitamin D deficiency, whereas quantification of 25(OH)D₂ and 25(OH)D₃ fractions may facilitate treatment monitoring. For example, in patients without clinical improvement after D₂ or D₃ supplementation, lack of increase in the corresponding 25(OH)D₂ or 25(OH)D₃ and total 25(OH) D levels may indicate inadequate dosing, nonadherence, or malabsorption. Some laboratory assays for vitamin D cannot differentiate between 25(OH)D₂ and 25(OH)D₃ and will only report a total 25(OH)D level. Some laboratory assays underdetect D₂ metabolites, which may give the appearance of ineffective D₂ supplementation.

In people with healthy kidneys and bones, normal serum levels of calcium and phosphorus are maintained predominantly through the interaction of 2 hormones: parathyroid hormone (PTH) and calcitriol. In the setting of vitamin D deficiency, secondary HPT causes both release of calcium stored in bone and resorption of calcium by the kidney to maintain normal serum calcium and phosphorus levels. Thus, vitamin D deficiency is usually accompanied by normal blood levels for calcium and phosphorus, high-normal or elevated levels of PTH, normal to elevated levels of total alkaline phosphatase, a low 24-hour urine calcium excretion rate, and low levels of total 25(OH)D. Patients with severe and long-standing vitamin D deficiency may present with overt hypocalcemia and/or hypophosphatemia, but this is the exception. Clinicians should not measure 1,25(OH)₂D levels to diagnose hypovitaminosis D. Doing so can lead to an erroneous interpretation of vitamin D status because calcitriol levels are often normal or even elevated in patients with vitamin D deficiency as a result of elevated PTH levels.

What Is an Optimal 25(OH)D Level?

A wide "optimal" range for 25(OH)D is reported (25-80 ng/mL), and differences of opinion exist as to the definitions of vitamin D insufficiency (sometimes reported as <30 ng/mL) and deficiency (<20 ng/mL). Mild-to-modest deficiency can be associated with osteoporosis and/or secondary HPT. Severe deficiency may lead to failure to mineralize newly formed osteoid in bone, resulting in rickets in children and osteomalacia in adults. Most cells have vitamin D receptors. The consequences of vitamin D deficiency for organs other than bone are not fully known but may include impaired immunity, increased autoimmunity, myopathy, diabetes mellitus, and an increased risk of colon, breast, and prostate cancers.¹³ Higher vitamin D levels have also been associated with increased longevity.^14,15 Thus, an optimal vitamin D level might depend on the health outcome in question. The vitamin D levels in Table 4 are those reported by Mayo Medical Laboratories and represent clinical decision-making values that apply to men and women of all ages rather than population-based reference values.

TABLE 4.

Mayo Medical Laboratories Reference Ranges for Total Serum 25-hydroxyvitamin D [25(OH)D]^a

Population reference ranges for vitamin D vary widely depending on ethnic background, age, geographic location of the population, and the sampling season. In northern latitude locations in particular, up to 73% of the population may have levels of less than 20 ng/mL during winter.¹⁶ Thus, it is important to be aware that vitamin D levels are affected by both geographic and seasonal variability and that a person with an "optimal" level in the summer may well become "deficient" in the winter without any change in diet and as a result of changes in sun exposure.

HOW TO PREVENT AND TREAT VITAMIN D DEFICIENCY

Many patients and physicians think that adequate vitamin D intake can be obtained via diet alone. This assumption is erroneous. With the exception of fatty fish, the vitamin D content of most foods, including fortified dairy products, is relatively low to nonexistent. Even some dairy products in the United States are not fortified, making it important to read food labels to ensure the vitamin D content of foods.

Vitamin D supplementation is safe¹⁷ and inexpensive, but vitamin D deficiency often remains undiagnosed or is undertreated. Possible explanations for this disparity include (1) the recommended age-dependent adequate intake (AI) of vitamin D was established before publication of studies suggesting that 25(OH)D levels of greater than 30 ng/mL are needed to ensure PTH suppression into the normal range; (2) the current AI for vitamin D can easily be met by diet and/or a daily multivitamin,¹⁸ but this intake level may still be inadequate to reach optimal levels in many people, especially those at risk; and (3) physicians may be uncomfortable recommending larger doses of vitamin D. That fear is generally unmerited given the dearth of reports of vitamin D toxicity compared with the expansive literature on vitamin D deficiency. The rarity of reports of vitamin D toxicity can be explained in part by the kidney's ability to limit production of active calcitriol. Increased calcitriol levels inhibit PTH both directly (through the vitamin D response element on the PTH gene) and indirectly (by increasing intestinal calcium absorption), causing calcitriol production in the kidney to decrease. Renal 24-hydroxylase activity further limits the availability of calcitriol by creating inert metabolites of both calcitriol (1,24,25-trihydroxyvitamin D) and calcidiol (24,25-dihydroxyvitamin D). The 24-hydroxylase gene is under the transcriptional control of calcitriol, thereby providing tight negative feedback.

Vitamin D₂ Vs Vitamin D₃ Supplements: How Much Is Enough?

Both D₂ (ergocalciferol) and D₃ (cholecalciferol) are available as dietary supplements. The relative efficacy of D₂ vs D₃ in humans continues to be debated, although both appear to be effective for preventing or treating disease, provided that an adequate total 25(OH)D blood level is obtained. The variable efficacy of D₂ vs D₃ may relate primarily to differences in serum half-life and is clinically relevant for dosing and monitoring frequency. A single dose of 50,000 IU of D₂ or D₃ produces a similar increase in the total 25(OH)D concentration, but the apparent longer half-life of D₃ suggests that less frequent dosing may be needed.¹⁹ A daily dosing study of 1000 IU of D₂ vs D₃ showed no difference in any resulting vitamin D level [25(OH)D₂, 25(OH)D₃, or total 25(OH)D].²⁰ However, a recent study comparing 1600 IU of D₂ once daily vs 1600 IU of D₃ once daily vs 50,000 IU of D₂ once monthly vs 50,000 IU of D₃ once monthly suggested that D₃ is superior in that it showed slightly higher levels of 25(OH)D₃ at the end of 1 year. An important caveat of this study was that the mean total 25(OH)D level at the beginning of the study was already in the reference range (33 ng/mL), and those with hypovitaminosis D may respond differently.²¹ We recommend the use of D₃, particularly if dosing is infrequent (ie, less than once weekly). One situation in which D₂ may be preferred is a vegetarian or vegan diet. It is recommended that both D₂ and D₃ be taken with a meal containing fat to ensure maximum absorption.

Since 1997, the Food and Nutrition Board has advised an AI of vitamin D of 200 to 600 IU/d.¹⁸ The AI is "believed to cover the needs of all individuals" but "lack of data or uncertainty in the data" limit the ability to confidently determine a recommended daily allowance. The AI for vitamin D is based on maintenance of a total serum 25(OH)D level of at least 11 ng/mL.¹⁸ Although these recommendations are the basis for the amounts of vitamin D used to fortify foods and provided in many supplements, it is widely accepted that they are outdated.²² Revised dietary reference intakes from the Institute of Medicine are expected in 2010.

How much vitamin D is needed to correct severe vitamin D deficiency (<10 ng/mL)? Although not validated by clinical trials, a commonly applied strategy is to prescribe a "loading dose" (eg, 50,000 IU of vitamin D orally once weekly for 2-3 months, or 3 times weekly for 1 month). A review of multiple loading algorithms suggested that a minimum total dose of 600,000 IU best predicted an end-of-treatment 25(OH)D level greater than 30 ng/mL.²³ It is important to note that none of the studied patients developed hypercalcemia. For mild to moderate deficiency (11-25 ng/mL), a shorter treatment interval or lower dose may be effective. Although many different strategies may be used in treating vitamin D deficiency, a common oversight in management is to stop treatment or provide inadequate vitamin D maintenance dosing once the 25(OH)D level reaches the optimal range. Regardless of initial vitamin D therapy, and assuming no change in lifestyle or diet, a maintenance/prevention daily dose of 800 to 2000 IU or more will be needed to avoid recurrent deficiency (Table 3).²⁴ A maintenance dose averaging 2000 IU/d meets the current safe upper limit guidelines and is well below safe upper limits reported by others.¹⁷

Special mention is needed for patients who have malabsorption or require tube feeding or parenteral nutrition. Patients receiving tube feeding (but without malabsorption) have vitamin D dosing requirements similar to persons with oral intake. However, ergocalciferol capsules contain D₂ in oil, which can clog the feeding tube and therefore should not be used. Cholecalciferol capsules and tablets contain D₃ in powder form and can be used without clogging the feeding tube. Patients with malabsorption often require larger maintenance dosing of vitamin D. For example, patients with malabsorptive gastric bypass procedures may require 50,000 IU of D₂ or D₃ maintenance dosing from once weekly to as frequently as daily to maintain sufficiency. Standard multivitamin preparations for intravenous parenteral nutrition provide only 200 IU, a dose that helps maintain normal 25(OH)D levels in the short term but may not correct vitamin D deficiency. In extreme malabsorptive states, UVB exposure (ie, sunlight or phototherapy) can be effective for those who do not respond to large oral doses.²⁵ Vitamin D for intramuscular administration is not commercially available in the United States; however, it can be compounded in specialty pharmacies for limited local use.²⁶

THE IMPORTANCE OF CALCIUM AND VITAMIN D TOXICITY

What Role is Played by Calcium Nutrition?

Maintenance of normal serum calcium levels results from an array of interrelated processes, including intestinal calcium absorption, calcium uptake and release from the skeleton, and renal calcium handling. As previously noted, vitamin D plays a critical role in each of these processes. Hypovitaminosis D impairs intestinal calcium absorption and leads to secondary HPT and risk of bone loss. Heaney et al²⁷ found that maximal calcium absorption in men occurs when 25(OH)D levels are in the range of 30 to 40 ng/mL, consistent with vitamin D levels needed to suppress PTH. However, even in the presence of vitamin D sufficiency, inadequate oral calcium intake may cause secondary HPT. The National Osteoporosis Foundation guidelines recommend that men and women younger than 50 years ingest 1000 mg/d of elemental calcium, and those older than 50 years ingest 1200 mg/d (http://www.nof.org/prevention/calcium_and_VitaminD.htm, accessed December 24, 2009).

Clinicians should be mindful of several important caveats when considering calcium supplementation.

First, up to 500 to 600 mg of elemental calcium can be efficiently absorbed in any single dose, with excess calcium passing unabsorbed through the gut.

Second, gastric acidity is necessary for calcium absorption. However, even in patients with achlorhydria, calcium absorption is reported to occur adequately if taken with meals. For patients with achlorhydria due to gastric reduction or bariatric surgery, or during gastric acid suppressive therapy (eg, protein pump inhibitor use), calcium supplementation with the more acidic calcium citrate is preferred over calcium carbonate. However, calcium citrate can clog feeding tubes and should not be administered via any feeding tube.

Third, during vitamin D sufficiency, approximately 30% of calcium intake is normally absorbed regardless of the dietary or supplement source.²⁷ Thus, if 1000 mg of calcium is ingested and 30% (300 mg) is absorbed, and assuming that 50 mg is required for daily bone health, the remaining 250 mg will be renally excreted (normal 24-hour urine calcium excretion approximates 100-250 mg/d). With vitamin D deficiency, as little as 10% of ingested calcium may be absorbed. Thus, calcium excretion would be low (only 50 mg for a dose of 1000 mg). Although cumbersome, 24-hour urine calcium excretion is an effective test to assess adequacy of both calcium and vitamin D intake. When assessing urine calcium values, it is important to note that thiazide diuretics, lithium, and a low-sodium diet decrease renal calcium excretion, whereas excess sodium intake increases it.

Fourth, as already noted, low 25(OH)D levels may be associated with secondary HPT and abnormal bone mineralization. Thus, increased levels of PTH, increased total or bone alkaline phosphatase levels, and low 24-hour urine calcium levels should prompt suspicion for vitamin D deficiency in some patients. For example, vitamin D deficiency should be suspected in an otherwise healthy person found to have an elevated alkaline phosphatase level, especially if findings on other liver enzyme tests are normal.

What About Vitamin D Toxicity?

Vitamin D toxicity should not be diagnosed solely on the basis of an elevated 25(OH)D level; instead, it should be recognized as a clinical syndrome of both hypervitaminosis D and hypercalcemia, in which hyperphosphatemia and hypercalciuria also commonly (although not always) occur. Patients with vitamin D toxicity could present with clinical symptoms and signs of hypercalcemia (eg, nausea, dehydration, and constipation) and hypercalciuria (eg, polyuria and kidney stones). Hypervitaminosis D in the absence of hypercalcemia may prompt further investigation to evaluate the etiology of increased vitamin D levels; however, unlike hypercalcemia, it is not a medical emergency. Although excess vitamin D supplementation can lead to hypercalcemia, vitamin D toxicity is extremely rare and generally occurs only after ingestion of large doses of vitamin D (>10,000 IU/d) for prolonged periods in patients with normal gut absorption or in patients who may be concurrently ingesting generous if not excessive amounts of calcium. A 25(OH)D level of 80 ng/mL is the lowest reported level associated with toxicity in patients without primary HPT with normal renal function. Most patients with vitamin D toxicity have levels greater than 150 ng/mL.²⁸ Binkley et al²¹ have recently reported that vitamin D supplementation with 1600 IU/d or 50,000 IU monthly was not associated with any laboratory parameters of toxicity [eg, 25(OH)D, PTH, bone alkaline phosphatase, and 24-hour urine calcium] and even failed to increase total 25(OH)D levels above 30 ng/mL in 19% of participants.

CONCLUSION

Vitamin D is important for skeletal and nonskeletal health. It is now well established that many people have vitamin D levels that are less than currently recommended for optimal health. Worldwide, vitamin D is predominantly obtained through exposure to UVB radiation in the form of sunlight and cutaneous vitamin D production. Latitude, cultural dress habits, season, sun avoidance, and sunscreen protection can all limit vitamin D production. Gastrointestinal, hepatic, and renal disease may be related to low vitamin D levels, but hypovitaminosis D most commonly results from inadequate intake. Hypovitaminosis D resulting from lack of UVB exposure is not easily corrected by dietary intake alone in the absence of supplementation. Food fortification with vitamin D is based on outdated recommendations for daily AI. Supplementation with 800 to 1000 IU/d of vitamin D or 50,000 IU monthly is safe for most people and can ensure levels of vitamin D within the optimal range. This intake is within the currently recommended safe upper tolerable limit for vitamin D of 2000 IU/d for those aged 1 year and older. Revised recommended dietary intake values for vitamin D, which are needed to guide patients and physicians alike, are expected to be published in 2010.

Supplementary Material

Notes

On completion of this article, you should be able to (1) recognize patients at risk for vitamin D deficiency, (2) optimally use and interpret serum vitamin D testing, and (3) determine the optimal vitamin D therapy required to treat or prevent vitamin D deficiency in adults.

CME Questions About Vitamin D Deficiency in Adults

1. Which one of the following patients is at greatest risk for vitamin D deficiency?

   1. A formula-fed infant

   2. A teenaged girl eating an unrestricted diet and taking a multivitamin

   3. A 30-year-old male nursing home resident treated with phenytoin for epilepsy

   4. A 70-year-old woman with osteopenia taking a calcium carbonate with vitamin D supplement

   5. A 43-year-old male farmer

2. Which one of the following biochemical tests provides the best initial assessment of a person's vitamin D status?

   1. Serum parathyroid hormone (PTH)

   2. Serum 25-hydroxyvitamin D (calcidiol) [25(OH)D]

   3. Serum 1,25-dihydroxyvitamin D (calcitriol) [1,25(OH)₂ D]

   4. Serum bone alkaline phosphatase

   5. 24-hour urine calcium excretion

3. Which one of the following sets of laboratory test findings (reference ranges provided parenthetically) is most suggestive of vitamin D toxicity?

   1. Serum calcium, 9.7 mg/dL (8.9-10.1 mg/dL); serum phosphorus, 4.0 mg/dL (2.5-4.5 mg/dL); 24-hour urine calcium, 250 mg/spec (25-300 mg/spec); 25(OH)D, 120 ng/mL (25-80 ng/mL); and PTH, 30 pg/mL (15-50 pg/mL)

   2. Serum calcium, 10.4 mg/dL (8.9-10.1 mg/dL); serum phosphorus, 4.8 mg/dL (2.5-4.5 mg/dL); 24-hour urine calcium, 450 mg/spec (25-300 mg/spec); 25(OH)D, 120 ng/mL (25-80 ng/mL); and PTH, 20 pg/mL (15-50 pg/mL)

   3. Serum calcium, 11.0 mg/dL (8.9-10.1 mg/dL); serum phosphorus, 2.2 mg/dL (2.5-4.5 mg/dL); 1,25(OH)₂D, 85 pg/mL (22-67 pg/mL); and PTH, 95 pg/mL (15-50 pg/mL)

   4. Serum calcium, 10.6 mg/dL (8.9-10.1 mg/dL); serum phosphorus, 4.0 mg/dL (2.5-4.5 mg/dL); 24-hour urine calcium, 450 mg/spec (25-300 mg/spec); 25(OH)D, 26 ng/mL (25-80 ng/mL); 1,25(OH)₂D, 85 pg/mL (22-67 pg/mL); and PTH, 12 pg/mL (15-50 pg/mL)

   5. Serum calcium, 15 mg/dL (8.9-10.1 mg/dL); serum phosphorus, 4.0 mg/dL (2.5-4.5 mg/dL); 24-hour urine calcium, 450 mg/spec (25-300 mg/spec); 25(OH)D, 35 ng/mL (25-80 ng/mL); 1,25(OH)₂D, <10 pg/mL (22-67 pg/mL); and PTH, <6 pg/mL (15-50 pg/mL)

4. Which one of the following treatment strategies is most likely to be safe and effective to achieve optimal vitamin D levels in a person with little sun exposure?

   1. Daily supplementation with 400 IU of vitamin D₃ (D₃) via a multivitamin

   2. Daily supplementation with 800 to 1000 IU of vitamin D₂ (D₂) or D₃

   3. Daily supplementation with 50,000 IU of D₃

   4. Monthly supplementation with 50,000 IU of D₂

   5. One daily serving of fortified milk

5. Which one of the following statements about measuring 25(OH)D levels is correct?

   1. All patients should be tested for vitamin D deficiency before supplementation

   2. A patient with a 25(OH)D level of 10 ng/mL who is beginning treatment with 800 IU/d of D₃ should be rechecked after 1 month

   3. A patient with a 25(OH)D level of 10 ng/mL who is beginning treatment with 50,000 IU of vitamin D 3 times weekly for 1 month to be followed by 50,000 IU once monthly should be rechecked after 1 month

   4. A patient with a 25(OH)D level of 10 ng/mL who is beginning treatment with 2000 IU/d of D₃ should be rechecked after 6 months

   5. A patient with generous summertime sun exposure living at a high latitude with a low 25(OH)D level in spring should be supplemented and retested in the fall

This activity was designated for 1 AMA PRA Category 1 Credit(s).™

Because the Concise Review for Clinicians contributions are now a CME activity, the answers to the questions will no longer be published in the print journal. For CME credit and the answers, see the link on our Web site at mayoclinicproceedings.com.

REFERENCES

1. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357:266-281 [PubMed] [Google Scholar]

2. Plotnikoff GA. Weather or not: the importance of vitamin D status monitoring and supplementation. Minn Med. 2009;92(11):43-46 [PubMed] [Google Scholar]

3. Khoja SO, Khan JA, Berry JL, Maimani AR, Woolf AD, Lanham-New SA. Nutritional influences on bone in Saudi Arabian women: widespread vitamin D deficiency Presented at the 6th International Symposium on Nutritional Aspects of Osteoporosis; Lausanne, Switzerland; May4-6, 2006 [Google Scholar]

4. Lips P. Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications. Endocr Rev. 2001;22:477-501 [PubMed] [Google Scholar]

5. Glerup H, Mikkelsen K, Poulsen L, et al. Commonly recommended daily intake of vitamin D is not sufficient if sunlight exposure is limited. J Intern Med. 2000;247:260-268 [PubMed] [Google Scholar]

6. Ginde AA, Liu MC, Camargo CA., Jr Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Arch Intern Med. 2009;169:626-632 [PMC free article] [PubMed] [Google Scholar]

7. Bischoff HA, Stahelin HB, Dick W, et al. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res. 2003;18:343-351 [PubMed] [Google Scholar]

8. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D3 and calcium to prevent hip fractures in the elderly women. N Engl J Med. 1992;327:1637-1642 [PubMed] [Google Scholar]

9. Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B. Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials. JAMA 2005;293:2257-2264 [PubMed] [Google Scholar]

10. Holick MF. High prevalence of vitamin D inadequacy and implications for health. Mayo Clin Proc. 2006;81:353-373 [PubMed] [Google Scholar]

11. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc. 2003;78:1463-1470 [PubMed] [Google Scholar]

12. Arvold DS, Odean MJ, Dornfeld MP, et al. Correlation of symptoms with vitamin D deficiency and symptom response to cholecalciferol treatment: a randomized controlled trial. Endocr Pract. 2009;15:203-212 [PubMed] [Google Scholar]

13. DeLuca HF. Overview of general physiologic features and functions of vitamin D. Am J Clin Nutr. 2004;80:1689S-1696S [PubMed] [Google Scholar]

14. Autier P, Gandini S. Vitamin D supplementation and total mortality: a meta-analysis of randomized controlled trials. Arch Intern Med. 2007;167:1730-1737 [PubMed] [Google Scholar]

15. Ginde AA, Scragg R, Schwartz RS, Camargo CA., Jr Prospective study of serum 25-hydroxyvitamin d level, cardiovascular disease mortality, and all-cause mortality in older U.S. Adults. J Am Geriatr Soc. 2009;57:1595-1603 [PubMed] [Google Scholar]

16. Reusch J, Ackermann H, Badenhoop K. Cyclic changes of vitamin D and PTH are primarily regulated by solar radiation: 5-year analysis of a German (50 degrees N) population. Horm Metab Res. 2009;41:402-407 [PubMed] [Google Scholar]

17. Hathcock JN, Shao A, Vieth R, Heaney R. Risk assessment for vitamin D. Am J Clin Nutr. 2007;85:6-18 [PubMed] [Google Scholar]

18. Institute of Medicine Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride Washington, DC: National Academy Press; 1999:71-145 [Google Scholar]

19. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89:5387-5391 [PubMed] [Google Scholar]

20. Holick MF, Biancuzzo RM, Chen TC, et al. Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D. J Clin Endocrinol Metab. 2008;93:677-681 [PMC free article] [PubMed] [Google Scholar]

21. Binkley N, Gemar D, Engelke J, Gangnon R, Ramamurthy R, Krueger D. Dosing with ergocalciferol or cholecalciferol, 1,600 IU daily or 50,000 IU monthly, is safe but does not assure vitamin D adequacy. J Bone Miner Res. 2009;24 (suppl 1). [Google Scholar]

22. Yetley EA, Brule D, Cheney MC, et al. Dietary reference intakes for vitamin D: justification for a review of the 1997 values. Am J Clin Nutr. 2009;89:719-727 [PMC free article] [PubMed] [Google Scholar]

23. Pepper KJ, Judd SE, Nanes MS, Tangpricha V. Evaluation of vitamin D repletion regimens to correct vitamin D status in adults. Endocr Pract. 2009;15:95-103 [PMC free article] [PubMed] [Google Scholar]

24. Heaney RP. The Vitamin D requirement in health and disease. J Steroid Biochem Mol Biol. 2005;97:13-19 [PubMed] [Google Scholar]

25. Chandra P, Wolfenden LL, Ziegler TR, et al. Treatment of vitamin D deficiency with UV light in patients with malabsorption syndromes: a case series. Photodermatol Photoimmunol PhotoMed. 2007;23:179-185 [PMC free article] [PubMed] [Google Scholar]

26. Bertino JS, Reed MD, Lambert PW, Halpin TC. Stability of an extemporaneous formulation of injectable cholecalciferol. Am J Hosp Pharm. 1981;38:1932-1933 [PubMed] [Google Scholar]

27. Heaney RP, Dowell MS, Bierman J, Hale CA, Bendich A. Absorbability and cost effectiveness in calcium supplementation. J Am Coll Nutr. 2001;20:239-246 [PubMed] [Google Scholar]

28. Jones G. Pharmacokinetics of vitamin D toxicity. Am J Clin Nutr. 2008;88:582S-586S [PubMed] [Google Scholar]

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How To Read Vitamin D Lab Results

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912737/

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