Foods To Eat While On Low Carb Diet

Foods To Eat While On Low Carb Diet

"People Food" Your Dog Can & Can't Eat

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Although it's hard to resist those puppy dog eyes at the dinner table, it may not always be safe to feed your canine companion the same foods you eat. Dogs have different digestive systems than humans, which means some "people food" that seems harmless may actually be dangerous for your pet.

Read on to find out which foods — from avocados to eggs — are safe bets for your dog and which snacks could result in a trip to the vet — or worse.

Turkey: Yes

Yes, dogs can enjoy a helping of turkey on Thanksgiving — or on any old day of the year. However, experts suggest you remove excess fat as well as the turkey's skin before tossing it in your dog's bowl. Any meat with excessive seasonings or salt can upset a dog's stomach, and onions and garlic should be avoided at all cost.

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But the most important tip? Be sure to check the meat for bones and remove them. Dogs can easily swallow fine bones, which could then splinter during the digestive process, leading to blockages or tears in your pet's intestines.

Peanut Butter: Yes

Yes, peanut butter makes a great treat for both humans and dogs alike. This tasty source of protein also contains important vitamins — B and E — as well as niacin, a nutrient that helps lower cholesterol. Everyone has their own peanut butter preference, from smooth to crunchy to extra crunchy.

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For your pup, purchase a peanut butter that's raw, unsalted and not full of added sugars. Those added sugars could contain xylitol, a substance found in chewing gum and candy that is toxic for canines.

If peanut butter is A-okay, then that means peanuts are also a "yes." Contrary to popular belief, peanuts are actually a type of legume that just happens to be known for its delicious seeds.

Ice Cream: No

I scream, you scream, the dog howls for ice cream — but too bad. Nope, dogs should not eat ice cream. Surprisingly, this isn't necessarily a dairy issue. It's true that dogs aren't quite built to digest milk after they have been weaned as puppies, but the bigger issue is that the frozen treat contains loads of sugar.

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The American Kennel Club recommends freezing chunks of strawberries, raspberries or apples (without seeds) and then giving those to your dog on a hot day. Of course, these frozen fruits also contain some sugar, but they have far more nutritional value and can be doled out in small portions.

Honey: Yes

Though sweet, honey still lands in the "yes" column. First, it contains a whole alphabet soup of vitamins as well as nutrients. Honey also has other health benefits for both dogs and humans. It can be used topically to treat burns and minor scrapes.

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Allergy sniffles get you down? Consuming honey — particularly honey that's locally-made — can help you and your pooch build up an immunity to seasonal allergies. Because honey contains a bit of pollen from those pesky, allergy-inducing plants, your body gets acclimated to those would-be allergens.

Tuna & Salmon: Yes

Although cats are often portrayed as the fish lovers, dogs can also benefit from chowing down on certain waterbound critters, particularly tuna and salmon. Cooked fresh tuna promotes heart health, thanks to its bounty of omega-3 fatty acids. However, avoid canned tuna, which contains trace amounts of mercury and more sodium.

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Chock full of healthy fats and amino acids, salmon is also a great protein for your dog. As with poultry, it's important to de-bone all fish properly. Yes, it's tedious work, but you don't want to rush your pooch pal to the vet after a delicate bone gets lodged somewhere it shouldn't.

Cinnamon: No

Nothing says "winter" like a healthy dose of cinnamon. Whether it's in drinks or baked goods, it's often the star of the season. However, you should find a different way to add some holiday cheer to your dog's life. Although cinnamon isn't toxic, the oils in it can irritate a dog's mouth, making them super uncomfortable.

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Additionally, cinnamon can cause more than just discomfort. It can lower your pet's blood sugar, causing fluctuations in heart rate, vomiting and diarrhea. And rest assured that a dog losing its kibble all over the Christmas tree skirt doesn't scream "Happy Holidays."

Quinoa: Yes

Yes, feel free to dish out the quinoa to your pet. Gluten-free and highly trendy, quinoa seeds are packed with protein. Even better, they also contain decent amounts of all nine essential amino acids as well as fiber, iron, calcium and Vitamin E.

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Long before it became the foundational element in a hipster's take on a burrito bowl, quinoa was used to make kibble — high-quality kibble, of course. The more common corn, wheat and soy were used to fuel most big-name brands.

Pork: Yes

At this point, almost everyone is familiar with that overplayed Beggin' Strips ad, right? For the unindoctrinated, it begins with a dog dreaming about bacon strips. Upon waking, the dog races downstairs, chanting either "bacon bacon bacon" or "beggin' beggin' beggin'," depending on your interpretation for a bacon-flavored treat.

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While a flavored treat or dried out rawhide is fine, experts don't recommend feeding your dog a ton of bacon. Laced with fat, bacon should be eaten in moderation. A less fatty cut of pork is a better protein, loaded with amino acids.

Milk: Not Really

Surprisingly, there's not a clear-cut answer for this one. Like all mammals, puppies drink their mother's milk for sustenance, but that doesn't mean they are equipped to handle the cow's milk you bring home from the store. A lick or two of milk won't seriously harm your pet, but maybe just stick with water.

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According to PetMD, Doctor Heather Brausa of New York's Animal Medical Center explains, "Puppies generally have the enzyme [to break down lactose] in abundance, as it is used to break down their mother's milk while nursing." However, once weaned, mature dogs don't produce lactase as readily. Like humans, dogs can become lactose intolerant.

Garlic: No

Garlic is a huge N-O. And not just because you want your dog to avoid that tell-tale bad breath. Onions, chives, leeks and garlic are all part of a family of plants that are toxic to dogs. Garlic, however, takes things to a whole new level: It is five times more toxic than its fellow members of the Allium family.

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If your dog accidentally chows down on a bit of garlic or onion, monitor him closely for a few days. Some side effects, like elevated heart rate and weakness,set in immediately, but others, such as gum disease and anemia, take longer to appear.

Shrimp: Yes (Cooked)

If you fire up the barbecue on a summer afternoon, feel free to give your dog a little surf to go with the turf. Cooked shrimp are not just okay for your dog to eat; the little shellfish contain tons of antioxidants and vitamin B-12. Bonus: They are also low in fat and calories, making them a lighter alternative to the usual meat products and treats you may feed your pet.

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Like with poultry and fish, a little extra prep is needed. In addition to fully cooking prawns, be sure to remove the tail, head and legs. Unlike some meat products that owners give to dogs raw and bloody, refrain from tossing your pup bacteria-filled, uncooked shrimp.

Popcorn: Yes

Next time you and your pooch decide to stay in for the night and watch some Netflix, feel free to offer your pet a few kernels of popcorn. As long as it's unsalted, unbuttered and air-popped, the treat is fine in moderation. Of course, be sure to check the kernels to make sure they are fully popped before handing the bowl over to your dog.

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Regular old corn is also a fine snack for your pet. In fact, it's a super common ingredient in most manufactured dog foods. The cob may seem like a veggie alternative to a rawhide bone, but it's always a good idea to take the corn off the cob before feeding it to your dog.

Coconut: Yes

Coconut is generally okay for dogs to ingest, but you should probably stick to feeding it to your pet in moderation. According to the American Kennel Club (AKC), owners are encouraged to add coconut oil to their dogs' diets. As far as the meat of this tropical fruit goes, it's also a pretty beneficial treat.

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However, AKC writers note that coconut, though non-toxic, "contains medium chain triglycerides, which may cause some gastrointestinal upset and bloating." In layman's terms, check with your vet. Added benefits of eating coconut include better breath, clearer skin and a healthier immune system.

Chocolate: No

You've probably heard all your life that dogs shouldn't eat chocolate, and that urban legend is not a fable at all — it's a cold, hard fact. Dogs should not even taste it. Chocolate contains toxic (to dogs) methylxanthines, which impact a canine's metabolic process. In fact, these substances halt the process altogether.

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Just a tiny chocolate chip can cause diarrhea and vomiting. And a large amount could incite seizures and heart issues. In some cases, dogs have even died as a result of eating chocolate. If your pooch gets his paws on some chocolate, you should seek medical help as soon as possible.

Eggs: Yes

Yes, eggs are totally fine for dogs — as long as they are fully cooked. Raw egg whites can cause a biotin deficiency, and your dog needs biotin to take food and translate it into energy. Vets even recommend adding cooked eggs to your dog's food as a treat and for an added protein boost.

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In addition to protein, eggs also contain riboflavin, or vitamin B, as well as other immune system boosters. Writers at the American Kennel Club also recommend feeding your dog eggs to help settle an upset stomach.

Rice: Yes

Plain white rice is one of those comfort foods that just always hits the spot. A great side and a great remedy for an upset stomach, it's a truly versatile food. Plain cooked rice (white or brown) is okay for your dog to chow down on as well.

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Because rice is very easy to digest, it's often a go-to choice when dogs have stomach issues. Similar to when you're feeling under the weather, your dog may need a little plain rice and broth or a bit of protein-packed chicken to put him firmly on the road to recovery.

Nuts: Mostly No

As mentioned earlier, peanuts are technically legumes, which makes them okay for dogs. Nuts, on the other hand, pose more of a problem. While some nuts, such as cashews, are technically fine in moderation, others are potentially harmful.

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Almonds, a popular treat in trail mix and on their own, are a firm no. They aren't toxic, but they can definitely block a dog's esophagus or cause internal tears. The amount of salt is also a problem: Not only will salt mean more trips outside, it can also lead to sodium ion poisoning, vomiting, tremors and seizures.

According to the American Kennel Club, other nuts, such as pecans, walnuts and macadamias, are all considered harmful.

Cherries: Yes (Pitted)

Cherries are a seriously underrated snack. Perfect for nibbling while lounging on the couch or hanging out poolside, cherries require a lot less prep work than other fruits. Luckily, your dog can also enjoy fresh pitted cherries in small amounts. There aren't any huge health benefits, but if your dog has a sweeth tooth one or two pitted cherries may be the answer.

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Definitely be aware when purchasing a bag of cherries from the store. Dogs should never eat cherry pits. The pits contain cyanide, which is highly poisonous to dogs, especially when consumed in large amounts.

Coffee: No

There's nothing like a hot cup of coffee in the morning to kickstart the day, so who could blame you for wanting to share that feeling with your furry best friend? Coffee — and anything containing caffeine — should not be given to your dog. Caffeine stimulates a dog's nervous system, and that can lead to a whole host of issues.

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From the expected vomiting and diarrhea to serious symptoms like an erratic heart rate and seizures, the fallout is not good for your pooch. Although humans can deal with coffee's more unpleasant effects, dogs just aren't equipped to do so. Even small amounts could lead to lung failure and heart issues related to death.

Grapes: No

Grapes and raisins seem like pretty benign foods. But, sadly, you should not feed grapes or raisins to your pup. Both versions of this fruit contain toxic compounds that could lead to rapid kidney failure and, in some cases, death.

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In fact, even just a taste can make your dog wildly sick. As with chocolate and garlic, it's important to have a vet on hand if your dog mistakenly gets its paws on a bunch of grapes. It's not just sour grapes talking here. Even if your dog really wants to try one, the answer is no.

Cheese: Yes

From brie to cheddar to a nice mozzarella, cheese comes in a lot of delicious varieties. As with milk, some dogs handle cheese better than others. Some develop an intolerance to lactose after being weaned off their mother's milk, while others have a hard time digesting dairy from another species.

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If you choose to let your dog snack on cheese, be sure to monitor your pet's reaction. If your pup comes away from the treat with an upset stomach, it could be a sign of intolerance. If not, something lean, like mozzarella or cottage cheese, makes a great snack.

Carrots: Yes

Carrots have an alleged superpower — the ability to improve your eyesight. While they do contain vitamin A, which promotes good eye health and helps you see better in low-light environments, they don't necessarily improve your ability to see.

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But the realistic good news is this low-calorie snack is also great for your dog. Both raw and cooked carrots are okay, making this a pretty versatile treat. A great source of vitamin A, various minerals and fiber, carrots make much better snacks for your pet than fatty choices.

Onions: No

Although onions make you cry and give you bad breath, they cause a far worse fate for your dog. Like garlic and leeks, onions are highly toxic to dogs. From the flesh to the juice, all parts of the onion are equally harmful. Even onion powder, a common additive, can cause huge issues.

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But why are onions so toxic? They contain something called N-propyl disulfide, which causes red blood cells to break down. This can lead to severe cases of anemia in dogs — meaning their red blood cells can't provide adequate oxygen for their body's tissues. Real 'ruff stuff.

Watermelon: Yes (Seedless)

Low in calories and loaded with vitamins A and C, it's a healthy alternative to fatty foods. According to Dog Time, although watermelon contains sugar, "the fiber content in the fruit insulates the sugar and prevents it from being released into the bloodstream too quickly," making it a better alternative to various other fruits as well.

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However, experts suggest removing the seeds and not letting your dog gets its paws on the fruit's rind. Both the seeds and rinds pose an obvious choking hazard, but, more importantly, some claim they can also cause digestive problems and intestinal blockages.

Apples: Yes (Seedless)

An apple a day keeps the doctor away, but does the same hold true for vets? You should still take your pet in for regular check-ups, but it's true that apples can be good for dogs to snack on. Packed with vitamins, minerals and antioxidants, apples also contain fiber to help your dog's digestive system.

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Because apple skin can be difficult to swallow, you should peel the apples and cut them into slices before handing them over to your pooch. It's also critically important to remove the seeds from the apple, as they contain the highly poisonous chemical cyanide.

Avocado: No

According to some salty folks, avocado toast is allegedly getting in the way of millennial home ownership (see the McMansion section for more). One thing that's certain: If your pet gets its paws on this trendy food item, it could land you in the doghouse. To be clear, regardless of how Instagrammable the moment might be, a dog should never eat avocado.

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And it's not about saving all the extra guac for yourself. Avocados contain a toxin called persin, which is super harmful to your four-legged friend. Persin is contained not just in the fruit, but also in the avocado's pit and leaves. It can cause a buildup of fluid in a dog's lungs and chest, leading to breathing issues, oxygen deprivation and, in some cases, death.

Citrus Fruits: Yes & No

True to form, there's some sweet news and some sour news when it comes to dogs and citrus fruits. First, the sour: Lemons and limes can be toxic to your dog. The skins of these fruits contain psoralen, a substance that can cause severe vomiting and diarrhea. If a dog consumes too much psoralen, it could even lead to muscle tremors, liver failure and death.

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Meanwhile, oranges, clementines and tangerines can all be eaten by dogs, although experts recommend only feeding them a few segments a day. While the citric acid doesn't pose a threat to dogs, the high amount of sugar can lead to an upset stomach.

Bananas: Yes

Rich in potassium, vitamin B6 and vitamin C, bananas make a great, healthy snack for your dog — in moderation. According to the American Kennel Club, a lot of veterinarians actually recommend this fruit as an alternative to foods that are high in fat or salt. Another great benefit is the high fiber, meaning it's great for your dog if your pet is experiencing an upset stomach.

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Banana peels, on the other hand, aren't toxic, but they are difficult for dogs to digest. In order to avoid the messiness, try mixing a mashed banana in with your dog's food or serving it up with a dollop of peanut butter. If you choose the latter, feel free to make yourself the same delicious treat. If you choose the former, we may need to talk…

Bread: Yes

Yes, dogs can enjoy a little bit of bread, but only if it's plain bread — no spices and no fancy add-ins. (Obviously avoid chocolate bread, cinnamon bread, raisin bread, garlic bread and any other options with toxic ingredients.) Freshly baked bread makes a much better choice than breads preservative-filled ones from supermarket shelves.

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Although bread doesn't harm your dog's digestive system, it also won't do much to improve it.

However, never feed your dog uncooked dough. The yeast can expand in your pet's stomach, leading to a whole mess of issues. As you may recall from chemistry class, yeast produces an alcohol called ethanol — and nobody wants to give a dog alcohol poisoning.

Tomatoes: Yes & No

Tomatoes are another tricky one. Their leaves and stems — basically any green part of a tomato plant — contain a substance called solanine, which is harmful to dogs and can cause an upset stomach and even seizures. This also means that unripened, green tomatoes pose a threat.

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As for ripened, red tomatoes, experts have given them the green light. This is good news for quite a few reasons. Substances found in tomatoes are shown to promote strong bones, muscle health and low blood pressure. Low in calories and high in fiber, tomatoes also boost your dog's digestive system.

Foods To Eat While On Low Carb Diet

Source: https://www.reference.com/pets-animals/dog-food?utm_content=params%3Ao%3D740005%26ad%3DdirN%26qo%3DserpIndex

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Is Vitamin D Good For Hair Loss

Is Vitamin D Good For Hair Loss

• Definition
  • What Is Vitamin D?
• Benefits
  • What Are the Benefits of Vitamin D?
• Balding Treatment
  • Does Vitamin D Help with Hair Thinning?
• Diet
  • What Are Good Sources of Vitamin D?
• Guide
  • Does Vitamin D Help with Hair Thinning? Topic Guide

What Is Vitamin D?

Vitamin D is essential for cell reproduction in the hair and skin, and also benefits the immune system. Vitamin D deficiency contributes to hair loss in some cases.

Vitamin D is a fat-soluble vitamin that helps the body absorb dietary calcium and phosphorus from the intestines and suppresses the release of parathyroid hormone, a hormone that causes bone resorption. This serves to keep the bones healthy. Vitamin D is also believed to improve muscle and immune function.

Vitamin D is made in the skin when it is exposed to sunlight. Vitamin D is also naturally occurring in certain foods such as fatty fish, cod liver oil, and eggs. It is also found on fortified foods such as milk.

What Are the Benefits of Vitamin D?

Health benefits of vitamin D include:

• Strong bones
• Prevention of falls
• Supports immune function
• Reduces inflammation
• May help protect against some cancers such as colon, prostate, and breast cancers
• May help prevent and treat:
  • Diabetes
  • High blood pressure (hypertension)
  • Glucose intolerance
  • Multiple sclerosis

Does Vitamin D Help with Hair Thinning?

Getting adequate vitamin D intake or supplementation may help prevent hair loss.

• Vitamin D may be important for cell proliferation in the hair growth cycle
• Vitamin D may reduce inflammation, which may also help keep hair follicles healthy
• Vitamin D helps support immune function which can protect the scalp from infection

Vitamin D deficiency may contribute to hair loss in some cases. Talk to your doctor about the right dose for your condition.

What Are Good Sources of Vitamin D?

Foods that are good sources of vitamin D include:

• Seafood
  • Trout
  • Salmon
  • Sardines
  • Tuna
• Meat and poultry
  • Beef liver
  • Chicken breast
  • Ground beef
• Vegetables
  • Mushrooms (white and Portabella)
• Dairy products
  • Milk, vitamin D fortified
  • Cheddar cheese
• Other
  • Cod liver oil
  • Plant-based milks (e.g. soy, almond, oat), vitamin D fortified
  • Eggs
  • Ready-to-eat cereals, vitamin D fortified

Exposure to sunlight is also another source for vitamin D but too much sun exposure can lead to sunburns, premature skin aging, eye damage, heat exhaustion or heat stroke, or skin cancer. Talk to your doctor about how much sun exposure you may need and how to get exposure safely.

SLIDESHOW

Your Hair and Scalp Can Say a Lot About Your Health See Slideshow

Reviewed on 8/31/2020

References

Medscape Medical Reference

Is Vitamin D Good For Hair Loss

Source: https://www.emedicinehealth.com/does_vitamin_d_help_with_hair_thinning/article_em.htm

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How To Take Vitamin D Injection Orally

How To Take Vitamin D Injection Orally

Effect of a Single Oral Dose of 600,000 IU of Cholecalciferol on Serum Calciotropic Hormones in Young Subjects with Vitamin D Deficiency: A Prospective Intervention Study

Cristiana Cipriani,

1Departments of Clinical Sciences (C.C., E.R., M.L.M., S.M.) University of Rome "Sapienza," 00161 Rome, Italy;

*Address all correspondence and requests for reprints to: Cristiana Cipriani, M.D., Department of Clinical Sciences, University of Rome "Sapienza", Viale del Policlinico 155, 00161 Rome, Italy.

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Elisabetta Romagnoli,

1Departments of Clinical Sciences (C.C., E.R., M.L.M., S.M.) University of Rome "Sapienza," 00161 Rome, Italy;

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Alfredo Scillitani,

3Units of Endocrinology (A.S., C.B., R.V.), Instituto di Ricovero e Cura a Carattere Scientifico (IRCCS) "Casa Sollievo della Sofferenza" Hospital, 71013 San Giovanni Rotondo, Italy;

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Iacopo Chiodini,

6Department of Medical Sciences (I.C., C.E.-V.), University of Milan, Fondazione Policlinico IRCCS, 20122 Milan, Italy

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Rita Clerico,

2Dermatology (R.C.), University of Rome "Sapienza," 00161 Rome, Italy;

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Vincenzo Carnevale,

4Internal Medicine (V.C.), Instituto di Ricovero e Cura a Carattere Scientifico (IRCCS) "Casa Sollievo della Sofferenza" Hospital, 71013 San Giovanni Rotondo, Italy;

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Maria Lucia Mascia,

1Departments of Clinical Sciences (C.C., E.R., M.L.M., S.M.) University of Rome "Sapienza," 00161 Rome, Italy;

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Claudia Battista,

3Units of Endocrinology (A.S., C.B., R.V.), Instituto di Ricovero e Cura a Carattere Scientifico (IRCCS) "Casa Sollievo della Sofferenza" Hospital, 71013 San Giovanni Rotondo, Italy;

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Raffaella Viti,

3Units of Endocrinology (A.S., C.B., R.V.), Instituto di Ricovero e Cura a Carattere Scientifico (IRCCS) "Casa Sollievo della Sofferenza" Hospital, 71013 San Giovanni Rotondo, Italy;

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Mauro Pileri,

5Clinical Chemistry (M.P.), Instituto di Ricovero e Cura a Carattere Scientifico (IRCCS) "Casa Sollievo della Sofferenza" Hospital, 71013 San Giovanni Rotondo, Italy;

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... Show more

Published:

01 October 2010

Context: Effects of vitamin D repletion in young people with low vitamin D status have not been investigated so far.

Objective: We evaluated the effect of a single massive dose of cholecalciferol on calcium metabolism at 3, 15, and 30 d, compared to baseline.

Design and Setting: We conducted a prospective intervention study in an ambulatory care setting.

Participants: Forty-eight young subjects with vitamin D deficiency participated in the study.

Intervention: A single oral dose of 600,000 IU of cholecalciferol was administered to each subject.

Main Outcome Measures: We evaluated serum changes of 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D, calcium, and PTH induced by a single load of cholecalciferol.

Results: The 25(OH)D level was 15.8 ± 6.5 ng/ml at baseline and became 77.2 ± 30.5 ng/ml at 3 d (P < 0.001) and 62.4 ± 26.1 ng/ml at 30 d (P < 0.001). PTH levels concomitantly decreased from 53.0 ± 20.1 to 38.6 ± 17.2 pg/ml at 3 d and to 43.4 ± 14.0 pg/ml at 30 d (P < 0.001 for both). The trends were maintained in a subgroup followed up to 90 d (P < 0.001). Mean serum Ca and P significantly increased compared to baseline, whereas serum Mg decreased at 3 d. 1,25-Dihydroxyvitamin D significantly increased from 46.8 ± 18.9 to 97.8 ± 38.3 pg/ml at 3 d (P < 0.001) and to 59.5 ± 27.3 pg/ml at 60 d (P < 0.05).

Conclusions: A single oral dose of 600,000 IU of cholecalciferol rapidly enhances 25(OH)D and reduces PTH in young people with vitamin D deficiency.

Vitamin D depletion has been reported as a very common condition worldwide, with many implications for health (1–4). Although elderly institutionalized patients are at high risk, several studies have also shown a high prevalence of vitamin D deficiency among healthy postmenopausal free-living women and among the general adult population (5–13). Well-known consequences of hypovitaminosis D are secondary hyperparathyroidism, bone loss, proximal muscle weakness, increase in body sway, falls, and fractures (7). Moreover, nonskeletal consequences of vitamin D deficiency have been associated with an enhanced risk of chronic disease and cancer (1–4, 14), and the association between intake of vitamin D supplements and decrease in all-cause mortality has been reported (15). Sunlight exposure is widely recognized as the main source of vitamin D, but prolonged sun exposure is usually discouraged because of an increased risk of skin cancer. A recent evidence-based review (16) actually recognized that a threshold of sun exposure sufficient to maintain a healthy vitamin D status without measurable cancer risk is difficult to define. Hence, current guidelines recommend a daily intake of at least 1000 IU of vitamin D. To reach this supplementation, an adequate food fortification and oral supplementation are widely suggested (1, 17). However, clinical recommendations concerning the optimal dose and the frequency of administration of vitamin D to achieve and maintain the target vitamin D serum level [usually expressed in terms of serum 25-hydroxyvitamin D or 25(OH)D] and to decrease the PTH secretion are still lacking. The majority of the studies (18–22) investigated the response of serum 25(OH)D to large doses of cholecalciferol in the elderly, which are considered the population at highest risk of vitamin D deficiency. Trivedi et al. (18) found that a single oral 100,000 IU dose of cholecalciferol is safe and effective in reducing fractures in community-dwelling people over age 65 yr. Ilahi et al. (19) suggested that a single oral dose of 100,000 IU of cholecalciferol every 2 months is useful in increasing and maintaining 25(OH)D concentration above baseline in the elderly. Recent data from our group (20) reported the greater potency (and the safety) of a single, large, oral 300,000-IU dose of cholecalciferol, compared with ergocalciferol, in enhancing serum 25(OH)D concentration with concomitant decrease in PTH secretion. Bacon et al. (22) reported in the elderly a normalization of 25(OH)D values 1 month after an oral dose of 500,000 IU of cholecalciferol. However, to our knowledge, despite several papers carried out in elderly subjects, data on younger people are still limited. In particular, Tangpricha et al. (23) observed an increase of 150% in serum 25(OH)D and a decrease of 25% in serum PTH concentration from baseline to the 12th week in healthy adults who daily received orange juice fortified with 1000 IU of vitamin D₃. We instead performed a prospective intervention study to evaluate the effect of a single loading oral dose of cholecalciferol (600,000 IU) on the vitamin D-PTH axis in a sample of young subjects with vitamin D deficiency.

Subjects and Methods

We studied 48 free-living subjects (35 females and 13 males; mean age ± sd, 36.04 ± 8.46 yr; age range, 25–56 yr; body mass index, 24 ± 3.52 kg/m²) with limited sun exposure because of poor tolerability, skin cancer, or other skin diseases. None of them had diseases or took drugs affecting bone metabolism, nor did they consume calcium or vitamin D supplements. The study was performed between January and March 2009. All subjects were placed on a standardized diet with 1000–1500 mg of elemental calcium per day starting 2 months before the beginning of the study. All participants received a single oral dose of 600,000 IU of cholecalciferol, which equals two vials of commercially available cholecalciferol in Italy. Fasting blood samples were collected at baseline and 3, 15, and 30 d after cholecalciferol administration in all participants. A subgroup of 20 female subjects (mean age, 33.2 ± 6 yr; range, 25–50 yr; body mass index, 23.8 ± 4.01 kg/m²) agreed to continue the follow-up and were also assessed at 60 and 90 d. In all subjects, the following serum biochemical parameters were measured: total calcium (Ca), phosphorus (P), magnesium (Mg), 25(OH)D, and PTH. In the subgroup of 20 subjects who were followed for 90 d, serum 1,25-dihydroxyvitamin D [1,25(OH)₂D] levels were also assessed. Moreover, in this subgroup of subjects, serum 25-hydroxyvitamin D₃ [25(OH)D₃] was measured with HPLC at baseline and at 3 and 60 d to selectively measure 25(OH)D₃, but not other vitamin D metabolites. In 28 participants, a morning fasting 3-h urinary collection was also taken to measure calcium and magnesium excretion; tubular reabsorption was expressed as excretion per unit of creatinine clearance [mg/dl of glomerular filtration rate (GFR)]. Serum 25(OH)D concentrations were measured by RIA (Diasorin Inc., Stillwater, MN); the intra- and interassay coefficients of variation (CVs) were 8.1 and 10.2%, respectively. Serum 25(OH)D₃ level was measured by solid phase extraction/isocratic HPLC-reverse phase with spectrophotometric detection at 265 nm UV (Eureka Lab Division, Chiaravalle, Ancona, Italy). The sensitivity of the method was 2 ng/ml (24). Serum 1,25(OH)₂D concentrations were determined by RIA (IDS; Nordic, Herlev, Denmark); the intra- and interassay CVs were 9.3 and 9.6%, respectively. Serum PTH levels were assessed by IRMA (N-tact PTHSP; Diasorin Inc.); the intra- and interassay CVs were 3 and 5.5%, respectively. Blood samples were then stored at −70 C, and the assays were performed in one batch at the end of the study.

Written, informed consent was obtained from all participants. The protocol was approved by the "Sapienza" University of Rome Ethics Committee.

Statistics

Patient's biochemical measures according to time from vitamin D load were reported as mean ± sd, and differences were assessed via repeated measurements ANOVA models. Comparisons between groups at baseline and between baseline and follow-up values at each time point were performed by unpaired and paired t test. Significance was set at a P value of 0.05. SigmaStat version 3.5 (Systat Software, London, UK) was used for statistical calculations.

Results

Biochemical parameters of all the participants at baseline and at all time points are reported in Table 1. Basal values of 25(OH)D and PTH did not differ between the whole group and the 20 subjects followed up to 90 d.

TABLE 1.

Biochemical parameters of all subjects at each time point

Parameter		Baseline	3 d	15 d	30 d	60 d	90 d	P a
Ca (mg/dl)	A	9.3 ± 0.4	9.5 ± 0.3	9.4 ± 0.3	9.4 ± 0.3			<0.05
	B	9.3 ± 0.3	9.5 ± 0.3	9.4 ± 0.3	9.4 ± 0.3	9.4 ± 0.3	9.5 ± 0.4	NS
P (mg/dl)	A	3.8 ± 0.6	4.0 ± 0.6	3.8 ± 0.5	3.8 ± 0.6			<0.01
	B	3.5 ± 0.4	3.8 ± 0.6	3.6 ± 0.4	3.6 ± 0.6	3.4 ± 0.5	3.5 ± 0.5	<0.01
Mg (mg/dl)	A	2.0 ± 0.2	1.9 ± 0.2	2.0 ± 0.2	2.0 ± 0.2			<0.001
	B	1.8 ± 0.1	1.7 ± 0.1	1.8 ± 0.1	1.8 ± 0.1	1.9 ± 0.2	1.8 ± 0.1	<0.05
25(OH)D (ng/ml)	A	15.8 ± 6.5	77.2 ± 30.5	76.5 ± 27.9	62.4 ± 26.1			<0.001
	B	17.2 ± 6.3	73.7 ± 16.9	70.9 ± 14.9	63.5 ± 12.5	42.8 ± 8.9	31.9 ± 12.6	<0.001
PTH (pg/ml)	A	53.0 ± 20.1	38.6 ± 17.2	40.6 ± 15.8	43.4 ± 14			<0.001
	B	57.0 ± 21.6	39.2 ± 15.9	36.7 ± 14.5	39.2 ± 13	42.8 ± 19.1	37.7 ± 15.1	<0.001
1,25(OH)2D (pg/ml)	A
	B	46.8 ± 18.9	97.8 ± 38.3	90.7 ± 46.9	74.9 ± 36.8	59.5 ± 27.3	52.9 ± 23.3	<0.001
CaEx (mg/dl GFR)	C	0.08 ± 0.06	0.10 ± 0.08	0.10 ± 0.05	0.08 ± 0.04			<0.05
MgEx (mg/dl GFR)	C	0.04 ± 0.02	0.06 ± 0.03	0.05 ± 0.02	0.05 ± 0.03			NS

Parameter		Baseline	3 d	15 d	30 d	60 d	90 d	P a
Ca (mg/dl)	A	9.3 ± 0.4	9.5 ± 0.3	9.4 ± 0.3	9.4 ± 0.3			<0.05
	B	9.3 ± 0.3	9.5 ± 0.3	9.4 ± 0.3	9.4 ± 0.3	9.4 ± 0.3	9.5 ± 0.4	NS
P (mg/dl)	A	3.8 ± 0.6	4.0 ± 0.6	3.8 ± 0.5	3.8 ± 0.6			<0.01
	B	3.5 ± 0.4	3.8 ± 0.6	3.6 ± 0.4	3.6 ± 0.6	3.4 ± 0.5	3.5 ± 0.5	<0.01
Mg (mg/dl)	A	2.0 ± 0.2	1.9 ± 0.2	2.0 ± 0.2	2.0 ± 0.2			<0.001
	B	1.8 ± 0.1	1.7 ± 0.1	1.8 ± 0.1	1.8 ± 0.1	1.9 ± 0.2	1.8 ± 0.1	<0.05
25(OH)D (ng/ml)	A	15.8 ± 6.5	77.2 ± 30.5	76.5 ± 27.9	62.4 ± 26.1			<0.001
	B	17.2 ± 6.3	73.7 ± 16.9	70.9 ± 14.9	63.5 ± 12.5	42.8 ± 8.9	31.9 ± 12.6	<0.001
PTH (pg/ml)	A	53.0 ± 20.1	38.6 ± 17.2	40.6 ± 15.8	43.4 ± 14			<0.001
	B	57.0 ± 21.6	39.2 ± 15.9	36.7 ± 14.5	39.2 ± 13	42.8 ± 19.1	37.7 ± 15.1	<0.001
1,25(OH)2D (pg/ml)	A
	B	46.8 ± 18.9	97.8 ± 38.3	90.7 ± 46.9	74.9 ± 36.8	59.5 ± 27.3	52.9 ± 23.3	<0.001
CaEx (mg/dl GFR)	C	0.08 ± 0.06	0.10 ± 0.08	0.10 ± 0.05	0.08 ± 0.04			<0.05
MgEx (mg/dl GFR)	C	0.04 ± 0.02	0.06 ± 0.03	0.05 ± 0.02	0.05 ± 0.03			NS

All values are expressed as mean ± sd. A, Whole sample (n = 48); B, subgroup of subjects followed up to 90 d (n = 20); C, subgroup of subjects collecting urine samples (n = 28); CaEx, calcium excretion; MgEx, magnesium excretion; NS, not significant.

^a

RM ANOVA.

TABLE 1.

Biochemical parameters of all subjects at each time point

Parameter		Baseline	3 d	15 d	30 d	60 d	90 d	P a
Ca (mg/dl)	A	9.3 ± 0.4	9.5 ± 0.3	9.4 ± 0.3	9.4 ± 0.3			<0.05
	B	9.3 ± 0.3	9.5 ± 0.3	9.4 ± 0.3	9.4 ± 0.3	9.4 ± 0.3	9.5 ± 0.4	NS
P (mg/dl)	A	3.8 ± 0.6	4.0 ± 0.6	3.8 ± 0.5	3.8 ± 0.6			<0.01
	B	3.5 ± 0.4	3.8 ± 0.6	3.6 ± 0.4	3.6 ± 0.6	3.4 ± 0.5	3.5 ± 0.5	<0.01
Mg (mg/dl)	A	2.0 ± 0.2	1.9 ± 0.2	2.0 ± 0.2	2.0 ± 0.2			<0.001
	B	1.8 ± 0.1	1.7 ± 0.1	1.8 ± 0.1	1.8 ± 0.1	1.9 ± 0.2	1.8 ± 0.1	<0.05
25(OH)D (ng/ml)	A	15.8 ± 6.5	77.2 ± 30.5	76.5 ± 27.9	62.4 ± 26.1			<0.001
	B	17.2 ± 6.3	73.7 ± 16.9	70.9 ± 14.9	63.5 ± 12.5	42.8 ± 8.9	31.9 ± 12.6	<0.001
PTH (pg/ml)	A	53.0 ± 20.1	38.6 ± 17.2	40.6 ± 15.8	43.4 ± 14			<0.001
	B	57.0 ± 21.6	39.2 ± 15.9	36.7 ± 14.5	39.2 ± 13	42.8 ± 19.1	37.7 ± 15.1	<0.001
1,25(OH)2D (pg/ml)	A
	B	46.8 ± 18.9	97.8 ± 38.3	90.7 ± 46.9	74.9 ± 36.8	59.5 ± 27.3	52.9 ± 23.3	<0.001
CaEx (mg/dl GFR)	C	0.08 ± 0.06	0.10 ± 0.08	0.10 ± 0.05	0.08 ± 0.04			<0.05
MgEx (mg/dl GFR)	C	0.04 ± 0.02	0.06 ± 0.03	0.05 ± 0.02	0.05 ± 0.03			NS

Parameter		Baseline	3 d	15 d	30 d	60 d	90 d	P a
Ca (mg/dl)	A	9.3 ± 0.4	9.5 ± 0.3	9.4 ± 0.3	9.4 ± 0.3			<0.05
	B	9.3 ± 0.3	9.5 ± 0.3	9.4 ± 0.3	9.4 ± 0.3	9.4 ± 0.3	9.5 ± 0.4	NS
P (mg/dl)	A	3.8 ± 0.6	4.0 ± 0.6	3.8 ± 0.5	3.8 ± 0.6			<0.01
	B	3.5 ± 0.4	3.8 ± 0.6	3.6 ± 0.4	3.6 ± 0.6	3.4 ± 0.5	3.5 ± 0.5	<0.01
Mg (mg/dl)	A	2.0 ± 0.2	1.9 ± 0.2	2.0 ± 0.2	2.0 ± 0.2			<0.001
	B	1.8 ± 0.1	1.7 ± 0.1	1.8 ± 0.1	1.8 ± 0.1	1.9 ± 0.2	1.8 ± 0.1	<0.05
25(OH)D (ng/ml)	A	15.8 ± 6.5	77.2 ± 30.5	76.5 ± 27.9	62.4 ± 26.1			<0.001
	B	17.2 ± 6.3	73.7 ± 16.9	70.9 ± 14.9	63.5 ± 12.5	42.8 ± 8.9	31.9 ± 12.6	<0.001
PTH (pg/ml)	A	53.0 ± 20.1	38.6 ± 17.2	40.6 ± 15.8	43.4 ± 14			<0.001
	B	57.0 ± 21.6	39.2 ± 15.9	36.7 ± 14.5	39.2 ± 13	42.8 ± 19.1	37.7 ± 15.1	<0.001
1,25(OH)2D (pg/ml)	A
	B	46.8 ± 18.9	97.8 ± 38.3	90.7 ± 46.9	74.9 ± 36.8	59.5 ± 27.3	52.9 ± 23.3	<0.001
CaEx (mg/dl GFR)	C	0.08 ± 0.06	0.10 ± 0.08	0.10 ± 0.05	0.08 ± 0.04			<0.05
MgEx (mg/dl GFR)	C	0.04 ± 0.02	0.06 ± 0.03	0.05 ± 0.02	0.05 ± 0.03			NS

All values are expressed as mean ± sd. A, Whole sample (n = 48); B, subgroup of subjects followed up to 90 d (n = 20); C, subgroup of subjects collecting urine samples (n = 28); CaEx, calcium excretion; MgEx, magnesium excretion; NS, not significant.

^a

RM ANOVA.

Figure 1A shows changes in serum 25(OH)D levels induced by vitamin D supplementation in the whole sample. We found a significant change in 25(OH)D levels throughout the entire observation period [P < 0.001, by repeated measures (RM) ANOVA]. In particular, a sharp and significant increase was observed already at 3 d, attaining average values of 77.1 ± 30.5 ng/ml (P < 0.001), with an absolute increment above baseline of 61.3 ± 28 ng/ml (P < 0.001). Subsequently, there was a slow but not significant decrease; at the end of the observation period, mean 25(OH)D serum levels, as well as the 30-d basal difference, remained significantly higher than baseline (P < 0.001) (Fig. 1, A and B). Noteworthy, the highest 25(OH)D level achieved at the third day in a female subject was 136 ng/ml.

Fig. 1.

Effect of vitamin D supplementation on 25(OH)D serum changes. A and B, Mean values and respective basal difference of serum 25(OH)D at each time point in the whole sample (n = 48). B, Mean ± se values of 25(OH)D basal difference at 3, 15, and 30 d were 61.4 ± 4, 60.7 ± 3.8, and 46.7 ± 23.9 ng/ml, respectively. *, P < 0.001 vs. baseline. C and D, Mean values and the respective basal difference of serum 25(OH)D at each time point in the subgroup (n = 20). D, Mean ± se values of 25(OH)D basal difference at 3, 15, 30, 60, and 90 d were 56.5 ± 3.4, 53.7 ± 3.6, 46.3 ± 3, 25.6 ± 2, and 14.7 ± 3.3 ng/ml, respectively. *, P < 0.001 vs. baseline. The dashed lines (A and C) represent the threshold level for vitamin D adequacy, settled at 32 ng/ml.

Fig. 1.

Effect of vitamin D supplementation on 25(OH)D serum changes. A and B, Mean values and respective basal difference of serum 25(OH)D at each time point in the whole sample (n = 48). B, Mean ± se values of 25(OH)D basal difference at 3, 15, and 30 d were 61.4 ± 4, 60.7 ± 3.8, and 46.7 ± 23.9 ng/ml, respectively. *, P < 0.001 vs. baseline. C and D, Mean values and the respective basal difference of serum 25(OH)D at each time point in the subgroup (n = 20). D, Mean ± se values of 25(OH)D basal difference at 3, 15, 30, 60, and 90 d were 56.5 ± 3.4, 53.7 ± 3.6, 46.3 ± 3, 25.6 ± 2, and 14.7 ± 3.3 ng/ml, respectively. *, P < 0.001 vs. baseline. The dashed lines (A and C) represent the threshold level for vitamin D adequacy, settled at 32 ng/ml.

Vitamin D load induced a significant decrease in serum PTH concentration (P < 0.001, by RM ANOVA), which was already significant at 3 d (P < 0.001). Thereafter, PTH values slowly increased, but at each time point they remained significantly lower compared with baseline (P < 0.001) (data not shown).

Serum Ca and P levels significantly changed throughout the entire period (P < 0.05 and P < 0.01, respectively, by RM ANOVA) (Table 1). However, the increase with respect to baseline was significant only at 3 d after supplementation (Ca, 0.1 ± 0.3 mg/dl; P, 0.2 ± 0.5 mg/dl; P < 0.01 for both). Moreover, there was a significant change in Mg serum levels (P < 0.001), whose values were significantly reduced only on the third day (−0.05 ± 0.1 mg/dl, P < 0.01). In subjects collecting urine samples, calcium excretion significantly changed (P < 0.05). The increase of calcium excretion was significant both 3 d (0.03 ± 0.04 mg/dl GFR; P < 0.01) and 15 d (0.02 ± 0.04 mg/dl GFR; P < 0.05) after cholecalciferol supplementation. Magnesium excretion was significantly increased only at 3 d (0.02 ± 0.02 mg/dl GFR; P < 0.01).

The changes of serum 25(OH)D levels in the subgroup of 20 subjects followed up to 90 d were similar to those found in the sample as a whole (Fig. 1, C and D). In particular, mean values of 25(OH)D were still significantly higher with respect to baseline at both 60 and 90 d. Noteworthy, at 90 d, nine of 20 patients had 25(OH)D levels over the threshold of vitamin D sufficiency. The increase of serum 25(OH)D at 3 d was confirmed using a HPLC assay, which separates 25(OH)D₃ from all other vitamin D metabolites. Indeed, 25(OH)D₃ serum levels at 3 d were significantly higher with respect to baseline (56.6 ± 15.9 vs. 12.7 ± 6.9 ng/ml; P < 0.001); at 60 d serum levels decreased, mean values being still significantly higher than baseline (28.5 ± 8.1 mg/dl; P < 0.001). Percentage changes with respect to baseline between the two methods were not significantly different at 3 and 60 d (data not shown). A significant positive correlation was found between HPLC and RIA assays (r = 0.81; P < 0.0001) (Fig. 2).

Fig. 2.

Correlation between the concentration of 25(OH)D assessed by HPLC method and RIA assay.

Fig. 2.

Correlation between the concentration of 25(OH)D assessed by HPLC method and RIA assay.

The concomitant changes of PTH and 1,25(OH)₂D serum levels, expressed as absolute differences from basal values, are reported in Fig. 3. We found a significant decrease of serum PTH already at 3 d (P < 0.001). The lowest values were reached at 15 d (−20.3 ± 17.8 pg/ml; P < 0.001). The decrease was statistically significant throughout the entire period of observation. The reduction of serum PTH was mirrored by the concomitant increase in 1,25(OH)₂D values (Table 1). In fact, we observed a rapid increase of 1,25(OH)₂D levels at 3 d (P < 0.001). This increase was statistically significant up to 60 d, whereas at 90 d 1,25(OH)₂D levels returned to baseline.

Fig. 3.

Effect of vitamin D supplementation on the basal difference of serum 1,25(OH)₂D (upper panel) and of PTH (lower panel) in the subgroup of 20 subjects. Mean ± se values of 1,25(OH)₂D basal difference at 3, 15, 30, 60, and 90 d were 51 ± 9, 43.8 ± 9.3, 28.2 ± 7.5, 12.7 ± 5.5, and 6.1 ± 4.7 pg/ml, respectively. Mean ± se values of PTH basal difference at 3, 15, 30, 60, and 90 d were −17.8 ± 3.3, −20.3 ± 4, −17.8 ± 3.4, −14.2 ± 4, and −19.3 ± 2.7 pg/ml, respectively. *, P < 0.001; **, P < 0.01; ***, P < 0.05.

Fig. 3.

Effect of vitamin D supplementation on the basal difference of serum 1,25(OH)₂D (upper panel) and of PTH (lower panel) in the subgroup of 20 subjects. Mean ± se values of 1,25(OH)₂D basal difference at 3, 15, 30, 60, and 90 d were 51 ± 9, 43.8 ± 9.3, 28.2 ± 7.5, 12.7 ± 5.5, and 6.1 ± 4.7 pg/ml, respectively. Mean ± se values of PTH basal difference at 3, 15, 30, 60, and 90 d were −17.8 ± 3.3, −20.3 ± 4, −17.8 ± 3.4, −14.2 ± 4, and −19.3 ± 2.7 pg/ml, respectively. *, P < 0.001; **, P < 0.01; ***, P < 0.05.

Changes in Ca, P, and Mg levels in the subgroup followed up to 90 d were similar to those observed in the whole sample, with a significant increase in Ca and P levels after 3 d (P < 0.01) and a concomitant significant Mg decrease (P < 0.50) (data not shown).

Discussion

Available evidence in the elderly suggests that at least 800-1000 IU of vitamin D per day are needed to achieve mean serum 25(OH)D levels of 32 ng/ml (25). This value, associated with the optimal calcium absorptive performance (26), is currently considered by many authors as the threshold of adequate vitamin D status (25, 27–29). However, there are limited and nonconclusive data about the optimal dose and dosing intervals needed to achieve and maintain these levels and to reduce secondary hyperparathyroidism (30). Several studies reported safety and efficacy of supplementation with large doses of vitamin D, particularly in the elderly (18–22, 31). It has been suggested that a single high dose of cholecalciferol is effective in rapidly increasing 25(OH)D levels, namely in patients with severe vitamin D deficiency. Moreover, higher intermittent doses of cholecalciferol were proposed to improve adherence to treatment (20, 22, 25). New guidelines claimed the reevaluation of the upper limit of safe vitamin D daily intake, with a trend to shift to 2000 IU/d (1).

In this study, we evaluated the effect of a single very large oral dose of cholecalciferol (600,000 IU) on serum levels of 25(OH)D and other calciotropic hormones in young subjects with vitamin D deficiency. Our results demonstrate that an oral dose of 600,000 IU of cholecalciferol is able to rapidly increase serum 25(OH)D levels in patients with severe vitamin D depletion. A peak of 25(OH)D concentration was already attained as soon as 3 d after vitamin D administration, probably due to the strikingly higher dose employed compared with previous reports (20). Remarkable increments of 25(OH)D serum levels were also attained at 3 d when 300,000 IU of cholecalciferol were given to elderly subjects (20). Noteworthy, the highest value attained in the present study by an individual subject was 136 ng/ml, which is well below the widely accepted toxic blood levels of 200 ng/ml (32). This result was likely due to the low pretreatment vitamin D status of our sample. Moreover, 25(OH)D levels remained significantly higher than baseline up to 30 d, and in the subgroup of 20 subjects followed up to 90 d, 25(OH)D basal difference was still significant at 90 d. In this group, at the end of observation, half of the patients had 25(OH)D levels still over 32 ng/ml. Overall, our findings demonstrate that a high oral dose of cholecalciferol rapidly enhances and maintains adequate 25(OH)D levels up to 90 d after administration in young subjects with vitamin D deficiency. These results are in line with data obtained in elderly subjects and probably rely on a rapid absorption and conversion of the oral load of cholecalciferol to the 25-hydroxy metabolite. Heaney et al. (31) demonstrated that vitamin D administration induces a biphasic response, with a rapid increase of serum 25(OH)D at low serum vitamin D₃ concentrations and a slower response at higher levels. Hence, we can hypothesize that the huge increase of 25(OH)D levels after supplementation could probably be due to the low basal vitamin D₃ concentration. Ilahi et al. (19) also reported a peak of 25(OH)D concentration 7 d after a single oral dose of 100,000 IU of cholecalciferol, whereas others obtained similar results 1 month after giving an oral dose of 500,000 IU of cholecalciferol to subjects with initial 25OHD levels of 20 ng/ml or less (22, 33). However, the authors did not give any data at 3–10 d after cholecalciferol loading. On the other hand, a single im dose of 600,000 IU of cholecalciferol may enhance 25(OH)D levels above the threshold of sufficiency only at 4 months in subjects with vitamin D deficiency (34). This finding confirms that, faced with the physiological skin production, the oral administration is a valuable alternative route of vitamin D supplementation. This is also supported by previous results from our group showing that a dose of 300,000 IU of cholecalciferol given orally but not im can sharply and significantly increase 25(OH)D levels in vitamin D-deficient elderly people (20). In that study, the highest 25(OH)D concentration was found at 30 d, and it remained significantly higher than baseline up to 2 months. We can therefore conclude that both 600,000 and 300,000 IU of oral cholecalciferol determine a sharp and significant increase in 25(OH)D levels, maintaining adequate vitamin D status for at least 2 months. Moreover, a single oral dose of 600,000 IU administered to younger and less deficient subjects induced a faster increase of 25(OH)D levels, and a good vitamin D status was maintained up to 90 d.

The results obtained by the RIA method were further strengthened by those obtained with HPLC, separating 25(OH)D₃ from all other vitamin D metabolites. Indeed, the huge increase measured by RIA at 3 d is confirmed by the HPLC results. However, we found an apparent discrepancy between the mean 25(OH)D levels measured by RIA and 25(OH)D₃ assessed by HPLC. Indeed, looking at Fig. 2, it is apparent that RIA measurement overestimated values below 40 ng/ml, whereas it underestimated values above 40 ng/ml with respect to HPLC. Such a difference was not significant, namely at 3 d, and it might be due to the small size of the sample assessed by both methods. Also, considering this limit, we showed that a loading dose of oral cholecalciferol rapidly and significantly improved vitamin D status as soon as 3 d.

The significant increase in serum calcium levels 3 d after supplementation could probably depend on an increase of calcium absorption due to the rise in 25(OH)D values (26). This hypothesis is confirmed by a significant increase in urinary calcium excretion at 3 d, because intestinal calcium daily absorption implicitly equates to urinary calcium daily excretion (32). However, urinary data were not collected in all the participants and unfortunately were not informative about the effect of a very large dose of cholecalciferol on 24-h calcium excretion, which is considered a more sensitive indicator of vitamin D adverse effects (35). It was also shown that a loading dose of 600,000 IU of cholecalciferol rapidly enhanced magnesium urinary excretion, probably because of the concomitant increase in serum and urinary calcium levels. Indeed, renal magnesium reabsorption is proportional to calcium excretion and dependent on calcemia. Alternatively, the reduction in renal Mg reabsorption could be due to suppressed levels of PTH. However, noteworthy, serum Ca and Mg levels remained in the physiological range during the entire observation period.

Significant reduction of serum PTH was observed already 3 d after administration of 600,000 IU of cholecalciferol and persisted throughout the entire period of observation (30 d); in the group followed up to 90 d, serum PTH levels were suppressed up to 3 months. On the other hand, Diamond et al. (34) reported a significant decrease in PTH levels only 12 months after administration of the same amount of cholecalciferol by im route. In line with our previous study, our current results confirm the greater potency of an oral cholecalciferol load in rapidly reducing PTH levels (20).

Also concerning 1,25(OH)₂D serum changes, the current results confirm our previous data (20). This finding could be explained by a rapid conversion of the 25-hydroxy metabolite to 1,25(OH)₂D because the initial secondary hyperparathyroidism promotes a marked increase of 1,25(OH)₂D levels when these patients ingest vitamin D (36). It is also possible that a high concentration of serum vitamin D metabolites may displace 1,25(OH)₂D from the circulating vitamin D-binding protein (32). However, we cannot exclude that the observed relevant change of 1,25(OH)₂D levels at 3 d could depend on the relatively low specificity of the employed assay, and these results will require verification with a more specific assay.

We believe that our results have some clinical implications. The potency of a very large dose of cholecalciferol, given orally, is an important finding in patients with high risk of vitamin D deficiency and high fracture risk. A rapid vitamin D repletion is also desirable to prevent hypocalcemia in vitamin D-deficient patients before treatment with iv bisphosphonates. Moreover, we believe that a loading intermittent dose of cholecalciferol could also be associated with a better adherence to treatment, also in young people with vitamin D deficiency.

Our data regarding PTH changes also deserve emphasis because elevated PTH secretion due to vitamin D deficiency is not only associated with increased bone turnover and fracture risk, but may also result in increased mortality, at least in elderly vitamin D-deficient people (37). Although our study was performed in young people, a rapid reduction of PTH levels could be expected to occur also in elderly patients (38). Moreover, the time-related pattern of PTH change deserves interest because a marked decrease was already obtained at the third day and maintained until 90 d, despite no concomitant changes of serum calcium levels. At the latter time point, the reduction of PTH serum levels still persists, although Ca and 1,25(OH)₂D levels returned to baseline values. This finding, in line with previous results from our group (20, 39), supports the hypothesis that 25(OH)D could also have a direct role in modulating PTH secretion, regardless of both 1,25(OH)₂D and calcium levels.

In conclusion, our results demonstrate that the administration of a single very large oral dose of 600,000 IU of cholecalciferol is useful in rapidly and safely enhancing 25(OH)D levels and in reducing serum PTH in young people with vitamin D deficiency.

Acknowledgments

Disclosure Summary: The authors have nothing to disclose.

Abbreviations:

• CVs,

  Coefficients of variation;

• GFR,

  glomerular filtration rate;

• 1,25(OH)₂D,

• 25(OH)D,

• 25(OH)D₃,

• RM,

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