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No “Bones” About It…

Essential Fatty Acids and BonesEssential Fatty Acids may be a key ingredient in supporting bone health.

Essential fatty acids (EFAs) do not come to mind as the first thought in searching for nutritional answers regarding bone health.  “Recent evidence-based research, however, supports intervention with adequate amounts of specific nutrients including vitamin D, strontium, vitamin K, and essential fatty acids in the prevention and primary management of osteoporosis” (Genius, Clin Nutr. 2007).  Osteoporosis has become an epidemic in the Western World in recent years.  How do EFAs fit into this problem that plagues us especially as we get older?

When we think about osteoperosis, we think calcium.  Calcium and bone go together like salt and pepper.  Add in some vitamin D and that’s about it.  However, looking into it deeper we came up with a number of studies that say that EFAs should be right up front and strongly considered in our first line of bone defense.

Essential fatty acids are necessary to human survival, and are called essential because they must come from the diet; they cannot be made by the body.  The omega-6 and omega-3 fatty acids are the best known.  Learning that they are also important for bone health is something we need to know.

In vivo studies (that means in a living animal) have shown that supplementation with long chain n-6 poly-unsaturated fatty acids (PUFAs) in rats causes increases in intestinal Calcium absorption (Haag 2001).  Haag and his colleagues reported a higher total calcium balance and bone calcium content just by adding in either sunflower or safflower oil in their diet.

In another study pregnant female rats were made diabetic. They use a chemical called streptozotocin to duplicate the disorder in the animals.  They were then fed evening primrose oil (GLA) at 500 mg/kg/d throughout their pregnancy and found an almost complete restoration of bone ossification (process of laying down new bone) occurred just by adding in the primrose oils (Braddock, Pediatr Res. 2002).

Claassen et al, Prostaglandins 1995, found that the supplementation of essential fatty acids (EFAs) leads to increased intestinal calcium absorption and calcium balance. The main dietary EFAs they used were linoleic acid (LA) from sunflower oil and alpha-linolenic acid (ALA) from flax seed oil.  They were administered in a ratio of 3:1 which is very close to our 4:1 BodyBio Balanced oil.  The calcium balance (mg/24 h) and bone calcium (mg/g bone ash) increased significantly in the group that were on the EFAs as compared to the animals that were not given the oils.

Schlemmer et al, Prostaglandins 1999, found that if you make animal’s essential fatty acid deficient they flat out develop osteoporosis.  He then added in evening primrose oil (GLA) and completely reversed the loss of bone and reported positive effects on bone metabolism in both the growing male and female rat.

It certainly goes against what you might think.  Oils are thin, some of them even squishy, while bone is completely hard as a rock.  But leaning on our visual senses doesn’t work with body chemistry, obviously.

Bone remodeling is a life-long process where mature bone tissue is removed from the skeleton and is called resorption, while new bone tissue is formed.  It’s a process called ossification or new bone formation. These processes go on all the time and are managed by special cells that crawl along our bones and chew up excess bone growth, osteoclast.  There is another cell osteoblast, that busily does the opposite, laying down new growth where it’s needed.

In the first year of life, almost 100% of the skeleton is replaced.  In adults, remodeling proceeds at about 10% per year (Wheeless).  That means that in a span of 10 years our skeleton is brand new,  If the process is continuous those cells that do the work must be directly influenced by essential fatty acids, and if EFAs are needed to get the job done, well…

References

Genuis SJ, Schwalfenberg GK. Picking a bone with contemporary osteoporosis management: Nutrient strategies to enhance skeletal integrity. Clin Nutr. 2007 Apr;26(2):193-207

Haag M, Kearns SD, Magada ON, Mphata PR, Claassen N, Kruger MC. Effect of arachidonic acid on duodenal enterocyte ATPases. Prostaglandins Other Lipid Mediat. 2001 Aug;66(1):53-63

Braddock R, Siman CM, Hamilton K, Garland HO, Sibley CPGamma-linoleic acid and ascorbate improves skeletal ossification in offspring of diabetic rats. Pediatr Res. 2002 May;51(5):647-52.

Claassen N, Coetzer H, Steinmann CM, Kruger MC. The effect of different n-6/n-3 essential fatty acid ratios on calcium balance and bone in rats. Prostaglandins Leukot Essent Fatty Acids. 1995 Jul;53(1):13-9.

Schlemmer CK, Coetzer H, Claassen N, Kruger MC. Oestrogen and essential fatty acid supplementation corrects bone loss due to ovariectomy in the female Sprague Dawley rat. Prostaglandins Leukot Essent Fatty Acids. 1999 Dec;61(6):381-90

Wheeless Textbook of Orthopedics, Clifford R. Wheeless, III, MD.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Special Vitamin K?

Eat Your GreensMany people think that vitamin K is used by the body only to clot blood after getting a cut.  That’s true, but this nutrient is much more complicated than that.  Because it’s fat-soluble, it requires fat to be absorbed, but unlike some other fat-soluble vitamins, it doesn’t get stored anywhere in large amounts.  Its name came from the German word koagulation in 1929, immediately after its newly discovered function.

Vitamin K is not a single substance, but a group of structurally similar vitamins that are necessary for the regulation of several proteins involved in metabolic pathways other than blood clotting, including bone and coronary health.  If all it did was to clot blood, vitamin K would be one of the more boring substances related to body function.  There are two natural forms of vitamin K—K1, also known as phylloquinone, and K2, also called menaquinone.   The former is made by plants; the latter, by animals, including humans.

The main dietary source of vitamin K as phylloquinone is plants, the bioavailability of which is questionable and lower than generally assumed.  The absorption of phylloquinone from plants is about one and a half times slower than the vitamin K from a supplement.  (Gijsbers, et al. 1996)  The liver absorbs it quickly and maintains the highest concentration, though significant amounts may be found in the heart.  Whether it is secreted by the liver and transported to other tissue is not known.  (Davidson. 1998)  Green leafy vegetables are rich in K1, and contribute almost half of the total dietary intake.

Vitamin K2, or menaquinone, is a collection of a few vitaminers, the most publicized of which are MK-4 and MK-7, although there are several other MK forms.  Found in egg yolks, butter, liver, certain cheeses and fermented soy products, K2 is also produced by bacteria that live in the gut.  The amount contributed by intestinal microflora is unclear, but dietary contribution of K2 is considerably less than that of K1.  The MK numeration refers to the number of side units that are attached to the main ring-like body of the molecule— MK-4 has four units; MK-7 has seven.  They range from one to ten.  These side chains are called isoprenoids, and are made from two or more hydrocarbons, each containing five carbon atoms.  MK-4 is not produced in significant amounts by bacteria, but appears to be made from phylloquinone.  There are at least three synthetic forms of vitamin K: K3, K4, and K5.  Vitamin K3, known as menadione and metabolized to vitamin K2, has demonstrated moderate toxicity, although it is being used in pet food.  Concentrations of menaquinones in tissue are higher than the phylloquinones, especially menaquinone-4 (MK-4), which is the major tissue-bound form.   Despite the difference, the origin of MK-4 is somewhat elusive.  Investigators in Japan determined that MK-4 is converted from phylloquinone by a metabolic removal of a side chain.  (Okano. 2008)

Deficiencies of vitamin K are uncommon, but are more likely to happen as a result of drug therapy or some diseases.  The most significant instances of deficiency manifest in newborns as an acquired disease, the hemorrhagic activity of which is quelled by oral and intramuscular administration of vitamin K at birth.  Efficiency of vitamin K absorption covers a wide range, from 10% to 80%.  The recommended allowances for this nutrient are set to forestall deficiency diseases, which concern themselves with blood clotting and little else.  The optimal amounts needed to address skeletal and arterial needs have been ignored.

The most studied subtypes of vitamin K2 are MK-4 and MK-7.  MK-4 comes from K1, where its conversion may occur in the testes, pancreas, and arterial walls.  Because scientists have seen the conversion in germ-free mice (having no intestinal microflora), they concluded that bacterial activity is not necessary to make MK-4.  (Ronden. 1998)

Antibiotics are generally non-selective, and will kill the intestinal microflora upon which we depend to manufacture vitamin K from plants.  This can reduce vitamin K (menaquinone) production by more than 70% when compared to those who are not taking antibiotics.  (Conly. 1994)

Vitamin K helps to regulate calcium in both bone and the arteries, working by way of an amino acid called “Gla,” which stands for gamma-carboxyglutamic acid, or gamma-carboxyglutamyl.  Gla responds to changes in dietary intake, an age-dependent process, but several days are needed to observe any alterations.  (Ferland. 1993)   Vitamin K has a modulating effect on several proteins, where it performs an action called carboxylation.  This gives the proteins a kind of claw-like function that enables them to hold on to calcium and move it around.  Without enough vitamin K, the proteins lack their claws.  If this happens, calcium migrates away from bones and teeth, and degradation becomes an issue.  Of all the Gla proteins, osteocalcin (OC) is best known.  It’s synthesized by osteoblasts, the bone-forming cells.  Although everything about osteocalcin is not known, it is believed to be related to bone mineralization.  Osteocalcin that is under-carboxylated, labeled ucOC, is a marker for vitamin K status. High levels of ucOC are indicative of reduced bone mineral density (BMD) and increased risk for fractures.  Vitamin K intake of the general population may not be sufficient to guarantee the carboxylation needed to maintain osteocalcin activity.  (Bach. 1996)  The player in the background of all this activity is vitamin D, which regulates osteocalcin transcription.

(Lian.  1989)  Lian and his team found a large region of nucleotides directly upstream from the transcription start area that supports a ten-fold stimulation of transcription of the OC gene by 1,25-dihydroxy vitamin D.

The vitaminer MK-4 has demonstrated the capacity to reduce bone fracture risks, and even to reverse bone loss.  The synergy of vitamins K and D was recognized in studies performed by the University of California, where MK-4 received the nod as the leader of the pack.  (Kidd. 2010)  Japanese researchers who preceded that study reported that a dose of 45 mg a day of vitamin K, accompanied by calcium supplementation, would increase BMD and lead to the prevention of nonvertebral fractures. (Sato. 2005)  Additionally, K2 was found to reduce the incidence of vertebral fractures without having a substantial effect on BMD.  (Iwamoto. 2006)

Not to be outdone by its analog MK-4, MK-7, sourced from fermented soy, has been found to stimulate osteoblastic bone formation while inhibiting osteoclastic bone resorption, all the while limiting calcium depletion by modulating prostaglandin E2.
(Yamaguchi. 2006)   (Tsukamoto. 2004)

Some individuals with osteoporosis are likely to have an excess of calcium in their arteries.  Vascular calcification might even be viewed as vascular ossification—the formation of bone inside an artery.  The appearance of atherosclerotic plaques in arterial walls is a hallmark of cardiovascular disease (CVD).  The plaques cause decreased elasticity of the affected vessel and increased risk of clot formation.  In Dutch studies it was discovered that women with atherosclerotic calcifications have a lower bone mass, which, of course, puts them at greater risk for fractures.  Deficiency of vitamin K causes an increase of ucOC, leading to deposition of calcium in arteries, an activity that would be halted by carboxylated OC.  Menaquinone, including MK-4, but probably not phylloquinone, is associated with reduced coronary calcification.  (Beulens. 2009)  (Geleijnse. 2004)  These studies show that those who ingested the greatest amounts of vitamin K2 experienced a 57% reduction in cardiac fatalities.  No such relationship was found for K1.  In these studies, though, MK-4 and MK-7 were not separately analyzed, but were grouped together.  But in earlier studies it was learned that MK-4 has a distinct effect on plaque prevention in warfarin treatment, where MK-4 was three times more efficiently utilized in the aorta than vitamin K1, mostly by virtue of its bioavailability and use in carboxylation.  (Spronk. 2003)

Warfarin and other anticoagulants interfere with the activity of vitamin K.  Unfortunately, warfarin has the capacity to cause arterial calcification in the long run.  (Price. 1998)  (Danziger. 2008)   Generally, there are enough data to suggest that a constant dietary intake of 65-80 mcg of vitamin K a day during warfarin therapy is an acceptable practice, while avoiding fluctuations in vitamin K intake that would interfere with the activity of the drug.  (Booth. 1999)  It is strongly recommended that such patients work closely with their physicians to monitor prothrombin time, perhaps better known as INR.  It is accepted that vitamin K replacement is an important part of warfarin therapy. (Patriquin. 2011)  In some instances, aspirin may be the better choice.  (Chimowitz. 2005)

The activities of the special K vitamin extend beyond the scope of this newsletter.  Maybe that can be addressed another time.

References

Adams J, Pepping J.
Vitamin K in the treatment and prevention of osteoporosis and arterial calcification.
Am J Health Syst Pharm. 2005 Aug 1;62(15):1574-81.

Arunakul M, Niempoog S, Arunakul P, Bunyaratavej N.
Level of undercarboxylated osteocalcin in hip fracture Thai female patients.
J Med Assoc Thai. 2009 Sep;92 Suppl5:S7-11.

Bach AU, Anderson SA, Foley AL, Williams EC, Suttie JW.
Assessment of vitamin K status in human subjects administered “minidose” warfarin.
Am J Clin Nutr. 1996 Dec;64(6):894-902.

Berkner KL.
The vitamin K-dependent carboxylase.
J Nutr. 2000 Aug;130(8):1877-80.

Beulens JW, Bots ML, Atsma F, Bartelink ML, Prokop M, Geleijnse JM, Witteman JC, Grobbee DE, van der Schouw YT.
High dietary menaquinone intake is associated with reduced coronary calcification.
Atherosclerosis. 2009 Apr;203(2):489-93. Epub 2008 Jul 19.

Booth SL, Centurelli MA
Vitamin K: a practical guide to the dietary management of patients on warfarin.
Nutr Rev. 1999 Sep;57(9 Pt 1):288-96.

Brody T. Nutritional Biochemistry. 2nd ed. San Diego: Academic Press; 1999.

Chatrou ML, Reutelingsperger CP, Schurgers LJ.
Role of vitamin K-dependent proteins in the arterial vessel wall.
Hamostaseologie. 2011 Nov;31(4):251-7.

Cheung AM, Tile L, Lee Y, Tomlinson G, Hawker G, Scher J, Hu H, Vieth R, Thompson L, Jamal S, Josse R.
Vitamin K supplementation in postmenopausal women with osteopenia (ECKO trial): a randomized controlled trial.
PLoS Med. 2008 Oct 14;5(10):e196.

Marc I. Chimowitz, M.B., Ch.B., Michael J. Lynn, M.S., Harriet Howlett-Smith, R.N., Barney J. Stern, M.D., Vicki S. Hertzberg, Ph.D., et al
Comparison of Warfarin and Aspirin for Symptomatic Intracranial Arterial Stenosis
N Engl J Med 2005; 352:1305-1316 March 31, 2005

Conly J, Stein K.
Reduction of vitamin K2 concentrations in human liver associated with the use of broad spectrum antimicrobials.
Clin Invest Med. 1994 Dec;17(6):531-9.

Danziger J.
Vitamin K-dependent proteins, warfarin, and vascular calcification.
Clin J Am Soc Nephrol. 2008 Sep;3(5):1504-10.

Davidson RT, Foley AL, Engelke JA, Suttie JW.
Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria.
J Nutr. 1998 Feb;128(2):220-3.

Ferland G, Sadowski JA, O’Brien ME.
Dietary induced subclinical vitamin K deficiency in normal human subjects.
J Clin Invest. 1993 Apr;91(4):1761-8.

Feskanich D, Weber P, Willett WC, Rockett H, Booth SL, Colditz GA.
Vitamin K intake and hip fractures in women: a prospective study.
Am J Clin Nutr. 1999 Jan;69(1):74-9.

Geleijnse JM, Vermeer C, Grobbee DE, Schurgers LJ, Knapen MH, van der Meer IM, Hofman A, Witteman JC.
Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study.
J Nutr. 2004 Nov;134(11):3100-5.

Gijsbers BL, Jie KS, Vermeer C.
Effect of food composition on vitamin K absorption in human volunteers.
Br J Nutr. 1996 Aug;76(2):223-9.

Iwamoto J, Takeda T, Sato Y.
Menatetrenone (vitamin K2) and bone quality in the treatment of postmenopausal osteoporosis.
Nutr Rev. 2006 Dec;64(12):509-17.

Iwamoto J, Sato Y, Takeda T, Matsumoto H.
High-dose vitamin K supplementation reduces fracture incidence in postmenopausal women: a review of the literature.
Nutr Res. 2009 Apr;29(4):221-8.

Je SH, Joo NS, Choi BH, Kim KM, Kim BT, Park SB, Cho DY, Kim KN, Lee DJ.
Vitamin K supplement along with vitamin D and calcium reduced serum concentration of undercarboxylated osteocalcin while increasing bone mineral density in Korean postmenopausal women over sixty-years-old.
J Korean Med Sci. 2011 Aug;26(8):1093-8.

Jie KG, Bots ML, Vermeer C, Witteman JC, Grobbee DE.
Vitamin K status and bone mass in women with and without aortic atherosclerosis: a population-based study.
Calcif Tissue Int. 1996 Nov;59(5):352-6.

Jin DY, Tie JK, Stafford DW.
The conversion of vitamin K epoxide to vitamin K quinone and vitamin K quinone to vitamin K hydroquinone uses the same active site cysteines.
Biochemistry. 2007 Jun 19;46(24):7279-83.

Kanai T, Takagi T, Masuhiro K, Nakamura M, Iwata M, Saji F.
Serum vitamin K level and bone mineral density in post-menopausal women.
Int J Gynaecol Obstet. 1997 Jan;56(1):25-30.

Kidd PM.
Vitamins D and K as pleiotropic nutrients: clinical importance to the skeletal and cardiovascular systems and preliminary evidence for synergy.
Altern Med Rev. 2010 Sep;15(3):199-222.

Knapen MH, Schurgers LJ, Vermeer C.
Vitamin K2 supplementation improves hip bone geometry and bone strength indices in postmenopausal women.
Osteoporos Int. 2007 Jul;18(7):963-72.

Lian J, Stewart C, Puchacz E, Mackowiak S, Shalhoub V, Collart D, Zambetti G, Stein G.
Structure of the rat osteocalcin gene and regulation of vitamin D-dependent expression.
Proc Natl Acad Sci U S A. 1989 Feb;86(4):1143-7.

Luo LZ, Xu L.
Vitamin K and osteoporosis.   [Article in Chinese]
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2003 Jun;25(3):346-9.

Patriquin C, Crowther M.
Treatment of warfarin-associated coagulopathy with vitamin K.
Expert Rev Hematol. 2011 Dec;4(6):657-67.

Price PA, Faus SA, Williamson MK.
Warfarin causes rapid calcification of the elastic lamellae in rat arteries and heart valves.
Arterioscler Thromb Vasc Biol. 1998 Sep;18(9):1400-7.

Price PA, Faus SA, Williamson MK.
Warfarin-induced artery calcification is accelerated by growth and vitamin D.
Arterioscler Thromb Vasc Biol. 2000 Feb;20(2):317-27.

Ronden JE, Drittij-Reijnders MJ, Vermeer C, Thijssen HH.
Intestinal flora is not an intermediate in the phylloquinone-menaquinone-4 conversion in the rat.
Biochim Biophys Acta. 1998 Jan 8;1379(1):69-75.

Sato Y, Kanoko T, Satoh K, Iwamoto J.
Menatetrenone and vitamin D2 with calcium supplements prevent nonvertebral fracture in elderly women with Alzheimer’s disease.
Bone. 2005 Jan;36(1):61-8. Epub 2004 Nov 24.

Shiomi S, Nishiguchi S, Kubo S, Tamori A, Habu D, Takeda T, Ochi H.
Vitamin K2 (menatetrenone) for bone loss in patients with cirrhosis of the liver.
Am J Gastroenterol. 2002 Apr;97(4):978-81.

Spronk HM, Soute BA, Schurgers LJ, Thijssen HH, De Mey JG, Vermeer C.
Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats.
J Vasc Res. 2003 Nov-Dec;40(6):531-7. Epub 2003 Dec 3.

Toshio Okano, Yuka Shimomura, Makiko Yamane, Yoshitomo Suhara, Maya Kamao, Makiko Sugiura and Kimie Nakagawa
Conversion of Phylloquinone (Vitamin K1) into Menaquinone-4 (Vitamin K2) in Mice
TWO POSSIBLE ROUTES FOR MENAQUINONE-4 ACCUMULATION IN CEREBRA OF MICE

The Journal of Biological Chemistry, April 25, 2008, 283, 11270-11279

Tsukamoto Y.
Studies on action of menaquinone-7 in regulation of bone metabolism and its preventive role of osteoporosis.
Biofactors. 2004;22(1-4):5-19.

Yamaguchi M.
Regulatory mechanism of food factors in bone metabolism and prevention of osteoporosis.
Yakugaku Zasshi. 2006 Nov;126(11):1117-37.

Vermeer C, Schurgers LJ.
A comprehensive review of vitamin K and vitamin K antagonists.
Hematol Oncol Clin North Am. 2000 Apr;14(2):339-53.

Wallin R, Schurgers L, Wajih N.
Effects of the blood coagulation vitamin K as an inhibitor of arterial calcification.
Thromb Res. 2008;122(3):411-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Vitamin C For Bone Health?

skeleton-vitamin-cHow many bones are in the human skeleton? How come it’s on the inside? What does it do? Does anybody really care? Sometimes.

The human skeleton offers shape and protection to the body. It supplies a place for organs to attach or to be supported. It comprises 206 bones, the largest of which is the thigh (femur). It makes up about 15% of your body weight, part of which is water. This fifteen percent refers to ideal body weight, not to a 400-pound behemoth who is less than six feet tall. Infants have more than 206. The skull starts out with more than twenty bones, some of which fuse together during development. Besides helping you to move, bones make red and white blood cells in their marrow, and act as a storage house for minerals. It takes about twenty years to develop completely.

Bone is actually a type of connective tissue, obviously denser than cartilage, which is the flexible stuff at the flap of your ear (tragus) and the tip of your nose. Cartilage also makes the discs that separate your vertebrae from each other and the femur from the tibia at the knee. Bone tissue is heavily mineralized by a form of calcium called hydroxyapatite. Calcium is the mineral found in the greatest amount in the body, about ninety-nine percent of which is in bone. Phosphorus works with calcium to maintain bone health by combining to make hydroxyapatite. This aggregation helps bone to remodel—to break down and then to redeposit. Trace amounts of other minerals, including magnesium, boron, copper and zinc, stimulate bone growth. But there’s one element of bone health that is overlooked because it’s thought of as nothing more than an anti-oxidant—vitamin C, aka ascorbic acid.

In a study of prepubescent females done in Philadelphia, it was learned that specific bone parameters were positively affected by vitamin C, especially in combination with zinc. For every milligram a day of vitamin C intake, there was an increase in trabecular bone area (Laudermilk, 2012). That’s the porous part of a bone found in the center and at the end of a long bone, like the femur. It’s important to the manufacture of blood cells inside the red marrow. Because it’s porous, trabecular bone is not as strong as the harder cortical outer layer. As hormones change with development, bone requirements also change. This is why it’s necessary to lay down as much bone as possible in one’s early years. By the time a girl reaches thirty, she will have laid down all the bone she ever will, which is probably why a DXA scan compares/contrasts a patient’s bone density to that of a thirty-year-old. You can read about this at the NIH Osteoporosis and Related Bone Diseases National Resource Center website,
http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/bone_mass_measure.asp

If vitamin C intake promotes bone, then deficiency must degrade it. Too little vitamin C causes scurvy, the condition that once affected seamen who were deprived of fresh fruits and vegetables for prolonged periods. That doesn’t happen anymore; at least it shouldn’t. The sailors’ joints and muscles would hurt, they bruised easily, their gums would bleed, and their teeth would sometimes fall out. Since vitamin C is responsible for the formation of connective tissue, these occurrences seem relevant.  Spontaneous fractures caused by low bone mineral density, and considered to be induced by a failure of collagen synthesis, also characterize scurvy (Park, 2012). Deficiency of vitamin C is implicated in scurvy by the inhibition of osteoblast activity. You remember osteoblasts.  They’re the cells responsible for making new bone material.

Most animals do not require external sources of vitamin C because they can get it from glucose through their enzyme systems. Humans and other primates, guinea pigs, and fruit bats lack this ability, so they have to get it from their diets. Since fast foods have replaced fruits and vegetables, many of us may be vitamin C deficient in the absence of supplementation.  Lettuces, onions, apples and bananas don’t help. Citrus fruits, cruciferous vegetables and strawberries do. Besides diet, other lifestyle factors influence vitamin C status, especially smoking, a habit that seriously affects the neck of the femur (Sahni, 2008) unless ascorbic acid intake is considerably greater than the RDA. The dietary recommendation for vitamin C is that amount needed to prevent a condition caused by its lack, in this case, scurvy and its aftermath. Sixty milligrams a day is hardly enough to meet a human’s physiological and metabolic needs. The 400-pound gorilla at the zoo gets 4000 milligrams a day. Shouldn’t a 200-pound human get 2000, then?

Speaking of the femur…This is where the hip joint is, at the top of the thigh bone.  In a seventeen-year follow-up study conducted by Tufts University, those elderly (70-80 yrs.) in the highest third of vitamin C intake had significantly fewer hip and non-vertebral fractures than those in the bottom third, suggesting a protective effect of vitamin C on bone health (Sahni, 2009). It’s important to note that oral contraceptives may adversely affect vitamin C accumulation. Women who fail to supplement while taking hormones as oral contraceptives have lower plasma levels of vitamin C than those who do supplement (Kuo, 2002). This, however, would seem to be the case regardless of contraceptive use.  Concerning sex steroids, both estrogen and testosterone are important for developing peak bone mass (Riggs, 2002). In the case of hypogonadism, where sex glands produce little or no hormones, vitamin C stimulates bone formation (Zhu, 2012), allowing bone recovery in light of hormone deficit. This finding is particularly important to those at risk for osteoporosis, as may be such in developing countries, among the food insecure, and in men who have had certain treatments for prostate disease, including one called gonadotropin-releasing hormone, abbreviated GnRH  (Mittan, 2002).

Despite having lost the ability to synthesize vitamin C, humans can take supplements or increase dietary intake to avert the onset of osteoporosis, realizing that ascorbic acid can block osteoclast proliferation and bone loss while promoting osteoblast activity and bone remodeling.

References

Fain O.
Musculoskeletal manifestations of scurvy.
Joint Bone Spine. 2005 Mar;72(2):124-8.

Gabbay KH, Bohren KM, Morello R, Bertin T, Liu J, Vogel P.
Ascorbate synthesis pathway: dual role of ascorbate in bone homeostasis.
J Biol Chem. 2010 Jun 18;285(25):19510-20.

Kuo SM, Stout A, Wactawski-Wende J, Leppert PC.
Ascorbic acid status in postmenopausal women with hormone replacement therapy.
Maturitas. 2002 Jan 30;41(1):45-50.

Laudermilk MJ, Manore MM, Thomson CA, Houtkooper LB, Farr JN, Going SB.
Vitamin C and Zinc Intakes are Related to Bone Macroarchitectural Structure and Strength in Prepubescent Girls.
Calcif Tissue Int. 2012 Oct 18.

Lean JM, Davies JT, Fuller K, Jagger CJ, Kirstein B, Partington GA, Urry ZL, Chambers TJ.
A crucial role for thiol antioxidants in estrogen-deficiency bone loss.
J Clin Invest. 2003 Sep;112(6):915-23.

Mittan D, Lee S, Miller E, Perez RC, Basler JW, Bruder JM.
Bone loss following hypogonadism in men with prostate cancer treated with GnRH analogs.
J Clin Endocrinol Metab. 2002 Aug;87(8):3656-61.

NIH Osteoporosis and Related Bone Diseases National Resource Center
Bone Mass Measurement: What the Numbers Mean
January, 2012
http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/bone_mass_measure.asp

Park JK, Lee EM, Kim AY, Lee EJ, Min CW, Kang KK, Lee MM, Jeong KS.
Vitamin C deficiency accelerates bone loss inducing an increase in PPAR-γ expression in SMP30 knockout mice.
Int J Exp Pathol. 2012 Oct;93(5):332-40.

B. Lawrence Riggs, Sundeep Khosla and L. Joseph Melton II
Sex Steroids and the Construction and Conservation of the Adult Skeleton
Endocrine Reviews June 1, 2002 vol. 23 no. 3 279-302

Sahni S, Hannan MT, Gagnon D, Blumberg J, Cupples LA, Kiel DP, Tucker KL.
High vitamin C intake is associated with lower 4-year bone loss in elderly men.
J Nutr. 2008 Oct;138(10):1931-8.

Sahni S, Hannan MT, Gagnon D, Blumberg J, Cupples LA, Kiel DP, Tucker KL.
Protective effect of total and supplemental vitamin C intake on the risk of hip fracture–a 17-year follow-up from the Framingham Osteoporosis Study.
Osteoporos Int. 2009 Nov;20(11):1853-61.

Markus J. Seibel, Colin R. Dunstan, Hong Zhou, Charles M. Allan and David J. Handelsman
Sex Steroids, Not FSH, Influence Bone Mass
Cell. 2006 Dec 15;127(6):1079

Simon JA, Hudes ES.
Relation of ascorbic acid to bone mineral density and self-reported fractures among US adults.
Am J Epidemiol. 2001 Sep 1;154(5):427-33.

Zhu L-L, Cao J, Sun M, Yuen T, Zhou R, Mne Zaidi, et al.
Vitamin C Prevents Hypogonadal Bone Loss.
PLoS ONE (2012); 7(10): e47058.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.