Hydrogenating vitamin K-rich oils negatively impacts bone health - Nutrition and Bone Health - Brief Article

Nutrition Research Newsletter, Jan, 2002

Hydrogenated fats have been shown to increase LDL-cholesterol concentrations, hence increasing the risk of developing cardiovascular disease. However, the effect of the hydrogenation process on vegetable oil components other than fatty acids has received little attention. One fat-soluble vitamin found in hydrogenated oils is vitamin K. Vitamin K nutrition has been proposed as a modifiable risk factor for osteoporosis. At least three vitamin K-dependent proteins have been identified in bone or cartilage, including osteocalcin. Previous research has shown that the side chain of vitamin K is partially saturated during the hydrogenation process and can be absorbed from the gastrointestinal tract. The biological activity of this hydrogenated form of vitamin K is yet to be determined. Phylloquinone (vitamin [K.sub.1]) is the primary dietary form of vitamin K and is abundantly found in green, leafy vegetables and certain plant oils, such as soybean and canola. The process of hydrogenation of phylloquinone-rich oils promotes conversion to 2',3'-dihydrophylloquinone.

Recently, investigators set out to study the effects of vitamin K status on bone turnover markers after phylloquinone depletion and subsequent repletion with dihyrophylloquinone and phylloquinone while controlling for other dietary factors, such as calcium and vitamin D, known to impact bone status. Fifteen, healthy young adults (aged 20-40 years) served as subjects in this randomized, crossover-designed study. Each subject resided in the Metabolic Research Unit at the Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University for two 30-day residency periods. Each residency period consisted of three diets: a 5-day control diet, a 15-day depletion diet, and a 10-day repletion diet. The control and depletion diets were identical in each residency period. The repletion diet contained either phylloquinone or dihyrophylloquinone. The primary criterion in designing the 5-day control diet was to approximate the adequate intake for vitamin K by providing subjects with approximately 100 microgram phylloquinone per day. There was no dihyrophylloquinone in the control diet. The depletion diet was designed to provide as little phylloquinone and dihyrophylloquinone as possible. For the two repletion diets, purified sources of phylloquinone or dihyrophylloquinone were added to corn oil in muffins. Blood samples were collected on multiple days following a 12-hour fast. Plasma phylloquinone, serum total and undercarboxylated osteocalcin, prothrombin time, and activated partial thromboplastin time were assessed for all days on which blood samples were collected. Other blood measures included protein induced by vitamin K absence or antagonism (PIVKA-II). parathyroid hormone (PTH), bone-specific alkaline phosphatase (BAP), 25-hydroxyvitamin D. and 1,25-dihydroxyvitamin D. Twenty-four-hour urine collections were analyzed for urinary gamma-carboxyglutamic acid and creatinine.

Investigators found an increase and subsequent decrease in measures of bone formation and resorption after dietary phylloquinone restriction and repletion, respectively. When compared with phylloquinone, dihyrophylloquinone was less absorbed and had no measurable biological effect on the measures of bone formation and resorption.

The ingestion of hydrogenated plant oils not only increases LDL-cholesterol concentrations but also appears to decrease the absorption and biological effect of vitamin K in the bone. This effect may prove to negatively impact bone health and should be further investigated.

S. Booth, A. Lichtenstein, M. O'Brien-Morse, et al. Effects of a hydrogenated form of vitamin K on bone formation and resorption. American Journal of Clinical Nutrition 74: 783-790 (December 2001) [Correspondence: S. L. Booth, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111. E-mail: sbooth@hnrc.tufts.edu.]