sealPurdue News

August 30, 1996

'Good' fat may be bad to the bone, study concludes

WEST LAFAYETTE, Ind. -- Parents may have another bone to pick with fast foods, says a Purdue University food scientist.

His research shows that eating too much of the polyunsaturated fat common in convenience and fast food may inhibit bone growth.

In work reported in the September 1996 issue of the Journal of Bone and Mineral Research, Professor Bruce A. Watkins compared the bone growth of chicks that got all their dietary fat from vegetable oil rich in n-6 polyunsaturated fat (n-6 PUFA) to bone growth of chicks fed a combination of fish oil (rich in n-3 polyunsaturates) and vegetable oil. Chick bones built with a combination of fats grew faster than bones of chicks fed diets in which the fat came from vegetable oil alone.

"Balance is the key," Watkins says. "My research suggests that lowering dietary n-6 PUFA by increasing either saturated fat or n-3 PUFA might benefit bone growth in the young."

Earlier work reported by Watkins showed that combining saturated fat with vegetable fat in chicks' diets led to faster bone growth than did vegetable fat alone. It's apparently the overabundance of n-6 PUFA that gets bones in trouble.

"If we eat only convenience food, fast food or snack food and avoid meat, dairy products, and fresh vegetables or fruits, we're getting a large percentage of our fat from n-6 PUFA," Watkins says. "And while no particular food is bad in itself, my research suggests that eating foods rich in n-6 PUFA exclusively or in great abundance could be bad for bones. This is another vote for a balanced diet."

Statistics from the U.S. Department of Agriculture indicate that, compared to a typical American diet in the 1960s, the '90s American diet is richer in n-6 PUFA. When heart disease studies in the '50s painted saturated fat as a villain, food processors began switching from saturated, animal fat to polyunsaturated vegetable oil in many baked and processed foods, Watkins says. Because of that switch, the percentage of our total fat intake that comes from n-6 PUFA has risen dramatically.

Watkins' work has won him a USDA grant to continue studying the effects of fat on human nutrition for optimal health. Because his work supports other findings that saturated fat intake is associated with greater bone density in children, it also has caught the interest of companies that produce infant formulas.

Although he can't yet be sure why large amounts of n-6 polyunsaturates cause trouble for bones, Watkins' recent research leads him to suspect that part of the problem has to do with hormone regulation and free radicals.

Bones can convert n-6 polyunsaturated fats into the hormone prostaglandin E2 (PGE2), which influences bone formation and breakdown to control the shape of bone in animals and humans.

Small amounts of PGE2 in bone have promoted bone growth in human and animal studies. Large amounts of the hormone inhibit bone growth, however, according to studies done by Watkins and others. The more n-6 PUFA an animal eats, the more PGE2 it produces.

The PGE2 produced by our bodies also appears to influence the concentration and action of insulin-like growth factor 1 (IGF-1), another hormone found in bone.

IGF-1 is needed for bone regeneration and is found in abnormally low levels in women with osteoporosis, according to Watkins. Estrogen therapy to reduce bone mineral loss also increases levels of IGF-1 in women's bodies. If Watkins and others can figure out how the amounts and types of fat we eat change our bones' production of IGF-1, nutritionists may be able to develop diets that increase IGF-1 levels and decrease the risk of osteoporosis, he says.

In addition to affecting hormone levels, polyunsaturates often get tangled up with free radicals, molecules that can react with and damage other important molecules in our bodies.

Our bodies manufacture some free radicals naturally, but environmental stresses such as smoke, radiation and chemicals add more to the mix. Free radicals are believed to contribute to disease problems such as cancer and arteriosclerosis. They cause bone breakdown and may hamper bone formation. Free radicals also break down certain polyunsaturated fats into reactive molecules that are nearly as damaging as the free radicals themselves.

Watkins suspected that because broken-down polyunsaturates disrupt cell processes, cartilage cells (where bone growth takes place) work to keep certain polyunsaturates out. If a large amount of broken-down polyunsaturated fat surrounded and entered growing bone, he thought, it could inhibit bone growth.

Watkins tested his idea by feeding chicks a diet rich in polyunsaturated fat plus supplemental vitamin E. Vitamin E is an antioxidant, which means it ties up and counteracts the effects of free radicals. If the polyunsaturated fat indeed was inhibiting bone growth by increasing oxidative stress, Watkins thought, vitamin E should counteract its negative effects.

Vitamin E did the job. Bones of chicks fed large amounts of polyunsaturates plus vitamin E grew as well as bones of chicks fed a combination of moderate amounts of polyunsaturated and saturated fat.

Watkins stresses that researchers can't directly extrapolate results of work done with animals to humans, but he notes that other investigators report that vitamin E decreases bone loss in rats and might benefit bone health in elderly men.


Source: Bruce Watkins (765) 494-5802; e-mail,

Writer: Rebecca Goetz (765) 494-0461; e-mail,


Dietary (n-3) and (n-6) Polyunsaturates and Acetylsalicylic Acid Alter Ex Vivo PGE2 Biosynthesis, Tissue IGF-I Levels, and Bone Morphometry in Chicks

Bruce A. Watkins, Chwan-L. Shen, Kenneth G.D. Allen, and Mark F. Seifert

This study examined the effects of dietary (n-6) and (n-3) polyunsaturated fatty acids (PUFA) and acetylsalicylic acid (ASA) on bone ash content, morphometry, fatty acid composition, ex vivo PGE2, biosynthesis, tissue IGF-I concentration, and serum alkaline phosphatase (ALPase) activity in chicks. Newly hatched chicks were fed a semipurified diet containing soybean oil (S) or menhaden oil + safflower oil (M) at 90 g/kg. At 4 days of age, chicks were divided into four equal treatment groups receiving 0 mg (-) or 500 mg (+) of ASA/kg of diet: S-ASA, M-ASA, S+ASA, and M+ASA. Lipids and ASA treatments did not affect bone length, bone ash, or bone mineral content in chicks. Chicks fed M had increased fractional labeled trabecular surface and tissue level bone formation rates, independent of ASA treatment, compared with those given S. A significant fat x ASA interaction effect was found for trabecular bone volume, thickness, separation, and number. Chicks fed S had higher 20:4 (n-6) but lower 20:5 (n-3) concentrations in liver and bone compared with those given M. Ex vivo PGE2 biosynthesis was higher in liver homogenates and bone organ cultures of chicks fed S compared with the values for those given M at 17 days. ASA treatment decreased ex vivo PGE2 production in liver homogenates and bone organ cultures of chicks, independent of the dietary lipids. Chicks fed ASA had a lower concentration of IGF-I in tibiotarsal bone compared with those not given ASA at 19 days. Serum ALPase activity was higher in chicks given M compared with those fed S, but the values were reversed with ASA feeding. This study demonstrated that both dietary fat and ASA modulated bone PGE2 biosynthesis, and that (n-3) PUFA and fat x ASA interactions altered bone morphometry. (J. Bone Miner Res 1996; 11:9, 1321-1332)

* To the Purdue News and Photos Page