Anti-Stiffness Factor

Author unknown

Summary: The facts behind the Wulzen factor—an important fat-soluble nutrient found in raw milk and sugarcane juice—have been lost to modern science. Also known as the “anti-stiffness factor” because it combats arthritis and relieves pain, swelling, and stiffness, the Wulzen factor was considered an actual vitamin by a number of early nutrition investigators, but it was never accepted as such by medical or government “authorities.” To acknowledge it would have required the admission that pasteurization of dairy products is a causative factor in arthritis, and such an admission would never be made by those who so vigorously promoted and enforced pasteurization laws. From Annual Review of Biochemistry, 1951. Part of Lee Foundation for Nutritional Research reprint 27A. (To read reprint 27A in its entirely, including an in-depth discussion of the negative effects of milk pasteurization, see “A Fresh Look at Milk” in these archives.)

The following is a transcription of the original Archives document. To view or download the original document, click here.

Anti-Stiffness Factor[spacer height=”20px”]

A critical review has been presented by Dasler.1

Chemical Nature  

Ross, van Wagtendonk, and Wulzen8 reported the preparation, from cane juice, of a compound with a tentative formula C28H46O that alleviates the stiffness induced in guinea pigs on certain experimental diets. From the ultraviolet spectrum, they conclude that the substance is a sterol. Dasler1 doubted the purity of the product.

Oleson, Van Donk, Bernstein, Dorfman, and SubbaRow6 had previously found ergostanyl acetate to be active, a finding that was confirmed by Petering, Stubberfield, and Delor,7 although they had to use much higher doses. Dasler and Bauer2 could not confirm the anti-stiffness activity of ergostanyl acetate, and Dasler1 points to the great difficulties involved in the assay.


Perhaps the most interesting recent development is the observation by Wulzen and Plympton10,11 that guinea pigs reared on stiffness-producing diets finally become deaf, as demonstrated by the inability to react with ear flicking to suitable auditory stimuli. Krueger, Wulzen, and Leveque4 showed that the deafness is due to distortion and pathological calcification of the auditory complex.

Among these abnormalities were reduction and irregularity of the depression for the paraflocculus; reduction of the size of the internal acoustic meatus and of the facial canal; thickening of the wall of the bulla and of the cochlea; obliteration of the tympanic cavity; and elongation of the external acoustic meatus by a second or even a third white, hard, incomplete annulus around the meatus. The auditory ossicles were often deformed and sometimes embedded in a hard, white, amorphous, papillated mass having the appearance of sugar-candy concretions. A series of skulls of guinea pigs exhibiting these malformations was exhibited at the 18th International Physiological Congress in Copenhagen in 1950.

Harris and Wulzen3 described the following anatomical changes in guinea pigs reared on the stiffness-inducing diet: a peculiar type of arteriosclerosis, necrosis, and calcification of the skeletal muscle and myocardium; deposition of calcium salts in the smooth muscle of the gastrointestinal tract; [and] in kidneys and liver, development adjacent to bones and joints of abscesses that frequently become calcified. Hamsters reared on the same diet did not develop these symptoms.

Weimar and Wulzen9 described blood changes belonging to the syndrome: hypocythemic, normochromic, and normocytic or macrocytic anemia; reduction in number of red cells in circulating blood; increased sedimentation rate for erythrocytes; leucocytosis.

Possible Relation to Human Pathology

Lansbury, Smith, Wulzen, and van Wagtendonk5 state that experimental production of a collagen necrosis disease with calcinosis by means of a deficiency diet is of interest to the rheumatologist and suggests the possibility of a nutritional factor in the pathogenesis of some of the collagen diseases.

Author unknown. Reprinted from Annual Review of Biochemistry, Volume 20, 1951, as part of Lee Foundation for Nutritional Research reprint 27A.


1. Dasler, W. Chicago Med. School Quart., 11, 70–73, 1950.
2. Dasler, W. and Bauer, C.D. Proc. Soc. Exptl. Biol. Med., 70, 134–35, 1949.
3. Harris, P.N., and Wulzen, R, Am. J. Path., 26, 595–615, 1950
4. Krueger, H., Wulzen, R., and Leveque, P. Abstracts Communs. 18th Intern. Physiol. Congr., 316–17, Copenhagen, 1950.
5. Lansbury, J., Smith, L.W., Wulzen, R., and van Wagtendonk, W.J. Ann. Rheumatic Diseases, 9, 97–108, 1950.
6. Oleson, J.J., Van Donk, E.C., Bernstein, S., Dorfman, L., and SubbaRow, Y. J. BioI. Chem., 171, 1–7, 1947.
7. Petering, H.G., Stubberfield, L., and Delor, R.A. Arch. Biochem., 18, 487–94, 1948.
8. Ross, L.E., van Wagtendonk, W.J., and Wulzen, R. Proc. Soc. Exptl. Biol. Med., 71, 281–83, 1949.
9. Weimar, V. and Wulzen, R. Federation Proc., 9, 134, 1950.
10. Wulzen, R. and Plympton, A.B. Proc. Soc. Exptl. BioI. Med., 72, 172–74, 1949.
11. Wulzen, R. and Plympton, A.B. Federation Proc., 8, 173, 1949.

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