How saturated fats may be a causative factor in multiple sclerosis and other diseases.
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Biomedical subjects
Publications and source records attributed to R L Swank.
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It is of interest that, aside from starvation, the nutrition catastrophes of the past, including scurvy (vitamin C deficiency) resulting from lack of fresh vegetables and fruit and beriberi (vitamin B1 deficiency) from consumption of polished rice, are forgotten and only of interest as history. The problems of vitamins were largely considered settled by the 1950s. With the appearance on the market of multiple-vitamin-and-mineral tablets, the public was also satisfied and considered the problem of deficiencies solved. Now we are faced with unexpected nutrition problems primarily in the industrial West, which follow from the excess of dietary fats, the refining of grains to make white flour, and the alteration of other natural foods for general use. As we labor to understand and control these problems, new and unexpected "toxins," deficiencies, or excesses may develop. This article is a brief historical account of the past based largely on personal experiences and my concern for the future. The realization that the Western industrial world's high-fat diet was profoundly unhealthy has led to an attempt at correction by development of numerous low-fat foods. Unsaturated vegetable oils and saturated animal fats are being reduced or eliminated. In their place, other components and compounds are being substituted for their taste and consistency, without adequate concern for their nutritional value or freedom from toxicity. Before continuing this risk, the health of the world's population must be considered. Our past experiences with chemical and mechanical alteration of foods, and its effect on the nutrition of every man, woman, and child in the Western world, primarily in industrial North America, should not be forgotten.
144 multiple sclerosis patients took a low-fat diet for 34 years. For each of three categories of neurological disability (minimum, moderate, severe) patients who adhered to the prescribed diet (less than or equal to 20 g fat/day) showed significantly less deterioration and much lower death rates than did those who consumed more fat than prescribed (greater than 20 g fat/day). The greatest benefit was seen in those with minimum disability at the start of the trial; in this group, when those who died from non-MS diseases were excluded from the analysis, 95% survived and remained physically active.
Between 1949 and 1984, 150 multiple sclerosis patients consumed low-fat diets. Fats, oils, and protein intakes; disability; and deaths were determined. On daily fat consumption of less than 20.1 g (average 17 g), 31% died and deterioration was slight. Daily intakes of greater than 20 g (average of either 25 or 41 g) were attended by serious disability and deaths of 79% and 81%, respectively. Oil intakes bore an indirect relationship to fat consumption. Treatment early and before severe disability developed improved prognosis, and females tended to do better than males. High sensitivity to fats suggests they are involved in the genesis of multiple sclerosis.
Polystyrene latex particles were incubated in plasma from multiple sclerosis (MS) patients or normal subjects. Compared with plasma from healthy controls, MS plasma produced a significantly lower mean electrophoretic mobility of the latex particles after the addition of linoleic acid. The effect was similar to that found when erythrocytes were used as the indicator particle. However, the result with latex particles demonstrates that the phenomenon originates from a plasma component of MS patients rather than from an intrinsic difference in membranes of the red blood cell.
Regional cerebral blood flow (rCBF) was determined in 77 normal females and 53 normal males of different ages and in 26 men and 45 women with multiple sclerosis by the inhalation of radioactive Xe133 method. In the normal subjects the CBF was relatively high in the teens and fell, at first rapidly and then slowly in both sexes with age. During adult life the flow in females was significantly higher than in males. The delivery of packed red cells (RCD) was determined by multiplying the CBF by the percentage concentration of red cells (HCT). The RCD for both sexes was nearly the same. In the patients with multiple sclerosis there occurred a progressive generalized decrease in CBF and in RCD with age which was significantly greater than observed in normal subjects. The rate of decrease in CBF and RCD correlated directly with the rate of progress of the disease.
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We have confirmed the red cell electrophoretic mobility-unsaturated fatty acid test for multiple sclerosis, which involves measuring the change in electrophoretic mobility of erythrocytes in Medium 199 upon the addition of linoleic acid. Using defibrinated blood samples, the average decrease in the mobility of red cells upon the addition of linoleic acid of 57 multiple sclerosis patients was 6.7 +/- 2.1% and that of 23 normal control subjects was .09 +/- 1.2% (p less than 0.001). In addition, blood anticoagulated with trisodium citrate was found to give similar test results, and such preparations were found to be simpler and quicker to use.
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Patients with multiple sclerosis (MS) have been shown to have a measurable deterioration in the ability to perceive temporal variations of light. Compared to the traditional critical flicker fusion (CFF) measure, a modified flicker fusion test showed an improved sensitivity for denoting neurological deficit in temporal vision. One hundred twenty-two patients with MS were examined. The traditional CFF test exhibited abnormalities in 48%; the modified test exhibited abnormalities in 78% of the same patients. These results appear to be independent of whether or not the demyelinating disease clinically involved the visual system. Also, the percentage of abnormalities demonstrated by combining both techniques was unexpectedly high (60% to 80%) in patients with minimal evidence of neurological involvement.
A sensitive, antigen-specific rosetting technique was used to enumerate blood cells that bind myelin basic protein (BP) in MS patients and controls. Sixteen of 23 MS patients in exacerbation but only 7 of 48 in remission formed elevated numbers of rosettes. Five of the latter 7 patients had recovered from an exacerbation within four months of the laboratory evaluation. Eight of 20 patients with progressive MS, all of whom had had disease for more than four years, had BP rosette-forming cells. None of the 16 normal volunteers and 1 of 8 neurological controls had BP rosette-forming cells. These results suggest that BP-binding cells in MS are confined to patients in acute exacerbation or within four months of activity, and those who have had progressive disease for at least four years.
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