Hyperlipemia fat-induced

I. Familial fat-induced hyperlipemia. Plasma creamy Xanthomatosis eruptive, tuberous Hepato-splenomegaly Chylomicrons on any fat intake Post-heparin lipolytic activity low Glucose tolerance normal. 

Fat-induced hyperlipemia (FIHL), hyperchylomicronemia, type I of Fredrickson and Lees, alimentary hyperglyceridemia]. 

Fig. 2. Exogenous (fat-induced) hyperlipemia. Intake of any of a variety of fats in this boy resulted in progressive hyperglyceridemia. Fat-free (high carbohydrate) diets were associated with rapid fall of plasma glyceride levels toward normal. Glycerides in this study were determined by difference from total lipids. Values are higher as compared with those of other figures...

FIHL = fat-induced hyperlipemia, CIHL = carbohydrate-induced hyperlipemia. 

On the basis of our own experience and to some degree that of others, it seems probable that pure carbohydrate-induced hyperglyceridemia is a relatively rare entity, although by no means as rare as pure fat-induced hyperlipemia (hyperchylomicronemia). 

The importance of the calorie level in carbohydrate and fat inducible hyperlipemia (group 2) has been emphasized. In this group the lowest feasible calorie intake will result in lowest plasma lipid levels. Unsaturated at the expense of saturated fat should be emphasized. 

Administration of heparin has frequently been tried in EHL. Whereas no significant effect on plasma lipids was reported by Kuo et al. (1959) and in a heparin unresponsive subject with fat-induced hyperlipemia by Furman et al. (1961), the latter authors demonstrated significant improvement in plasma lipid levels of two other patients with carbohydrate-induced hyperlipemia. One might anticipate unresponsiveness to long term heparin administration with low postheparin lipolytic activity found with the in vitro assay of Fredrickson et al. (1963) (see Table 1). Such a correlation is not necessarily present as evidenced by the response in a child with the fat-induced variety, whom we have observed (Kinsell and Schlierf 1965). 

In heterozygotes of fat-induced hyperlipemia the statistical mean of plasma neutral fat concentration is increased as compared with controls. Clearing after... 

The problems in explaining the basic pathogenetic mechanism are well demonstrated by an observation of Fredrickson et al. (1963). In one family with fat-inducible hyperlipemia these authors found an affected girl who in the heparin test showed the expected markedly diminished lipolytic activity, and an equally... 

That a number of subjects with carbohydrate-induced hyperlipemia will exhibit significant hyperglyceridemia even on low carbohydrate, high fat diets, is already evident from Fig. 6 given by Ahrens et al. in 1961 and from Table 1 of Knittle and Ahrens (1964). Other authors therefore have used the term carbohydrate-accentuated rather than induced to describe such patients. 

In pure carbohydrate-induced hyperlipemia, restriction of carbohydrate compatible with acceptability of the diet and prevention of ketosis is recommended. Thus 50—70% of calories may be given as fat with a carbohydrate content below 25%. If a significant amount of the fat comes from unsaturated sources, it may be cleared from plasma faster than saturated fats (Engelberg 1964) and hypercholesterolemia may be further reduced. Such a regimen should also be optimal in the combination of essential hypercholesterolemia and hyperhpemia. 

About this time Ahrens et al. (1961) postulated that there were two kinds of hyperlipemia in man one was fat-induced, and the other was carbohydrate-induced. The latter was associated widi a raised serum glyceride concentration, and this carbohydrate-induced type of lipemia is now well-established. 

More studies have been made in this field in man largely because an increase in serum lipid level is associated with ischemic heart disease and Ahrens et al. (1961) advanced the hypothesis that hyperlipemia could be carbohydrate-induced. This was confirmed in diabetics where the isocaloric substitution of carbohydrate for fat in the diet resulted in an increase in the serum lipid level (Bierman and Hamlin, 1961). 

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