Booyens J, Maguire L, Katzeff I E
Med Hypotheses. 1985 Aug;17(4):351-62. doi: 10.1016/0306-9877(85)90094-5.
The mono-unsaturated non-essential fatty acid oleic acid (OA) has been shown to stimulate malignant cell proliferation in culture significantly. In contrast, the essential fatty acids (EFAs) linoleic acid (LA) and alpha-linolenic acid (ALA) and their longer chain metabolic derivatives have been shown to have potent proliferation suppressive effects on malignant cells in culture. OA is normally synthesized in the body and present in most vegetable oils and therefore also in most experimental polyunsaturated fatty acid diets used for assessing the effects of dietary fatty acids on tumorigenesis in rats. Dietary OA could therefore specifically account for the general observation that diets containing polyunsaturated fatty acids (PUFAs) are tumorigenic (1). It has been repeatedly demonstrated that many EFAs and EFA metabolites suppress proliferation of a wide range of malignant cells in culture. These cytotoxic effects of EFAs do not inhibit the proliferation of nonmalignant cultured cells. The EFAs which have proliferation-suppression activities are components of cell membranes and many are also eicosanoid precursors. It is proposed that the membranes of malignant cells are inherently unstable. Thus the EFAs may have effects which either fluidise or stabilise these membranes. This results in either cytolysis or inhibition of proliferation. The relative quantities of the different EFAs may be critical for these effects. Eicosanoid metabolites may further compound these actions. It is suggested that one pathway for these actions could be a metabolic imbalance of EFA metabolites and their eicosanoid products. This would arise due to a combination of inhibited desaturase enzymes and a concomitant free cellular supply of dietary arachidonic acid (AA). This imbalance also could be causally involved in the promotion of malignancy. A simple procedure, which only involves dietary supplementation with gamma-linolenic acid (GLA) and eicosapentaenoic acid (EPA), is proposed as prophylaxis against the possible tumorigenic effect of dietary fats. "By some estimates, as much as 90% of all cancer in humans has been attributed to various environmental factors, including diet. The evidence reviewed by the committee suggests that cancers of most of the major sites are influenced by dietary patterns. The committee concluded that of all the dietary components it studied, the combined epidemiological and experimental evidence is most suggestive for a causal relationship between fat intake and the occurrence of cancer" - (1).
单不饱和非必需脂肪酸油酸（OA）已被证明能在培养中显著刺激恶性细胞增殖。相比之下，必需脂肪酸（EFAs）亚油酸（LA）和α-亚麻酸（ALA）及其长链代谢衍生物已被证明对培养中的恶性细胞具有强大的增殖抑制作用。OA通常在体内合成，存在于大多数植物油中，因此也存在于大多数用于评估膳食脂肪酸对大鼠肿瘤发生影响的实验性多不饱和脂肪酸饮食中。因此，膳食中的OA可能特别解释了一个普遍观察结果，即含有多不饱和脂肪酸（PUFAs）的饮食具有致瘤性（1）。反复证明，许多必需脂肪酸和必需脂肪酸代谢产物在培养中抑制多种恶性细胞的增殖。必需脂肪酸的这些细胞毒性作用并不抑制非恶性培养细胞的增殖。具有增殖抑制活性的必需脂肪酸是细胞膜的组成部分，许多也是类花生酸前体。有人提出，恶性细胞的膜本质上是不稳定的。因此，必需脂肪酸可能具有使这些膜流化或稳定的作用。这导致细胞溶解或增殖抑制。不同必需脂肪酸的相对数量可能对这些作用至关重要。类花生酸代谢产物可能进一步加剧这些作用。有人认为，这些作用的一条途径可能是必需脂肪酸代谢产物及其类花生酸产物的代谢失衡。这是由于去饱和酶的抑制和膳食花生四烯酸（AA）的细胞内自由供应同时存在而产生的。这种失衡也可能因果性地参与恶性肿瘤的促进。提出了一种简单的程序，仅涉及膳食补充γ-亚麻酸（GLA）和二十碳五烯酸（EPA），作为预防膳食脂肪可能的致瘤作用的措施。“据一些估计，人类所有癌症中多达90%归因于各种环境因素，包括饮食。委员会审查的证据表明，大多数主要部位的癌症受饮食模式影响。委员会得出结论，在其研究的所有膳食成分中，综合的流行病学和实验证据最表明脂肪摄入与癌症发生之间存在因果关系” - （1）。
