In Nutrition and Evolution, Michael Crawford and David Marsh make the following statement (page 238):
“The library shelves groan with data showing that feeding saturated fats increases blood cholesterol, damages the arteries, stimulates the blood clotting mechanism, and, indeed, affects blood pressure and the immune system. By contrast, the essential polyunsaturated fatty acids are needed for reproduction, brain growth, vascular system development, cholesterol excretion, control of blood lipids, blood pressure, and other important regulatory functions.”
So I decided to check PubMed for the data on fats and blood coagulation. I found a number of very interesting articles.
In 1954, Cullen and Swank (1, full text), seeking to understand their finding that a low-fat diet can improve multiple sclerosis in humans (2, 3, 4 abstracts, see also Swank's Multiple Sclerosis Diet Book), reported that feeding hamsters with cream produced marked aggregation of red blood cells:
“In many vessels the flow of blood became extremely slow, and frequently the flow stopped completely in some vessels. These changes became first evident and remained most pronounced in the venules.”
Cullen and Swank provided these photos of the process:
|Click for larger version|
Row A shows normal circulation in hamsters on a low fat diet. Rows B and C show clumping of red blood cells in a hamster after a high fat feeding. The photos are enlargements of frames from a colored motion picture taken during the experiments. In the discussion, the authors state:
“The underlying mechanism of the circulatory changes produced by a high fat intake is not clear. Previous darkfield microscopic observations and the cinephotomicrographs taken in the present study leave no doubt that an adhesive envelope develops around the red blood cells. In all likelihood this is the principal cause of the aggregation of the red blood cells and of the slowed circulation.”
After discussing the possible mechanism for formation of this adhesive envelope, Swank and Cullen make other comments including this:
“A high fat diet has long been thought to increase the coagulability of the blood. Moolton and colleagues have shown that a diet rich in animal fat causes a distinct rise in the adhesiveness of the platelets and in some cases in the count as well. He has isolated a lipid substance, present in all fatty tissue, which when injected increases the platelet cound and adhesiveness and the coagulability of the blood. The efficacy of a high fat diet in relieving bleeding disorders has been reported, and a diet poor in fat has been utilized to combat the thrombotic tendency in surgical patients and in patients following coronary thrombosis. Of interest also is the reported decrease in vascular thrombosis in Norway during the recent war when the fat intake was reduced by about 50 per cent.”
You might object that this study involved hamsters, not humans or an animal adapted to meat-eating. Swank actually performed a similar study using humans and dogs, with a similar result (5, abstract), about which the authors comment:
“In an attempt to determine the mechanism by which the fat intake influences multiple sclerosis, studies have been made of the effects of large fat meals on the blood of dogs and humans. Six to nine hours after large fat meals the red blood cells observed in vitro in darkfield illumination have a tendency to aggregate, become adhesive to one another and be distorted. These changes in the suspension stability of the blood occur about an hour after the peak of the alimentary lipemia and finally disappear 9 to 12 hours after the fat meal when the lipemia clears.”
This would suggest that someone eating one high fat meal daily would have this stagnation of blood circulation for half of that day, and two to three high fat meals could result in virtually round-the clock sluggish circulation. As Swank and Cullen note, this could have adverse effects on the nervous system because of its dependence on nutrients and oxygen.
In Nutrition and Evolution, Crawford and Marsh make a similar point, noting that the nervous and vascular systems coevolved, such that the more developed the nervous system in any species, the more developed the nervous system. For example, the human vascular system must serve the nervous system innervating the five digits of each hand, whereas in the hooved animals, both vascular and nervous systems are less complex in the extremities. Anything that adversely affects the vascular system will perforce adversely affect the nervous system. The Swank research suggests that dietary impairment of circulation causing neural ischemia or malnourishment may cause neural damage leading to M.S. and other neural diseases.
In 1976, O’Brien et al reported in the Lancet (6, abstract):
“Large amounts of saturated fats (S.F.) or unsaturated fats (U.S.F.) were given to healthy volunteers at a single meal. The heparin thrombin clotting-time, which may measure platelet factor 4 released from platelets into the plasma, was shortened after S.F. and prolonged after U.S.F. The antithrombin clotting activity decreased after S.F. and increased after U.S.F. The platelet-count decreased and the platelet volume increased after both S.F. and U.S.F.”
Hence, in this study, blood was more prone to clot with high intake of saturated fats, and less prone to clot with unsaturated fats. Other studies (9, full text) indicate that the effect of unsaturated fats depends on dose and background diet, with low doses (low fat diets) reducing coagulability, and high doses increasing coagulability if consumed against a background diet high in saturated fats.
Silveria et al fed 33 heart disease (myocardial infarction) patients and 10 controls a fat load consisting of soybean oil in a dose of 50 g/m2 body surface area.(7, full text) This oil contained about 14% saturated fats, 23% monounsaturated fats, and 62% polyunsaturated fats. The subjects all had increases in serum triglycerides from the dietary fat load. The fat load increased coagulant activity, and Silveria et al concluded:
“Alimentary lipemia is a procoagulant state that is likely to promote formation of occlusive thrombi on fissured atherosclerotic plaques that evolve through other mechanisms. A hypercoagulable state may also predispose to increased fibrin deposition on injured intimal surfaces, fibrin incorporation, and subsequent evolution and growth of atherosclerotic plaques. Since most of our lives are spent in the postprandial state, disturbances of lipoprotein metabolism leading to postprandial triglyceridemia may thus have both atherogenic and thrombotic consequences.”
Elmas et al (8, abstract) investigated “Activation of coagulation during alimentary lipemia under real-life conditions.” They fed 33 healthy physicians and 27 heart disease patients a large meal containing liversausage, bacon, lard, goose, and chocolate as main fat sources; rye bread, potatoes, and sugar were the main carbohydrate sources. The whole meal provided 57 percent of calories from fat, 28 percent from carbohydrate, and 13 percent from protein. They found a roughly threefold increase in fibrinopeptide A levels in both healthy subjects and patients. Fibrinopeptide is released as a part of the blood clotting process.
Elmas et al concluded:
“Fat-rich meals may cause procoagulant episodes, which may promote vascular complications such as myocardial infarction, transient ischemia attacks in susceptible persons.”
Some may respond that this meal was high in carbohydrate, wondering if that rather than the fat caused the hypercoagulability. This is not likely because studies have clearly shown that low fat high carbohydrate diets reduce coagulability of the blood in humans. (9, full text)
Blood circulation to all tissues keeps those tissues alive. Anything that impairs circulation impairs delivery of oxygen and nutrients to tissues, and removal of wastes from those tissues. I'll let you imagine what happens to cells that experience nearly continuous deprivation of nutrients combined with build up of waste products due to impaired circulation.