davebrown10
Serum levels of saturated fat are not related to dietary saturated fat intake. https://news.osu.edu/study-doubling-saturated-fat-in-the-die...
What puts a person at risk for chronic inflammatory diseases is excessive polyunsaturated fatty acid intake; in particular, arachidonic acid. Excerpt: "The Mediterranean diet is low in arachidonic acid and rich in healthy fats such as monounsaturated fats found in extra-virgin olive oil (EVOO), nuts and omega-3 fatty acids from fish, which has been shown to lower the risk of inflammation, heart disease, cancer, diabetes and obesity, and other degenerative diseases." https://advancedmolecularlabs.com/blogs/news/new-red-meat-st...
In the middle decades of the 20th Century the heart attack rate was extremely high. Much of that mortality is likely attributable to the release of heavy metals into the environment. Heavy metals such as lead tend to cause arterial plaques to rupture. Excerpt: It must be theoretically expected that there will be a synergistic (multiplicative) interaction between low Se intake (leading to undersaturation of the blood plasma with selenoprotein P), large exposure to toxic heavy metals (which may be expected to lead to simultaneous inhibition of selenoprotein P and extracellular thioredoxin reductase), a high dietary LA/oleic acid intake ratio and high rates of superoxide anion radical production from endothelial NADPH oxidase as causes of more rapid LDL oxidation - with a high rate of LDL oxidation leading in turn to high rates of atheromatosis development. Against this background it is not unreasonable to speculate that excessive exposure to a number of toxic metals from a wide range of different sources may have been one of the main causes of the post-war epidemic of coronary heart disease both in North America and Western Europe. These include lead from car exhaust and from drinking water (especially in the British Isles), as well as mercury and silver from dental amalgam fillings and cadmium from acid rain, commercial fertilizers and tobacco smoke...This hypothesis would appear to be in reasonably good agreement with what is known about the historical curves both for coronary heart disease mortality and for the use of lead as an additive in gasoline in Western Europe, compared to North America. The use of lead as an additive in gasoline started earlier and ended earlier in the United States than it did in the countries of Western Europe. And the epidemic of coronary heart disease has followed a similar time course with both its start and its culmination occurring earlier in the United States than in Western Europe." https://pmc.ncbi.nlm.nih.gov/articles/PMC3031257/
(1996) "Excessive signaling of arachidonic acid (AA) metabolites has been associated with various chronic degenerative or autoimmune diseases, and intervention with the metabolism of AA is widely employed therapeutically in these afflictions. In essence, AA is the most biologically active unsaturated fatty acid in higher animals. Its concentration in membranes and its magnitude of effects depend on its amount, or that of its precursors and analogues, in the diet. The tendency of the field of nutrition to ignore the role of dietary AA will optimistically be reversed in the future." The article also said, "The underlying rationale for this symposium is that dietary AA is perhaps the single most important nutritional determinant in regulating AA levels in Americans. This may ultimately account in part for the striking differences in chronic diseases between strict vegetarians and the bulk of the omnivorous population." https://pubmed.ncbi.nlm.nih.gov/8642436/
Vijay p. Singh says, "Separately, on analyzing global COVID-19 mortality data and comparing it with 12 risk factors for mortality, they found unsaturated fat intake to be associated with increased mortality. This was based on the dietary fat patterns of 61 countries in the United Nations' Food and Agricultural Organization database. Surprisingly, they found saturated fats to be protective."https://www.medpagetoday.com/reading-room/aga/lower-gi/86940
It's interesting that fasting and exercise furnish some protection from excessive polyunsaturated fatty acid intake. For example, "The increased proportional intake of dietary fat, decrease in feeding frequency and increased physical activity in free-ranging compared to captive cheetahs are all predicted to result in enhanced mitochondrial FA oxidation through the lowering of circulating glucose concentrations and insulin:glucagon ratios. During fasting/refeeding cycles and increased levels of exercise, tissue PUFA concentrations have been shown to deplete rapidly in both humans and rats. These studies show that most PUFAs, including α-linolenic acid (ALA) and linoleic acid (LA), are preferentially oxidized in periods of exercise or fasting. During refeeding, SFAs and monounsaturated fatty acids (MUFAs), such as palmitic acid and oleic acid, are also more rapidly replaced than any of the PUFAs. Similarly, the concentrations of most plasma PUFAs and MUFAs have been shown to be significantly lower in rats fed a high fat ketogenic diet than in controls. The predicted increase in FA oxidation in free-ranging cheetahs is therefore likely to also skew their serum FA profiles toward lower proportional serum concentrations of PUFAs and MUFAs relative to SFA." https://pmc.ncbi.nlm.nih.gov/articles/PMC5167222/
In the final analysis, dietary saturated fats are benign, if not outright beneficial over a wide range of intakes as long as they are consumed in the context of healthy nutrient configuration as in whole foods. https://pmc.ncbi.nlm.nih.gov/articles/PMC7846167/
I refer to the very readable review by Philip Calder “A systematic review of the effects of increasing arachidonic acid intake on PUFA status, metabolism and health-related outcomes in humans.” His final statement is that an increase in arachidonic acid intake up to 1.5 grams per day does not significantly change the parameters associated with inflammation, blood clotting or atherogenesis. In this very interesting observation, I was astonished by the fact that the background diet was not taken into account. Although the intake of arachidonic acid with the background diet is reported several times, the resulting metabolic consequences are not discussed.
From the data provided, it can be concluded that the background diet in all studies included in the review was a Western diet, the proportion of arachidonic acid being estimated at 200 to 400 mg per day. Our studies on healthy volunteers were carried out with formula diets and allowed a precisely defined supply of arachidonic acid over a period of 6 weeks. These studies have shown that the exclusion of arachidonic acid from the diet (vegan diet) causes a progressive decrease of this fatty acid from 11 + 3% of the total fatty acids in the cholesterol esters of the plasma to 8 + 2% after 6 weeks. The later studies on patients with rheumatoid arthritis have shown that an intake of arachidonic acid amounting to not more than 80 mg/day does not increase the concentration of arachidonic acid in the phospholipids of the plasma and in the erythrocyte lipids. From these findings I have concluded that the body's own production of arachidonic acid is around 80 mg per day. This means that the Western Diet provides approximately 2.5 to 5 times the estimated need for arachidonic acid.
This intake that is higher than the requirement primarily has no negative consequences. We know from many studies that the "silent inflammation" characteristic for the prevalent diseases of western societies has a latency period of more than 10 years before the consequences such as arteriosclerosis and myocardial infarction become apparent. The body is evidently able to avert the consequences of an unfavorable diet for a long time. To do this, there are numerous regulatory options, such as substrate or product inhibition in the case of enzymes or the inhibition of transport to or incorporation into cells. Arachidonic acid has a very special metabolic pathway that offers possibilities for regulating absorption from the intestine, transport in the chylomicrons, metabolism via the enzymes involved and also for incorporation into the cells. For example, we have found a completely different efficiency for the uptake of arachidonic acid into the cell membrane for platelets compared to erythrocytes or granulocytes. It is therefore very likely that regulation options on the metabolic pathway of arachidonic acid can, to a certain extent, compensate for changes in intake.
Only when too much arachidonic acid is present in the food for a prolonged time do these protective mechanisms apparently fail and inflammation and the manifestation of lifestyle diseases is seen. This explains the long latency period with which the diseases of civilization occur. It is documented in the literature that unhealthy supplementation, such as megadoses of vitamin E, has no deleterious effects on health-related outcomes for humans in the short term. Only long-term observations and meta-analyzes have been able to prove the increased overall mortality. These protective functions with which our body is endowed are very important, because our body is often confronted with megadoses of vitamins or other food stuff or unreasonable diets. Otherwise humans would already be extinct.
In summary, I would like to note that the human metabolism has many opportunities to compensate for unreasonable interventions for a limited time. The studies available so far relate to arachidonic acid intake with the Western Diet. This condition may already have provoked defense mechanisms that delay the occurrence of Western Diet diseases. We all agree that the Western Diet is too meat-based. The studies included in the review gave me the impression that an attempt had been made to further aggravate an already bad situation, present in Western civilizations. The negative result of these studies is reassuring for me, but does not mean that this supplementation has to be harmless and without long-term effects.
From my point of view, it would have been more productive from the experimental approach if vegans had been given the doses of arachidonic acid employed in the studies that are included in the review. This would come closer to the desired goal of the effects of arachidonic acid on PUFA status, metabolism and health-related outcomes in humans. Then one could also come to a result for the desirable intake of arachidonic acid, which I estimate for patients with inflammatory rheumatic diseases at 80 mg per day, corresponding to 560 mg per week. This corresponds to a diet with 5 vegan days and 2 days with consumption of animal products per week.