Primary prevention in cardiovascular disease: moving out of the shadows of the truth about death W.E.M. Lands - 2003 - Great 11 page full-text review on n-6 PUFAs causing heart disease.

https://sci-hub.se/10.1016/s0939-4753(03)80175-880175-8)

Primary prevention in cardiovascular disease: moving out of the shadows of the truth about death W.E.M. Lands

Abstract

Aim: This review identifies deficits in current educational efforts for the primary prevention of cardiovascular disease. Data synthesis: Essential fatty acids in the foods we eat have a subtle but powerful influence on hundreds of different processes in the life and death of humans, understanding of which has been delayed by two attitudes in the biomedical community. One involves a bias towards expensive curative/treatment interventions that neglect prevention of initial nutritional causes of disease and death, and the other mvolves careless logic in interpreting evidence of causes of disease and death. Both attitudes interfere wtth translation of published science of essential fatty acids into effective prevention of cardiovascular deaths, a sttuatton made worse by a widespread wish for simple descriptions of complex interactions m disease. Some clinical signs and risk factors may be only shadows of true causal factors. For example, attention to cholesterol ignored important evidence that nutritional imbalances in expenditure~intake of energy and in omega3~omega-6 essential fatty acids cause cardiovascular disease. Balancing the few percentage of dady calories m omega3~omega-6 nutrients is not a questton of obesity or blood cholesterol Effective preventton through education will requtre targeting the causal risk factors that are known beyond the shadow of a doubt, but seldom discussed by health professionals and the public.

Conclusions: Death from coronary heart disease comes from acute ischemia and arrhythmia, often following long term chronic inflammatory vascular damage that predisposes to acute fatal thrombosis and arrhythmia. The three processes involve excessive self-healing acttons of natural n-6 atttacoids (auto=self, akos=healing) produced from tissue essential fatty acids that come only from foods. Readily corrected nutritional imbalances in expenditure/intake of energy and in omega-3/omega-6 essential fatty acids are causal risk factors with plausible mechanisms contributing to fatal events which can be prevented. Nutr Metab Cardiovasc Dis (2003) 13:154-164

Beyond a shadow of a doubt

​

Modern molecular medicine grew explosively throughout the twentieth century. Each newly identified compound accelerated discovery of more previously unknown compounds and functions. Now, there is no doubt that a large complex network of signaling interactions inside cells and between cells participate in a balanced life (and in its cessation, death). A hundred years ago, scientists debated whether potent signaling molecules made in the body should be named hormones (hormain=stir or excite) or autacoids (auto=self, akos=healing). Today's concept of signaling networks regulating body functions includes autacoids and hormones as well as intercellular signaling by cytokines, selectins, and integrins, plus intracellular signaling by protein kinases, protein phosphatases and scaffolding proteins. Some essential nutrients that the body cannot make are called vitamins (vital amines) and others are just essential nutrients. The vitamin-like essential fatty acids (both omega-3 and omega-6) deserve careful attention because many tissues of the body convert them into potent hormone-like autacoids called eicosanoids. We now know beyond a shadow of a doubt that:

• Fatal heart attacks and thrombotic strokes are caused by excessive platelet omega-6 thromboxane formation and diminished by aspirin-like inhibitors.

• Fatal heart arrhythmias are made worse by the omega-6 arachidonate that forms pro-arrhythmic omega-6 eicosanoids, and they are diminished by many non-esterified fatty acids, especially omega-3 acids.

• Formation and action of omega-6 prostaglandins amplify inflammatory events that are treated worldwide by nonsteroidal anti-inflammatory drugs (NSAIDs).

• Inflammation is amplified by positive feedback from released inflammatory mediators at various stages of pathology in vascular atherosclerosis and endothelial dysfunction.

• Inflammatory vascular pathology begins accumulating in adolescents and progresses throughout life, with the current number of inflammatory sites predicting greater future pathology.

• Eicosanoid formation requires initiating and amplifying local hydroperoxides, and elevated tissue hydroperoxides enhance rates of eicosanoid formation.

• Omega-6 eicosanoids amplify natural responses rapidly enough to make some reversible events shift towards irreversible ones, whereas omega-3 eicosanoids are less vigorous in causing irreversible events.

• Stimulated tissues make eicosanoids from non-esterified omega-3 and omega-6 HUFA released from tissue membrane phospholipids.

• The proportions of omega-3 and omega-6 in tissue HUFA are determined by the relative amounts of dietary EFA that compete for incorporation into tissue HUFA.

• Large meals that elevate blood triglycendes, non-esterifled fatty acids, and glucose create transient postprandial oxidant stress and increase endothelial dysfunction.

• Four major risk factors (obesity, hypertension, diabetes, smoking) predictive for cardiovascular mortality are themselves associated with endothelial dysfunction, oxidant stress, inflammatory processes, high postprandial blood fat and non-esterified acids, and insulin resistance.

• Higher blood levels of acute phase reactant or stressreactive proteins (C-reactive protein; heat-shock proteins; orosomucoid; fibrinogen; PAI-1; gamma globulin; angiotensinogen) are systemic markers associated with inflammatory/immune events and oxidant stress.

Summary

The immediate cause of cardiovascular death is thrombosis and arrhythmia that is made worse by excessive omega-6 eicosanoid actions. The chronic vascular inflammation that predisposes to these acute events may be triggered by oxidant stress from postprandial elevations in triglycerides, free fatty acids and glucose, and made worse by a tissue imbalance of omega-3 and omega-6 highly unsaturated fatty acids. The pro-inflammatory imbalance can be prevented by careful choice of food that has more omega-3 and less omega-6. Excessive postprandial elevations of free fatty acids and glucose can be prevented by eating fewer calories per meal and by careful balance of overall energy intake and expenditure. Already, many people worldwide voluntarily choose foods that diminish excessive omega-6 eicosanoid actions and prevent cardiovascular death. Primary prevention nutrition recommendations by the American Heart Association in 2000 need more detailed revision and translation to decrease the postprandial inflammatory stress and excessive omega-6 eicosanoid actions that lead to cardiovascular death.

https://ift.tt/31TNbhl prevention in cardiovascular disease: moving out of the shadows of the truth about death W.E.M. LandsAbstractAim: This review identifies deficits in current educational efforts for the primary prevention of cardiovascular disease. Data synthesis: Essential fatty acids in the foods we eat have a subtle but powerful influence on hundreds of different processes in the life and death of humans, understanding of which has been delayed by two attitudes in the biomedical community. One involves a bias towards expensive curative/treatment interventions that neglect prevention of initial nutritional causes of disease and death, and the other mvolves careless logic in interpreting evidence of causes of disease and death. Both attitudes interfere wtth translation of published science of essential fatty acids into effective prevention of cardiovascular deaths, a sttuatton made worse by a widespread wish for simple descriptions of complex interactions m disease. Some clinical signs and risk factors may be only shadows of true causal factors. For example, attention to cholesterol ignored important evidence that nutritional imbalances in expenditure~intake of energy and in omega3~omega-6 essential fatty acids cause cardiovascular disease. Balancing the few percentage of dady calories m omega3~omega-6 nutrients is not a questton of obesity or blood cholesterol Effective preventton through education will requtre targeting the causal risk factors that are known beyond the shadow of a doubt, but seldom discussed by health professionals and the public.Conclusions: Death from coronary heart disease comes from acute ischemia and arrhythmia, often following long term chronic inflammatory vascular damage that predisposes to acute fatal thrombosis and arrhythmia. The three processes involve excessive self-healing acttons of natural n-6 atttacoids (auto=self, akos=healing) produced from tissue essential fatty acids that come only from foods. Readily corrected nutritional imbalances in expenditure/intake of energy and in omega-3/omega-6 essential fatty acids are causal risk factors with plausible mechanisms contributing to fatal events which can be prevented. Nutr Metab Cardiovasc Dis (2003) 13:154-164Beyond a shadow of a doubt​Modern molecular medicine grew explosively throughout the twentieth century. Each newly identified compound accelerated discovery of more previously unknown compounds and functions. Now, there is no doubt that a large complex network of signaling interactions inside cells and between cells participate in a balanced life (and in its cessation, death). A hundred years ago, scientists debated whether potent signaling molecules made in the body should be named hormones (hormain=stir or excite) or autacoids (auto=self, akos=healing). Today's concept of signaling networks regulating body functions includes autacoids and hormones as well as intercellular signaling by cytokines, selectins, and integrins, plus intracellular signaling by protein kinases, protein phosphatases and scaffolding proteins. Some essential nutrients that the body cannot make are called vitamins (vital amines) and others are just essential nutrients. The vitamin-like essential fatty acids (both omega-3 and omega-6) deserve careful attention because many tissues of the body convert them into potent hormone-like autacoids called eicosanoids. We now know beyond a shadow of a doubt that:• Fatal heart attacks and thrombotic strokes are caused by excessive platelet omega-6 thromboxane formation and diminished by aspirin-like inhibitors.• Fatal heart arrhythmias are made worse by the omega-6 arachidonate that forms pro-arrhythmic omega-6 eicosanoids, and they are diminished by many non-esterified fatty acids, especially omega-3 acids.• Formation and action of omega-6 prostaglandins amplify inflammatory events that are treated worldwide by nonsteroidal anti-inflammatory drugs (NSAIDs).• Inflammation is amplified by positive feedback from released inflammatory mediators at various stages of pathology in vascular atherosclerosis and endothelial dysfunction.• Inflammatory vascular pathology begins accumulating in adolescents and progresses throughout life, with the current number of inflammatory sites predicting greater future pathology.• Eicosanoid formation requires initiating and amplifying local hydroperoxides, and elevated tissue hydroperoxides enhance rates of eicosanoid formation.• Omega-6 eicosanoids amplify natural responses rapidly enough to make some reversible events shift towards irreversible ones, whereas omega-3 eicosanoids are less vigorous in causing irreversible events.• Stimulated tissues make eicosanoids from non-esterified omega-3 and omega-6 HUFA released from tissue membrane phospholipids.• The proportions of omega-3 and omega-6 in tissue HUFA are determined by the relative amounts of dietary EFA that compete for incorporation into tissue HUFA.• Large meals that elevate blood triglycendes, non-esterifled fatty acids, and glucose create transient postprandial oxidant stress and increase endothelial dysfunction.• Four major risk factors (obesity, hypertension, diabetes, smoking) predictive for cardiovascular mortality are themselves associated with endothelial dysfunction, oxidant stress, inflammatory processes, high postprandial blood fat and non-esterified acids, and insulin resistance.• Higher blood levels of acute phase reactant or stressreactive proteins (C-reactive protein; heat-shock proteins; orosomucoid; fibrinogen; PAI-1; gamma globulin; angiotensinogen) are systemic markers associated with inflammatory/immune events and oxidant stress.SummaryThe immediate cause of cardiovascular death is thrombosis and arrhythmia that is made worse by excessive omega-6 eicosanoid actions. The chronic vascular inflammation that predisposes to these acute events may be triggered by oxidant stress from postprandial elevations in triglycerides, free fatty acids and glucose, and made worse by a tissue imbalance of omega-3 and omega-6 highly unsaturated fatty acids. The pro-inflammatory imbalance can be prevented by careful choice of food that has more omega-3 and less omega-6. Excessive postprandial elevations of free fatty acids and glucose can be prevented by eating fewer calories per meal and by careful balance of overall energy intake and expenditure. Already, many people worldwide voluntarily choose foods that diminish excessive omega-6 eicosanoid actions and prevent cardiovascular death. Primary prevention nutrition recommendations by the American Heart Association in 2000 need more detailed revision and translation to decrease the postprandial inflammatory stress and excessive omega-6 eicosanoid actions that lead to cardiovascular death. https://ift.tt/eA8V8J https://ift.tt/3oIF15u