Why do trans-fatty acids wreak so much havoc on the cardiovascular system when compared to regular fats?
What Are TransFatty Acids and Where Do They Come From?
Trans fatty acids contain at least one double bond in the trans configuration. The carbon/carbon double bonds of fatty acids can exist in either the cisor transconfiguration. When the two hydrogen atoms are on opposite sides of the double bond, the configuration is termed trans; when the two hydrogen atoms are on the same side of the double bond, the configuration is termed cis. Lack of rotational mobility precludes interconversion of configurations under normal circumstances. The bond angle is larger for a trans than a cisdouble bond. Therefore, the presence of a trans, relative to a cis, double bond results in acyl chains that can pack together more tightly.
Trans double bonds occur in nature as such. They are the result of anaerobic bacterial fermentation in ruminant animals and are thereby introduced into the food chain. Humans consume them in the form of meat and dairy products. Trans double bonds are also formed during the hydrogenation of either vegetable or fish oils. Oils are hydrogenated to increase their plasticity and chemical stability, hence their potential use in food products. It is important to note that hydrogenation results in a number of changes in the acyl chain of the fatty acid moiety, all of which can impact physiological parameters: conversion of cis to trans double bonds, saturation of double bonds, and migration of double bonds along the acyl chain resulting in multiple positional isomers.
What Is the Current Intake of Trans Fatty Acids in the United States?
Although numbers for the intake of trans fatty acids in the United States exist, they are only estimates. The lack of a complete database for trans fatty acid levels in foods has significantly impeded efforts to assess current intakes accurately and reliably. In addition, without such data it is difficult to evaluate the magnitude of the impact of trans fatty acid or hydrogenated fat intake on plasma lipid levels or other parameters. Estimates of intake are based on availability or disappearance data (that which disappears from available supplies), food-questionnaire data, and analysis of self-selected diets.All have inherent limitations in estimating food intake independent of the availability of reliable data on the trans fatty acid content of foods and are beyond the scope of this statement. Reported intakes range from 2.6 g/d to 12.8 g/d. High-range estimates are drawn from availability or disappearance data, low-range estimates from analysis of self-selected diets. Variability of food intake patterns among population subgroups further confounds putting a precise number on trans fatty acid intakes.
Effect of Trans Fatty Acids or Hydrogenated Fat Relative to Cis Fatty Acids, Native Oil, or Saturated Fat on Plasma Lipid Levels Clinical Data
The data on trans fatty acid intake and plasma lipid levels are relatively consistent; trans fatty acids or hydrogenated fat result in higher plasma cholesterol levels than native oil and lower plasma cholesterol levels than more saturated fat.Effects on triglyceride levels are highly variable. These results have persisted despite the marked difference among study designs, levels of trans fatty acids consumed by study subjects, and the actual source of transfatty acids. Not withstanding these data, a pivotal study published in 1990 refocused attention on trans fatty acids from total cholesterol levels to effects on specific lipoprotein particles. When a relatively high level of a trans fatty acid, 11% of energy as elaidic acid (18:1 trans 9), was substituted for a cisfatty acid, oleic acid (18:1 cis 9), or a saturated fatty acid, stearic acid (18:0), total and low-density lipoprotein (LDL) cholesterol levels increased, whereas high-density lipoprotein (HDL) levels were comparable when the subjects consumed the oleic- or stearic acid-enriched diets. HDL levels were lower when they consumed the elaidic acid-enriched diet. These changes resulted in a less favorable total cholesterol/HDL cholesterol ratio. Using a similar study design but a lower level of transfatty acid, 7.7% of energy, this basic observation was made again. Subsequent confirmation of the independent effect of trans fatty acids on HDL cholesterol levels has been somewhat inconsistent. Variations in the level of trans fatty acids fed and whether a one-to-one substitution of a trans for a cis double bond containing fatty acid was made or hydrogenated fat was substituted for oil or butter has introduced critical variables into the experimental design, which may impact study outcome. The most recent plasma lipoprotein issue related to the effects of trans fatty acids is lipoprotein (a) (Lp[a]) levels. The majority of studies have reported that transfatty acid intake increases Lp(a) levels. A positive relationship has been reported between Lp(a) levels and risk of cardiovascular disease (CVD). Issues related to the magnitude of potential change in Lp(a) levels induced by transfatty acid intake and risk for disease need clarification.
Epidemiological Data
Data related to trans fatty acid intake and risk of developing CVD have been inconsistent. Beyond the usual caveats that association does not prove causation, difficulties inherent in estimating trans fatty acid intake, as detailed above, complicate interpretation of data. Data derived from food-frequency questionnaires and weighed records support a relationship between trans fatty acid intake and risk for CVD. More objective measures of transfatty acid intake, independent of reporting bias or data bank information such as plasma or adipose tissue levels, for the most part do not support an association between trans fatty acid intake and risk of CVD. How closely such measures truly reflect long-term food intake have yet to be adequately determined. Data on individual fatty acids suggest an association between risk of CVD and 16:1 trans, which comes to a great extent from animal sources, and not 18:1 trans,which comes to a great extent from hydrogenated fat. These data are opposite to the relationship between source of transfatty acids and disease risk suggested by the food-frequency questionnaire data, making it difficult to draw conclusions at this time.
Approaching the area of transfatty acid intake and CVD risk on the basis of epidemiological data is also difficult because of the potential for other dietary variables to confound the data. Although attempts are made to control for covariants, given the limitations in the information available and the very nature of dietary data, even the best attempts are somewhat limited.
Summary and Recommendations for Future Research Needs
Dietary trans fatty acids are derived from meat and dairy products and to a greater extent from products made from hydrogenated fat. Due to limitations in the data bank used to estimate the trans fatty acid content of food items, intake estimates in the United States are broad and somewhat dependent on the methods used to generate them. Before attempting to set guidelines for intake levels, it is imperative to standardize methods for determining trans fatty acid levels in food. Adequate and reliable information with which to assess current and future intake levels also must be available. Once these data are available, issues related to differences among positional isomers of trans double bond-containing fatty acids should be addressed.
Clinical studies have demonstrated that consumption of transfatty acids or hydrogenated fat result in higher blood cholesterol levels than consumption of cis fatty acids or naturally occurring oils. Relative to saturated fatty acids, trans fatty acids or hydrogenated fat result in lower blood cholesterol levels. Clarification is needed on issues related to the potentially detrimental effects of transfatty acids or hydrogenated fat compared with saturated fat with respect to decreasing HDL cholesterol levels and increasing Lp(a) levels alone and compared with their benefits in decreasing total and LDL cholesterol levels.
Data from epidemiological studies supporting a relationship between trans fatty acid or hydrogenated fat intake and risk for CVD are highly variable. Once again, difficulties inherent in estimating intake, especially long-term intake, are complicated, and those in use await validation. Establishing a relationship is further complicated by difficulties in teasing out confounding factors associated with all dietary data<.< />
On the basis of these data and reservations, it is prudent at this point to recommend that naturally occurring unhydrogenated oil be used when possible and attempts made to substitute unhydrogenated oil for hydrogenated or saturated fat in processed foods. Additionally, the recommendation to substitute softer for harder margarines and cooking fats seems justified.
How does one distinguish between the different stages of cardiovascular disease?
Which one? I have the Braunwald book of cardiovascular disease sitting on my desk right now and its about three inches thick. If you mean coronary artery disease then its the percentage of stenosis in the coronary arteries. THe heart lies anterior, inferior, sixty degrees to the left, thirty degrees from the horizontal in a typical biological patient with endless variation. There are three main arteries that sit atop the top heart. The right coronary which comes off of proximal aorta and feeds the right heart and inferior wall. The left main coronary artery also comes off the proximal aorta and supplies flow to the Left anterior descending or LAD and also the circumflex which truly normally feeds the inferior and posterior walls of the heart. The Left main thus feeds the majority of the heart and a blockage there is called a 'widowmaker'. The next worst blockage is an LAD stenosis b/c it feeds the left ventricle which is what pumps blood throughout the body and is much more muscular than the right heart. A myocardial infarction there prevents blood from reaching the rest of the body. LV function is what we use to look at mortality and morbidity. I calculate whats called the Ejection Fraction of the LV. Normal is 55-70% EF. Lower than that we just go by the percentage or more useful, I say it is normal, mildly reduced, moderately reduced or severely reduced left ventricular function. I do it by sight now that Ive seen thousands of hearts in an ultrasound test called an echocardiogram. There I look at the heart and see how well or poorly the heart or LV function is. So the answer to your question is I say mild, moderately or severely reduced function of the left ventricle to discuss ultimately the most important aspects of cardiac function. If you are talking CAD, then the only way to asssess the amount of stenosis in the artery is to do whats called an angiogram. This is where I take them to the cath lab and run a catheter directly into the coronary arteries, then inject a dye into them under fluoroscope(xray), this real time xraying, not a snapshot. There we can see a blackened picture of the dye within the artery denoting its shape and amount if any of obstructions. This is done by eyeball and assigned a percent stenosis, what artery and what location, ie the Lad mid 90% stenosis. If the lesion is that large we place a 'stent' in there which is a wire mesh stent and use a balloon to inflate the stent and reopen the artery. Its what Dick Cheney has had done several times. This is the treatment for severe CAD when possible. So, two different answers, LV function which may not be compromised yet or LV function post MI or during the progression of another issue such as cardiomyopathy or disease of the cardiac muscle. Also, the heart can be broken into at different basics. First off the electrical, this is the hearts rhythm, so they could have an arrhythmia, I read an EKG to see what the rhythm looks like and look at the form and structure of the electrical reading to classify what rhythm they are in. Then there is the plumbing, this is the coronary arteries, the arteries that feed the muscle the blood and just as important, carry away waste products from the muscle, this is what we are concerned with blockages. Then there are the structural components, the muscle. Diseases of the muscle can occur from various things, this affects the ability of the heart to contract, the muscle can be affect due to blockages of the arteries that feed it, lack of bloodflow cause death of the muscle or a heart attack as most think of it. But heart attack is broad and a fatal arrhythmia such as ventricular fibrillation can be included in that and VFIB can be as a result of irritated LV muscle from lack of blood flow so clearly all of these are interrelated and all can be discussed and differentiated. Then there are the valves that open and close, there are four of them. I look at how well they open but more often I look at how well they close or 'leak' called regurgitation, now they all leak to some degree and I classify it as mild moderate or severe by eyeball, sound subjective, it is. You can calculate it by doing an effective regurgitant orifice, but usually time consuming and doesnt offer much information so outside of universities its rarely done. So we mainly look at the left heart structures such as the aortic valve and how well it opens. You see older people can get calcification of the aortic valve called aortic stenosis. I use a calculation based on the velocities of blood prior to the valve and then the blood velocity after the valve to estimate the valve area. Thats used to say once again, mild,mod or severe aortic stenosis. Then I look at the mitral valve which is between the left ventricle and the left atrium, I look at doppler color flow analysis to see the size and shape of the regurgitant jet and describe it as mild, mod, or severe or trace mitral regurgitation. You see, there is a whole list of things that I evaluate in describing the function of the heart and its state of health. So when you say cardiovascular disease. Disease states can occur throughout all of the structures of the heart, so your question implicitly lacks specificity in order to answer. Clearly you do not know much about the heart. I figure you'd want to start with something simple such as what are heart palpitations, but more than you are challenging my knowledge of the heart which is my profession so you will fail at that. I think that about covers what I need to say about disease states until you come up with a better more specific question rather than openended silliness.
During the last stage of cardiovascular disease, if you were to happen upon someone what would be your method of treatment? This person has been lying around "coping" with their condition for years without treatment and they happen upon your treatment facility. What do you do? What is the short term fix for a long term problem?
Depends again on what disease state you speak of. Once a person's heart muscle is dead, its dead, there's no coming back from that. You see it as a section of heart that doesnt move. Nothing you can do. Now if its cardiomyopathy and you know whats causing it such as alcoholic cardiomyopathy the solution might be as simple as having the person cease alcohol consumption and the heart over months returns to normal contractility. For other reasons there are medications that can aid "somewhat" in contractility. It all depends on what you are talking about.
It's not as simple as using roto-rooter on their arteries to clear out the plaque.....but you've got to do something drastic, right?
err, we dont roto rooter anymore, we use stents. Depends on what you are referring to, if its a significant blockage then you open it up, itd be malpractice not to use a stent and reopen a significant lesion. If its prior to the point of needing stenting then you have them increase exercise, diet and precriptions such as statins and other blood lipid profile things. It all depends on what disease state you are talking about where something drastic has to be done. If you are talking poor function due to a myocardial infarction, then there is nothing you can do. The heart muscle is already dead, the horse is already out of the barn at that point. Your questions really do lack specificity enough to clearly answer. There are thousands of diseases of the heart, from electrical such as long QT syndrom, to muscular, cardiomyopathy, to valvular, aortic stenosis mitral regurgitation, to plumbing, coronary artery disease. There is no "ONE" cardiovascular disease and there are many overlaps depending on the criteria listed. I use a system to write my diagnosis commenting on several things.
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