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May 03, 2011

A Diet For Long-Term Weight Control And Optimal Health Part 5 - The Role of Modern Fats in Heart Disease, Cancer, and Obesity

HeaderPicJan11 In the early days of nutritional research, fat was seen as little more than a dense source of caloric energy.  Only when the biological activity of certain classes of fatty acids began to be investigated, did it become clear that some fatty acids play fundamental roles in cellular communication – including immune function, inflammation, reproduction, and cellular growth.

It was found that certain essential fatty acids acted as precursors for a wide range of inflammatory and immune–related chemicals called eicosanoids.  In the decades since this discovery was made, the breathtaking complexity of fatty acid metabolism has become a major focus of biological research.  Even today, however, the practical application of this research is still in its infancy.

The scientific and medical communities are still armed with little more than the most basic understanding of fatty acid metabolism, yet public health authorities have had a major hand in influencing the fatty acid intake of the American diet for decades.  Largely ignoring the overall nutrient composition of healthy traditional diets, modern authorities have advocated various unprecedented patterns of fat intake.  Saturated fats from meat, dairy and tropical oils were, and continue to be, demonized as contributors to heart disease.  The recommendation to consume polyunsaturated vegetable oils and vegetable oil–based margarine is still sometimes made, though it has gradually given way to the advice to consume more monounsaturated fats such as those found in olive oil.  Today, omega–3 fatty acid supplements like fish oil have largely received the approval of mainstream and “alternative” medical practitioners alike.  As a whole, however, such imprecise recommendations have largely failed to improve public health, and are instead likely to be causing unique and unprecedented health disturbances.  Numerous controlled and epidemiological studies show that, even in surprisingly low amounts, the omega–6 fatty acid, linoleic acid may be a powerful contributor to heart disease, cancer, and obesity.  From the research, it’s reasonable to conclude that the optimal dose of linoleic acid for adult humans is near or below 2% of calories.  At this intake of linoleic acid, the omega–6–to–omega–3 fatty acid ratio of the diet will automatically be lowered, meaning that only minute amounts of omega–3 fats will suffice to properly balance the production of linoleic acid–derived inflammatory eicosanoids.  Low overall intakes of PUFA (polyunsaturated fatty acids, omega–3 and omega–6) will also result in less harmful oxidative damage to these lipids in vivo.

Because even a small change in the fatty acid composition of the diet can have a profound biological impact, health–conscious people will be well served to calculate the amount, and relative ratios of certain fatty acids in their diet.  Though the concepts of omega–6 and omega–3 “essential fatty acids” are widely bandied about in food and supplement marketing, the overwhelming majority of people (even those who take fatty acid supplements) have no idea what amount of these fatty acids they’re taking in, or what amounts (and ratios) are likely to be needed for optimal health.

Judging by the research, it’s likely that the first fundamental guiding principle of healthy fat intake is to reduce linoleic acid consumption to as low a level as is reasonably possible.

Excess Linoleic Acid and Heart Disease

Though historically hypothesized to reduce the risk of cardiovascular disease by lowering serum cholesterol and triglyceride levels, vegetable oils rich in linoleic acid have often proven harmful when incorporated into the diet as a replacement for the more–saturated (and less chemically–reactive) animal fats.  In the 1960’s, a two–year study of individuals with existing heart disease investigated the use of corn oil (containing ~59% linoleic acid) as a replacement for animal fat.  In contrast to expectations at the time, the corn oil–users fared worse than those eating a standard diet.  The study found that the percentage of corn–oil users remaining alive and free of heart attack at the end of two years was 52%.  In the control group eating their regular diet, this number was 75%:

Study Link – Corn oil in the treatment of ischaemic heart disease.

Quote from the above study:

The patients receiving the key treatment (corn oil) fared worse than those in the other two groups: two years from the start of treatment infarction or death had occurred in one quarter more of the corn–oil than of the control group… It is concluded that under the circumstances of this trial corn oil cannot be recommended as a treatment of ischaemic heart disease. It is most unlikely to be beneficial, and it is possibly harmful.

Numerous studies in the scientific literature show that corn oil may contribute to heart disease and cancer, but it’s especially interesting to note that one group in the above study replaced animal fat with olive oil – an oil widely promoted for its health benefits.  The percentage of this group remaining alive and free of heart attack after two years was 57% — a result remarkably similar to that of corn oil, and far below the 75% in the control group.  Olive oil contains far less linoleic acid than corn oil (~10%), and does contain some protective polyphenols, but this study suggests that it’s incorporation into the diet in high amounts (or at the expense of animal–based lipids) may not necessarily reduce the rate of heart attack or mortality.

Such research may be particularly meaningful, as many health–conscious people today avoid industrial vegetable oils and opt for olive oil for home–cooking uses.  This is generally a beneficial trend, but it may not necessarily be enough to reduce heart disease risk in the Western world.

The scientific literature on the role of certain fats in heath and disease can often seem contradictory – many studies show olive oil, for example to have a beneficial impact on markers of health, levels of disease, or mortality.  Other studies (like the one above), show the opposite.  Similarly contradictory findings can be found for many sources of fats including fish oils, and saturated fats from meat or dairy.  Clearly, there’s a level of complexity which is largely being ignored by public health authorities in their determinations of what constitute “healthy” and “unhealthy” fats.

Though it’s rarely stated explicitly, the most important factor in engineering a healthy fat intake is that the overall amount of PUFA in the diet be kept low.  It’s probably also important that the omega–6–to–omega–3 ratio of our diet be lowered to one mimicking traditional diets.  It’s uncertain exactly what ratio is optimal, but this is a secondary issue, as lowering the overall PUFA intake will automatically lower the omega–6–to–omega–3 ratio to a more balanced level.  Keeping these factors in mind helps to explain some of the seemingly contradictory findings in the scientific literature relating to dietary fat.

Olive oil is a part of traditional and healthy diets in the Mediterranean region, but unlike the American diet, these diets are also low in other sources of omega–6 linoleic acid.  The fish consumed in the Mediterranean region is also likely to contribute small, but meaningful amounts of omega–3 fatty acids to the diet, thus lowering the omega–6–to–omega–3 ratio.  In other words, in our culture, it’s still entirely possible for both the overall level of linoleic acid, and the omega–6–to–omega–3 ratio of the diet to remain dangerously elevated despite the regular use of olive oil.

The Mediterranean Diet

Beginning in the late 1950s, researcher Ancel Keys began a large–scale study of dietary patterns in relation to cardiovascular disease.  More than 12,000 men of Finland, Greece, Italy, Japan, Holland, the United States, and Yugoslavia were studied in what was called The Seven Countries Study.  Ultimately, men of Finland and the United States had the highest rates of heart disease, whereas men from Mediterranean countries and Japan had the lowest.

Interpreting the results of this study led many researchers to advocate a Mediterranean–style diet with particular emphasis on foods like olive oil, fish, and red wine.  Of course, the average American’s conception of the Mediterranean Diet is often quite different than the health–promoting diet actually consumed in traditional Mediterranean cultures.  The true Mediterranean diet is a varied mixture of nutrient–rich and minimally–processed foods, and while some of these foods may have become accepted into American culinary culture, it’s naïve to think that these foods, alone, will confer the benefits of the overall Mediterranean diet.  Case in point, the widespread use of olive oil among health–conscious Americans is certainly a beneficial trend relative to the use of many other types of industrial vegetable oils, but it can hardly be expected to act as the sort of magical cardio–protective elixir it’s often made out to be.  We find a similar scenario with the currently–fashionable use of fish oil supplements.

Often, when meaningful research such as the Seven Countries Study is distilled through the filter of the popular media, the only messages that survive are messages geared towards selling products (buy olive oil, buy fish oil, buy red wine, buy resveratrol pills, etc.). The benefits of the Mediterranean diet, however, are likely to stem from a wide variety of nutrient–rich foods.  More importantly, what the Mediterranean diet lacks may be equally as important as what it contains.

If the actual Mediterranean diet (and not just isolated aspects of it), does reduce heart disease risk, it’s important to investigate which aspects of the diet are most responsible.  Recent controlled studies (where diets were purposefully manipulated to test the effects) have shed even more light on the issue.  One such study is the Lyon Diet Heart Study – one of the most successful dietary interventions ever conducted in terms of reducing cardiovascular and overall mortality.

In the study which took place in Lyon, France, 605 men and women with pre–existing heart disease were instructed to follow either a control diet similar to the one advocated by the American Heart Association (i.e., < 30% fat, < 10% saturated fat) or a “Mediterranean” diet defined as “low in total fat and saturated and omega–6 fatty acids, but rich in omega–3 fatty acids, oleic acid, fiber, antioxidants, vegetable proteins, and vitamins of the B group.”

The effects of consuming the Mediterranean diet were so favorable, that what was to be a five–year study was halted after 27 months (when an intervention is so clearly effective, it’s deemed unethical to continue it for the benefit of the control group not receiving the treatment, or in this case, diet).   

Article Link – Dietary Prevention of Coronary Heart Disease.  The Lyon Diet Heart Study.

Quote from the above study:

The initial report was published in Lancet in 1994 after the study was terminated by its Scientific and Ethics Committee at 27 months mean follow–up time of what had been planned as a 5–year study, because the benefits in the experimental group at that time were so favorable.

Study Link – Mediterranean Diet, Traditional Risk Factors, and the Rate of Cardiovascular Complications After Myocardial Infarction Final Report of the Lyon Diet Heart Study.

All told, the specifically–constructed Mediterranean diet was associated with a 76% reduction in cardiovascular deaths, and a 70% reduction in overall mortality.

As relates specifically to lipids, the experimental diet in the above study was characterized by the use of olive oil and a canola oil–based margarine to replace butter.  Participants in this study did, therefore consume more monounsaturated oleic acid (from olive oil) and a slightly higher amount of omega–3s (from canola oil). However, it’s notable that they also consumed significantly less linoleic acid than the control group.

The graphic below shows that the linoleic acid content of the Mediterranean diet was 3.6% of calories – significantly less than the 5.3% in the control group. As we shall see, many of the detrimental effects of linoleic acid may begin to manifest when this fatty acid comprises above 4% of the diet.

In addition to olive oil consumption, the Mediterranean diet is also characterized by fish (and therefore, omega–3 fatty acid) consumption.  The omega–3 linolenic acid content of the experimental diet, at 0.84% was slightly higher than the 0.29% of the control group.  This 0.84% translates into 1.8 grams of omega–3 per day in a 1,947 calorie–per–day Mediterranean diet – an amount of omega–3s easily obtainable on any diet of whole foods.  Despite marketing efforts to the contrary, this study does not provide evidence of the need for omega–3 supplementation – as such supplementation may increase the omega–3 percentage of the diet to historically unprecedented and potentially harmful levels. What it does provide is evidence for a diet low in linoleic acid – an environment in which trace amounts of dietary omega–3s are then able to function optimally.  This is the same principle at work in numerous healthy traditional diets, as we saw in the previous edition of the Integrated Supplements Newsletter.

Damage to PUFAs in Heart Disease

Why shouldn’t an excess of omega–6 fatty acids like those found in the modern American diet be “balanced out” with additional omega–3s as is often advocated by the sellers of omega–3 supplements?  The reason has to do with the chemical instability of both omega–6 and omega–3 fatty acids.  We’ll delve into this topic in greater detail in subsequent Integrated Supplements Newsletters, but for now, we’ll look at how the chemical instability of polyunsaturated oils has major implications for heart disease.

The ability of polyunsaturated fats to increase heart disease risk is easier to understand with a bit of knowledge of the chemical structure of fatty acids.  In molecules of saturated fatty acids, each carbon atom is attached to as many hydrogen atoms as its chemical nature can support.  In other words, the carbon atoms are “saturated” with hydrogen atoms.  By contrast, unsaturated fatty acids contain double–carbon bonds in their structure.  When these double bonds are formed, hydrogen atoms are eliminated, so the carbon atoms aren’t saturated with hydrogen as they are in saturated fatty acids.  As their names suggest, monounsaturated fatty acids contain one double bond whereas polyunsaturated fatty acids contain more than one double bond.  Each double bond in a fatty acid’s structure is chemically reactive; and though this chemical reactivity gives unsaturated fats important biological functions, it also makes them prone to damage when spontaneously reacting with other substances such oxygen.

Generally, the greater the amount of unsaturated lipids in the diet (and therefore body’s tissues), the more fragile and easily damaged all tissues of the body become.  This is one reason why excess PUFA consumption has implications for heart disease and all other age–related disorders.

Heart disease mortality in the U.S. reached its peak between 1950 and 1975 – a time in which saturated and animal fat consumption decreased, at the same time unsaturated vegetable fat consumption increased significantly.  Vegetable oil proponents (and purveyors) likely over–emphasized the ability of vegetable oils to lower serum cholesterol.  Not only is this effect short–lived, but serum cholesterol is a remarkably poor indicator of cardiovascular risk to begin with.  A far more important indicator of cardiovascular risk may be the tendency of cholesterol–carrying lipoproteins to oxidize.

As their name suggests, lipoproteins are proteins which contain lipid structures.  They often serve to transport fat soluble lipids such as cholesterol through the watery environment of the blood.  Fats in the diet directly influence the lipid composition of lipoproteins, and the ingestion of lipids which are prone to oxidative damage (i.e., PUFAs) create lipoproteins which are prone to oxidative damage as well.

Oxidized low density lipoprotein (oxLDL) has been shown to attract immune cells, called macrophages, to the vascular intima.  These macrophages engulf oxidized (and only oxidized) products of LDL , which leads to the production of foam cells and the eventual development of atherosclerotic plaque characteristic of heart disease. Where polyunsaturated fatty acids of the omega–6 and omega–3 class are both inherently prone to spontaneous oxidation due to the double bonds in their structure, the consumption of each is associated with increased levels of oxidized LDL :

Study Link – Dietary polyunsaturates and peroxidation of low density lipoprotein.

Quote from the above study:

Omega–6 polyunsaturated fatty acids enhance the susceptibility of low density lipoprotein to oxidation compared with monoenes [monounsaturated fatty acids]. Most studies on omega–3 fatty acids also exhibit increased peroxidation of low density lipoprotein, although these data are more conflicting.

In studies where saturated fat was replaced with canola oil and sunflower oil (including low–trans–fat margarine made from these oils), levels of oxidized LDL and another cardiovascular disease risk marker, lipoprotein(a), both increased – even though the diet was high in antioxidants:

Study Link – Changes in Dietary Fat Intake Alter Plasma Levels of Oxidized Low–Density Lipoprotein and Lipoprotein(a).

Quote from the above study:

In conclusion, we found that a diet traditionally considered to be anti–atherogenic (low in saturated fat and high in polyunsaturated fat and naturally occurring antioxidants) increased plasma levels of circulating oxidized LDL and Lp(a).

In the above study, the dietary changes made were not extreme.  Compared to baseline intakes, the two study groups decreased their saturated fat intake from 15% to between 9.5% and 11% of overall calories.  The two study groups also increased their polyunsaturated fat intake from 6% to between 7% and 9.5% of overall calories.

In the Mediterranean diet of the Lyon Diet Heart study, omega–3 lipids from canola oil were added to the diet as they were in the above study.  However, unlike the above study, the overall PUFA intake in the Lyon Diet Heart Study was under 5% of calories.  In the above study, the overall PUFA intake was between 7% and 9.5% of calories.  The Lyon Diet Heart Study was associated with reductions in cardiovascular and overall mortality, yet the above study found increased markers of cardiovascular risk.  Together, these studies provide evidence that increasing the PUFA intake of the diet (from either omega–6s or omega–3s) is likely to have negative consequences once a certain threshold is crossed.

Note: It’s important to note that the harmful effects of polyunsaturated oils in the above study were probably not due to trans fats, as the study specifically indicates that low–trans–fat oils were chosen.  Trans fats are created when unsaturated oils are chemically stabilized (as by hydrogenation) to give liquid oils different physical characteristics (i.e., the ability to be spread, as in margarine, or the ability to withstand cooking temperatures as in vegetable shortening).  With the recent backlash against trans fats, many consumer products are currently promoted on the basis that they are trans fat–free, but the toxicity and metabolic destruction caused by the unsaturated oils isn’t necessarily a function of trans fats.  It’s the chemically–reactive double bond in the structure of unsaturated fatty acids which is largely responsible for their toxicity.  As such, even fresh, “unrefined,” or “cold–pressed” sources of polyunsaturated fatty acids are liable to cause damage when consumed in excess.  When the diet contains a high amount of polyunsaturated fats, there is simply no practical way to avoid the spontaneous oxidative damage these lipids undergo in the human body – even in the presence of an antioxidant–rich diet.

Excess Linoleic Acid and Cancer

Though excess linoleic acid is likely to play a role in the development of heart disease, a more major concern may be the fatty acid’s ability to cause or support the development of cancer.

Multi–year studies in which animal fats were replaced with unsaturated oils showed some benefit with regard to cardiovascular mortality, but no benefit with regard to overall mortality.  This is likely to be because groups consuming polyunsaturated oils experienced a greater incidence of fatal cancer:

Study Link – Incidence of cancer in men on a diet high in polyunsaturated fat.

Quote from the above study:

…total mortality was similar in the two groups: 178 controls v. 174 experimentals, demonstrating an excess of non–atherosclerotic deaths in the experimental group.  This was accounted for by a greater incidence of fatal carcinomas in the experimental group.

Many animal studies clearly show that linoleic acid increases cancer risk.  In the following study, even 5% of calories as linoleic acid increased the development of chemically–induced colon cancer in rats:

Study Link – Effect of Dietary Unsaturated and Saturated Fats on Azoxymethane–induced Colon Carcinogenesis in Rats.

Quote from the above study:

The rats were fed two types of semipurified diets consisting of 5% linoleic acid or 4.7% stearic acid plus 0.3% essential fatty acid as dietary fats. The rats were treated with azoxymethane (7.4 mg/kg body weight) s.c. once a week for 11 weeks and sacrificed 15 weeks after the last injection of the carcinogen. The rats fed unsaturated fat diet demonstrated a significantly higher incidence of colon tumors [100%], more tumors per rat [2.68 ± 1.60 (S.D.)], and greater malignant differentiation histologically than did those fed saturated fat diet [76%, 1.79 ± 1.59, respectively].

And similarly:

Study Link – The essential fatty acid requirement for azoxymethane–induced intestinal carcinogenesis in rats.

Quote from the above study:

Large bowel tumor incidence showed a dependence on the essential fatty acid content of the diet.

In the following study, human breast cancer cells implanted into mice grew and metastasized to a greater extent when mice were fed a diet containing 12% linoleic acid versus a diet containing 2% linoleic acid:

Study Link – Effects of Linoleic Acid on the Growth and Metastasis of Two Human Breast Cancer Cell Lines in Nude Mice and the Invasive Capacity of These Cell Lines in Vitro.

Quote from the above study:

…the mean weight of mammary fat pad MDA –MB–231 cell tumors in 12% LA–fed mice was significantly higher (6.7 ± 1.4 g) than that of the mice fed 2% LA; also, it was higher than that of MDA–MB–435 cell tumors in the 12% LA–fed mice (3.6 ± 0.1 g) or the 2% LA–fed mice (3.3 ± 0.1 g) (each P < 0.001). Mice fed the 12% LA diet had a higher incidence of grossly visible MDA–MB–435 cell pulmonary metastatic nodules than those fed the 2% LA diet (67% versus 33%; P < 0.02), more metastatic lesions (5.7 ± 1.6 versus 2.3 ± 0.8; P < 0.05), and greater total volumes (62.0 ± 25.9 versus 24.8 ± 9.0 mm3; P < 0.02) per mouse.

Studies in rats have found that the maximal cancer–promoting dose of linoleic acid was 4.4% of the diet by weight, which amounts to approximately  8% of the diet when measured as a percentage of calories:

Study Link – Requirement of essential fatty acid for mammary tumorigenesis in the rat.

Quote from the above study:

Mammary tumorigenesis was very sensitive to linoleate intake and increased proportionately in the range of 0.5 to 4.4% of dietary linoleate. Regression analysis indicated that a breakpoint occurred at 4.4%, beyond which there was a very poor linear relationship, suggesting the possibility of a plateau. From the intersection of the regression lines in both the upper and lower ranges, the level of linoleate required to elicit the maximal tumorigenic response was estimated to be around 4%.

In an animal study which may have particular relevance for human nutrition, the following rat study found that when corn oil exceeded 3% of the diet, any subsequent increase in total fat intake caused tumors to develop more quickly.  When corn oil comprised less than 3% of the diet, however, the development of tumors was slowed, and there was a decrease in the overall incidence of tumor development:

Study Link – Dietary lipid effects on the growth, membrane composition, and prolactin–binding capacity of rat mammary tumors.

Quote from the above study:

Our results indicated that 1) when the polyunsaturated lipid component (corn oil) of the diet exceeded 3%, it was the quantitative level of total lipid, rather than the level of polyunsaturated lipid alone, that best correlated with the observed reduction in tumor latent period; 2) when the polyunsaturated lipid content of the diet fell below 3%, there was a decrease in tumor incidence and an increase in the mean latent period.

Remember that the amount of linoleic acid in the average American diet is approximately 9% of calories.  From the above studies, it’s clear that the dose of linoleic acid which has repeatedly been shown to maximize cancer development in laboratory animals is significantly less than the dose of linoleic acid consumed in the typical American diet.

In animal studies of cancer like those above, cancer cells or cancer–causing chemicals are injected, and the diet can be meticulously controlled to examine the effects of different types of diets on the subsequent development of cancer.  For ethical reasons, of course, human studies can’t involve the induction of cancer.  This is why human studies of cancer must rely on epidemiological data – population data which, in the realm of nutritional science, examines how populations generally eat, and relates this to their overall incidence of cancer or other disorders.  Hypotheses are then formed about the association between nutrient status and the development of disease.

Some studies have shown evidence that omega–6 linoleic acid is associated with cancer in humans.  The following study even found that the relatively stable fats from dairy were protective against prostate cancer in smokers:

Study Link – (n–6) PUFA Increase and Dairy Foods Decrease Prostate Cancer Risk in Heavy Smokers.

But although many animal studies clearly show that linoleic acid increases cancer incidence, human studies are far more equivocal.  In human studies, overall fat intake is more closely associated with cancer incidence than is linoleic acid intake per se.  But, from the  rodent studies above, we can see that as little as 3–5% of dietary calories as linoleic acid is sufficient to increase cancer incidence, whereas 2% did not.  In industrialized human populations, however, it’s rare to find any significant number of people not consuming at least 3–5% of their daily calories from linoleic acid.  In humans, as in the rat study previously mentoned, it’s likely that once a certain threshold of linoleic acid is reached in the diet, any subsequent increase in fat intake increases cancer risk.

Using the diet of traditional cultures (for whom cancer incidence is low) as a guide, we may want to construct our diet to contain ~2% linoleic acid.  All evidence suggests that this dose easily prevents omega–6 deficiency, and lower doses than this are quite difficult to achieve on any whole–food diet.

From the accumulated research, we can see clear evidence that unprecedented intakes of polyunsaturated fats in industrialized nations may predispose us to increased incidence of heart disease and cancer.  Yet the related disorders of industrialization, obesity and diabetes, may also owe much to our uniquely high polyunsaturated fat intake.

Multigenerational Effects of Excess PUFA in Obesity

Long–term studies in which unsaturated fats replaced saturated fats in the diet clearly show that the fatty acid composition of the body’s tissues changes commensurately.  Logically, a greater amount of chemically–unstable and pro–inflammatory lipids in the body’s tissues can set the stage for major metabolic disruption.  The following study is one of the few in the scientific literature which investigated the long–term (up to five years) effects of replacing saturated fats with polyunsaturated fats:

Study Link – Composition of lipids in human serum and adipose tissue during prolonged feeding of a diet high in unsaturated fat.

In the above study, elderly men consuming increased amounts of PUFA exhibited serum lipids (i.e., triglycerides and lipoproteins) in which linoleic acid was incorporated commensurately with dietary intake (thus predisposing these blood lipids to increased oxidation as seen earlier).  By the end of five years, the linoleic acid content of adipose tissue had risen from 11% at the start of the study to 32% – in essence, building a nearly limitless storehouse of this inflammatory lipid.  The high–PUFA group was shown to gain weight compared to those eating the normal diet (those eating the normal diet actually lost weight).  While there’s reason to believe that their higher PUFA intake inhibited metabolism somewhat, the degree of weight gain in the high–PUFA group wasn’t remarkably pronounced.  There are several additional factors to consider, however, when investigating the role of polyunsaturated lipids in causing weight gain.

This study was conducted on elderly men, and was published in 1966 – the men in this study were born, and experienced their formative years, before the massive influx of PUFA into the American food supply.  It’s quite likely that a high–PUFA intake during childhood may fundamentally alter metabolic rate and increase the propensity to gain fat in the long–term.

As evidence, It’s helpful to investigate what happens when animals are fed high–PUFA, or high omega–6 diets in the long–term – including their formative years when adipocyte number (and subsequent risk of obesity) is largely determined.

Studies have found that different dietary lipids can influence the rate of weight gain, even independent of caloric intake.  Rats fed beef tallow (a source of saturated and relatively stable fats) exhibited less weight gain than those fed either olive oil or safflower oil.  All groups were also fed omega–3 fats from linseed (flaxseed) oil, and only in the rats fed beef tallow was the incorporation of these omega–3s into tissue phospholipids not inhibited.  This is further evidence that linoleic acid intake must be kept low in order for omega–3s to exert their beneficial effects:

Study Link – Dietary Lipid Profile Is a Determinant of Tissue Phospholipid Fatty Acid Composition and Rate of Weight Gain in Rats.

Quote from the above study:

Despite isocaloric feeding, weight gain was lower (P < 0.001) in rats fed the more highly saturated ET–L diet (69 ±8 g) than in those fed either the high (n–9) fatty acid OL–L diet (93 ±2 g) or the high (n–6) fatty acid SAF–L diet (108 ±4 g).

In adulthood, fat cells can expand to hold more lipids, but the overall number of fat cells remains largely constant.  It’s during gestation and early childhood that the quantity of the body’s fat cells is largely determined.  Linoleic acid appears to stimulate the production of fat cells at this critical time in development, and animals exposed to large amounts of linoleic acid during gestation and lactation appear to be particularly prone to obesity:

Study Link – Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern?

Quote from the above study:

During the pregnancy–lactation period, mother mice were fed either a high–fat diet rich in linoleic acid, a precursor of arachidonic acid (LO diet), or the same isocaloric diet enriched in linoleic acid and alpha–linolenic acid (LO/LL diet). Body weight from weaning onwards, fat mass, epididymal fat pad weight, and adipocyte size at 8 weeks of age were higher with LO diet than with LO/LL diet. In contrast, prostacyclin receptor–deficient mice fed either diet were similar in this respect, indicating that the prostacyclin signaling contributes to adipose tissue development. These results raise the issue of the high content of linoleic acid of i) ingested lipids during pregnancy and lactation, and ii) formula milk and infant foods in relation to the epidemic of childhood obesity.

Similar evidence from animal studies suggests that the obesity–inducing effects of omega–6–rich oils may even increase across generations.  Animals fed vegetable oils produce offspring which are more apt to have both larger and more numerous fat cells and greater fat mass, even with no change in caloric intake.  Several generations of such feeding has been shown to result in offspring exhibiting marked obesity.  If even a similar phenomenon occurs in humans, this would go a long way towards explaining the rapidly increasing rate of obesity (especially childhood obesity) found in recent decades:

Study Link – A Western–like fat diet is sufficient to induce a gradual enhancement in fat mass over generations.

Quote from the above study:

Offspring showed, over four generations, a gradual enhancement in fat mass due to combined hyperplasia and hypertrophy with no change in food intake.

Study Link – Fatty acid composition as an early determinant of childhood obesity.

Quote from the above study:

…changes over decades in the fatty acid composition of dietary fats observed in breast milk and formula milk, i.e. a high increase in [linoleic acid] with slight or no change in [linolenic acid], may be responsible, at least in part, of the dramatic increase in the prevalence of childhood overweight and obesity.

Researchers involved in the above studies have thus postulated that our unique fatty acid intake may have much to do with dramatic increases in the prevalence and degree of obesity in industrialized countries.  The role of linoleic acid as a precursor to various inflammatory and proliferative signaling molecules has been noted, as has the historical over–estimation of the true human linoleic acid requirement:

Study Link – An emerging risk factor for obesity: does disequilibrium of polyunsaturated fatty acid metabolism contribute to excessive adipose tissue development?

Quote from the above study:

Recent human and animal studies suggest that by altering rates of adipocyte differentiation and proliferation, differences in the composition of dietary fat may also contribute to adipose tissue development. At least in rodent models, the relative intake of n–6 to n–3 PUFA is clearly emerging as a new factor in this development …One factor potentially contributing to oversight about the apparent role of dietary n–6 PUFA (especially excess dietary linoleate) in adipose tissue development is the historical overestimation of linoleate requirements and the enthusiasm for higher intake of 'essential fatty acids'. More research is needed to address whether disequilibration of dietary PUFA intake contributes to the risk of obesity in humans.

In the next edition of the Integrated Supplements Newsletter, we’ll examine more ways in which an excess of linoleic acid and other polyunsaturated fats may cause major metabolic disruption.  We’ll see how a diet containing low levels of polyunsaturated fats may be particularly beneficial for various health concerns, and we’ll examine practical aspects of analyzing and constructing a low–PUFA diet.

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