The Whole Fat Story: Exposing The Myth That Fat Makes You Fat, Raises Cholesterol, Blocks Arteries, And Causes Heart Disease
Dietary fat, and especially saturated fat, has become a controversial and deeply misunderstood issue.
Despite being an integral and essential dietary element for every animal and mammal, including humans, over the course of evolution, since the 1950’s public awareness and understanding of the issues surrounding fat intake and its effects on health have changed dramatically.
Despite an astounding lack of supporting scientific evidence, and any attempt to explain the nuance of this is at times a complex issue, the food industry, government, and organised medicine have demonised dietary fat to the extent that in Western society, fat has come to be perceived not only as undesirable, but detrimental and even dangerous to human health.
After all, everyone (including the government and your medically qualified doctor) knows that eating fat will make you fat, raise your cholesterol, clog your arteries, and cause heart disease.
So how did something that has always been, and remains, an essential element of the human diet come to be viewed by large sections of the population in this way?
The trouble with powerful, popular, myths is that once established, and especially when validated by powerful individuals, institutions and industry which enjoy positions of authority and trust in our society, they can become very difficult to displace, even in the face of the available evidence.
Winding the clock back on human evolution perhaps provides an interesting vantage point from which we can start to think about historical and evolutionary human nutrient intake.
The human genome has changed 0.02% in the last 40,000 years, and our genetics have changed little in the past 120,000 years.
It seems reasonable to suggest that given relatively recent changes in nutrition and lifestyle as a result of our recent shift to modernity (recent in terms of human evolution), a discordance exists between our genetically determined biology, and modern nutrition and lifestyle factors.
At the same time, modern populations leading a ‘Western’ existence have exhibited a rapid increase in mortality from conditions which have been absent, or have not been significantly evidenced, at any other point in human history.
A 2004 paper notes:
“There is growing awareness that the profound changes in the environment (eg, in diet and other lifestyle conditions) that began with the introduction of agriculture and animal husbandry ≈10000 y ago occurred too recently on an evolutionary time scale for the human genome to adjust. In conjunction with this discordance between our ancient, genetically determined biology and the nutritional, cultural, and activity patterns of contemporary Western populations, many of the so-called diseases of civilization have emerged. In particular, food staples and food-processing procedures introduced during the Neolithic and Industrial Periods have fundamentally altered 7 crucial nutritional characteristics of ancestral hominin diets:
1) glycemic load
2) fatty acid composition
3) macronutrient composition
4) micronutrient density
5) acid-base balance
6) sodium-potassium ratio
7) fiber content
The evolutionary collision of our ancient genome with the nutritional qualities of recently introduced foods may underlie many of the chronic diseases of Western civilization”. 
In historic hunter-gatherer societies, evidence suggests[4,5]a macronutrient profile of:
A 1984 study evaluated the caloric intake of Australian aboriginals who returned to a traditional hunter-gatherer lifestyle, following them through a number of geographical settings, noting a macronutrient profile of:
The variability of macronutrient intake is reflective of the availability of food sources based on the immediate geographical environment, and is indicative of the fact that rather than there being a one size fits all macronutrient profile that is suitable for a population or particular individual, human metabolism is both complex an flexible – over short periods of time at least.
So if bone isotope, and more recent ethnographic studies, suggest that fat intake has been higher throughout human evolution than current government guidelines suggest is healthy, what changed, and how is this linked to current research on the impact on human health?
Two trends present themselves; the modern politics of fat, and new fats which have been introduced to the human diet for the first time.
The politics of fat, and especially saturated fat
The politicisation of saturated fat (leading to the politicisation of fat in general) began in earnest in 1953, when Ancel Keys, Ph.D, a physiologist, published a paper entitled ‘Atherosclerosis, a Problem in Newer Public Health’.
Keys hypothesised that fat intake was directly correlated with the incidence of heart disease. His data, looking at fat intake and heart disease mortality in the United States, Canada, Australia, England, Italy, and Japan, appeared to prove his hypothesis to be correct.
The trouble is that Keys selectively picked his data to match his hypothesis.
In 1957, a biostatistician named Jacob Yerushalmy, along with Herman Hilleboe, published a paper noting that while data from the six countries analysed supported Keys’ hypothesis, Keys had actually collected data from 22 countries, and that when the data from all 22 countries was analysed, the apparent link between fat intake and heart disease was not found.
In fact, by selectively analysing data from six other countries Keys collected data from, Yerushalmy and Hilleboe showed that the incidence of mortality from heart disease decreases with higher fat consumption:
Further, Keys did not show direct causality between fat intake and heart disease in the six countries he did select, only a correlation (it was an epidemiological study). As well as eating more fat than their Japanese counterparts, were Americans engaging in other activities that led to increased mortality from heart disease, such as consumption of sugar and refined carbohydrates, and a more sedentary lifestyle?
Crucially, such factors were not analysed.
Nor, at the time, was Keys’ hypothesis the only theory behind rising heart disease mortality. In 1957, John Yudkin, a British physiologist, put forward the theory that dietary sugar was to blame for rising mortality from heart disease.
However, while Yudkins research was left unpublicised, Keys was popularised, as evidenced on the Jan 13th 1961 Time magazine cover:
Keys study was seized upon by the sugar industry and wider food industry. Low sugar guidelines presented a disaster for a burgeoning processed, high sugar food industry, low fat presented an opportunity for a whole new range of manufactured products.
Then in 1970, Keys published his Seven Countries Study, which suggested that in the seven countries selected (the United States, Japan, Italy, Yugoslavia, Greece, the Netherlands and Finland), animal fat intake was a predictor of the incidence of heart attacks. Importantly, Keys also noted a correlation between total cholesterol and heart disease mortality, which led him to conclude that intake of saturated animal fat, rather than other fats, lead to raised levels of total cholesterol and therefore lead to heart disease.
Again, this study was epidemiological in nature, and the data was far from convincing in suggesting a causative link between saturated animal fat and heart disease.
For a start, there is a suggestion that Keys biased the study design by selecting countries he knew would support his hypothesis.
Even given that possibility, Yugoslavia, Greece and Finland showed poor correlation, and the incidence of heart disease, and cardiac arrest fatalities, among populations who consumed similar levels of animal fat varied to significant degrees (Eastern and Western Finland showed significant divergences in the incidence of heart disease and cardiac arrest mortality despite similar intake of animal fat – suggesting that the causal factor may not have been saturated animal fat intake).
While the data noting these points was included in the final publication, the variances seen were not covered in detail in the study findings.
Importantly, the assumption that saturated fat had a negative effect on cholesterol levels was made.
The diet-heart hypothesis was born.
In 1977, despite only epidemiological evidence and support from diet-heart hypothesis supporters, and opposition from within the scientific community as well as the American Medical Association, US Congress made the recommendation of a low fat diet, government policy.
What are fats?
To understand the differences between different types of fats, we need to look at the molecular structure. The three main groups of fats are saturated, monounsaturated and polyunsaturated fatty acids.
Saturated fatty acids are ‘saturated’ with hydrogen atoms (and have no double bonds) whereas monounsaturated have one double bond and polyunsaturated have many.
There are different sub-types of fats within each group which are metabolised and utilised differently in the body, for example a medium-chained saturated fatty acid is shuttled directly to the liver and oxidised (burned) for energy. Long-chain saturated fatty acids (16 carbon atoms or longer) are almost insoluble in water so are metabolised differently – bile is required for their digestion and absorption and they are eventually transported as fatty acids to adipose and muscle tissue for energy or storage.
The biochemistry of fats – what are they used for?
Fats are essential for hormone production, as is cholesterol, which is the precursor for all of our steroid hormones, which includes sex hormones and stress hormones. A low-fat (high-fibre) diet has shown to reduce circulating androgens (anabolic hormones) in men, whereas a high fat diet (41% of calories) with a higher intake of saturated fat, can increase testosterone levels. Dietary fat intake has a significant impact on testosterone levels, from a 12% reduction in testosterone older men following a low-fat diet, to a 13% increase in testosterone levels in young men who increased their fat intake.
Good fats increase satiety, and keep you feeling fuller for longer. They signal to the brain that you feel satiated and help regulate appetite through several mechanisms, including the release of appetite hormones, and the inhibition of gastric emptying and intestinal transit. The length of the fatty acid can determine which appetite hormones are stimulated, so for example only fatty acids with a chain length of greater than 12 carbons are able to stimulate cholecystokinin (CCK), gastric inhibitory peptide (GIP), neurotensin and pancreatic polypeptide (PP).[15,16,17]
Fats can also help lower the blood glucose and insulin response following a meal (when combined with the other macronutrients, carbohydrates and protein, in an ideal ratio).
The satiety promoting effects of fats, through hormonal responses as discussed above, is one of the strategies that when applied correctly, can help promote weight loss. Neuropeptide YY is a hormone that suppresses appetite[18,19] and fats per se are more effective than carbohydrates, and possibly proteins, at increasing levels of this hormone after a meal.
When considering caloric intake, replacing some calories from carbohydrates with those from good fats can help reduce post-prandial insulin response. Chronically high insulin levels can be pro-inflammatory as well as increasing the risk of insulin resistance, resulting in poor blood sugar control and weight gain.
Omega 3 fatty acids (specifically, EPA) are anti-inflammatory, an effect exerted by eicosanoids (a hormone like substance). The most powerful effect of omega 3’s in inflammation is down to its ability to inhibit the release of arachidonic acid from cell membranes. Arachidonic acid (AA) is the precursor for eicosanoids involved in a pro-inflammatory pathway. Omega 3’s also have an immune modulation role, where they can reduce the release of pro-inflammatory cytokines and adipocytokines and therefore reduce adipose tissue inflammation and oxidative stress.
Fish oils (omega 3’s) have been found to increase the breakdown of fats in between cells in adipose tissue (fat tissue), heart and skeletal muscle, and increase a process called beta-oxidation, where fatty acids are burned for energy. This occurs through a process called thermogenesis (heat production), which prevents the energy from being stored.
In this way, good fats can help burn unwanted fat.
Countless studies have shown the beneficial health benefits of good fats on cognitive structure and function. The include visual and cognitive development in infancy[23,24], improved mood and memory, prevention/delay in cognitive decline in Alzheimer’s disease, increased IQ in children, and improved cognitive function (and sleep) in ADHD[28,29].
This should come as no surprise, considering that around 60% of brain tissue is fat[30,31]. But since not all types of fats are synthesized in the body, it is critical for optimal brain function that essential fatty acids are consumed in the diet.
These are the omega 3 polyunsaturated fatty acids and omega 6 polyunsaturated fatty acids. Most of the health benefits shown in clinical trials are a result of increased omega 3’s or an improved omega 3 to omega 6 ratio.
Docosahexaenoic acid (DHA) and Eicosapentaenoic acid (EPA) are the two key omega 3 fatty acids. Of these, DHA is believed to be the nutrient which has played the most integral role in the evolution of human intelligence.
An important point to note is that even though brain structure and development is almost complete by the age of 5-6 years[32,37], the intake of dietary fatty acids in later life can influence the fatty acid composition of the brain.
Cell membrane integrity – phospholipids
All human cell membranes consist of a thin phospholipid bilayer that covers the whole circumference of the cell. Dietary fats can influence the fatty acids that are used to form this cell membrane phosolipid bilayer, and the significance of this to health is huge.
Let’s look at the critical functions of the cell membrane, which can be grouped into four categories;
1. maintenance of membrane fluidity
2. lignand binding to receptors
3. cell signalling and gene expression, and
4. eicosanoid and docosanoid synthesis.
Higher levels of polyunsaturated fatty acids incorporated into cell membranes can increase the flexibility, or ‘fluidity’ of the cell wall, which allows nutrients to diffuse in and out of cells with greater efficiency; transporter functions are improved and cell communication is enhanced.
The most important factor for cell membrane structure and function may be attributable to an inadequate proportion of DHA (an omega 3 fatty acid) in membrane phospholipids, driven largely by excessive consumption of omega-6 fatty acids.
Molecular dynamic modelling of phospholipid bilayers have consistently demonstrated increased membrane flexibility when DHA is present compared with other fatty acids. These highly flexible membranes are less sensitive to mechanical stress than saturated fatty acids.
Cells are highly metabolically active and a significant by-product of this activity is the release of reactive oxygen species (ROS), which cause oxidative stress. When cell membranes have a ‘healthy’ phospholipid bilayer, DHA can provide protection against ROS, acting as antioxidant and inhibiting inflammatory responses.
Omega 3’s can also be oxidised to signalling molecules called resolvins and protectins, collectively known as docosanoids, and may be released from phospholipids to be converted into resolvins, during conditions of tissue stress.
Resolvins actively promote resolution of inflammatory processes, making DHA and EPA great anti-inflammatory nutrients to help reduce systemic inflammation, which is common in adult populations (something we regularly test at Optimised Personal Wellness is high-sensitivity C-reactive protein (hs-CRP), a marker for systemic inflammation).
DHA is also the precursor for protectin, or neuroprotectin when found in the nervous system, where it induces nerve regeneration and reduces pro-inflammatory signaling. It is primarily DHA which provides benefit in neurocognitive conditions such as Alzheimer’s, and in the “normal” cognitive decline seen in ageing.
Due to the well understood anti-inflammatory effects of omega 3 fatty acids, their therapeutic application in chronic inflammatory conditions has been widely studied. The consumption of oily fish (rich in omega 3 fatty acids) is recommended to reduce low-grade systemic inflammation in adults with one or more feature of metabolic syndrome. Signs of metabolic syndrome include high blood pressure, high LDL:HDL ratio, high triglycerides, obesity and insulin resistance.
A meta-analysis in 2012 reviewing 10 randomised controlled trials found that omega 3’s at dosages greater than 2.7g/day for more than 3 months, reduced non-steroidal anti-inflammatory drug doses (NSAIDS) in rheumatoid arthritis patients. The health benefits of any reduction in NSAID medications (such as aspirin, ibuprofen, diclofenac, indometacin, naproxen and mefenamic acid) are significant in our opinion when considering the potential side-effects of long term use.
The beneficial effects of omega 3 and 6 fatty acids in skin health have also been extensively explored.
Since these ‘good’ fats are an important structural and functional component of skin cells (like all cells), in skin health they play a role in wound healing, permeability barrier integrity, production of new cells, inhibition of pro-inflammatory mediators, elevation of sunburn threshold, and promotion of cell death in malignant cells, including melanoma. The omega fatty acids can be of benefit in dermatitis, psoriasis, acne, systemic lupus erythematosus and eczema.
A very recent meta-analysis including 20,905 cases of breast cancer and 883,585 subjects, concluded that ‘higher consumption of dietary marine n-3 PUFA is associated with a lower risk of breast cancer’.
A detailed, unbiased, review of the available research clearly shows that there is no evidence that saturated fat intake is associated with an increased risk of heart disease.
There is evidence, however, that replacing some saturated fat with polyunsaturated fatty acids may reduce risk of coronary heart disease events as shown in a review paper published in 2010, which included randomised controlled trials where 13,614 participants with 1,042 CHD events, received increased PUFAs in place of saturated fats for at least one year. It seems that the type of polyunsaturated fat consumed is of key relevance, as omega 3 and omega 6 fatty acids have been shown to exert different effects when it comes to reducing risk of coronary heart disease.
There is strong evidence that omega 3 fatty acids are bioactive compounds that reduce the risk of cardiac death. The stiffness of arterial walls is a risk factor for cardiovascular disease in obese individuals and omega 3’s have been shown to protect blood vessels by improving the elastic qualities of arteries[44,45] and preventing fibrosis. Omega 3’s have also reduced blood pressure in a number of trials[46,47], and in one study there was a significant decline in systolic blood pressure in just 6 weeks.
Trans fats are one of the few food components that are widely accepted as being unhealthy, and for good reason. Industrial trans fats are created by pumping hydrogen molecules into liquid vegetable oil, changing the chemical structure and causing the oil to become a solid fat (a process called hydrogenisation). Naturally occurring trans fats such as those found in grass-fed meat, are different to industrially produced trans fats.
Trans fats are found in many processed foods such as margarine, biscuits, cakes, frozen foods, fried foods, and crisps and the negative health consequences are well understood and documented.
Trans fats have been found to be incorporated into both foetal and adult tissues, where they can cause cellular damage and lead to inflammation. ‘High’ levels of trans fats have been found to increase low-density lipoprotein (LDL) cholesterol and decrease high-density lipoprotein HDL) cholesterol compared with diets high in monounsaturated or polyunsaturated fatty acids.
The same study concludes that ‘the dietary levels of trans-fatty acids necessary to do this appear to be approximately 4% of energy or higher to increase low-density lipoprotein cholesterol and approximately 5% to 6% of energy or higher to decrease high-density lipoprotein cholesterol, compared with control diets essentially trans-free’.
The UK National Health Service list the negative health consequences of consuming ‘high’ levels of trans fats, and then go on to suggest that “we eat about half the recommended maximum of trans fats on average, which is why the more commonly eaten saturated fat is considered a bigger health risk”.
Our view is that if harmful trans fatty acids are not found naturally in foods, then the recommended daily intake should be 0g.
Does a high fat, especially saturated fat, diet cause heart disease?
A Japanese study followed more than 58,000 Japanese adults over a 14 year period, assessing the relationship between their saturated fat intake and risk of mortality from cardiovascular disease (including heart attack, cardiac arrest, heart failure, and stroke).
The study authors compared the risk of death with intake of saturated fat. Specifically, they compared outcomes between those consuming the least amount of saturated fat, and those consuming the most saturated fat.
Between the two groups, they found that the group with the highest saturated fat intake had:
– An 18% reduced risk of all cardiovascular disease
– A 31% reduced risk of all types of stroke
– A 42% reduced risk of ischaemic stroke
– A 52% reduced risk of intraparenchymal haemorrhage stroke
– No increased risk of death due to heart attack
– No increased risk of death due to heart failure
– No increased risk of death due to cardiac arrest
– No increased risk of death due to subarachnoid haemorrhage
A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease took into account every study published between 1950 and 2007.
The reviewers looked at prospective cohort studies (epidemiological in nature), and randomised trials.
What they found was:
– Tran fats were associated with an increased risk of heart disease
– Foods with a higher glycaemic index or load were associated with an increased risk of heart disease
– No evidence of an association between saturated fat intake and heart disease
– No evidence of an association between total fat intake and heart disease
– No evidence of an association between egg and meat intake and heart disease
– No evidence of an association between polyunsaturated fat intake and either a increase or a reduction in risk of heart disease (note: even though polyunsaturated fats lower cholesterol)
Evidence of protective factors against heart disease for:
– Mediterranean style diet
– Monounsaturated fats
– Marine derived omega 3 fatty acids
– Folate intake both from diet and supplements
– Whole grains
– Vitamin E
– Vitamin C
– Beta Carotene
Of these factors, the reviews found the strongest evidence for:
– Vegetable intake
– Mediterranean diet
– Nut consumption
– Trans fatty acid intake
– Intake of high glycaemic or high glycaemic load diet
Randomised controlled trials supported:
– A Mediterranean style diet
– Intake of marine derived omega 3 fatty acids
– Again, no randomised controlled trials that were identified supported a link between saturated fat and heart disease, or that lower intakes of saturated fat are associated with preventing heart disease.
In fact, the evidence from this review of every study published between 1950 and 2007 shows that a low fat, high carbohydrate diet is bad for heart health.
John Yudkin may have been right – sugar, both in refined form and from high glycaemic index and load foods has a causative link with heart disease.
A 2009 report published in the Annals of Nutrition and Metabolism covered a 2008 ‘expert consultation’ held by the World Health Organisation (WHO), and the Food and Agriculture Organisation (FAO) of the USA.
The consultation looked at both epidemiological studies and intervention studies.
The WHO/FAO report found that based on the epidemiological evidence:
“Intake of SFA [saturated fatty acids] was not significantly associated with CHD [coronary heart disease] mortality…”
“SFA intake was not significantly associated with CHD events”
Looking at intervention studies (where an intervention, such as medication, nutrition, lifestyle or exercise was performed), the report concluded that:
“The results of the meta-analyses showed that the RR [relative risk] of fatal CHD was not reduced by either the low-fat diets… or the high P/S [diets involving a change in the polyunsaturated to saturated fat (P/S) ratio of the diet, with or without a reduction in total fat intake] diets”
“low-fat diets did not affect CHD events”
Perhaps surprisingly given how prevalent, how deeply ingrained, and how often we are told that the saturated fat – cholesterol – heart disease link is true, the WHO/FAO report states that:
“According to the classic ‘diet-heart’ hypothesis, high intake of SFAs and cholesterol and low intake of PUFAs increase serum cholesterol levels and risk of CHD. However, few within-population studies have been able to demonstrate consistent associations with any specific dietary lipids, with the exception of trans fats and n–3 fatty acids.”
A 2010 meta-analysis, looking at 21 epidemiological studies covering 350,000 subjects over a period of between 5 and 23 years, assessed the relationship between saturated fat and heart disease.
What the study found was:
– No association between saturated fat and increased risk of heart disease
– No association between saturated fat and increased risk of stroke
The study authors did, however, note that:
More data are needed to elucidate whether CVD [cardiovascular disease] risks are likely to be influenced by the specific nutrients used to replace saturated fat.
Essentially, that what we have replaced saturated fat with in our diets might increase the risk of heart disease.
All of these studies combined have shown that there is no evidence of a link between saturated fat and heart disease.
But what of the notion that what we have erroneously reduced our saturated fat intake and replaced it with something that might actually increase our risk of heart disease?
Lowering saturated fat levels by swapping them for polyunsaturated omega 6 fats (found in vegetable oils) may increase overall risk of death in men:
“Advice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction. However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.”
Does cholesterol block arteries?
When it comes to arterial plaque, a study found that when assessing the composition of aortic plaques in those who had died of heart disease, 74% of the plaque content consisted of polyunsaturated fats (found in vegetable oils), and 26% saturated fat.
The study found a correlation between post-mortem serum (blood) polyunsaturated fat levels, adipose (fat) polyunsaturated fat levels, but no similar correlation for saturated fat.
The study authors noted that:
“No associations were found with saturated fatty acids. These findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered”
When it comes to cholesterol, is lower always better?
No. A long-term study found that individuals with low serum cholesterol maintained over a 20-year period had the worst outlook in terms of overall risk of death.
Another study conducted over 12 years in individuals aged 60-85, found that lower levels of cholesterol (< 170 mg/dl/4.4 mmol/l) were associated with a 36% increased risk of death.
Statin medications are widely prescribed for the treatment of ‘high’ cholesterol levels, however many researchers believe that the side-effects of statins such as memory loss and cognitive decline are down to cholesterol insufficiency.
Cholesterol levels are concentrated in the brain, where it contributes to the functioning of ‘synapses’ – tiny gaps between cells which allows nerves to communicate with each other. When statin medications lower cholesterol levels, it can potentially reduce the levels of cholesterol in the brain, leading to the adverse effects on cognitive function.
To your optimised wellness,
Matt & Dee
1. Cordain L (2002). The Paleo Diet. New Jersey: John Wiley & Sons, Inc.
2. Wolf R (2010). The Paleo Solution: The Original Human Diet. Las Vegas: Victory Belt Publishing.
3. Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, and Brand-Miller J (2005). Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nut 81:341-354.
4. Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD (2000). “Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets”. The American Journal of Clinical Nutrition 71 (3): 682–92
5. Cordain L, Eaton SB, Miller JB, Mann N, Hill K (2002). “The paradoxical nature of hunter-gatherer diets: meat based, yet non-atherogenic”. European Journal of Clinical Nutrition 56 (Suppl 1): S42–52.
6. O’Dea K Marked improvement in carbohydrate and lipid metabolism in diabetic Australian Aborigines after temporary reversion to traditional lifestyle (1984). Diabetes. 33596-603.
7. Keys A: Atherosclerosis: a problem in newer public health (1953). J Mt Sinai Hosp N Y 20(2):118-139.
8. Yerushalmy J, Hilleboe He (1957). Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med. Jul 15;57(14):2343-54.
9. Yudkin J (1957). Diet and coronary thrombosis: hypothesis and fact. Lancet 270:155-62.
10. Keys, A (1970). Coronary heart disease in seven countries. Circulation 41, suppl. 1, 1-211.
11. Wang C, et al (2005). Low-fat high-fiber diet decreased serum and urine androgens in men. J Clin Endocrinol Metab. Jun;90(6):3550-9.
12. Dorgan JF, et al (1996). Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. Am J Clin Nutr. Dec;64(6):850-5.
13. Meikle AW, et al (1990). Effects of a fat-containing meal on sex hormones in men. Metabolism. Sep;39(9):943-6.
14 Montmayeur JP, le Coutre J (2010). Fats and Satiety in Fat Detection: Taste, Texture, and Post Ingestive Effects. Chapter 15. Boca Raton (FL) : CRC Press [Online]. Available at: http://www.ncbi.nlm.nih.gov/books/NBK53550/ Accessed: 7 September 2013.
15. McLaughlin J, Grazia LM, Jones MN et al (1999). Fatty acid chain length determines cholecystokinin secretion and effect on human gastric motility. Gastroenterology. 116:46–53.
16. Barbera R, Peracchi M, Brighenti F et al (2000). Sensations induced by medium and long chain triglycerides: Role of gastric tone and hormones. Gut. 2000;46:32–36.
17. Drewe J, Mihailovic S, D’Amato M et al (2008). Regulation of fat-stimulated neurotensin secretion in healthy subjects. J Clin Endocrinol Metab. 93:1964–1970.
18. Karra E, Chandarana K, Batterham RL (2009). The role of peptide YY in appetite regulation and obesity. J Physiol. 15;587(Pt 1):19-25.
19. le Roux CW, Bloom SR. (2005). Peptide YY, appetite and food intake. Proc Nutr Soc. May;64(2):213-6.
20. Lomenick JP, et al (2009). Effects of meals high in carbohydrate, protein, and fat on ghrelin and peptide YY secretion in prepubertal children. J Clin Endocrinol Metab. Nov;94(11):4463-71.
21. Fan C, Zirpoli H, Qi K (2013). n-3 fatty acids modulate adipose tissue inflammation and oxidative stress. Curr Opin Clin Nutr Metab Care. Mar;16(2):124-32.
22. Shearer GC, Savinova OV, Harris WS (2012). Fish oil – how does it reduce plasma triglycerides? Biochim Biophys Acta. May;1821(5):843-51.
23. Tinoco SM, Sichieri R, Moura AS et al (2007) [The importance of essential fatty acids and the effect of trans fatty acids in human milk on fetal and neonatal development]. Cad Saude Publica. Mar;23(3):525-34.
24. Bourre JM (2007). Dietary omega-3 fatty acids in women. Biomed Pharmacother. Feb-Apr;61(2-3):105-12.
25. Heinrichs SC (2010). Dietary omega-3 fatty acid supplementation for optimizing neuronal structure and function. Mol Nutr Food Res. Apr;54(4):447-56.
26. Hashimoto M, Hossain S (2011). Neuroprotective and ameliorative actions of polyunsaturated fatty acids against neuronal diseases: beneficial effect of docosahexaenoic acid on cognitive decline in Alzheimer’s disease. J Pharmacol Sci. 116(2):150-62.
27. Yehuda S, Rabinovitz-Shenkar S, Carasso RL (2011). Effects of essential fatty acids in iron deficient and sleep-disturbed attention deficit hyperactivity disorder (ADHD) children. Eur J Clin Nutr. Oct;65(10):1167-9.
28. Yehuda S (2012). Polyunsaturated fatty acids as putative cognitive enhancers. Med Hypotheses. Oct;79(4):456-61.
29. Montgomery P, Burton JR, Sewell RP, Spreckelsen TF, Richardson AJ (2013). Low Blood Long Chain Omega-3 Fatty Acids in UK Children Are Associated with Poor Cognitive Performance and Behavior: A Cross-Sectional Analysis from the DOLAB Study. PLoS One. Jun 24;8(6):e66697.
30. Chang CY, Ke DS, Chen IY (2009). Essential fatty acids and human brain. Acta Neurol Taiwan. Dec;18(4):231-41.
31. J Bradbury (2011). Docosahexaenoic Acid (DHA): An Ancient Nutrient for the Modern Human Brain. Nutrients. May; 3(5): 529-554.
32. Singh M (2005). Essential fatty acids, DHA and human brain. Indian J Pediatr. Mar;72(3):239-42.
33. Feller S.E., Gawrisch K., MacKerell A.D., Jr (2002). Polyunsaturated fatty acids in lipid bilayers: Intrinsic and environmental contributions to their unique physical properties. J. Am. Chem. Soc.124:318–326.
34. Baldwin A.S., Jr. (1996). The NF-kappa B and I kappa B proteins: new discoveries and insights. Annu. Rev. Immunol.14:649–683.
35. Christie WW (2010). Fatty acids: Methylene-interrupted double bonds: Structures, occurrence and biochemistry.
36. Niemoller TD, Bazan NG (2010). Docosahexaenoic acid neurolipidomics. Prostaglandins Other Lipid Mediat. 91:85–89.
37. Bazan NG (2005). Neuroprotectin D1 (NPD1): A DHA-derived mediator that protects brain and retina against cell injury-induced oxidative stress. Brain Pathol. 15:159–166.
38. Robinson LE, Mazurak VC (2013). N-3 polyunsaturated fatty acids: relationship to inflammation in healthy adults and adults exhibiting features of metabolic syndrome. Lipids. Apr;48(4):319-32.
39. Lee YH, Bae SC, Song GG (2012). Omega-3 polyunsaturated fatty acids and the treatment of rheumatoid arthritis: a meta-analysis. Arch Med Res. Jul;43(5):356-62.
40. McCusker MM, Grant-Kels JM (2010). Healing fats of the skin: the structural and immunologic roles of the omega-6 and omega-3 fatty acids. Clin Dermatol. Jul-Aug;28(4):440-51.
41. Zheng JS, Hu XJ, Zhao YM et al (2013). Intake of fish and marine n-3 polyunsaturated fatty acids and risk of breast cancer: meta-analysis of data from 21 independent prospective cohort studies. BMJ. Jun 27;346:f3706.
42. Mozaffarian D, Micha R, Wallace S (2010). Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. Mar 23;7(3):e1000252.
43. Mozaffarian D, Wu JH (2011). Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events. J Am Coll Cardiol. Nov 8;58(20):2047-67.
44. Koziolova NA, Shilova IaÉ, Nikonova IuN, Agafonov AV, Polianskaia EA (2013). State of the structure and functions of the arterial wall in patients with chronic heart failure against the background of permanent atrial fibrillation and assessment of vasoprotective effect of omega-3 polyunsaturated fatty acids. Kardiologiia. 53(3):15-24.
45. Wong AT, Chan DC, Barrett PH, Adams LA, Watts GF (2013). Supplementation with n3 fatty acid ethyl esters increases large and small artery elasticity in obese adults on a weight loss diet. Nutr. Apr;143(4):437-41.
46. Iketani T, Takazawa K, Yamashina A (2013). Effect of eicosapentaenoic acid on central systolic blood pressure. Prostaglandins Leukot Essent Fatty Acids. Feb;88(2):191-5.
47. Abeywardena MY, Patten GS (2011). Role of ω3 long-chain polyunsaturated fatty acids in reducing cardio-metabolic risk factors. Endocr Metab Immune Disord Drug Targets. Sep 1;11(3):232-46.
48. Noreen EE, Brandauer J (2012). The effects of supplemental fish oil on blood pressure and morning cortisol in normotensive adults: a pilot study. J Complement Integr Med. Oct 23;9.
49. Larqué E, Zamora S, Gil A (2001). Dietary trans fatty acids in early life: a review. Early Hum Dev. Nov;65 Suppl:S31-41.
50. Hunter J.E (2005). Dietary levels of trans-fatty acids: Basis for health concerns and industry efforts to limit use. Nutr. Res. 25:499–513.
51.NHS Choices (2013). What are trans fats? [Online]. Available at: http://www.nhs.uk/chq/Pages/2145.aspx?CategoryID=51 (Accessed: 7 Sepetember 2013).
52. Yamagishi K, et al (2010). Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study. Am J Clin Nutri 92(4):759-765.
53. Mente A, et al. (2009). A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Arch Intern Med.169(7):659-669.
54. Fats and Fatty Acids in Human Nutrition (2009). Annals of Nutrition and Metabolism, 55 (1-3).
55. Siri-Tarino PW, et al (2010). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr Jan.
56. Ramsden CE, et al (2013). Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ 346:e8707.
57. Felton CV, Crook D, Davies MJ, Oliver MF (1994). Dietary polyunsaturated fatty acids and composition of human aortic plaques. Lancet. Oct 29;344(8931):1195-6.
58. Schatz IJ, et al (2001). Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. Lancet 358(9279):351-5.
59. Sarria Cabrera MA, et al (2012). Lipids and all-cause mortality among older adults: a 12-year follow-up study. Scientific World Journal May 1.
60. Vliet VP (2012). Cholesterol and late-life cognitive decline. J Alzheimers Dis. 30 Suppl 2:S147-62.