Introduction
Over the last decade, there has been and continues to be controversy about what constitutes a healthy diet. Saturated fats are at the center of this controversy as new perspectives challenge their role in causing cardiovascular disease. It’s approximately 41 years since the first dietary guidelines were issued to the American People and saturated fats were categorized as a causative factor in cardiovascular diseases. A few years later, the United Kingdom adopted comparable dietary standards to those in the United States. Overall fat consumption was limited to 30% of total calories, with saturated fat consumption limited to 10% of total calories in successive guidelines editions (Cassiday, 2021). However, new findings and reevaluation of previous research have cast doubt on whether dietary fat is as harmful as specialists have claimed over the past three decades.
Background
Cholesterol in our bodies is often carried by specific proteins called lipoproteins. Basically, lipoproteins are classified based on their densities with two of them being the most significant in causing heart and cardiovascular diseases. These include the high-density lipoprotein (HDL) and the low-density lipoprotein (LDL). On the other hand, coronary arteries are essentially hollow tubes with a very thin endothelium lining. The endothelium lining is constantly in touch with the blood, which transports lipoproteins like LDL. So, essentially the LDL particle does leave the bloodstream, pierce the endothelium, and enter the delicate arterial wall. On the other hand, High-Density Lipoproteins (HDL), and have the reverse effect as they drag cholesterol away from arterial walls, lowering the risk of cardiovascular diseases.
Following the increases evidence suggesting saturated fat and cholesterol don’t necessarily increase cholesterol levels in the blood for the majority of the population. A group of three researchers go further and propose the homeoviscous adaptation to dietary lipids (HADL) model, in an attempt to explain fluctuations in lipoprotein cholesterol as an adaptive homeostatic function that helps to maintain cell membrane fluidity for optimal cell function (University of Bergen, 2021). These scholars argue that when saturated fats replace polyunsaturated fats in the diet, less cholesterol is required to maintain cell membrane fluidity. The reverse is also true as polyunsaturated fats from our diet reach the cell membranes and cause them to become more fluid. In essence, cells incorporate cholesterol from circulation to regulate the fluidity of their membranes. According to the researchers’ methodology, a lot of polyunsaturated fats intake lowers blood cholesterol levels.
These authors argue that body cells modify their membrane fluidity in response to changes in their environment, such as access to different forms of fat in a phenomenon known as Homeoviscous adaptation. This phenomenon has also been seen in bacteria, animals, and human skin cells. This is quite fundamental in human physiology according to these authors.
Since nutrition research is predominantly focused on the interplay between foods, health, and disease, these researchers went a little bit further to understand the causation factors as well as why cholesterol changes occur. This is where the new HADL model, which is based on adaptable human physiology, comes into action arguing that cells need to modify their cholesterol content, and hence blood cholesterol, when dietary fats vary (University of Bergen, 2021).
Zinöcker and colleagues also discuss other causes of high LDL-cholesterol in persons with cardiovascular disease, such as low-grade inflammation and insulin resistance. For them, increased blood cholesterol due to metabolic disturbances must be distinguished from increased blood cholesterol due to a significant shift in dietary saturated fatty acid consumption. It also raises doubts about the value of decreasing blood cholesterol by eating more polyunsaturated fatty acids rather than treating the underlying reason.
The authors argue that the rationale behind the HADL model is that the effect of dietary lipids on blood cholesterol is not a pathogenic reaction, but rather a perfectly normal and even good adaptation to dietary changes.
Criticism
On the other hand, the homeoviscous adaptation to dietary lipids (HADL) model has received criticism in equal measure. Researchers Christensen et al (2021), argue that the HADL model is wrong as Lipoproteins transfer cholesterol from the bloodstream, and the bulk of it is present in apoB-100-containing LDL particles in humans. These apoB-100 originate from VLDLS and are continuously being secreted by the liver. Moreover, hepatocytes continuously remove LDL particles and thus LDL particles could pile up in the plasma in case of increased VLDL secretion or decreased LDL clearance. This implies that LDL particle components are distributed into various cellular pools after degradation in lysosomes. For example, cholesterol would be deposited as lipid granules, integrated into membranes, used for VLDL particle biosynthesis, or discharged into the bile ducts as bile salts or cholesterol to travel to the gut for reabsorption or eventual excretion.
Christensen et al (2021) also argue that, in variation to glucose homeostasis, no hormonal mechanism has developed to maintain a restricted range of plasma cholesterol concentrations. Since every cell can produce cholesterol, no cell has an absolute necessity for cholesterol absorption (6–8). As a result, plasma LDL-cholesterol concentrations can be very low (but not zero) with few side effects. Contemporary research shows that altered fatty acids trigger some changes in cell membrane lipids and this helps explain LDL-cholesterol changes in intervention studies.
Thirdly, it’s biologically proven that free cholesterol is poisonous and since human cells are unable to break down cholesterol granules, a balance between cholesterol input and outflow via nutrition and biosynthesis, as well as use and excretion occurs. Also, it’s an indisputable fact that all human body cells can produce cholesterol, and as such cellular cholesterol shortage arises only when cholesterol synthesis is faulty. Homozygous and Heterozygous familial hypercholesterolemia patients, for example, have a 50% and 100% reduction in cellular LDL uptake, respectively, but show no symptoms of cholesterol deficiency. On the other hand, cholesterol synthesis deficiency, as evidenced by Smith–Lemli–Opitz syndrome, is, harmful from the beginning of life.
Conclusion
In conclusion, these critics argue that the HADL model authors offered a skewed scientific explanation and ignored data that obviously contradicts their theory. According to these researchers, the HADL hypothesis contradicts existing information, and as a result, their hypothesis is wrong.
Illustrate the impact of food policy and regulation on food provision, food choice, and nutritional health relevant to your chosen nutrient. (1500 words)
Dietary Policy Guidelines
According to Cassiday (2021) the first dietary guidelines were announced in 1980 in the USA after a few clinical trials and some randomized epidemiological research. As a result, these guidelines were based almost entirely on epidemiological research. Some experts argue that it relied heavily on the work of renowned researcher Ancel Keys who had already published the Seven Countries Study that compared the diet and health of middle-aged men in Greece, Italy, Yugoslavia, Finland, Japan, the Netherlands, and the United States. Key’s research had concluded that those men who ate largely fish, grains, nuts, and vegetables lived longer than the group that took dairy or meat usually classified as saturated fats majorly from heart disease. There were other epidemiological studies and controlled clinical trials that yielded mixed results when it came to the role of saturated fat intake and the risk of heart disease. In recent years, individual researchers have produced inconsistent results on the link between dietary saturated fats and heart disease, and thus call for a more research on the link between different types of cholesterol particles in the body and unsaturated fats. However, when individual studies differ, researchers can use also use meta-analysis to combine data from several studies to uncover trends. Some of the notable meta-analysis researches include:
Siri-Tarino et al (2009) published a cohort studies focusing on healthy persons who differed in saturated fat intake. The findings showed that larger consumption of saturated fat was not connected with an increased risk of coronary heart disease, stroke, or cardiovascular disease among the participants.
Another study by Harcombe et al., (2015), found based on randomized controlled trials did not provide sufficient evidence that reducing saturated fat intake reduced heart disease fatalities. These authors, therefore, recommended a review of existing dietary advice as it should not have been adopted.
Moreover, Hooper et al (2015) included 15 randomized controlled trials studying over 59000 participants. The results of the study found no significant effect on reducing saturated fat when dealing with strokes or heart attacks. However, this study denoted that replacing some of it with polyunsaturated fat minimized the risk of cardiovascular diseases by 27%.
De Souza RJ, et al 2015, conducted a systematic observational review looking at the association of heart diseases, saturated fat, type 2 diabetes stroke, and death in 73 studies. The results of the analysis revealed that saturated fat intake wasn’t linked with heart diseases, stroke, or type 2 diabetes. The overall conclusion was that people who consumed more saturated fat were not more prone to these diseases as compared to those who ate less.
Lastly Chowdhury (2014) et al review looked at randomized controlled trials for the link between heart diseases or cardiac death and dietary fatty acids. The study conducted on over 550,000 participants in 49 observational studies found no link between saturated fat and the risk of death or heart disease
Despite the never-ending debate, most countries’ health organizations advise minimizing fat, particularly saturated fat, in the general population. According to UK dietary standards, fat should account for up to 35% of our daily energy (calories), whereas carbs should account for roughly 50%. (It’s worth emphasizing that this is a moderate-fat, moderate-carbohydrate diet, rather than a low-fat, high-carbohydrate diet.
The percentages are even lower when it comes to saturated fat. The United Kingdom advises that it should account for no more than 11% of our total food and beverage calories, whereas the United States and the World Health Organization advise that it should account for no more than 10%. Women should consume 20g per day (equal to 2.5 tablespoons butter or four supermarket sausages) and males should consume 30g per day (similar to 2.5 teaspoons butter or four supermarket sausages) (a quarter-pounder hamburger with cheese, plus four tablespoons of double cream)( Dowden,2021).
According to, nutritionists are concerned about the role saturated fat present in our diet in raising LDL cholesterol levels as discussed at the beginning of this paper. Mono- and polyunsaturated fats, on the other hand, have been found to reduce LDL cholesterol, perhaps the reason why the dietary guidelines in many countries advocate substituting unsaturated fats for saturated fats whenever possible. Saturated fats are believed to elevate HDL cholesterol far higher than other fats, perhaps counteracting the negative effects of LDL cholesterol. Tran’s fats, which are meant to replace saturated fats, elevate LDL cholesterol even higher than saturated fats while reducing HDL levels.
The significance of this is that and LDL particle number and LDL cholesterol levels are frequently concordant (i.e., when one is high, the other is high, and vice versa), which is likely why observational studies have shown a link between LDL cholesterol and heart disease. In these circumstances, high LDL cholesterol was a proxy indication for increased LDL particle number. However, recent studies show that this relationship can also be discordant. That is, if a person’s cholesterol is simply tested, not their particle number, they will be misled into thinking they have a low risk of heart disease. Worse, the people who are most likely to show this pattern are those who are at the worst risk: those who have metabolic syndrome or full-blown type 2 diabetes. According to Kathiresan et al (2006), the more metabolic syndrome components such as hypertension, abdominal obesity, insulin resistance, high triglycerides, and low HDL, the more probable LDL particle number will be raised. On the other end, patients with low LDL particle number (LDL-P) and high LDL cholesterol (LDL-C) do not have a high risk of heart diseases and perhaps this explains why they are often treated with statin drugs or cholesterol-lowering drugs. This is a cause for alarm as several studies have linked low cholesterol to the risk of death especially among women and the elderly.
The Petursson et al (2012) study found that women with cholesterol below 195mg/dl were at a greater risk of dying than women with higher cholesterol levels above the cut-off. Another study by Onder et al (2003), showed that elderly people aged over 70 with total cholesterol levels below 160mg/dl faced doubled risk of mortality than those with cholesterol levels between 160 and 199mg/dl. Definitely, this goes against the current belief on the real course of heart and cardiovascular diseases. Besides, low cholesterol is also associated with several health disorders.
Boscarino et al (2009), argue that men with low total cholesterol were seven times at risk of dying prematurely from unnatural causes such as accidents and suicide than other men in the study. An older study by Morgan, et al found that men with low cholesterol were three times at risk of suffering depression than those with high or normal cholesterol. More recently Seneff et al (2011), associated low cholesterol with Alzheimer’s disease.
It’s critical to highlight that most of these studies were observational thus do not prove low cholesterol was the principal cause of the increased risk of disease or death as observed. However, given that we understand the importance of cholesterol, it’s possible that low cholesterol could contribute to some of these diseases directly
The government’s guidelines have frequently been questioned due to a lack of consistency that consuming saturated fats increases the risk of heart diseases, as well as a better knowledge on the impact of fats on different types of cholesterol particles in the body. Some scholars believe it is time to raise, if not eliminate, the saturated fat limit set forth by UK dietary guidelines. Logically, this would bear significant repercussions, ranging from modifying school meals to readjusting manufacturer goals. The official standards for saturated fat would have to be set and incorporated in various foods across the board. Moreover, some scholars argue that existing saturated fat guidelines are not only unsuccessful in decreasing rates of obesity, cardiovascular disease, and type 2 diabetes but are also harmful to one’s health.
The set dietary guidelines could change soon, though research already shows that solidified dairy products like cheese are often avoided due to their highly saturated fat may contain beneficial saturated fatty acids ideal for healing some diseases.
According to Menshealth.com reducing saturated fat intakes, even more, would entail significant dietary adjustments. This is because dairy products, meat, and eggs account for 75% of all dietary saturated fat. Lowering the limit of saturated fat by at least 5% of total calories would require banning the items from the food table. Moreover, eliminating them would also deprive people of essential supplies of minerals, vitamins, proteins, and lipids, in addition to decimating the meat and dairy sectors.
Conclusion
It’s ideal to limit the consumption of saturated fats for people with specific medical illnesses or cholesterol issues. Most of the research findings chosen for this article show that saturated fat has no substantial link to heart disease in the average person. However, substituting unsaturated fat for saturated fat may provide significant health advantages. This isn’t to say that saturated fat is “evil”; but rather, it’s neutral with some unsaturated fats being beneficial.
References
University of Bergen (2021). New perspectives challenge the idea that saturated fats cause heart disease. Retrieved 18 December 2021, from https://www.uib.no/en/med/143134/new-perspectives-challenge-idea-saturated-fats-cause-heart-disease
Christensen, J. J., Telle-Hansen, V. H., Ulven, S. M., Kovanen, P. T., Jauhiainen, M., Öörni, K., & Holven, K. B. (2021). The homeoviscous adaptation to dietary lipids (HADL) hypothesis is probably incorrect. The American Journal of Clinical Nutrition, 113(6), 1711-1712.
Kathiresan, S., Otvos, J. D., Sullivan, L. M., Keyes, M. J., Schaefer, E. J., Wilson, P. W., … & Robins, S. J. (2006). Increased small low-density lipoprotein particle number: a prominent feature of the metabolic syndrome in the Framingham Heart Study. Circulation, 113(1), 20-29.
Davidson, M. H., Ballantyne, C. M., Jacobson, T. A., Bittner, V. A., Braun, L. T., Brown, A. S., … & Dicklin, M. R. (2011). Clinical utility of inflammatory markers and advanced lipoprotein testing: advice from an expert panel of lipid specialists. Journal of clinical lipidology, 5(5), 338-367.
Petursson, H., Sigurdsson, J. A., Bengtsson, C., Nilsen, T. I., & Getz, L. (2012). Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years of prospective data from the Norwegian HUNT 2 study. Journal of evaluation in clinical practice, 18(1), 159-168.
Onder, G., Landi, F., Volpato, S., Fellin, R., Carbonin, P., Gambassi, G., & Bernabei, R. (2003). Serum cholesterol levels and in-hospital mortality in the elderly. The American journal of medicine, 115(4), 265-271.
Morgan, R. E., Palinkas, L. A., Barrett-Connor, E. L., & Wingard, D. L. (1993). Plasma cholesterol and depressive symptoms in older men. The Lancet, 341(8837), 75-79.
Seneff, S., Wainwright, G., & Mascitelli, L. (2011). Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet. European Journal of Internal Medicine, 22(2), 134-140.
Dowden, A. (2021). The truth about saturated fat. Retrieved 18 December 2021, from https://www.bbc.com/future/article/20190712-saturated-fat-worse-than-unsaturated-fat
Boscarino, J. A., Erlich, P. M., & Hoffman, S. N. (2009). Low serum cholesterol and external-cause mortality: potential implications for research and surveillance. Journal of psychiatric research, 43(9), 848-854.
Hooper L, et al. Reduction in saturated fat intake for cardiovascular disease Trusted Source. Cochrane Database Systematic Review, 2015.
Cassiday, L. (2021). Big fat controversy: changing opinions about saturated fats. Retrieved 18 December 2021, from https://www.aocs.org/stay-informed/inform-magazine/featured-articles/big-fat-controversy-changing-opinions-about-saturated-fats-june-2015?SSO=True
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