HIGH INTAKE OF OMEGA-6 RICH VEGETABLE OILS CAUSES OBESITY AND INSULIN RESISTANCE
by admin | October 6, 2021 | Health

Summary: Reducing total fat consumption did not considerably help reduce the prevalence of abdominal fat accumulation, and obesity has increased. Studies suggest that this rise is more due to higher consumption of linoleic acid (LA) rich omega-6 fatty acids. It occurred as humans switched to greater consumption of vegetable oils from animal fat consumption. It also resulted in lower omega-3 in the diet. Experimental studies confirm that reducing the dietary intake of LA may considerably help lower the risk of obesity. Additionally, adding omega-3 to the diet may have additional benefits of countering LA’s adverse effects, thus helping lower obesity prevalence.

Keywords: linoleic acid (LA), omega-6 fatty acids, omega-3 fatty acids, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), endocannabinoid system

Introduction

 

New experimental data indicate that high dietary intake of omega-6 and relatively low omega-3 intake has more to do with obesity, accumulation of visceral fat, and insulin resistance than total fat intake to fulfill energy needs. Correction of omega-6: omega-3 ratio in diet may be the key to countering obesity.

Abdominal obesity has grown at an alarming rate in the last 40-50 years in the US. Historical data shows that in men, it rose from 12.7% to 38.3%. Whereas, in women, it grew from 19.4% to almost 60% between 1960 -2000. This tripling of abdominal obesity is difficult to explain solely based on the total fat content of the diet1.

Researchers think that increase in abdominal obesity has more to do with the quality of fats consumed. Some researchers suggest that humans have evolved to consume omega-6 and omega-3 fatty acids almost in equal ratios. However, in the modern diet, its proportions are from ~10:1 to 25:1. That’s a severe disbalance2.

If that is the case, correcting the omega-6 to the omega-3 ratio by consuming more omega-3 and less omega-6 may solve the problems of obesity to a great extent. However, before making any firm recommendation, there has to be strong evidence supporting the theory.

Researchers think that some evidence comes from watching the historical changes in dietary patterns. For example, data shows that consumption of omega-6 fatty acids rose considerably from 1900 onwards, when people in the western world switched from butter or lard to consuming more vegetable oils, like soybean oil. This resulted in a two-fold increase of linoleic acid (LA), the primary omega-6 fatty acid in vegetable oils, and it makes now 8 to 10% of total calorie intake3.

These assumptions are further supported by a systemic review of studies indicating that LA content in subcutaneous tissues in the US has increased by 2.5 times.

Experiments confirm that reducing LA intake or increasing omega-3 intake may help counter obesity

Researchers carried out lab experiments in mice to understand the effect of LA on obesity and further understand the role of a high-fat diet4.

Firstly, they divided mice into two groups, one to be fed with a medium-fat diet (35% of total calorie intake) and another on a high-fat diet (65% of the total calorie intake). They further divided mice into two groups, with one fed with diet having 1% LA and another with 8% LA diet (meaning 1% and 8% of energy from LA, respectively).

Interestingly enough, they found that higher fat consumption was not much related to obesity, as there is not much difference in the group a and d.

However, there is a clear and high association between obesity and high LA consumption irrespective of total fat intake; thus, both group b and e mice developed severe abdominal obesity.

Next, they wanted to understand the role of omega-3 fatty acids in the diet. Thus, they added omega-3 (eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) to the diet of the mice on the 8% LA group.

They found that omega-3 enriched diet may help prevent obesity and thus metabolic disorders. To their surprise, omega-3 could help control obesity in mice on an 8% LA diet, and total fat in the diet had not much impact on it. Thus omega-3 fatty acids prevented fat accumulation in the 8% LA and medium fat diet group (Figure 2 C) and 8% LA and high-fat diet group (Figure 2 F)

It confirmed the following things:

• LA is the primary cause of abdominal obesity, be it low fat or a high-fat diet. Thus, a need to limit LA consumption.

• Consuming a diet rich in omega-3 fatty acids (EPA+DHA) may help counter obesity-causing effects of LA.

Understanding the underlying mechanism

Researchers think that this ability of LA to cause obesity can be explained by changes that happened at the cellular level due to high LA consumption. It primarily stimulates the endocannabinoid system leading to impaired fat storage, altered behavior, appetite, and thus greater risk of obesity.

Although total calorie intake counts, perhaps how many calories a body gets from fats is less relevant. Even a high-fat diet will not cause obesity if it is low in LA containing fats. Further, adding omega-3 fatty acids rich in EPA and DHA may help counter these obesity-causing effects of LA.

References

 

1. Okosun IS, Chandra KMD, Boev A, et al. Abdominal adiposity in US adults: prevalence and trends, 1960–2000. Preventive Medicine. 2004;39(1):197-206. doi:10.1016/j.ypmed.2004.01.023

2. Simopoulos AP. Evolutionary Aspects of the Dietary Omega-6/Omega-3 Fatty Acid Ratio: Medical Implications. In: Alvergne A, Jenkinson C, Faurie C, eds. Evolutionary Thinking in Medicine: From Research to Policy and Practice. Advances in the Evolutionary Analysis of Human Behaviour. Springer International Publishing; 2016:119-134. doi:10.1007/978-3-319-29716-3_9

3. DiNicolantonio JJ, O’Keefe JH. Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis. Open Heart. 2018;5(2):e000898. doi:10.1136/openhrt-2018-000898

4. Alvheim AR, Malde MK, Osei-Hyiaman D, et al. Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity. Obesity (Silver Spring). 2012;20(10):1984-1994. doi:10.1038/oby.2012.38

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