Lesson 5: Fat

Table of Contents


In the last lesson I discussed protein and recommendations regarding quantity, quality, and other relevant aspects for overall health and dieting.

In this lesson I will do the same with dietary fat. Unlike with protein, there are no specific reasons why fat intake will be additionally beneficial for weight loss. However, fat intake is still important for general health purposes.(Liu, 2017) As discussed below, there is lots of controversy regarding the topic of dietary fat and the different types. While there isn’t necessarily a “right” answer, I will try to provide a fair overview of the points of contention as well as general recommendations with the various controversies in mind.


Standard dietary guidelines suggest: 

  • 2-3 years old: 30-40% of one’s calories come from fat
  • 4-18 years old: 25-35% of one’s calories come from fat
  • ≥19 years old: 20-35% of one’s calories come from fat

While protein discussed previously has literature suggesting certain amounts per kilogram of body weight, there is no strong evidence base supporting fat be considered in the same manner.

There is much talk of low fat vs low carbohydrate diets, but a 2020 Cochrane review indicates that lower vs higher fat intake makes at most a small difference in weight outcomes when not attempting to lose weight (-1.4 kg when lowering one’s fat intake).(Hooper, 2020a) When losing weight, there are no meaningful differences between low fat and low carbohydrate diets when calories are matched.(Blaak, 2021; Yang, 2021)

A 2021 umbrella review of systematic reviews found low fat diets may improve total cholesterol and low density lipoprotein cholesterol (LDL, the “bad” type) compared to low carbohydrate diets, while high fat diets may improve triglycerides and high density lipoprotein cholesterol (HDL, the “good” type).(Schwingshackl, 2021) These cholesterol effects were also seen in a 2021 systematic review and meta-analysis (SR/MA) performed more recently than those included in the prior umbrella review (though no impact on triglycerides was seen).(Yang, 2021) Thus, an argument can be made for lower or higher fat diets. Importantly, this does not consider the source of carbohydrates or fats; as different types of fats have different health implications I will discuss this in more detail below.

Reasons for a minimum daily fat intake

The only two essential fatty acids are linoleic acid and linolenic acid, and one of the reasons for the minimum threshold listed above is to ensure that the recommended intakes for these are met:

  • Linoleic acid (“LA”, an “ω-6” (“omega-6”) or “n-6” polyunsaturated fatty acid) is recommended at 7 grams/day age 1-3 years and then 10-17 grams/day beyond that depending on age and gender.
  • α-Linolenic acid (“ALA”, an ω-3 or n-3 polyunsaturated fatty acid) is recommended at 0.7 grams/day age 1-3 years and then 0.9-1.6 grams/day beyond that depending on age and gender.

However, you can likely get away with consuming considerably less than those recommended amounts. See the note below.

Note: For a full overview of where these and many other recommended dietary intakes come from, read through here.
Briefly, for LA there seems to be very few cases of clinical deficiency. In children there was no data to inform how much is needed to prevent or treat deficiency, and in adults being fed entirely by parenteral nutrition (meaning being fed through an intravenous catheter), as little as 8.0 grams daily was able to correct signs of deficiency. As this is not applicable to the general population, the recommendation for all age groups was set as the median intake in the general population.
For ALA in children there are only a handful of case reports of deficiency in medical patients, and supplementation with 1-1.5 grams daily reversed this. In adults several cases of deficiency in medical patients were seen with intakes of <0.1 grams daily, while in one study ~0.3 grams daily prevented deficiency. Given the paucity of evidence overall, the recommendation for all age groups was set as the median intake in the general population.
So in both cases the recommended amount is simply the median of what the general population consumed at the time those recommendations were made. As very few cases of deficiency occur in the general population it seems reasonable to me to conclude that intakes far lower than the median intakes will still prevent any signs of deficiency.

There are a handful of other reasons to consume dietary fat:

  • Fat is additionally helpful for absorption of the four fat-soluble vitamins: A, D, E, and K.
  • There is some evidence that fat intake below the above recommendations for extended periods can decrease hormone levels (ie, testosterone), but it is unclear if this will impact skeletal muscle mass in a negative way.(Iraki, 2019)
  • Lastly, some sources of fats are associated with beneficial health properties, (ie, nuts, olive oil, fatty fish). If daily fat intake was set too low these beneficial foods would have to be excluded.

Tip: As mentioned previously, you can plug a single day of eating into cronometer.com to see if you are meeting these essential fatty acid recommendations. However, as indicated in the prior note you can likely consume considerably less than the recommended intakes without significant risk of harm. Thus, I would not burden yourself too significantly to meet the recommended fat intake levels if it would otherwise prove troublesome to do so, especially when actively losing weight and thus consuming relatively few calories.

However, over the long run there are likely benefits to consuming the healthier food groups that have significant amounts of fat. For example, a recent (SR/MA) found that higher vs. lower consumption of LA is associated with decreased mortality.(Li, 2020)

Example: If a person wants to consume 2,000 kcal/day, 20% of this is 400 kcal. Considering 9 kcal/gram of fat, this equates to a minimum of 400/9 = 44 grams of fat daily. Of this, ~1-1.5 grams of ALA and ≥10 grams of LA daily are likely sufficient to meet health requirements in adults.

Reasons for a maximum daily fat intake

There is nothing inherently wrong with a high fat diet that goes beyond the upper limits of the ranges listed above. The upper limits were set with the thought that going higher will make it harder to get the essential and healthy nutrients needed from sources of protein and carbohydrates while still limiting total calories to an appropriate amount for body weight management. Thus, if you can meet your total nutritional needs and calorie target while increasing your fat intake above the previously mentioned upper limit this should be safe. However, limits regarding saturated and trans fatty acids should be kept in mind (see below).

Note: Ketogenic diets are an example of a dietary strategy with fat intake considerably above the upper limit listed above. There are pros and cons of ketogenic diets; for example one pro is appetite suppression(Gibson, 2015; Roekenes, 2021) while one con is difficulty maintaining or building skeletal muscle.(Vargas, 2018; Ashtary-Larky, 2021) The health implications of sustaining a ketogenic diet for extended periods of time are unclear. I will discuss ketogenic diets in more detail in Lesson 13.

Types of dietary fat

There are four chemical structures of fatty acids: saturated (SFA), monounsaturated (MUFA), polyunsaturated (PUFA), and trans (TFA). Higher intakes of PUFA and MUFA have been associated with lower risk of mortality, while higher intakes of SFA and TFA have been associated with higher risk of mortality.(Kim, 2021) There is also research indicating that replacing SFA with MUFA or especially PUFA can improve blood lipids and measures of blood glucose control(Schwingshackl, 2021) as well as decrease the risk of cardiovascular events when replacing SFA with PUFA.(Hooper, 2020b) However, this does not consider potential differences between the subtypes of each classification. There are many controversies as well as open questions in the literature regarding the health effects of different types and quantities of the various fatty acids.(Visioli, 2020) I will discuss relevant aspects of each type below.

Saturated fatty acids (“SFA”)

The general health recommendation is to keep SFA intake at <10% of total calories. The American Heart Association recommends keeping saturated fat intake at <7% of total calories. There are several authors who disagree with this recommendation, and the overall literature base is riddled with controversy.(Liu, 2017; Harcombe, 2019; Kaur, 2020; Heileson, 2020; Astrup, 2021; Lawrence, 2021 – this has been critiqued (citations included below); Johnson, 2023; Teicholz, 2023) For a formal overview of this controversy, see the cited article series designed as an Oxford-style debate.(Kris-Etherton, 2020; Krauss, 2020a; Krauss, 2020b)

Part of this controversy is likely attributable to individual variability within the cholesterol response to SFA.(Griffin, 2021) There is also evidence that different saturated fats have different health properties (example: saturated fat from dairy seems less harmful than saturated fat from meat).(Unger, 2019; Brouwer, 2020) This is likely due in part to structural differences as well as differences in the food matrices (see note below) within which various SFAs are found.(Astrup, 2020) In fact, an argument can even be made that the 15 carbon odd-chain SFA pentadecanoic acid should be considered an essential fatty acid.(Dornan, 2021)

a table of LDL particle sizes
Reproduced from (Froyen, 2021)

In addition to overall cholesterol, saturated fatty acids seem to have variable impacts on the size and density of the LDL cholesterol particles. There are many subclasses of LDL particles as shown in the table to the right, and generally the small, dense type are found to be more harmful from a cardiovascular disease perspective. A 2021 review indicates that overall increased SFA intake may shift the LDL particle size in a health-beneficial direction, but when looking at individual saturated fatty acids there are variable responses.(Froyen, 2021) Additionally, when normalizing the subclasse distribution for the number of LDL particles the distribution itself seems less relevant for risk determination, and it has been generally shown that decreasing SFA intake will decrease the total quantity of LDL particles.(Maki, 2021b) We will need more research to truly determine the health impact of the various types of saturated fatty acids.

At this point I agree with the notion of attempting to limit SFA intake to <10% of your daily calories, though going over this occasionally and especially with dairy (preferably excluding butter and hard margarines)(Brouwer, 2020) or dark chocolate(Morze, 2020) is unlikely to pose any significant health risk. I do think the evidence is pointing towards moving away from this specific type of recommendation and moving more towards recommendations that also consider the underlying food source and matrix; more research is needed to generate confident recommendations with this in mind.

It also may be more important to keep SFA intake on the lower side when eating in a caloric surplus. In this circumstance increasing SFA intake does seem more harmful and I recommend keeping the intake to<10% of your total calories (which is easier when in a surplus as you are able to consume more total calories).(Rosqvist, 2014)

As the saturated fat molecules are relatively linear, it is easy for them to stack on top of each other and thus they tend to be solids at room temperature. OF note, some SFAs have branching points; these will not stack as well and will thus potentially have different properties (more in line with MUFA and PUFA).(Astrup, 2020)

Note: While the saturated fat from dairy seems less harmful than from other sources, a recent study replacing the saturated fat from dairy with unsaturated fat yielded improved health markers.(Vasilopoulou, 2020) Of note, rather large amounts of dairy were provided during this trial and it will need to be replicated with more realistic quantities.

Example: If a person wants to eat a 2,000 kcal/day diet and keep SFA intake at <10% of their total calories, 10% of 2,000 is 200 kcal, and this would be generated from 200/9 = 22 grams of fat. Thus, they should aim to keep their saturated fat intake under 22 grams. If they have significant cardiovascular risks and want to follow the American Heart Association guidelines then they should keep their saturated fat intake under 2,000 * 0.07 / 9 = 16 grams daily.

Monounsaturated fatty acids (“MUFA”)

There are no specific recommendations for monounsaturated fat intake and the evidence overall is mixed regarding a benefit to purposely including more of this in your diet in lieu of other nutrients.(Fattore, 2018) A 2021 SR/MA of prospective cohort studies found that increased MUFA consumption yields a small benefit for reducing all-cause mortality (a 3% decreased risk for an additional 5% of total energy intake by MUFA) with no benefit for cardiovascular mortality or cancer mortality.(Lotfi, 2021) The lack of significant benefits and overall mixed evidence base may stem from the source of the MUFA as a recent study (with associated commentary) indicated a beneficial health impact when this is predominantly consumed from plant sources as opposed to animal sources.(Guasch-Ferré, 2019; Ros, 2019) Thus, it is possible MUFA do not have significant health implications themselves but rather reflect the overall food matrix (see the note below) within which they are present.

With both of the adjacent carbons of the double bond on the same side, this molecule is much less linear than saturated fat. These molecules thus stack together less well and tend to form a liquid at room temperature.

Note: The term “food matrix” alludes to the full food source of the nutrients in question. Many studies are done on isolated nutrients but generally we do not consume nutrients in isolation. When we consume whole foods the health impact is not necessarily just the sum of the individual parts. This is due to potentially competing effects of nutrients within a food that can alter absorption as well as the many micronutrients and phytonutrients contained within a full food source that are generally not considered in studies of individual nutrients. This can lead to the differences seen in the plant vs animal sources of MUFA and potentially the differences in SFA from dairy vs nondairy sources (though the chemical structure of the SFA may play a role in those differences as well).

Polyunsaturated fatty acids (“PUFA”)

Polyunsaturated fat is generally considered to have either positive or neutral effects on overall health. There is a body of evidence suggesting replacing SFA with PUFA leads to better cardiovascular and overall health outcomes.(Siri-Tarino, 2015) The two essential fatty acids mentioned above, LA & ALA, are both polyunsaturated. Overall, most data indicates a potential benefit of increased PUFA intake (particularly in lieu of SFA or refined carbohydrates). This may extend to changes in body composition as well.(Monnard, 2020)

However, not all research supports health benefits, and controversy persists.(Fattore, 2018, Forouhi, 2018) This is in part due to the fact that by the nature of being polyunsaturated these compounds have multiple double bonds in their structures; there are many opportunities for oxidation and peroxidation of these compounds and this may exert negative health effects.(Hu, 2021; Lawrence, 2021 – this has been critiqued (citations included below)) Ultimately it may come down to the food preparation itself as methods that yield greater oxidation (ie, frying in oil) may yield more harmful products.(Addis, 2021) Thus, while overall the evidence does suggest health benefits from increased intake of PUFA, it may be most helpful to use cooking processes with lower risk of oxidation (principally by preparing them with low heat/light/air exposure, as well as minimal storage time prior to consumption; I briefly discuss this in Lesson 10).

See a note below for discussion of the various PUFAs, particularly ϖ-3 fatty acids, and the research regarding supplementing them directly.

Similar to MUFA, PUFA do not stack well together and also tend to be liquids at room temperature.

Note: It can be a bit confusing to keep straight the differences between the various PUFA. There are a lot of them. The body can utilize LA, an ω-6 fatty acid, to synthesize many more ω-6 fatty acids. One of these is arachidonic acid (“AA” or “ARA”). The body can utilize ALA, an ω-3 fatty acid to synthesize many more ω-3 fatty acids. Two of these include eicosapentaenoic acid (“EPA”) and docosahexaenoic acid (“DHA”). However, the conversion of ALA to these other compounds is not very efficient, and thus it is commonly recommended to directly consume additional EPA and DHA specifically. EPA and AA both utilize the same enzymes for further metabolism.

Prior concerns of unhealthy ratios of ω-6 to ω-3 intake seem generally unfounded and may reflect inadequate ω-3 intake rather than excessive ω-6 intake.(Marventano, 2015; Maki, 2018; Monnard, 2020) For example, as indicated above, higher LA intakes have been associated with decreased mortality.(Li, 2020) There is some evidence that the AA:EPA ratio is more meaningful, but more research is needed to confirm this and to determine its full prognostic value in prospective cohorts.(Davinelli, 2021)

Another potential biomarker is the n-3 index, defined by calculating the amount of EPA + DHA as a percentage of total fatty acids (typically in red blood cell membranes). This also seems to be a useful marker with better health outcomes when the n-3 index is higher, however, similar to the AA:EPA ratio more research is needed to determine its full prognostic value.(Davinelli, 2021)

Thus, at this point in time it is difficult to determine an optimal level of intake of EPA and DHA. As discussed in Lesson 11, there is ample evidence that consuming fish that contain these compounds is beneficial for overall health. I discuss direct supplementation in the next section.

Supplementation of ω-3 fatty acids

Below I have included 5 of the most recent meta-analyses and general review articles on ω-3 fatty acid supplementation. I provide conclusions that I draw from this body of research underneath this (you can skip to my conclusions and not read through the 5 analyses if desired).

In the data analyses I include relative risks and confidence intervals. A relative risk describes the percent change in risk of an event occurring as a result of a given intervention. The 95% confidence interval denotes the uncertainty in this estimate; in general, larger sample sizes and more consistent data between studies will yield smaller confidence intervals. If the confidence interval crosses 1.00 then most people would consider this to not be statistically significant. The Cochrane review included below actually uses a different definition of significance, but this is not a standard approach (they state that if the relative risk is far enough from 1.00 (ie, 8% off, or 0.92) then they find it to be meaningfully significant even if they 95% confidence interval crosses 1.00).

As an example, I write 0.80 [0.70, 0.90] if the relative risk is 0.80 with a 95% confidence interval of 0.70-0.90. This implies a 20% decrease in the relative risk of an event occurring with a 95% confidence interval of 10-30%. You can take this to mean there is a 95% chance that the true relative risk is within 10-30%.*

*Confidence intervals have a slightly more technical definition but usually this is close enough to the true meaning that a more detailed understanding is not necessary.

In 2019 a meta-analysis of 13 randomized controlled trials (this updated a prior meta-analysis of 10 studies with 3 new trials published near the end of 2018) regarding the impact of marine ω-3 fatty acid supplementation in trials with a sample size of at least 500 and at least 1 year follow-up was published.(Hu, 2019) The authors performed analyses with and without the REDUCE-IT trial as this latter trial used a much higher supplementation dose (4 grams of EPA) than the other trials (max 1.8 grams of EPA+DHA).

  • In the analysis without the REDUCE-IT trial the pooled relative risks and 95% confidence intervals were:
    • myocardial infarction (MI): 0.92 [0.86, 0.99], coronary heart disease (CHD): 0.95 [0.91, 0.99], CHD death: 0.92 [0.86, 0.98], cardiovascular disease (CVD): 0.97 [0.94, 0.99], CVD death: 0.93 [0.88, 0.99], major vascular events: 0.97 [0.94, 1.00]
    • For every 1000 milligram per day (mg/d) supplementation there was a decrease in CVD by 17% and major vascular events by 17%.
  • When including the REDUCE-IT trial the results were more significant:
    • MI: 0.88 [0.83, 0.94], CHD: 0.93 [0.89, 0.96], CVD: 0.95 [0.92, 0.98], CVD death: 0.92 [0.88, 0.97], major vascular events 0.95 [0.93, 0.98]
    • For every 1000 mg/d supplementation there was a decrease in CHD by 7%, major vascular events by 8%, MI by 9%, CVD by 9%, and stroke by 11%.

In 2020 a Cochrane review on the impact of ω-3 fatty acids for the primary and secondary prevention of cardiovascular disease examined 86 randomized controlled trials of at least 12 months duration, looking at studies with direct supplementation as well as studies that used enriched foods or dietary advice.(Abdelhamid, 2020) Regarding EPA & DHA the authors found no impact on all-cause mortality, cardiovascular events, stroke, or arrhythmia. They found evidence of a small impact on:

  • CVD mortality: 092 [0.86, 0.99], CHD events: 0.91 [0.85, 0.97], CHD mortality: 0.90 [0.81, 1.00]
  • a decrease in triglycerides of ~15% in a dose-dependent manner

In 2021 an updated meta-analysis and meta-regression of intervention trials was published.(Bernasconi, 2021) Here the authors used the same search criteria as the above Cochrane review except they only looked at supplementation trials, not studies that incorporated dietary advice. There were 40 included studies. They found no impact on CVD events but did see a decrease in:

  • MI: 0.87 [0.80, 0.96], fatal MI: 0.65 [0.46, 0.91], CHD events: 0.90 [0.84, 0.97], CHD mortality 0.91 [0.85, 0.98]
  • For each additional 1 gram intake per day they did find:
    • a decrease in CVD events of 5.8% and a decrease in MI of 9.0%
    • no linear relationship for CHD events, fatal MI, and CHD mortality
  • They did not find evidence that supplementation of EPA alone is superior to EPA+DHA.

In 2021, a general review article discussing the above analyses and two more recent trials (the STRENGTH and OMEMI trials) not included in any of the prior analyses ultimately concluded that it is too soon to start to recommend high dose supplementation of EPA, DHA, or both for the primary or secondary prevention of various cardiovascular diseases.(Khoukaz, 2021)

  • The authors note that in the REDUCE-IT trial the control group was provided mineral oil, and while the authors of the REDUCE-IT trial have provided evidence that this did not confound the results it is not completely clear if the mineral oil in the control group may have generated some risk of harm.
  • The STRENGTH trial, not included in the above analyses, tested 4 grams daily supplementation of DHA+EPA in individuals on high-intensity statin therapy with at least 1 additional cardiovascular risk factor. This trial was stopped early as there was no evidence of benefit but there was a small increased risk of atrial fibrillation (2.2% vs 1.3% in the control group).
  • The OMEMI trial was published more recently and examined the impact of supplementing 930 mg EPA with 660 mg DHA. Subjects were elderly patients with a recent MI who were receiving statin therapy; no benefit was found but there was a trend towards an increased risk of atrial fibrillation.
  • The authors note that studies finding benefit frequently did not include individuals on statin therapy when they likely should have been based on baseline health risks; had they been on statins then benefits of DHA+EPA may not have been seen.
  • The authors also note that many of the benefits are seen with secondary analyses or subgroup analyses rather than in primary endpoint analysis (this increases the risk of multiple hypothesis testing leading to spurious associations).

A separate 2021 review article from the same authors of the 2021 meta-analysis above (that did not include the more recent STRENGTH and OMEMI trials) discusses the totality of the literature including these new trials and takes a favorable viewpoint towards supplementing ω-3 fatty acids.(Elagizi, 2021) They state they are in the process of updating their prior meta-analysis to include the new trials and there is still an overall benefit to supplementing.

A 2022 meta-analysis found essentially no benefit towards ω-3 supplementation of any dose for all-cause mortality, MI, or stroke.(Markozannes, 2022) The authors acknowledge we need more research on high dose EPA supplementation.

A 2022 meta-analysis found mild benefit of ω-3 supplementation for major adverse cardiovascular events, cardiovascular disease mortality, and myocardial infarction at relative risks of 0.95, 0.94, and 0.90, respectively, but these findings were heavily influenced by the REDUCE-IT trial.(Yan, 2022) There was a 25% increased risk of atrial fibrillation and when using the more effective EPA supplements there was an increased risk of bleeding.

A 2023 meta-analysis summarized much of the above evidence, placing it in the figure I have included below.(Bae, 2023) Panel A shows evidence regarding experiencing any of fatal or nonfatal heart attack, fatal or nonfatal stroke, and cardiovascular death. Panel B shows evidence regarding the risk of developing new-onset atrial fibrillation.

Reproduced from: Bae JH, Lim H, Lim S. The Potential Cardiometabolic Effects of Long-Chain ω-3 Polyunsaturated Fatty Acids: Recent Updates and Controversies. Adv Nutr. 2023 Jul;14(4):612-628. doi: 10.1016/j.advnut.2023.03.014. Epub 2023 Apr 7. PMID: 37031750; PMCID: PMC10334139.

So what can we conclude from all of this? Similar to many other topics in nutrition, it’s hard to make definitive conclusions. At this point, it’s not clear if the REDUCE-IT trial shows a true benefit with high-dose EPA supplementation (4 grams daily) or if the concerns of mineral oil being used for the control, plus the additional trends towards increased atrial fibrillation and significant bleeding events in the EPA group, negate the potential health benefits that are seen. The STRENGTH trial did not find benefits of 4 grams of DHA+EPA, but perhaps EPA alone is the way to go. As has been discussed, more research is needed to evaluate this.(Maki, 2021a; Hamilton-Craig, 2023)

It’s also not clear if the higher dose supplements will be more beneficial in populations that have little fish intake at baseline. Otherwise, benefits across the board seem small with the confidence intervals of most relative risk estimates being close to 1.

Thus, overall, I am not confident there is any merit to supplementing high dose ω-3 fatty acids, as the overall benefit seems mild if it even exists. There does seem to be a risk of harm regarding atrial fibrillation (an 11% increased risk per 1 gram of intake per a 2021 SR/MA(Gencer, 2021)) and bleeding events. The actual benefit of supplements may disappear in individuals who are following healthy dietary practices and taking medications as advised in recent guidelines for cardiovascular disease risk reduction. I would favor increasing one’s fish intake (recommendations discussed in Lesson 11) instead.

Trans fatty acids (“TFA”)

TFA are typically categorized as either industrial (a byproduct of baking or cooking certain products with high temperatures) or ruminant (produced by certain animals (ie, cows) and then absorbed with their consumption). The research almost universally indicates that industrial TFA are harmful to human health and should be avoided. The research on ruminant TFA is less clear with evidence generally suggesting they do not impart a harmful effect.(de Souza, 2015) One caveat here is that people typically consume ~2.5x more industrial than ruminant TFA, and this makes it harder to pick up a harmful signal with the ruminant TFA. Overall, I would not worry about consuming ruminant TFA while industrial trans TFA should be avoided.

Similar to SFA, TFA have a mostly linear conformation, making them stack together more easily and more likely to be a solid fat at room temperature.


Dietary fat is important for a number of reasons, and the full range of positive and negative health impacts of the various types are not completely clear:

  • Industrial trans fat is universally regarded as harmful.
  • Ruminant trans fat does not seem harmful in typically consumed quantities but may be harmful in larger quantities.
  • Saturated fat from processed meats and unprocessed red meats as well as baked goods are generally considered harmful, though some disagree with this sentiment.
  • Saturated fat from dairy (with a possible exception of butter and hard margarines) seems less harmful than from other sources.
  • Monounsaturated fat may be neutral towards health overall but beneficial and harmful when consumed from plant and animal sources, respectively.
  • Polyunsaturated fat is generally considered neutral or beneficial towards health, though consideration of potential oxidation and peroxidation should be kept in mind.
  • The jury is still out regarding ω-3 fatty acid supplementation, but there is likely at most a mild benefit, if any at all, for individuals who include healthy sources of fish in their diet.

Similar to the last lesson where studies on isolated protein sources were not necessarily applicable to people eating food items and mixed meals, studies on isolated fatty acids are not necessarily applicable to whole food consumption. It is apparent with the significant controversy alluded to above that the sources of the fats play a large role in their overall health impact. For this reason, much of the literature is starting to shift towards consideration of overall dietary patterns and food sources as opposed to just individual nutrients. With this in mind, I will discuss food groups in Lessons 10 and 11 and various diets in Lesson 13.

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