Tag Archives: Omega-3

In Part I of this series, we looked at the longstanding recommendations of many governmental health organizations to reduce dietary saturated fat and replace it with omega-6 fats. Doing so supposedly, these organizations claim, reduces cardiovascular disease (CVD) risk. As we saw in Part I, however, there is considerable controversy within the nutrition science community concerning this claim. There’s a case to be made for decreased saturated fat, but there’s also a case for decreased omega-6. Since the current science is far less black-and-white than the recommendations would lead you to believe, with Part II of this series, we’ll be looking at the debate from a paleolithic perspective, with the hope of gaining a broader and more balanced perspective on optimal consumption levels of both saturated and polyunsaturated fats.

 

Paleo PUFA Consumption

Although conclusive scientific studies are lacking, we can gain valuable insight by examining the diets of our Paleolithic ancestors. How much of these nutrients did they consume? How do current PUFA recommendations compare to PUFA consumption by our Paleolithic ancestors?

To know how much saturated fat and PUFAs they ate, we first must estimate how much total fat they ate. As always, Paleolithic diets varied based on geography and access to certain foods, but in general, our ancestors ate relatively more fat, more protein, and less carbohydrate, compared to contemporary diets. In 2000, Dr. Cordain and his colleagues estimated the following macronutrient ratios for Paleolithic diets:[1]

  • Fat: 28-58% of calories
  • Protein: 19-35% of calories
  • Carbohydrates: 22-40% of calories

They arrived at these estimates, in part, by analyzing the diets of 229 hunter-gather societies, assessing their specific foods, and measuring their ratios of plant to animal food consumption. The vast majority (73%) of these societies derived more than 50% of their calories from animal foods [2].

Next, we need to estimate how macronutrients are distributed within the specific foods our ancestors ate. Figures 1 and 2 below compare the meat of wild animals with the meat of commercially raised animals. Figure 1 shows the percentage of calories from protein, fat, and carbohydrate (note that carbs are negligible in animal meat) whereas Figure 2 shows each type of fat as a percentage of total fat. We can assume, with a reasonable degree of certainty, that wild animals today are similar to those hunted and consumed by our ancestors, with respect to body composition.

Macronutrient Calories in Animal Foods

Figure 1. Percent of calories from macronutrients (protein, fat and carbohydrate) in wild and commercial animal foods.

Proportion of Fatty Acids in Animal Foods

Figure 2. Proportions of fatty acids in wild and commercial animal foods.

 

Examining these figures, two dominant trends emerge:

1. Wild meat is proportionally higher in protein and lower in fat compared to commercially raised meat.
2. The fat portion of wild meat is proportionally higher in PUFAs – both omega-6 and omega-3 – compared to commercial meat.

Additionally, we can say that grass-fed beef is closer to wild meat than grain-fed beef, but both grass-fed beef and grain-fed beef poorly approximate wild meat.

The above observations are based on data from the USDA Nutrient Database and are substantiated by numerous studies comparing wild and domesticated animals [3], [4], [5], [6], [7].

Additionally, scientists have recently extracted frozen, Paleolithic-era animal carcasses from the Siberian tundra. Tissue analyses of these carcasses further highlight the similarities between Paleolithic meat and modern wild meat, particularly with respect to n-6/n-3 ratios [8], [9].

 

The Ever-Important Omega Ratio

As we saw in part I, many RCTs, observational studies, and meta-analyses addressing omega-6 consumption fail to properly account for omega-3 consumption (and the n-6/n-3 ratio). For our Paleolithic ancestors, this ratio was approximately 1/1 (and probably no higher than 3/1) [10]. Today, however, the ratio approaches 20/1 for people consuming typical Western diets [11].

This disparity is critical to the entire debate about saturated fat and its replacement with omega-6. Recent studies show saturated fat isn’t a health menace, as previously believed [12][13][14][15]. On the other hand, our reliance on commercially raised meat has probably skewed our fat consumption by over-representing saturated fat and under-representing PUFAs. We’ve compensated by consuming large quantities of vegetable oils, which are rich in omega-6, but omega-3 consumption has fallen by the wayside.

The consequences of our dramatically elevated n-6/n-3 ratios include the following:[16]

  • Increased inflammation
  • Increased leptin and insulin resistance
  • Increased risk for diabetes
  • Increased weight gain and risk for obesity

 

Keeping it Real

Just as previous generations shunned saturated fat, we would be foolish to shun omega-6 completely. After all, omega-6 is an essential fatty acid (EFA), meaning our body requires it and can only obtain it from food. That being said, some sources of are better than others.

It’s easy to get good quality omega-6 from olive oil, avocados, nuts, and from certain animal foods. By following the Paleo Diet template, you’ll get a good balance of omega-6 and omega-3, plus a good distribution of SFAs, MUFAs, and PUFAs.

With respect to omega-6, our best advice would be to eliminate all vegetable and seed oils from your diet. These include, among others:

  • Soybean oil
  • Corn oil
  • Safflower oil
  • Sunflower oil
  • Canola oil
  • Grapeseed oil

The problem with these oils is they contain very high amounts of omega-6. Consuming them increases your n-6/n-3 ratio, while also introduces potentially dangerous free radicals.

 

Unstable Seed Oils

The industrial processing of vegetable seed oils involves high-heat and the use of various chemical solvents – a guaranteed recipe for free radical oxidation and lipid peroxidation [17].

Cooking with PUFA-rich oils creates lipid oxidation products known as alkenals, some of which are toxic [18].

Olive oil, which contains some PUFAs, but is mostly comprised of MUFAs, has been shown to be more heat-stable and better for cooking compared to vegetable oils [19],[20]. It’s best to avoid high-heat cooking with any oils, but those containing higher amounts of SFAs and MUFAs are more stable than those with higher amounts of PUFAs.

 

Conclusion

Saturated fat isn’t unhealthy, but it needn’t be over represented in our diets. Many health authorities recommend replacing saturated fat with omega-6, and although some studies support this recommendation, most fail to differentiate between omega-6 and omega-3. Replacing some saturated fat with PUFAs could be beneficial, particularly if doing so lowered the n-6/n-3 ratio. For most people, this would mean eliminating all vegetable seed oils, while increasing oily fish (omega-3) consumption.

It’s also important to recognize that meat from game animals is better than commercially raised meat, but since obtaining wild meat is impractical for most people, pasture-raised meat (grass-fed, etc.) should always be favored.

Don’t over complicate things too much. You don’t need to meticulously track your fat consumption. By following The Paleo Diet template and listening to your body, you’ll get a healthy mix.

 

References

[1] Cordain L, et al. (2000). Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. American Journal of Clinical Nutrition, 71(3). Retrieved from (link).

[2] Cordain L, et al. (2000). Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. American Journal of Clinical Nutrition, 71(3). Retrieved from (link).

[3] Davidson B, et al. (Mar-Apr 2011). Meat lipid profiles: a comparison of meat from domesticated and wild Southern African animals. In Vivo, 25(2). Retrieved from (link).

[4] Rule DC, et al. (2002). Comparison of muscle fatty acid profiles and cholesterol concentrations of bison, beef cattle, elk, and chicken. J Anim Sci., 80(5). Retreived from (link).

[5] Cordain, et al. (Mar 2002). Fatty acid analysis of wild ruminant tissues: evolutionary implications for reducing diet-related chronic disease. Nature, 56(3). Retrieved from (link).

[6] Cordain, et al. (2001). Fatty acid composition and energy density of foods available to African hominids. Evolutionary implications for human brain development. World Rev Nutr Diet., 90. Retrieved from (link).

[7] Fine LB, et al. (2008). Comparison of lipid and fatty acid profiles of commercially raised pigs with laboratory pigs and wild-ranging warthogs. South African Journal of Science, 104. Retrieved from (link).

[8] Guil-Guerrero JL, et al. (2014). The Fat from Frozen Mammals Reveals Sources of Essential Fatty Acids Suitable for Palaeolithic and Neolithic Humans. PLoS One., 9(1). Retrieved from (link).

[9] Guil-Guerrero JL, et al. (2015). The PUFA-Enriched Fatty Acid Profiles of some Frozen Bison from the Early Holocene found in the Siberian Permafrost. Scientific Reports, 5. Retrieved from (link).

[10] Eaton SB, et al. (1998). Dietary intake of long-chain polyunsaturated fatty acids during the paleolithic. World Rev Nutr Diet., 83. Retrieved from (link).

[11] Simopoulos AP. (2016). An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity. Nutrients, 8(3). Retrieved from (link).

[12] Ruiz-Nunez, B., D.A.J. Dijck-Brouwer, and F.A.J. Muskiet, The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease. Journal of Nutritional Biochemistry, 2016. 36: p. 1-20.

[13] Chowdhury, R., et al., Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk A Systematic Review and Meta-analysis. Annals of Internal Medicine, 2014. 160(6): p. 398-+.

[14] Astrup, A., et al., The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? American Journal of Clinical Nutrition, 2011. 93(4): p. 684-688.

[15] Hoenselaar, R., Saturated fat and cardiovascular disease: The discrepancy between the scientific literature and dietary advice. Nutrition, 2012. 28(2): p. 118-123.

[16] Simopoulos AP. (2016). An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity. Nutrients, 8(3). Retrieved from (link).

[17] Kanner J, et al. (2007). Dietary advanced lipid oxidation endproducts are risk factors to human health. Mol Nutr Food Res., 51(9). Retrieved from (link).

[18] Halvorsen BL, et al. (2011). Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements. Food Nutr Res., 55. Retrieved from (link).

[19] Halvorsen BL, et al. (2011). Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements. Food Nutr Res., 55. Retrieved from (link).

[20] Silva L, et al. (2010). Oxidative stability of olive oil after food processing and comparison with other vegetable oils. Food Chemistry, 121(4). Retrieved from (link).

FOOD-official-meatFor over a decade now, a debate has been raging within the nutrition science community. One side views saturated fat as generally unhealthy; they recommend replacing these fats, at least to some degree, with omega-6 polyunsaturated fats. The other side views saturated fat as health-supportive, or at least health-neutral; likewise, they regard omega-6 as somewhat unhealthy and typically recommend decreasing its consumption. So, who has it right? The truth seems to be grey and somewhere in between.

 

The Modern Diet

Americans have largely followed the US government’s dietary advice for the past 40 years. For example, following official dietary advice in the 80s to reduce fat in our diets, we decreased our fat consumption from 45 to 34% of calories, on average, while increasing our carbohydrate consumption from 39 to 51% of calories [i].

We made these changes because doing so – or so we were told – would decrease cardiovascular disease (CVD), which was and still remains the number one cause of death in the western world.

However, there are also different types of fats (see Figure 1) and both international and US government guidelines have made recommendations about the types of fats we should consume. Current recommendations suggest reducing saturated fat to a maximum of 10% of total calories while increasing omega-6 to somewhere between five and 10% of total calories  [ii], [iii].

Figure 1. The basic types of fat.

Different Types of Fats

 

As a population, we’re pretty much within these recommended zones. We get 11% of our calories from saturated fat and 8% from polyunsaturated fat (primarily the omega-6 variety)[iv], [v].

CVD mortality has declined since its peak in the 1950s, but CVD prevalence remains very high. For example, the total number of inpatient cardiovascular operations and procedures increased 28% between 2000 and 2010 (from 5.9 million to 7.6 million procedures) [vi]. Moreover, prevalence of metabolic syndrome, a precursor to CVD, has reached a staggering 34% of the population [vii].

If the advice to replace saturated fat with omega-6 was designed to reduce CVD, then what went wrong? Was the advice misguided? Let’s look at the evidence.

 

The Pro-PUFA Studies

Numerous recently published meta-analyses support the conclusion that replacing saturated fat with polyunsaturated fat (though not necessarily omega-6) leads to modest CVD risk reductions. For example:

 

  • Mozaffarian D, et al. (2010) pooled data from 8 randomized controlled trials (RCTs) encompassing 13,614 participants and 1,042 coronary heart disease (CHD) events. They determined that for every 5% caloric increase in polyunsaturated (PUFA) fat there is a corresponding 10% decrease in CHD risk [viii].

Study Limitations: PUFA consumption for this study included both omega-6 and omega-3. Therefore, it’s possible the positive results may have been primarily from omega-3; negative effects from omega-6 could have been masked.

 

  • Hooper L, et al. (2015) pooled data from 13 long-term RCTs encompassing 53,300 participants. They found “a small but potentially important reduction in cardiovascular risk when saturated fat intake was lowered,” particularly by replacing saturated fat with PUFAs, but not by replacing it with carbohydrates [ix]. However, the study found no clear effect of reducing saturated fat on total mortality.

Study Limitations: Among these RCTs, omega-6 and omega-3 PUFAs were grouped together. Therefore, analyzing the individual impact of either PUFA was not possible.

 

  • Farvid MS, et al. (2014) conducted a meta-analysis of 11 studies pertaining to omega-6 (LA) intake and CHD. They concluded “a 5% of energy increment in LA intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events and a 13% lower risk of CHD deaths”.

Study Limitations: (1) Whereas this study did specifically measure omega-6, it didn’t account for the ratio of omega-6 to omega-3 (referred to as “n-6/n-3” hereafter), (2) the meta-analysis only included observational studies, not RCTs, and (3) the meta-analysis measured cardiovascular disease mortality, but not all-cause mortality.

 

  • Yanping Li, et al. (2015) conducted a meta-analysis of two observational studies, the first of which followed 85,000 women for 24 years and the second of which followed 43,000 men for 30 years. In total, 7,667 cases of CHD were documented. The authors concluded that replacing 5% of the energy intake from saturated fats with equal energy from PUFAs was associated with a 25% reduced risk of CHD [xi].

Study Limitations: (1) The study was observational (no RCTs were included), (2) the study didn’t account for the n-6/n-3 ratio, and (3) the data was derived from food frequency questionnaires.

 

  • Wu JH, et al. (2015) conducted a cohort study of 2,792 older US adults (mean age, 74). To avoid the problems associated with food frequency questionnaires, they analyzed circulating omega-6 (LA only) blood levels, an objective biomarker of LA consumption[xii]. Those within the highest quintile of circulating LA had 13% lower all-cause mortality than those in the lowest quintile. Interestingly, when the authors stratified subjects based on combined LA and omega-3 PUFA concentrations, those in the highest quintile had a 54% lower all-cause mortality risk compared to those in the lowest quintile.

Study Limitations: This study was designed better than most, but didn’t completely demonstrate how changes to the n-6/n-3 ratio affect mortality.

 

The Anti-PUFA Studies

Christopher Ramsden, MD is a clinical investigator for the National Institutes of Health. During the past decade, Ramsden has been among the most prominent scientists challenging the mainstream narrative that omega-6 should replace saturated fat. Through a series of studies, most of which were published by the British Medical Journal, Ramsden and his colleagues have put forth an important antithesis [xiii], [xiv], [xv]. Some of their conclusions include:

  • Increasing omega-3 relative to omega-6 significantly reduces the risk of heart disease.
  • Diets rich in omega-6 increase risks of all CHD endpoints, while increasing all-cause mortality risk.
  • Substituting dietary omega-6 LA in place of SFA increases all-cause mortality risk, as well as risks from coronary heart disease.
  • Benefits previously attributed to greater intake of total PUFAs may be specifically attributable to omega-3 and not to omega-6 LA.

Some of the problems with the studies used to justify increased omega-6 consumption, according to Ramsden and his colleagues, include:

  • Failure to distinguish between trials that selectively increased omega-6 and those that substantially increased omega-3
  • Failure to acknowledge that omega-6 and omega-3 replaced not only SFAs, but large amounts of trans-fats in many trials used in the pro-PUFA meta-analyses
  • Failure to provide the specific compositions of the diets (particularly with respect to omega-6 and trans-fat) used in the pro-PUFA meta-analyses
  • Failure to analyze the impact of n-6/n-3 ratios


The Middle Ground

As you can see, the consumption of saturated fat and omega-6 are controversial, partly because we lack rigorous studies specifically designed to test the optimal balance between saturated fat, omega-6, and omega-3. This was precisely the conclusion of a 2015 Cochran review by Al-Khudairy L, et. al. [xvi].

The authors sought RCT data demonstrating the effectiveness of increasing or decreasing omega-6 for the prevention of cardiovascular disease. Additionally, they wanted to assess the impact of total omega-3 consumption and the n-6/n-3 ratio.

Unfortunately, “very few trials were identified with a relatively small number of participants randomized.” They concluded, (1) there is currently insufficient evidence to recommend either increased or decreased omega-6 consumption, and (2) larger, better RCTs on this topic are needed.

 

Conclusion

In Part 1 of this article series, we’ve seen that many critical questions about optimal saturated- and polyunsaturated fat consumption levels haven’t yet been answered by science. While we wait for better RCTs to be conducted, we can gain deeper insights and a better understanding of this issue by examining the fat consumption patterns of our Paleo ancestors. Be sure to check out Part II of this series, where we’ll do just that.

 

References

[i] Cohen E, et al. (2015). Statistical review of US macronutrient consumption data,

1965–2011: Americans have been following dietary guidelines, coincident with the rise in obesity. Nutrition, 31. Retrieved from (link).

[ii] US Department of Health and Human Services and U.S. Department of Agriculture. (Dec 2015). 2015–2020 Dietary Guidelines for Americans. 8th Edition. Retrieved from (link).

[iii] FAO. (2010). Fats and fatty acids in human nutrition: Report of an expert consultation. Rome: Food and Agriculture Organization of the United Nations. Retrieved from (link).

[iv] Ervin RB, et al. Centers for Disease Control. (Nov 2004). Advanced Data from Vital Health Statistics. Retrieved from (link).

[v] Wright JD, et al. Centers for Disease Control. (Nov 2010). Trends in Intake of Energy and Macronutrients in Adults. From 1999–2000 Through 2007–2008. NCHS Data Brief, 49. Retrieved from (link).

[vi] Mozaffarian D, et al. (2015). Heart Disease and Stroke Statistics—2015 Update. Circulation, 131. Retrieved from (link).

[vii] Aguilar M, et al. (2015). Prevalence of the Metabolic Syndrome in the United States, 2003-2012. JAMA, 313(19). Retrieved from (link).

[viii] Mozaffarian D, et al. (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, 7(3). Retrieved from (link).

[ix] Hooper L, et al. (Jun 2015). Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev., 10(6). Retrieved from (link).

Farvid MS, et al. (Oct 2014). Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies. Circulation, 130(18). Retrieved from (link).

[xi] Yanping Li, et al. (Oct 2015). Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease. Journal of the American College of Cardiology, 66(14). Retrieved from (link).

[xii] Wu JH, et al. (Oct 2015). Circulating Omega-6 Polyunsaturated Fatty Acids and Total and Cause-Specific Mortality: The Cardiovascular Health Study. Circulation, 130(15). Retrieved from (link).

[xiii] Ramsden CE, et al. (2010). n-6 Fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. British Medical Journal, 104(11). Retrieved from (link).

[xiv] 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. British Medical Journal, 346. Retrieved from (link)

[xv] Ramsden CE, et al. (Apr 2016). Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). British Medical Journal, 353. Retrieved from (link).

[xvi] Al-Khudairy L, et al. (2015). Omega 6 fatty acids for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev., 16(11). Retrieved from (link).

Healthy Eating | The Paleo Diet

Anyone who follows the U.S. nutritional guidelines has almost certainly been frustrated at some point or another by the conflicting advice and sometimes hopelessly outdated marketing material – think the Food Pyramid that still graces the walls of many elementary school classrooms.

The frustration has reached the point that cries of government corruption and inappropriate influence of big food industry lobbyists are frequently heard. Case in point, the February 2015 draft of the U.S. Dietary Guidelines,1 published every five years, prompted over 29,000 public comments compared to a couple thousand in 2010. The outcry has been so strong it has led to a Congressional review to start in October.

And just last week journalist Nina Teicholz published a scathing review of the guidelines in the high impact factor journal BMJ.2

Teicholz accused the Dietary Guidelines Advisory Committee (DGAC) of not listing their conflicts of interest, of using reviews from industry influenced professional associations, and of overall “weak scientific standards.” Which is scary considering the importance of the 2015 Dietary Guidelines can’t be understated.

According to Teicholz, “the guidelines have a big influence on diet in the U.S., determining nutrition education, food labeling, government research priorities at the National Institutes of Health (NIH) and public feeding programs.”

So what did the Committee recommend? The overall body of evidence examined by the 2015 DAC identifies that a healthy dietary pattern is higher in vegetables, fruits, whole grains, low- or non-fat dairy, seafood, legumes, and nuts; moderate in alcohol (among adults); lower in red and processed meats; and low in sugar-sweetened foods and drinks and refined grains.

Certainly not a win for the Paleo community, but also not anything we haven’t heard from these agencies for a long time.

Dr Barbara Millen, the Chair of the Committee, published an immediate response in BMJ claiming that “the procedures used to develop the DGAC scientific report are expansive, transparent, and thoughtful, with multiple opportunities for public input.”1

Millen pointed out that the committee was nominated by their peers and rigorously reviewed. She even fired back at Teicholz saying that she was just one individual with a clear bias herself having written the book The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet.

The biggest point of contention, however, was the methods for selecting the research the recommendations were based on.

In 2010, the US Department of Agriculture established the Nutrition Evidence Library (NEL) to help ensure the quality of nutritional recommendations by establishing standards for identifying and selecting research.3

Teicholz contends that the DGAC “did not use NEL reviews for more than 70 percent of the topics” and instead selected studies ad hoc often relying on reviews by external professional associations.

Millen defended the committee claiming that “you don’t simply answer these questions on the basis of the NEL. On topics where there were existing comprehensive guidelines, we didn’t do them.” Millen also contended that the bulk of their research came from the NIH and other federal agencies.

To her credit, the Guidelines detail four methods of research selection, most of which involved at the least consulting the NEL.

Ultimately, it is the recommendations themselves that will determine the integrity of the report and Teicholz had issues with several of them, all of which are highly relevant to those of us in the Paleo world:

THE CONTESTED RECOMMENDATIONS

Teicholz addressed the recommendation for lower dietary saturated fats first, pointing out that no NEL review of the research on saturated fat from the past five years was conducted. She claimed many conflicting studies were omitted, in particular a large controlled clinical trial known as the Women’s Health Initiative (WHI). No benefits of a lower saturated fat diet were observed in a cohort of 49,000 women over seven years.4

Millen responded that the report states “dietary advice should put the emphasis on optimizing the types of dietary fat and not reducing total fat.”

Next, Teicholz addressed the report’s failure to endorse a low carbohydrate diet claiming critical research was left out including a meta-analysis and a critical review demonstrating a benefit of low carb diets for type 2 diabetes.5, 6 Millen simply replied that there is limited evidence of the long-term health effects.

One of the biggest shifts in the new guidelines was a stronger emphasis on plant-based diets with the recommendation to reduce meat particularly red meat. The draft 2015 Guidelines added for the first time a “Healthy Vegetarian Pattern” to their three recommended diets that also include a “Healthy Mediterranean-Style Pattern” and a “Healthy U.S.-Style Pattern.”

Teicholz contends that there has been no review by the NEL of the health effects of red meat. While an NEL review of a vegetarian diet does exist and states that the evidence is limited for its disease fighting power.7 Yet, Teicholz holds that the report arbitrarily upgraded the rating of the evidence. She also claimed that the Guidelines left out three contradictory NIH studies including one from the WHI that found no significant advantage of a diet high in fruit, vegetables and grains for weight loss, diabetes, heart disease, or cancer.8-11 Even the Guideline’s sole diagram addressing red meat, according to Teicholz, showed that diets high in red meat were equivocal with diets lower in red meat.

Millen did not address the question of red meat in her response, but the report stated that the three recommended dietary patterns reaffirmed the 2010 DGAC recommendations and aligned with the American Institute for Cancer Research (AICR) and the American Health Association (AHA).1

A MORE MUNDANE EXPLANATION

A friend of mine, who by her own admission had a “cushy” well-paid job at a large government nutrition agency, once gave me her impression of government nutrition.

Her job was to follow the current research and take her findings to the higher-ups. She was quickly frustrated by the all-too-common response. They would thank her for bringing it to their attention, then tell her they already knew about it and they weren’t going to do anything. Did she experience, first hand, government corruption or industry influence at play?

My friend had a much more mundane answer. In a government nutrition agency, she said, there’s one unforgivable sin – to make a recommendation contrary to the decades old accepted cannon and end up being wrong. So was something this mundane going on with the DGAC?

The Report starts by asserting it was motivated by the current state of public health in the United States, a lot of which was a result of poor dietary patterns. Half of U.S. adults have a chronic disease and two-thirds are obese. It goes on to say these patterns “adversely affected the health of the U.S. public for decades and raise the urgency for immediate attention and bold action.”1

Yet that “bold action” consists of recommendations that by their own admission are consistent with past DGAC reports.

The few new recommendations they offer – replacing refined grain products with whole grain products and the reduction of refined sugar and sodium in the diet – are neither novel nor in any way controversial within the nutrition community.

Even in the Paleo world, while we would say to bypass the grains altogether, if you’re going to eat them, we’re still generally going to recommend whole grain products over refined empty-calorie snacks.

Perhaps Teicholz’s most poignant criticism of the report was her pointing out “a reluctance by the committee behind the report to consider any evidence that contradicts the last 35 years of nutritional advice.” She goes on to say that with the failure of existing intervention strategies, they should be welcoming new views.

Nowhere is the aging nature of the report potentially more obvious than in its handling of omega-3 fatty acids. As mentioned above, Millen responded to Teicholz by stating that the committee focused more on types of fats than absolute quantity. Which would imply that omega-3 fats were a focus.

Yet omega-3s are mentioned only three times in the 571-page report. Once in the context of wild vs farm raised fish. One paragraph under mental health where they briefly review the vast research showing the benefits of omega-3 for the brain and finally to point out the single study that found an association between nutrients in the diet and type 2 diabetes because it differentiated types of fats.12

The broad ranging health benefits of consuming omega-3 fatty acids, and the ratio of omega-3 to omega-6 fatty acids in the diet are some of the most heavily researched topics currently in nutrition.13 Yet the report made no recommendations about omega-3s. Instead it focused on a decades-old concept of “achieving better saturated fat to polyunsaturated fat ratios.”

IS MUNDANE ANY BETTER?

Teicholz herself concludes by admitting the mundane may be more at play than conflict of interest or industry pressure – “nearly all nutrition scientists accept funding from industry. Of far greater influence is likely to be bias in favor of institutionalized hypothesis.”

Nonetheless, does this really make the end result any better?

The report may very well answer that question itself. It has long been accepted that there is a big difference between refined sugar, refined grain products, and whole grain products despite all being grain-based. The report is careful and thorough in making this distinction and providing very different recommendations for each.

The report also admits to a difficulty in defining meat – “there was variability across the food groupings and this was particularly apparent in the meat group.” Red meats were clumped together with processed meat and chicken, fish was grouped with eggs and sausage.

Yet, after admitting to this issue, the report still stuck with traditional lines. Where it was careful to distinguish different categories of grains and plant foods it still ultimately lumped almost all meat together in its recommendation.

That is with the exception of a small footnote that ultimately contradicted its own recommendations:

As lean meats were not consistently defined or handled similarly between studies, they were not identified as a common characteristic across the reviews. However, as demonstrated in the food patterns modeling of the Healthy US-style and Healthy Mediterranean-style patterns, lean meats can be a part of a healthy dietary pattern.

Whether it was industry influence, conflict of interest, or simply mundane adherence to nutritional cannon, when it came to their final recommendations, they were unable to see the important implications of a distinction they themselves made.

REFERENCES

  1. United States. Department of Agriculture., Dietary Guidelines Advisory Committee. Scientific Report. v.
  1. Teicholz, N., The scientific report guiding the US dietary guidelines: is it scientific? BMJ, 2015. 351: p. h4962.
  1. Library, N.E., Frequently Asked Questions. 2015.
  1. Howard, B.V., et al., Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA, 2006. 295(6): p. 655-66.
  1. Feinman, R.D., et al., Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Nutrition, 2015. 31(1): p. 1-13.
  1. Ajala, O., P. English, and J. Pinkney, Systematic review and meta-analysis of different dietary approaches to the management of type 2 diabetes. Am J Clin Nutr, 2013. 97(3): p. 505-16.
  1. Library, N.E., How do the health outcomes of a vegetarian diet compare to that of a diet which customarily includes animal products?
  1. Beresford, S.A., et al., Low-fat dietary pattern and risk of colorectal cancer: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA, 2006. 295(6): p. 643-54.
  1. Knopp, R.H., et al., Long-term cholesterol-lowering effects of 4 fat-restricted diets in hypercholesterolemic and combined hyperlipidemic men. The Dietary Alternatives Study. JAMA, 1997. 278(18): p. 1509-15.
  1. Prentice, R.L., et al., Low-fat dietary pattern and risk of invasive breast cancer: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA, 2006. 295(6): p. 629-42.
  1. Prentice, R.L., et al., Low-fat dietary pattern and cancer incidence in the Women’s Health Initiative Dietary Modification Randomized Controlled Trial. J Natl Cancer Inst, 2007. 99(20): p. 1534-43.
  1. Fung, T.T., et al., A prospective study of overall diet quality and risk of type 2 diabetes in women. Diabetes Care, 2007. 30(7): p. 1753-7.
  1. Gomez-Candela, C., et al., The Role of Omega-3 Fatty Acids in Diets. J Am Coll Nutr, 2015. 34 Suppl 1: p. 42-7.

Inuit | The Paleo Diet

The Inuit have long been used as a shining example that low carbohydrate approaches to diet can work.1 2 3 4 In fact, traditionally they consumed very little vegetables or any other typically Western foods, and subsisted mainly on fish, sea mammals, and land animals.5 And despite this diet (which would horrify most mainstream dieticians) the Inuit traditionally had very low rates of disease.6

By contrast, the traditional Western diet has been correlated with a plague of health issues.7 8 9 As a further example of just how nutritionally poor the Western diet can be, one third of all cancer deaths have been linked to continued intake of low quality foods – which are everyday staples of the Western diet.10

Interestingly, when consumed in a very low carbohydrate version, a Paleo Diet looks very similar – if not identical – to the traditional Inuit diet. Since this way of eating is higher in fat than most North American diets, it is commonly presumed (erroneously) that high fat diets must somehow be “bad.”11 12 What gets (purposely) left out of these arguments is the fact that the type of fat consumed is very important.13 14 15 16 17 Consuming omega-3 fatty acids is highly beneficial for health – while consuming industrial trans fat is pretty much the worst thing you can do for your health.18

To bring all this background knowledge to a head, new research published last week, showed that the Inuit have special mutations in genes involved in fat metabolism.19 These genetic mutations may allow them to thrive on their very low carbohydrate diet. This is thought provoking because these genetic mutations are found in nearly 100% of the Inuit. By contrast, only a mere 2% of Europeans exhibit the same mutations. This means that those of us from European ancestry may synthesize omega-3 polyunsaturated fatty acids differently than the Inuit.

While the initial buzz of this paper was high, in practice it really doesn’t change anything we know about consuming a healthy Paleo Diet. Omega-3 fatty acids, like those found in wild-caught fish, are still extremely beneficial for our health. In fact, researchers have found that omega-3 fatty acids have widely beneficial anti-inflammatory properties.20 This proves beneficial for inflammatory and autoimmune diseases, in addition to maintaining good health for those without specific health conditions. The advice to consume omega-3 fatty acids is great for mitigating coronary heart disease, depression, aging, and cancer.21

Beyond this, arthritis, Crohn’s disease, ulcerative colitis and lupus erythematosis are autoimmune diseases which may be helped by adequate omega-3 consumption.22 Of the omega-3 fatty acids available, DHA (docosahexaenoic acid) is the best, for a variety of reasons.23 24 Look for foods naturally high in DHA (such as wild-caught fish) and avoid inflammatory seed oils – like those commonly used by most major restaurants. This crucial step will help you stay healthy in the long term – no matter what genes and ancestry you may have.

REFERENCES

[1] Dewailly E, Mulvad G, Sloth pedersen H, Hansen JC, Behrendt N, Hart hansen JP. Inuit are protected against prostate cancer. Cancer Epidemiol Biomarkers Prev. 2003;12(9):926-7.

[2] Bjerregaard P, Dewailly E, Young TK, et al. Blood pressure among the Inuit (Eskimo) populations in the Arctic. Scand J Public Health. 2003;31(2):92-9.

[3] Mulvad G, Pedersen HS, Hansen JC, et al. The Inuit diet. Fatty acids and antioxidants, their role in ischemic heart disease, and exposure to organochlorines and heavy metals. An international study. Arctic Med Res. 1996;55 Suppl 1:20-4.

[4] O’keefe JH, Harris WS. From Inuit to implementation: omega-3 fatty acids come of age. Mayo Clin Proc. 2000;75(6):607-14.

[5] Kuhnlein HV. Nutrition of the Inuit: a brief overview. Arctic Med Res. 1991;Suppl:728-30.

[6] Stefansson V. The friendly arctic. The MacMillan Co, NY. 1921.

[7] Manzel A, Muller DN, Hafler DA, Erdman SE, Linker RA, Kleinewietfeld M. Role of “Western diet” in inflammatory autoimmune diseases. Curr Allergy Asthma Rep. 2014;14(1):404.

[8] Myles IA. Fast food fever: reviewing the impacts of the Western diet on immunity. Nutr J. 2014;13:61.

[9] Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002;56(8):365-79.

[10] American Cancer Society. Cancer facts & figures 2004. Atlanta: American Cancer Society, 2004.

[11] Guldstrand MC, Simberg CL. High-fat diets: healthy or unhealthy?. Clin Sci. 2007;113(10):397-9.

[12] Schwingshackl L, Hoffmann G. Comparison of effects of long-term low-fat vs high-fat diets on blood lipid levels in overweight or obese patients: a systematic review and meta-analysis. J Acad Nutr Diet. 2013;113(12):1640-61.

[13] Abumrad NA, Piomelli D, Yurko-mauro K, Merrill A, Clandinin MT, Serhan CN. Moving beyond “good fat, bad fat”: the complex roles of dietary lipids in cellular function and health: session abstracts. Adv Nutr. 2012;3(1):60-8.

[14] Simopoulos AP. Omega-3 fatty acids in health and disease and in growth and development. Am J Clin Nutr. 1991;54(3):438-63.

[15] Daley CA, Abbott A, Doyle PS, Nader GA, Larson S. A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef. Nutr J. 2010;9:10.

[16] Loef M, Walach H. The omega-6/omega-3 ratio and dementia or cognitive decline: a systematic review on human studies and biological evidence. J Nutr Gerontol Geriatr. 2013;32(1):1-23.

[17] Swanson D, Block R, Mousa SA. Omega-3 fatty acids EPA and DHA: health benefits throughout life. Adv Nutr. 2012;3(1):1-7.

[18] Ip C. Review of the effects of trans fatty acids, oleic acid, n-3 polyunsaturated fatty acids, and conjugated linoleic acid on mammary carcinogenesis in animals. Am J Clin Nutr. 1997;66(6 Suppl):1523S-1529S.

[19] Fumagalli M, Moltke I, Grarup N, et al. Greenlandic Inuit show genetic signatures of diet and climate adaptation. Science. 2015;349(6254):1343-7.

[20] Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutr Rev. 2010;68(5):280-9.

[21] Harris WS, Dayspring TD, Moran TJ. Omega-3 fatty acids and cardiovascular disease: new developments and applications. Postgrad Med. 2013;125(6):100-13.

[22] Robinson DR, Knoell CT, Urakaze M, et al. Suppression of autoimmune disease by omega-3 fatty acids. Biochem Soc Trans. 1995;23(2):287-91.

[23] Horrocks LA, Yeo YK. Health benefits of docosahexaenoic acid (DHA). Pharmacol Res. 1999;40(3):211-25.

[24] Conquer JA, Holub BJ. Dietary docosahexaenoic acid as a source of eicosapentaenoic acid in vegetarians and omnivores. Lipids. 1997;32(3):341-5.

Vitamin D Omega 3 Supplements | The Paleo Diet

Choosing a Paleo diet and eating more in tune with how we’ve evolved provides the body with a robust amount of essential protein, healthy fats, gluten-free carbohydrates and nutrient dense veggies. An ancestral approach to eating also provides your body with key nutrients, vitamins and minerals the way nature intended. Does this mean that supplementation is unnecessary if you’re following a Paleo lifestyle? It’s a complicated question.

Most articles and blogs about supplements inevitably discuss the benefits or drawbacks of multi-vitamins. Research shows that if you eat a diet centered around the most nutrient dense foods – quality meats, veggies and fats – you’ll likely already be achieving a therapeutic dose for most vitamins and minerals. When intake is at a supra-physiological dose (that can never be found in nature), too many vitamins can actually put you at risk of chronic disease. Does this mean if you’re following a Paleo diet you don’t need any supplements?

Let’s look at the two most common instances where supplementation might still be a good idea, vitamin D and omega-3 fats. In both of these cases, although a Paleo diet is a great place to start, for many people this may not be enough.

SHOULD YOU SUPPLEMENT WITH VITAMIN D?

Vitamin D is classically known as an essential nutrient for bone health and immunity, however new research shows this fat-soluble vitamin has much more profound impacts on your health and well-being.

How important is vitamin D? Dr. Michael Holick, physician and vitamin D expert sums it up. “Imagine what would happen if a drug company came out with single pill that reduces the risk of cancer, heart attack, stroke, osteoporosis, PMS, depression and various autoimmune conditions? There would be a media frenzy the likes of which has never been seen before! Such a drug exists… it’s the sun.”1, 2, 3

Vitamin D is different than other vitamins because it’s created under your skin when ultraviolet light from the sun interacts with a specific enzyme to form cholecalciferol or vitamin D3. However, exposure to daily sunlight is no longer the norm as we are cooped up in cubicles all day and the deeply ingrained ancestral benefits of light exposure are overlooked.

It’s estimated that up to 70% of the American population is deficient in vitamin D (defined as blood levels below 20ng/mL or 50 nmol/L), or suffering from vitamin D insufficiency, a level above a diagnosed deficiency but still not sufficient for good health (measured as 20-32 ng/mL or 50-80nmol/L). 4

If you live in a northern climate with a true winter season, or north of the 49th parallel, it’s very difficult to achieve the required blood levels of vitamin D from food alone. While cold-water fatty fish, eggs and mushrooms are good foods sources of vitamin D, in the dead of winter they’re likely not enough. Adding a supplement can be highly beneficial.

The standard medical recommendation for vitamin D drops is 1,000-2,000 IU per day, however in the darkest winter months you may need a higher dose. Remember, always get your blood levels tested and work with a doctor if you’re thinking of supplementing with more than the recommended dose. The normal range is typically between 32-50ng/mL (80-125nmol/L) and for athletes new research suggests achieving levels greater than 40ng/mL (100nmol/L) to support superior performance and recovery.5 Be sure to take your vitamin D supplement with a meal that includes fat for optimal absorption.

SHOULD YOU SUPPLEMENT WITH FISH OILS?

Extra long-chain fats eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are the omega-3 ‘all-stars’ when it comes to supporting overall health and combating chronic disease. While most people know the benefits of omega-3 fats for cardiovascular health, many don’t realize they also help reduce the risk of diabetes and depression, protect against mental stress, and even support athletic performance by improving muscle protein synthesis and controlling excessive inflammation.

How important are omega-3 fats? In 2013, the Cardiovascular Healthy Study found that people with the highest omega-3 (e.g. EPA and DHA) levels in their blood had the lowest overall mortality rates.6 In short, the more omega-3 fats you consume, the less chance you have of dying from absolutely any cause. The good news is they are found in abundance in a Paleo diet (e.g. grass-fed meats, wild ocean fish, farm fresh eggs). However, modern day living and long, busy days might mean you’ll benefit from extra support.

If you’re prone to low mood or depression, or cope with regularly high stress levels fish oils could well be an important key to improving your brain health. A study in the Journal of Clinical Psychiatry found people experiencing depression had consistently lower levels of essential fatty acids in their blood. When subjects supplemented with fish oils they had significant improvements in their Hamilton Rating Scale, a recognized evaluation system for depression.7 The British Journal of Nutrition also discovered that supplementing with fish oils helps reduce the adrenal over-activation associated with high levels of mental stress.8

Rates of diabetes and pre-diabetes have never been higher, and constantly being on the go is just one factor that can lead to snacking on convenience foods that are high in processed carbs and sugars. A recent study of fish oil supplementation effects on blood sugar and insulin levels over a 3-week period found significant improvements in insulin function in those with elevated levels.9

Of course, it’s not enough just to increase your omega-3 intake. It’s far too easy to obtain excessive amounts of omega-6 type fats in today’s world, whether from processed foods, restaurant eating, or convenience snacks. The beauty of adopting a Paleo diet is that it often naturally restores this common imbalance. However, the impacts of modern living may still leave you short.

Unless you’re eating 1-2 pieces of cold, deep-water fatty fish daily, it’s best to add an omega-3 supplement rich in EPA/DHA. Fish oil is the richest in EPA and DHA, however krill oil, sea oil, and sea algae are all viable options as well. Aim to supplement with 1,000-1,500mg of combined EPA and DHA daily.

If you’re an athlete and training intensely fish oil supplementation can be a game changer. Supplementation can lead to an amazing 50% increase in the up-regulation of mTOR, the genetic signaling pathway that stimulates lean muscle growth, leading to significant increases in muscle protein synthesis and muscular hypertrophy.10  If you’re serious about your training, adding extra omega-3 fats to your sports nutrition arsenal is important.

A Paleo diet is a great way to cover all your bases on the nutrition front. However, depending on your genetics, where you live, how busy you are, and your lifestyle, diet may not be enough to correct low or insufficient levels of vitamin D and omega-3 fats. Adding these two supplements into your regime, particularly throughout the winter months, may be the fix you need to improve your health, productivity at work and performance in the gym.

REFERENCES

  1. Holick M.Vitamin D Deficiency:What A Pain It Is. Mayo Clin Proc 2003 78(12):1457-59
  1. Holick, M. Article Review: Vitamin D Deficiency. NEJM Medical Progress. 2007, 357:266-81.
  1. Holick, M. Shinning A Light On Vitamin D-Cancer Connection IARC Report. Dermato-Endocrinology, 2009 1(1):4-6
  1. Hanley D, Davison, K. Symposium: Vitamin D Insufficiency: A significant risk Factor in Chronic Disease and Potential Disease-Specific Biomarkers of Vitamin D Insufficiency: Vitamin D Insufficiency in North America. J Nutr 2005, 135:332-37.
  1. Koundourakis, N et al. Vitamin D and Exercise Performance in Professional Soccer Players. Plos One. 2014 Jul 3;9(7):e101659.
  1. Mozaffarian D, Lemaitre RN, King IB, et al. Plasma phospholipid long-chain omega-3 fatty acids and total and cause-specific mortality in older adults. A cohort study. Ann Intern Med 2013; 158:515-525.
  1. Su K, Huang S, Chiu C, Shen W. Omega-3 fatty acids in major depressive disorder. A preliminary double-blind, placebo-controlled trial. Eur Neuropsychopharmacol 2003;13(4):267-271.
  1. Delarue J et al. Fish oil attenuates adrenergic overactivity without altering glucose metabolism during an oral glucose load in haemodialysis patients. Br J Nutr. 2008 May;99(5):1041-7.
  1. Delarue J et al. Interaction of fish oil and a glucocorticoid on metabolic responses to an oral glucose load in healthy human subjects. Br J Nutr. 2006 Feb;95(2):267-72.
  1. Smith GI et al. Omega-3 polyunsaturated fatty acids augment the muscle protein anabolic response to hyperinsulinaemia-hyperaminoacidaemia in healthy young and middle-aged men and women. Clin Sci (Lond). 2011 Sep;121(6):267-78.

Boost Your Brain: Dopamine and Diet

There are many benefits of following a Paleo Diet.1, 2, 3, 4, 5, 6  The majority are aware of the physical effects of moving from a Western diet (full of processed foods, grains and sugar) to a Paleo Diet (rich with nutrients, anti-inflammatory fats, and healthy sources of carbohydrates).7, 8 However, most are likely unaware of the effects of diet on dopamine levels, and your brain.9, 10, 11, 12, 13 Numerous studies have examined the relationship, and all of the studies have fairly interesting results.14, 15, 16, 17, 18 One study showed mice fed a high fat diet during pregnancy had an increased preference for sucrose and fat.19 It must be noted, however, that what researchers refer to as a ‘high fat diet’ is instead a ‘high sugar and high fat diet.’20, 21, 22 On top of this, the diet consisted of poor sources of sugar and fat, not sweet potatoes and coconut oil.23

Boost Your Brain: Dopamine and Diet | The Paleo Diet

Wang, Gene-Jack et al. “Imaging of Brain Dopamine Pathways: Implications for Understanding Obesity.” Journal of addiction medicine 3.1 (2009): 8–18. PMC. Web. 6 Mar. 2015.

Boost Your Brain: Dopamine and Diet | The Paleo Diet

Volkow et al. “Overlapping Neuronal Circuits in Addiction and Obesity: Evidence of Systems Pathology.” Biological Sciences 363.1507 (2008): 3191.

More interesting, however, researchers ultimately found that diet actually altered the gene expression of dopamine and opioid-related genes.24 That is a pretty big find. Another study looked at the effect skipping breakfast had on dopamine levels.25 The authors of this study found breakfasts consumed with normal to higher amounts of protein, had increasingly positive effects on both dopamine secretion and reduced food cravings.

Boost Your Brain: Dopamine and Diet

Ahmad, S. Omar et al. “REDUCED NUMBERS OF DOPAMINE NEURONS IN THE SUBSTANTIA NIGRA PARS COMPACTA AND VENTRAL TEGMENTAL AREA OF RATS FED AN N-3 POLYUNSATURATED FATTY ACID-DEFICIENT DIET: A STEREOLOGICAL STUDY.” Neuroscience letters 438.3 (2008): 303–307. PMC. Web. 6 Mar. 2015.

If you’re having a hard time swallowing the idea that diet alters dopamine levels, this was only first “discovered” by researchers in 2003.26 Other researchers have stated that excessive intake of dietary fats leads to diminished brain dopaminergic function.27, 28, 29, 30 What must be noted here, again, is that they are not referring to healthier fats, but rather poor quality ones. By contrast, one can extrapolate that healthy fats (such as those included regularly in a Paleo Diet) will improve, or at the very least normalize, dopamine levels.31, 32, 33

As other researchers have also noted, sugar and fat bingeing have notable differences in addictive-like behavior.34 This, again, suggests we should avoid a Western diet at all costs, especially the unhealthiest versions, if you want to maximize dopaminergic function in the brain. Researchers have also found that the lack of opiate-like withdrawal signs after fat bingeing underscores the importance of opioid systems in differentiating sugars and fats and their subsequent effects on behavior.

While fat may not have the same effects on the brain as sugar,combining the two in one’s diet (especially in their worst forms) is akin to putting your brain in the freezer, or maybe even throwing it out in front of traffic.35, 36, 37 Healthy fats, like the omega-3 fatty acids found in abundance in a Paleo Diet, will help to maximize dopamine levels, as well as neuronal and physiologic functioning.38, 39, 40, 41, 42

Boost Your Brain: Dopamine and Diet

Teegarden, Sarah L., Eric J. Nestler, and Tracy L. Bale. “ΔFosB-Mediated Alterations in Dopamine Signaling Are Normalized by a Palatable High Fat Diet.” Biological psychiatry 64.11 (2008): 941–950. PMC. Web. 6 Mar. 2015.

In summary, proper dopamine levels are vital to leading a healthy life. A Paleo diet helps to optimize dopaminergic and neuronal health, meanwhile providing the multitude of healthful benefits. Check out the brand new The Real Paleo Diet Cookbook and check out over 250 delicious, healthy recipes that will help fuel your brain!

REFERENCES

[1] Kowalski LM, Bujko J. [Evaluation of biological and clinical potential of paleolithic diet]. Rocz Panstw Zakl Hig. 2012;63(1):9-15.

[2] Konner M, Eaton SB. Paleolithic nutrition: twenty-five years later. Nutr Clin Pract. 2010;25(6):594-602.

[3] Frassetto LA, Schloetter M, Mietus-synder M, Morris RC, Sebastian A. Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr. 2009;63(8):947-55.

[4] Jönsson T, Granfeldt Y, Lindeberg S, Hallberg AC. Subjective satiety and other experiences of a Paleolithic diet compared to a diabetes diet in patients with type 2 diabetes. Nutr J. 2013;12:105.

[5] O’keefe JH, Cordain L. Cardiovascular disease resulting from a diet and lifestyle at odds with our Paleolithic genome: how to become a 21st-century hunter-gatherer. Mayo Clin Proc. 2004;79(1):101-8.

[6] Cordain L, Eaton SB, Sebastian A, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2):341-54.

[7] Gutiérrez-fisac JL, Angel royo-bordonada M, Rodríguez-artalejo F. [Health-risks associated with Western diet and sedentariness: the obesity epidemia]. Gac Sanit. 2006;20 Suppl 1:48-54.

[8] Myles IA. Fast food fever: reviewing the impacts of the Western diet on immunity. Nutr J. 2014;13:61.

[9] Wang GJ, Volkow ND, Thanos PK, Fowler JS. Imaging of brain dopamine pathways: implications for understanding obesity. J Addict Med. 2009;3(1):8-18.

[10] Volkow ND, Wang GJ, Fowler JS, Telang F. Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. Philos Trans R Soc Lond, B, Biol Sci. 2008;363(1507):3191-200.

[11] Berthoud HR. Vagal and hormonal gut-brain communication: from satiation to satisfaction. Neurogastroenterol Motil. 2008;20 Suppl 1:64-72.

[12] Volkow ND, Wise RA. How can drug addiction help us understand obesity?. Nat Neurosci. 2005;8(5):555-60.

[13] Batterham RL, Ffytche DH, Rosenthal JM, et al. PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans. Nature. 2007;450(7166):106-9.

[14] Dallman MF, Pecoraro N, Akana SF, et al. Chronic stress and obesity: a new view of “comfort food”. Proc Natl Acad Sci USA. 2003;100(20):11696-701.

[15] Adam TC, Epel ES. Stress, eating and the reward system. Physiol Behav. 2007;91(4):449-58.

[16] Rada P, Avena NM, Hoebel BG. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 2005;134(3):737-44.

[17] Liang NC, Hajnal A, Norgren R. Sham feeding corn oil increases accumbens dopamine in the rat. Am J Physiol Regul Integr Comp Physiol. 2006;291(5):R1236-9.

[18] Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

[19] Vucetic Z, Kimmel J, Totoki K, Hollenbeck E, Reyes TM. Maternal high-fat diet alters methylation and gene expression of dopamine and opioid-related genes. Endocrinology. 2010;151(10):4756-64.

[20] Gibson SA. Are high-fat, high-sugar foods and diets conducive to obesity?. Int J Food Sci Nutr. 1996;47(5):405-15.

[21] Molteni R, Barnard RJ, Ying Z, Roberts CK, Gómez-pinilla F. A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience. 2002;112(4):803-14.

[22] Kuo LE, Czarnecka M, Kitlinska JB, Tilan JU, Kvetnanský R, Zukowska Z. Chronic stress, combined with a high-fat/high-sugar diet, shifts sympathetic signaling toward neuropeptide Y and leads to obesity and the metabolic syndrome. Ann N Y Acad Sci. 2008;1148:232-7.

[23] Axen KV, Dikeakos A, Sclafani A. High dietary fat promotes syndrome X in nonobese rats. J Nutr. 2003;133(7):2244-9.

[24] High-fat diet alters the dopamine and opioid systems: effects across development. International Journal of Obesity Supplements. 2012;:S25.

[25] Hoertel HA, Will MJ, Leidy HJ. A randomized crossover, pilot study examining the effects of a normal protein vs. high protein breakfast on food cravings and reward signals in overweight/obese “breakfast skipping”, late-adolescent girls. Nutr J. 2014;13(1):80.

[26] Montgomery AJ, Mctavish SF, Cowen PJ, Grasby PM. Reduction of brain dopamine concentration with dietary tyrosine plus phenylalanine depletion: an [11C]raclopride PET study. Am J Psychiatry. 2003;160(10):1887-9.

[27] Tellez LA, Medina S, Han W, et al. A gut lipid messenger links excess dietary fat to dopamine deficiency. Science. 2013;341(6147):800-2.

[28] Volkow ND, Wang GJ, Telang F, et al. Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: possible contributing factors. Neuroimage. 2008;42(4):1537-43.

[29] Wang GJ, Volkow ND, Logan J, et al. Brain dopamine and obesity. Lancet. 2001;357(9253):354-7.

[30] Thanos PK, Michaelides M, Piyis YK, Wang GJ, Volkow ND. Food restriction markedly increases dopamine D2 receptor (D2R) in a rat model of obesity as assessed with in-vivo muPET imaging ([11C] raclopride) and in-vitro ([3H] spiperone) autoradiography. Synapse. 2008;62(1):50-61.

[31] Meguid MM, Fetissov SO, Varma M, et al. Hypothalamic dopamine and serotonin in the regulation of food intake. Nutrition. 2000;16(10):843-57.

[32] Carlin J, Hill-smith TE, Lucki I, Reyes TM. Reversal of dopamine system dysfunction in response to high-fat diet. Obesity (Silver Spring). 2013;21(12):2513-21.

[33] Chalon S, Delion-vancassel S, Belzung C, et al. Dietary fish oil affects monoaminergic neurotransmission and behavior in rats. J Nutr. 1998;128(12):2512-9.

[34] Avena NM, Rada P, Hoebel BG. Sugar and fat bingeing have notable differences in addictive-like behavior. J Nutr. 2009;139(3):623-8.

[35] Gómez-pinilla F. Brain foods: the effects of nutrients on brain function. Nat Rev Neurosci. 2008;9(7):568-78.

[36] Rosales FJ, Reznick JS, Zeisel SH. Understanding the role of nutrition in the brain and behavioral development of toddlers and preschool children: identifying and addressing methodological barriers. Nutr Neurosci. 2009;12(5):190-202.

[37] Black MM. Effects of vitamin B12 and folate deficiency on brain development in children. Food Nutr Bull. 2008;29(2 Suppl):S126-31.

[38] Parletta N, Milte CM, Meyer BJ. Nutritional modulation of cognitive function and mental health. J Nutr Biochem. 2013;24(5):725-43.

[39] Singh M. Essential fatty acids, DHA and human brain. Indian J Pediatr. 2005;72(3):239-42.

[40] Horrocks LA, Yeo YK. Health benefits of docosahexaenoic acid (DHA). Pharmacol Res. 1999;40(3):211-25.

[41] Kidd PM. Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids. Altern Med Rev. 2007;12(3):207-27.

[42] Enslen M, Milon H, Malnoë A. Effect of low intake of n-3 fatty acids during development on brain phospholipid fatty acid composition and exploratory behavior in rats. Lipids. 1991;26(3):203-8.

Balancing Migraine Pain with a Paleo Diet | The Paleo DIet

As a migraine sufferer, I was all too excited several years ago when the local hospital hosted an expert panel on migraine remedies which included diet. The 45 minute presentation covered the basic physiology, briefly mentioned chocolate and alcohol, and then spent the bulk of the time on medications – Aspirin, Excederin, Midrin, and Fioricet. During the Q&A I asked about omega-3 PUFAs since they are known to inhibit COX-2. One expert replied that she was unaware of any research on PUFAs or COX-2 for migraine. I appreciated her congenial reply, but sat down disappointed. Most of the medication identified did only one thing in the body – inhibit COX-2.

Let’s start at the beginning. Migraine is a complex condition with many subclasses including with aura (Classic,) without aura (Common,) chronic, retinal, and hemiplegic migraine.1-3

Whatever the name, for the 10-15% of Americans who suffer from them, migraines mean episodic, intense headaches, often with nausea and light and sound sensitivity. In all cases, it affects our quality of life and ability to work.4, 5

While medication remains the primary focus of migraine treatment, its use as the primary treatment has its own concerns. There’s now a class of chronic migraine called medication overuse headache (MOH) where overuse of pain medication can actually cause near daily headaches.6-8

This has led many to seek alternative treatments.

Diet may help. Migraineurs – a term that makes it sound like an exclusive club with a very low voluntary applicant pool – often cite dietary triggers for their migraines. The most common are alcohol, chocolate, cheese, caffeine, MSG and fasting.9 On the other side of the coin, dietary elements such as magnesium and omega-3 fatty acids may be therapeutic.10

Unsurprisingly, all of these dietary elements fit with a healthy, Paleo Diet lifestyle. So let’s take a look at the physiology of a few key elements of the Paleo Diet that can help you spend less time at the ”Migraineur Club House.”

MIGRAINE 101: DON’T GET HYPEREXCITED

There are many theories about the cause of migraines, but the most widely accepted is the neural hyperexcitability theory. Backed by recent MRI studies, it proposes neurons in the trigeminal-vascular region of the brain’s cortex become inappropriately activated, releasing a series of neurotransmitters that cause vasodilation, mast cell degranulation, increased permeability, platelet aggregation, inflammation, and ultimately pain.2, 9, 11-14 Recently, some suggest hyperexcitability is a result of a dysfunction in sodium-potassium transporters.15

For some, their migraine is preceded by a visual aura. This aura is caused by an initial depolarization of the neurons referred to as Cortical Spreading Depression.2, 15

That’s a very short summary of a very complex process. The take home message: an imbalance in excitation signals, neurotransmitters, and electrolytes may be at the root of your migraine pain. Dive in deeper with the references listed below.

POLYUNSATURATED FATTY ACIDS: MIND YOUR 3S AND 6S

While living out of the medicine cabinet may not be the best long term strategy, it’s important to point out that NSAIDs, such as ibuprofen, are very effective at reducing acute migraine pain.1, 4, 16 They do one thing – prevent the formation of molecules called prostaglandins by inhibiting a key enzyme called cyclooxygenase (COX).

So, it’s not surprising prostaglandins have been linked to migraine.1, 17-21 Simply injecting prostaglandin E2 (PGE2) into both healthy subjects and migraine sufferers was enough to cause migraine pain.22-25 The fact that  pain was immediate, indicates that PGE2 may actually be the direct cause of pain for sufferers.22

But how does this relate to diet?

Prostaglandins are created from the polyunsaturated fatty acids (PUFAs) we eat.1 Our bodies are not particular – they will use whatever type of PUFA is available. But we end up with very different prostaglandins depending on whether we consume more omega-3 or omega-6 PUFAs.26

The figure below shows the types of prostaglandins (and other eicosanoids) formed from arachidonic acid (omega-6) verses EPA (omega-3).26

Balancing Migraine Pain with a Paleo Diet | The Paleo Diet

PGE3 and PGI3 from omega-3 PUFAs may actually help prevent both the inflammation and electrolyte imbalance that causes migraines.15, 26, 27 In fact, they have anti-inflammatory benefits for many chronic illnesses including cancer and heart disease.28-32

By contrast PGE2 and PGI2 from Omega-6 PUFAs are pain-causing. Hence they are the targets of most over-the-counter pain killers. These prostaglandins and their precursor arachidonic acid are elevated during migraines and may sensitize of the trigeminal nerve which is the location of migraine pain.1, 15, 19, 20, 33, 34 In fact, the highest level of PGE2 receptors in the body are found in the trigeminal nucleus caudalis.22

Fortunately, when diets are high in omega-3 fatty acids such as EPA from fish oil, the good prostaglandins tend to supplant the bad.26

So, why then was it that studies of omega-3 supplementation have had mixed results for migraine?35-37

The potential answer gets at a key tenant of the Paleo Diet – just popping a few fish oil supplements and calling yourself healthy isn’t enough. It’s all about balance.

Due to the huge increase in vegetable oils and grain fed livestock in the western world, the ratio of omega-6 to omega-3 PUFAs in our diets have risen to 10:1 from an estimated 3:1 or even 2:1 in Paleolithic times.26, 38-40

To see if the ratio influenced migraines, a 2013 study by Ramsden et al, not only increased omega-3 in Migraineurs’ diets, but reduced the omega-6 content. The pain improved significantly. Interestingly, the investigators included a second group that only reduced omega-6 PUFAs in their diet. While not as dramatic, this group also improved.35

Issues with the high ratio of omega-6 to omega-3 fatty acids in the western diet go beyond migraines. The ratio has been associated with many chronic conditions including depression (due to its influence on serotonin), rheumatoid arthritis, inflammatory bowel disease, asthma, heart disease and chronic inflammation.26, 27, 38, 41

A Paleo Diet promotes a better omega-3 to omega-6 ratio. The best source of omega-3 PUFAs is EPA from fish, but other sources include walnuts, lean meats, and some vegetables such as broccoli and spinach.42 Just remember that the shift from omega-3s to omega-6 PUFAs in our bodies takes time – from 6 – 18 weeks.43

MAGNESIUM: THE PAINFULLY FORGOTTEN ELECTROLYTE

Magnesium is sometimes referred to as the “forgotten electrolyte” since it is frequently overshadowed by calcium in the research.44-46 Magnesium is involved in over 300 functions in our body, which means it is not a nutrient we want to forget about. Yet almost 48% of Americans eat less than the RDA.15, 44

Most magnesium is found in our bones and cells with less than 1% in our blood,45 which means that a blood test for magnesium isn’t very effective.47 Up to 14% of the population may be deficient and this deficiency has been associated with many chronic conditions including heart disease.48

Evidently, magnesium deficiency has been clearly linked to migraines.9, 47, 49, 50 In multiple studies, migraine sufferers had lowered levels of magnesium in their blood, saliva, and cerebrospinal fluid during attacks.51-56

Magnesium affects many processes linked to migraine including neurotransmitter release, serotonin receptors, inflammatory mediators, and the inhibition of platelet aggregation.56-63 It may even block some of the inflammatory effects of omega-6 PUFAs.44

Magnesium supplements help migraine sufferers.51, 56 Even more strikingly, people going to the emergency room with migraine pain are frequently treated with an infusion of magnesium sulfate which is more effective than the pharmaceutical treatments dexamethasone and metoclopramide.47, 57

Unsurprisingly with current migraine research pointing to electrolyte imbalances, the “forgotten electrolyte” may play a key role in migraine hyperexcitability.15

Sodium-potassium imbalance may trigger migraines, but overactive calcium channels could be the cause.2 High levels of calcium in the brain make neurons easily excitable.2, 44 Magnesium is a key regulator of calcium and might be able to control this calcium-induced hyperexcitability.44

In fact, in a review of migraine hyperexcitability, Welch proposed that the changes in magnesium levels during a migraine may be an attempt by the brain to restore electrolyte balance.2

Here again, migraines show why a properly balanced diet is far more important than just popping supplements.

With the concern over osteoporosis, daily calcium consumption has been increasing over the past four decades.44 This Western focus on calcium has led to one of the biggest criticisms of the Paleo Diet for its elimination of dairy. This is in spite of recent research questioning the benefits of high calcium intake and worse, linking it to heart disease.64-68

What may be more important than the absolute calcium level is the ratio of magnesium to calcium in the diet which has been decreasing.44 Not something to overlook considering increased magnesium consumption reduced all-cause mortality associated with high calcium intake.69

Worse yet, consuming too much calcium can exacerbate magnesium deficiency.70

The higher calcium-magnesium ratio of the Western diet may contribute to a variety of chronic conditions beyond migraine, including stress, metabolic syndrome, Type II Diabetes, hypertension and vascular disease.44

The Paleo Diet promotes a better calcium-magnesium ratio through the consumption of foods high in both including almonds, cashews, green leafy vegetables, and fish. While research is limited, it is believed that alcohol and sugary drinks can limit magnesium absorption.

ELIMINATING DIETARY PAIN

Food sensitivity remains one of the most common migraine triggers,71, 72 but the foods tend to be highly individual. A food diary is one way for migraine sufferers to identify their triggers. Though this can be difficult since foods interact and sometimes the migraine appears a day or more after eating the culprit foods.9

Fortunately, there may be another way to identify your triggers. Food that causes an IgG antibody response has been associated with migraines.9 Studies eliminating these foods have produced dramatic results with up to 93% of participants becoming headache free.71, 73, 74

Balancing Migraine Pain with a Paleo Diet | The Paleo DietWhile the point of an IgG-elimination diet is individualization, the table to the left shows the most common IgG-inducing food groups.71

This study found that an IgG-elimination diet also helped Irritable Bowel Disease, another condition affected by dietary imbalance.71, 75 Up to 50% of people with IBS suffer from migraines76 with neural hypersensitivity77 and mitochondrial DNA mutations75 linked to both.

We frequently recommend Paleo Dieters suffering from chronic conditions try an elimination diet. Seeing your allergist to help you identify IgG-provoking foods may be a shortcut to help you get past migraine pain.

Certainly PUFAs and magnesium have dominated the literature on diet and migraines – to the point that they were used as a proof of concept for literature research.78 But this doesn’t mean they are the only dietary factors. Both low fat79 and ketogenic diets80 improved migraine symptoms. Migraine hyperexcitability can be affected by the sodium-potassium balance in the diet and hydration status (with dehydration and hypohydration causing migraines).15

The underlying message is migraine pain may be a disease of imbalance. So, while I’ve reached for the Excedrin bottle more than a few times to get through my day, a balanced diet more attune with our evolutionary make-up may ultimately be what keeps us Migraineurs away from the medicine cabinet altogether.

Trevor Connor | The Paleo DietTrevor Connor is Dr. Cordain’s last mentored graduate student and will complete his M.S. in HES and Nutrition from the Colorado State University this year and later enter the Ph.D. program. Connor was the Principle Investigator in a large case study, approximately 100 subjects, in which he and Dr. Cordain examined autoimmune patients following The Paleo Diet or Paleo-like diets.

 

REFERENCES

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2. Welch, K.M., Brain hyperexcitability: the basis for antiepileptic drugs in migraine prevention. Headache, 2005. 45 Suppl 1: p. S25-32.

3. Kaniecki, R.G., Basilar-type migraine. Curr Pain Headache Rep, 2009. 13(3): p. 217-20.

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8. Katsarava, Z., et al., Incidence and predictors for chronicity of headache in patients with episodic migraine. Neurology, 2004. 62(5): p. 788-90.

9. Sun-Edelstein, C. and A. Mauskop, Foods and supplements in the management of migraine headaches. Clin J Pain, 2009. 25(5): p. 446-52.

10. Crawford, P. and M. Simmons, What dietary modifications are indicated for migraines? Journal of Family Practice, 2006. 55(1): p. 62-+.

11. Kotas, R., Updated Insight into the Pathophysiology of Migraine – an Update. Ceska a Slovenska Neurologie a Neurochirurgie, 2011. 74(6): p. 654-661.

12. Moskowitz, M.A., The neurobiology of vascular head pain. Ann Neurol, 1984. 16(2): p. 157-68.

13. Battelli, L., K.R. Black, and S.H. Wray, Transcranial magnetic stimulation of visual area V5 in migraine. Neurology, 2002. 58(7): p. 1066-9.

14. Young, W.B., et al., Consecutive transcranial magnetic stimulation: phosphene thresholds in migraineurs and controls. Headache, 2004. 44(2): p. 131-5.

15. Harrington, M.G., et al., Capillary endothelial Na(+), K(+), ATPase transporter homeostasis and a new theory for migraine pathophysiology. Headache, 2010. 50(3): p. 459-78.

16. Levy, D., Endogenous mechanisms underlying the activation and sensitization of meningeal nociceptors: the role of immuno-vascular interactions and cortical spreading depression. Curr Pain Headache Rep, 2012. 16(3): p. 270-7.

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18. Maubach, K.A., et al., BGC20-1531, a novel, potent and selective prostanoid EP receptor antagonist: a putative new treatment for migraine headache. Br J Pharmacol, 2009. 156(2): p. 316-27.

19. Tuca, J.O., J.M. Planas, and P.P. Parellada, Increase in PGE2 and TXA2 in the saliva of common migraine patients. Action of calcium channel blockers. Headache, 1989. 29(8): p. 498-501.

20. Sarchielli, P., et al., Nitric oxide metabolites, prostaglandins and trigeminal vasoactive peptides in internal jugular vein blood during spontaneous migraine attacks. Cephalalgia, 2000. 20(10): p. 907-18.

21. Vardi, J., et al., Prostaglandin–E2 levels in the saliva of common migrainous women. Headache, 1983. 23(2): p. 59-61.

22. Antonova, M., et al., Prostaglandin E(2) induces immediate migraine-like attack in migraine patients without aura. Cephalalgia, 2012. 32(11): p. 822-33.

23. Sciberras, D.G., et al., Inflammatory responses to intradermal injection of platelet activating factor, histamine and prostaglandin E2 in healthy volunteers: a double blind investigation. Br J Clin Pharmacol, 1987. 24(6): p. 753-61.

24. Wienecke, T., et al., Prostaglandin E2(PGE2) induces headache in healthy subjects. Cephalalgia, 2009. 29(5): p. 509-19.

25. Wienecke, T., et al., Prostacyclin (epoprostenol) induces headache in healthy subjects. Pain, 2008. 139(1): p. 106-16.

26. Simopoulos, A.P., Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr, 2002. 21(6): p. 495-505.

27. Harel, Z., et al., Supplementation with omega-3 polyunsaturated fatty acids in the management of recurrent migraines in adolescents. J Adolesc Health, 2002. 31(2): p. 154-61.

28. Kris-Etherton, P.M., et al., Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation, 2002. 106(21): p. 2747-2757.

29. Simopoulos, A.P., Omega-3 fatty acids in inflammation and autoimmune diseases. Journal of the American College of Nutrition, 2002. 21(6): p. 495-505.

30. Simopoulos, A.P., OMEGA-3-FATTY-ACIDS IN HEALTH AND DISEASE AND IN GROWTH AND DEVELOPMENT. American Journal of Clinical Nutrition, 1991. 54(3): p. 438-463.

31. Simopoulos, A.P., The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomedicine & Pharmacotherapy, 2002. 56(8): p. 365-379.

32. Rose, D.P. and J.M. Connolly, Omega-3 fatty acids as cancer chemopreventive agents. Pharmacology & Therapeutics, 1999. 83(3): p. 217-244.

33. Moskowitz, M.A., Defining a pathway to discovery from bench to bedside: the trigeminovascular system and sensitization. Headache, 2008. 48(5): p. 688-90.

34. Durham, P.L., et al., Changes in salivary prostaglandin levels during menstrual migraine with associated dysmenorrhea. Headache, 2010. 50(5): p. 844-51.

35. Ramsden, C.E., et al., Targeted alteration of dietary n-3 and n-6 fatty acids for the treatment of chronic headaches: a randomized trial. Pain, 2013. 154(11): p. 2441-51.

36. Pradalier, A., et al., Failure of omega-3 polyunsaturated fatty acids in prevention of migraine: a double-blind study versus placebo. Cephalalgia, 2001. 21(8): p. 818-22.

37. Wagner, W. and U. Nootbaar-Wagner, Prophylactic treatment of migraine with gamma-linolenic and alpha-linolenic acids. Cephalalgia, 1997. 17(2): p. 127-30; discussion 102.

38. Cordain, L., et al., Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr, 2005. 81(2): p. 341-54.

39. Cordain, L., et al., Fatty acid analysis of wild ruminant tissues: evolutionary implications for reducing diet-related chronic disease. Eur J Clin Nutr, 2002. 56(3): p. 181-91.

40. Frassetto, L., et al., Diet, evolution and aging – The pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. European Journal of Nutrition, 2001. 40(5): p. 200-213.

41. Burr, M.L., et al., Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet, 1989. 2(8666): p. 757-61.

42. Raper, N.R., F.J. Cronin, and J. Exler, Omega-3 fatty acid content of the US food supply. J Am Coll Nutr, 1992. 11(3): p. 304-8.

43. Marangoni, F., et al., Changes of n-3 and n-6 fatty acids in plasma and circulating cells of normal subjects, after prolonged administration of 20:5 (EPA) and 22:6 (DHA) ethyl esters and prolonged washout. Biochim Biophys Acta, 1993. 1210(1): p. 55-62.

44. Rosanoff, A., C.M. Weaver, and R.K. Rude, Suboptimal magnesium status in the United States: are the health consequences underestimated? Nutr Rev, 2012. 70(3): p. 153-64.

45. Elin, R.J., MAGNESIUM – THE 5TH BUT FORGOTTEN ELECTROLYTE. American Journal of Clinical Pathology, 1994. 102(5): p. 616-622.

46. Gonzalez, W., et al., Magnesium: the forgotten electrolyte. Bol Asoc Med P R, 2013. 105(3): p. 17-20.

47. Mauskop, A. and J. Varughese, Why all migraine patients should be treated with magnesium. J Neural Transm, 2012. 119(5): p. 575-9.

48. Schimatschek, H.F. and R. Rempis, Prevalence of hypomagnesemia in an unselected German population of 16,000 individuals. Magnes Res, 2001. 14(4): p. 283-90.

49. Sun-Edelstein, C. and A. Mauskop, Role of magnesium in the pathogenesis and treatment of migraine. Expert Rev Neurother, 2009. 9(3): p. 369-79.

50. Innerarity, S., Hypomagnesemia in acute and chronic illness. Crit Care Nurs Q, 2000. 23(2): p. 1-19; quiz 87.

51. Peikert, A., C. Wilimzig, and R. Kohne-Volland, Prophylaxis of migraine with oral magnesium: results from a prospective, multi-center, placebo-controlled and double-blind randomized study. Cephalalgia, 1996. 16(4): p. 257-63.

52. Facchinetti, F., et al., Magnesium prophylaxis of menstrual migraine: effects on intracellular magnesium. Headache, 1991. 31(5): p. 298-301.

53. Schoenen, J., J. Sianard-Gainko, and M. Lenaerts, Blood magnesium levels in migraine. Cephalalgia, 1991. 11(2): p. 97-9.

54. Sarchielli, P., et al., Serum and salivary magnesium levels in migraine and tension-type headache. Results in a group of adult patients. Cephalalgia, 1992. 12(1): p. 21-7.

55. Ramadan, N.M., et al., Low brain magnesium in migraine. Headache, 1989. 29(9): p. 590-3.

56. Mauskop, A. and B.M. Altura, Role of magnesium in the pathogenesis and treatment of migraines. Clin Neurosci, 1998. 5(1): p. 24-7.

57. Shahrami, A., et al., Comparison of therapeutic effects of magnesium sulfate vs. dexamethasone/metoclopramide on alleviating acute migraine headache. J Emerg Med, 2015. 48(1): p. 69-76.

58. Mauskop, A., et al., Intravenous magnesium sulfate rapidly alleviates headaches of various types. Headache, 1996. 36(3): p. 154-60.

59. Bianchi, A., et al., Role of magnesium, coenzyme Q10, riboflavin, and vitamin B12 in migraine prophylaxis. Vitam Horm, 2004. 69: p. 297-312.

60. McCarty, M.F., Magnesium taurate and fish oil for prevention of migraine. Med Hypotheses, 1996. 47(6): p. 461-6.

61. Altura, B.M., B.T. Altura, and A. Carella, Magnesium deficiency-induced spasms of umbilical vessels: relation to preeclampsia, hypertension, growth retardation. Science, 1983. 221(4608): p. 376-8.

62. Turlapaty, P.D. and B.M. Altura, Magnesium deficiency produces spasms of coronary arteries: relationship to etiology of sudden death ischemic heart disease. Science, 1980. 208(4440): p. 198-200.

63. Mody, I., J.D. Lambert, and U. Heinemann, Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices. J Neurophysiol, 1987. 57(3): p. 869-88.

64. Bolland, M.J., et al., Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. BMJ, 2008. 336(7638): p. 262-6.

65. Bolland, M.J., et al., Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ, 2010. 341: p. c3691.

66. Paziana, K. and M. Pazianas, Calcium supplements controversy in osteoporosis: a physiological mechanism supporting cardiovascular adverse effects. Endocrine, 2015.

67. Meier, C. and M.E. Kranzlin, Calcium supplementation, osteoporosis and cardiovascular disease. Swiss Med Wkly, 2011. 141: p. w13260.

68. Weaver, C.M., Calcium supplementation: is protecting against osteoporosis counter to protecting against cardiovascular disease? Curr Osteoporos Rep, 2014. 12(2): p. 211-8.

69. Kaluza, J., et al., Dietary calcium and magnesium intake and mortality: a prospective study of men. Am J Epidemiol, 2010. 171(7): p. 801-7.

70. Bertinato, J., et al., Small increases in dietary calcium above normal requirements exacerbate magnesium deficiency in rats fed a low magnesium diet. Magnes Res, 2014. 27(1): p. 35-47.

71. Aydinlar, E.I., et al., IgG-based elimination diet in migraine plus irritable bowel syndrome. Headache, 2013. 53(3): p. 514-25.

72. Peatfield, R.C., et al., The prevalence of diet-induced migraine. Cephalalgia, 1984. 4(3): p. 179-83.

73. Arroyave Hernandez, C.M., M. Echavarria Pinto, and H.L. Hernandez Montiel, Food allergy mediated by IgG antibodies associated with migraine in adults. Rev Alerg Mex, 2007. 54(5): p. 162-8.

74. Egger, J., et al., IS MIGRAINE FOOD ALLERGY – A DOUBLE-BLIND CONTROLLED TRIAL OF OLIGOANTIGENIC DIET TREATMENT. Lancet, 1983. 2(8355): p. 865-869.

75. Chang, F.Y. and C.L. Lu, Irritable bowel syndrome and migraine: bystanders or partners? J Neurogastroenterol Motil, 2013. 19(3): p. 301-11.

76. Watson, W.C., et al., Globus and headache: common symptoms of the irritable bowel syndrome. Can Med Assoc J, 1978. 118(4): p. 387-8.

77. Cady, R.K., et al., The bowel and migraine: update on celiac disease and irritable bowel syndrome. Curr Pain Headache Rep, 2012. 16(3): p. 278-86.

78. Weeber, M., et al., Using concepts in literature-based discovery: Simulating Swanson’s Raynaud-fish oil and migraine-magnesium discoveries. Journal of the American Society for Information Science and Technology, 2001. 52(7): p. 548-557.

79. Bunner, A.E., et al., Nutrition intervention for migraine: a randomized crossover trial. J Headache Pain, 2014. 15: p. 69.

80. Di Lorenzo, C., et al., Migraine improvement during short lasting ketogenesis: a proof-of-concept study. Eur J Neurol, 2015. 22(1): p. 170-7.

Top 10 Paleo Foods for Heart Health | The Paleo Diet

One of the things I love most about a True Paleo regime is being able to enjoy so many of the foods I used to think were unhealthy choices.

And despite diet trends coming and going, many people get caught up with some of the less healthy versions along with the inaccurate hype that tends to surround them.

Some of the foods I now savor are ones I never would have dreamed of eating a mere decade ago, simply because I thought they were too high in fat (90’s mindset), didn’t provide enough carbohydrate (Endurance athlete? Go heavy on the carbs.), or simply because the sheer number of calories might exceed what I’d need in a given day (Exercise physiology thesis: Calories In vs. Out is the single, most important factor in determining whether you would lose weight, gain weight or stay the same), source of calories aside.

Testing and trying a number of ways of eating thankfully brought me back to a Paleo diet in 2005. Guess what? The many foods I didn’t consider are ones I’ve come to relish. It turns out they not only taste great, but are increasingly beneficial to our health.

February is National Heart Month and there is no better diet than a Paleo diet to promote heart health.

Salmon

One of the best sources of anti-inflammatory omega-3 fatty acids which can lower the risk of irregular heart beat as well as plaque build up in the arteries. 1  Stick with wild, not farmed.

Blueberries

Rich in anthocyanins and flavonoids, antioxidants that can decrease blood pressure and dilate blood vessels.2 Freezing wild berries makes for a surprisingly decadent treat, all on their own!

Citrus

High in flavonoids that are linked with a reduced rate of ischemic stroke caused by blood clots, and rich in vitamin C which has been associated with lower risk of heart disease, like atherosclerosis.3 Boost your heart health by adding tangerines to your spinach salad and quadruple the amount of iron you absorb.

Green Tea

Researchers estimate the rate of cardiac arrest decreases by 11% with consumption of three cups of tea per day.4 Green tea is rich in Theanine, the amino acid that will offset caffeine’s effect.

Tomatoes

Cardio-protective functions provided by the nutrients in tomatoes may include the reduction of low-density lipoprotein (LDL) cholesterol, homocysteine, platelet aggregation, and blood pressure.5 Go local and organic with this fruit in particular.

Extra Virgin Olive Oil

Rich in monounsaturated fats (MUFAs), EVOO may help lower your risk of heart disease by improving related risk factors. For instance, MUFAs have been found to lower your total cholesterol and low-density lipoprotein cholesterol levels.6  Promote heart health by upping your intake of this delicious fat in favor of relying too heavily on nuts.

Spinach

Lutein (a carotenoid); B-complex vitamins; Folate; magnesium; potassium; calcium; fiber.7  Looks like Popeye had the right idea!

Avocados

Consumption of ½ – 1½ avocados a day may help to maintain normal serum total cholesterol. More evidence that good fat is good!8

Wine (Sulfite-Free)

Rich in resveratrol, studies have shown that adults who drink light to moderate amounts of alcohol may be less likely to develop heart disease than those who do not drink at all or are heavy drinkers.9  Cheers to that!

Dark Chocolate

In humans, flavanol-rich cocoa counteracts lipid peroxidation and, therefore, lowers the plasma level.10  Just make sure to stick to the real stuff and go as close to 100% cacao as you can find!

And, just in time for Valentine’s Day, why not use this as the special occasion to enjoy my signature Paleo truffles!

While it’s no surprise wild salmon and leafy greens are included in my list of Top 10 Paleo Foods, when there’s room for the occasional glass of red wine and raw, dark chocolate on a lifelong Paleo regime too, it’s something that many people, myself included, enjoy wholeheartedly.

 

REFERENCES

[1] “The Role of Fish Oil in Arrhythmia Prevention”, Anand RG, Alkadri M, Lavie CJ, Milani RV. Mar-Apr 2008

[2] “Daily Blueberry Consumption Improves Blood Pressure and Arterial Stiffness in Postmenopausal Women with Pre- and Stage 1-Hypertension: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial”, Sarah A. Johnson, PhD, RD, CSO, Arturo Figueroa, MD, PhD, FACSM, Negin Navaei, Alexei Wong, PhD, Roy Kalfon, MS, Lauren T. Ormsbee, MS, Rafaela G. Feresin, MS, Marcus L. Elam, MS, Shirin Hooshmand, PhD, Mark E. Payton, PhD, Bahram H. Arjmandi, PhD, RD, October, 2014

[3] Woollard KJ, Loryman CJ, Meredith E, et al. Effects of oral vitamin C on monocyte: endothelial cell adhesion in healthy subjects. Biochem Biophys Res Commun. 2002 Jun 28;294(5):1161-8.

[4] Cooper R, Morre DJ, Morre DM. Medicinal benefits of green tea: Part I. Review of noncancer health benefits. J Altern Complement Med. 2005;11(3):521-8.

[5] Crit Rev Food Sci Nutr. 2003;43(1):1-18. Tomatoes and cardiovascular health. Willcox JK1, Catignani GL, Lazarus S.

[6] Lecerf JM. Fatty acids and cardiovascular disease. Nutrition Reviews. 2009;67:273.

[7] Ursula Arens, dietetician at the British Dietetic Association, Kathleen Zelman, WebMD director of nutrition. U.S. Highbush Blueberry Council. British Heart Foundation. British Dietetic Association. The Journal of the American Medical Association , July 23/30, 2003.

[8] Influence of avocados on serum cholesterol.[Proc Soc Exp Biol Med. 1960]

[9] Brien SE, Ronksley PE, Turner BJ, Mukamal KJ, Ghali WA. Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. BMJ. 2011;342:d636.

[10] Wiswedel I, Hirsch D, Kropf S, Gruening M, Pfister E, Schewe T, Sies H. Flavanol-rich cocoa drink lowers plasma F(2)-isoprostane concentrations in humans. Free Radic Biol Med. 2004; 37: 411–421.

Seafood Mercury Concerns Subside Amid New Research | The Paleo Diet

Fish and other marine life have been integral to human diets since the Paleolithic era. Some researchers even speculate that these foods “made us human” by enabling the rapid expansion of grey matter in the cerebral cortex. For three million years of evolution during the time of Australopithecus, brain capacity remained constant, but then curiously doubled during a one-million-year period between Homo erectus and Homo sapiens.1 The reasons for this great expansion are not entirely known, but increased dietary omega-3 from fish and shellfish was likely involved.

Fish consumption remains critically important today, but comes with complications unimaginable to our distant ancestors. Industrial pollution has greatly increased environmental mercury, much of which ends up in oceans and lakes, and finally, in small amounts, in the bodies of fish. In higher amounts, mercury is toxic and is especially problematic for developing babies. For years, the FDA was advising pregnant women to limit their fish consumption during pregnancy, but last year, they issued a draft revision encouraging prenatal fish consumption.2 This draft, which will eventually replace their previous recommendations, reflects a growing awareness, seen in the scientific literature, that fish is essential for developing babies and contains nutrients that limit, or even counter, the potentially harmful effects of mercury.

Recently published in the American Journal of Clinical Nutrition, a new study, representing 30 years of research in the Seychelles, is one of the longest and largest population studies regarding seafood and mercury.3 The Seychelles is a nation of islands clustered together in the Indian Ocean, where residents consume 10 times as much seafood as do Europeans and Americans, making it an ideal place to study the long-term impact of mercury exposure via seafood. The researchers concluded that high fish consumption by pregnant mothers, as much as 12 meals per week (the FDA recommends three), does not cause developmental problems in children.

To the contrary, fish is extremely beneficial for development, and contains special nutrients that protect against mercury. Lead author Dr. Sean Strain explained, “This research provided us the opportunity to study the role of polyunsaturated fatty acids [PUFAs] on development and their potential to augment or counteract the toxic properties of mercury.”4 Mercury is thought to damage the brain through oxidation and corresponding inflammation. Fish are rich in omega-3 PUFAs, which prevent inflammation, as opposed to omega-6 PUFAs, which promote inflammation. This was reflected in the study whereby children of mothers who had higher omega-6 blood levels performed worse on tests designed to measure motor skills.

This study builds upon an impressive body of research conducted by Dr. Nicholas Ralston and colleagues at the University of North Dakota. Ralston has demonstrated that selenium also protects against mercury toxicity and that foods with relatively higher amounts of selenium with respect to mercury, pose neither developmental nor neurological risks based on mercury toxicity.5 “This may explain,” Ralston says, “why studies of maternal populations exposed to foods that contain Hg [mercury] in molar excess of Se [selenium], such as shark or pilot whale meats, have found adverse child outcomes, but studies of populations exposed to MeHg [methylmercury] by eating Se-rich ocean fish observe improved child IQs instead of harm.”6

The vast majority of commonly consumed fish and shellfish contain far more selenium relative to mercury and many have significant amounts of omega-3 PUFAs. This means that fish and shellfish, two important components of the Paleo diet, should not be limited nor discontinued based on mercury concerns. Whether for pregnant women, babies, children, or adults, we encourage you to keep seafood on the menu.

Christopher James Clark, B.B.A.

@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

Christopher James Clark | The Paleo Diet TeamChristopher James Clark, B.B.A. is an award-winning writer, consultant, and chef with specialized knowledge in nutritional science and healing cuisine. He has a Business Administration degree from the University of Michigan and formerly worked as a revenue management analyst for a Fortune 100 company. For the past decade-plus, he has been designing menus, recipes, and food concepts for restaurants and spas, coaching private clients, teaching cooking workshops worldwide, and managing the kitchen for a renowned Greek yoga resort. Clark is the author of the critically acclaimed, award-winning book, Nutritional Grail.

REFERENCES

[1] Bradbury, J. (May 2011). Docosahexaenoic Acid (DHA): An Ancient Nutrient for the Modern Human Brain. Nutrients, 3(5). Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257695/

[2] U.S. Food and Drug Administration. (June 2014). Fish: What Pregnant Women and Parents Should Know. Draft Updated Advice by FDA and EPA. Retrieved from http://www.fda.gov/Food/FoodborneIllnessContaminants/Metals/ucm393070.htm

[3] Strain, JJ, et al. (January 2015). Prenatal exposure to methyl mercury from fish consumption and polyunsaturated fatty acids: associations with child development at 20 mo of age in an observational study in the Republic of Seychelles. American Journal of Clinical Nutrition, 101(1). Retrieved from http://ajcn.nutrition.org/content/early/2015/01/21/ajcn.114.100503

[4] University of Rochester Medical Center. (January 21, 2015). Fatty acids in fish may shield brain from mercury damage. ScienceDaily. Retrieved from www.sciencedaily.com/releases/2015/01/150121144835.htm

[5] Ralston, NV and Raymond, NJ. (November 2010). Dietary selenium’s protective effects against methylmercury toxicity. Toxicology, 278(1). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20561558

[6] Ibid, Ralston.

Paleo Diet Primer: Fats and Oils | The Paleo Diet

When it came to fats and oils, the choice was simple for our hunter gatherer ancestors. All dietary fats were consumed directly from the food source and were based on their geographic availablity. They ate the whole carcass of wild animals, including all of the organs and visceral fat, and foraged for fatty, high oil plants. These foods balanced the fatty acids in their diet. Today, as technology engineers oils from vegetable seeds, like mustard seed, cottonseed, and rapeseed (canola) oil, not only is the yield unnatural, it is also unsafe for consumption.

All animal fats, such as lard, tallow, duck and chicken fat, can withstand very high temperatures without oxidizing,1 and have prolonged shelf lives. However, navigating the bottled oil aisle at any grocery store can overwhelm even the most advanced label reader to decipher which  oils are safe and optimal for health.  A thorough explanation of the fatty acid composition of vegetables oils, as well as identifying the six vegetable oils (flaxseed, walnut, olive, macadamia, coconut, and avocado)  that are best suited for the Paleo Diet can be found HERE.  Yet, many of us still struggle with which cooking oil to select and how to heat it without compromising the nutritious benefits.

When heating any oil, it is important to keep them below their smoke point, (before oil burns to the point of smoking). Oils heated above their stability point begin to decompose, releasing free radicals along with toxic fumes. Oils are often refined to raise their smoke point. The refining process (heating, neutralization, filtering, and processing with chemicals and bleaching agents) removes the  oils from their pure state.2 Thus, despite their lower smoke point, unrefined virgin oils are preferential.

Flaxseed oil

If we look to hunter-gather-societies, we see they did not regularly use flaxseed oil. It was originally included in The Paleo Diet as a tool to balance out increased omega-6/omega-3 fatty acid ratio due to the excessive intake of omega-6 vegetable oils, especially linoleic acid, in the average western diet. Flaxseed oil is exceptionally high in alpha-linolenic acid (ALA), which is the parent fatty acid to Omega-3 fatty acids. Omega-3 fatty acids are extremely sensitive to heat, oxygen, and light,3 so refrigerate and never heat, but instead use in a salad dressing or as a finishing oil over cool vegetables.

Walnut Oil

Walnut oil possesses many antioxidants, including ellagic acid, which research suggests is antiatherogenic and supports osteoblastic activity.4 It’s a great source of omega-3 fatty acids 5 and although the refined version is often labeled safe for high-heat cooking, it is best not to heat it to high temperatures. Not only will the omega-3s be damaged, but the oil will also develop a bitter taste. The unrefined version can be heated to 320°F,6 so sauté vegetables in walnut oil  at low-to-medium heat, or drizzle on any salad.

Extra-Virgin Olive Oil

Olive oil contains at least 30 phenolic compounds.7 Phenols have been shown to reduce the amount of oxidative stress on the body8 and  protect the polyunsaturated fat in the olive oil from oxidizing. Olive oil is a great source of healthy monounsaturated fats, which help control cholesterol levels and have been linked with heart health. There are many varieties of olive oils, sourced from all over the world. Each has its own unique flavor and color that can be experimented with to highlight whatever dish you are cooking. And, while extra virgin olive oil has a smoke point of 325°F,9 it is fairly resistant to oxidation, even when used for high-heat deep-frying.10, 11

Macadamia Nut Oil

Macadamia nut oil is higher in monounsaturated fats than olive oil12 and provides the lowest level of omega-6 fats of any nut.13 It is high in phytochemicals, (qualene, tocotrienols and tocopherols), which protect against oxidation, making it suitable for room temperature storage for up to two years.14 Macadamia nut oil has been shown to improve the biomarkers of oxidative stress, inflammation, and reduce the risk factors for coronary artery disease.15

With a smoke point of 413°F, 16 macadamia oil can be used for almost any dish whether you’re grilling, sautéing or stir-frying. It can even be used a binder for homemade Paleo mayonnaise.

Coconut Oil

Coconut oil is more than 90% saturated fat; specifically it is high in medium chain triglyceride (MCT). MCTs do not require bile acids for digestion, which makes them easy to digest and available immediately as a fuel source.17 Coconut oil is also rich in lauric acid, a fatty acid found in mother’s milk that has anti-fungal, anti-bacterial and anti-viral properties.18 Unrefined coconut oil, which has not been bleached or filtered to remove impurities or natural flavors, has a smoke point of 320°F.19

Coconut oil, which is solid at room temperature, can be used as a replacement in any recipe that calls for butter, such as for coating a whole chicken before roasting. It also works well with Caribbean or Asian recipes, especially to those who aren’t quite accustomed to the flavor. We use it regularly to sauté vegetables, like kale or onions, as well as to grease the pan for cooking eggs.

Avocado oil

Avocados, thought classified as a fruit, are high in oil content. Cold pressing of avocados retains a high concentrations of vitamin E 20 and chlorophyll (40-60mg/kg), which gives the oil a green tint. 21 Research shows consuming avocado oil enhances carotenoid absorption from vegetables,22 and can decrease your risk of coronary artery disease.23 Similar to olive oil, avocado oil has a higher Omega 6:3 ratio (13.1:1).24 Avocado oil can withstand the heat. Virgin (unrefined) avocado oil has a smoke point of 40025 and can be used in any high heat cooking, dressing or as a finishing oil.

 

REFERENCES

[1] Sherwin, E. R. Oxidation and antioxidants in fat and oil processing. Journal of the American Oil Chemists’ Society 55.11 (1978): 809-814.

[2] Available at: http://www.business2community.com/health-wellness/the-danger-of-cooking-with-healthy-oils-past-their-smoke-point-0418150. Accessed on October 28, 2014.

[3] Choo, W. S., E. J. Birch, and J. P. Dufour. Physicochemical and stability characteristics of flaxseed oils during pan-heating. Journal of the American Oil Chemists’ Society 84.8 (2007): 735-740.

[4] Papoutsi, Z., et al. Walnut extract (Juglans regia L.) and its component ellagic acid exhibit anti-inflammatory activity in human aorta endothelial cells and osteoblastic activity in the cell line KS483. British journal of nutrition 99.04 (2008): 715-722.

[5] Available at: http://www.hsph.harvard.edu/nutritionsource/omega-3/.  Accessed on October 28, 2014.

[6]Available at: http://www.goodeatsfanpage.com/collectedinfo/oilsmokepoints.htm. Accessed on October 28, 2014

[7] Tuck, Kellie L., and Peter J. Hayball. Major phenolic compounds in olive oil: metabolism and health effects. The Journal of nutritional biochemistry 13.11 (2002): 636-644.

[8] Kim, Hwa-Young, Ok-Hee Kim, and Mi-Kyung Sung. Effects of phenol-depleted and phenol-rich diets on blood markers of oxidative stress, and urinary excretion of quercetin and kaempferol in healthy volunteers. Journal of the American College of Nutrition 22.3 (2003): 217-223.

[9]Available at: http://culinaryarts.about.com/od/culinaryreference/a/smokepoints.htm. Accessed on October 28, 2014.

[10] Casal, Susana, et al. Olive oil stability under deep-frying conditions. Food and Chemical Toxicology 48.10 (2010): 2972-2979.

[11] Sutherland, Wayne HF, et al. Effect of meals rich in heated olive and safflower oils on oxidation of postprandial serum in healthy men. Atherosclerosis 160.1 (2002): 195-203.

[12] Ako, H, Okuda D, and Gray D. Healthful new oil from macadamia nuts. Nutrition (Burbank, Los Angeles County, Calif.) 11.3 (1995): 286.

[13] Avaialable at: http://blog.lluniversity.com/nuts-and-oils-why-coconut-and-macadamia-nut-are-king/. Accessed on October 28, 2014.

[14] Wall, Marisa M. Functional lipid characteristics, oxidative stability, and antioxidant activity of macadamia nut (Macadamia integrifolia). Food chemistry 121.4 (2010): 1103-1108.

[15] Garg, Manohar L, et al. Macadamia nut consumption modulates favourably risk factors for coronary artery disease in hypercholesterolemic subjects. Lipids 42.6 (2007): 583-587.

[16] Available at: http://www.naturalnews.com/029202_olive_oil_smoke_point.html.  Accessed on October 14, 2014.

[17] Prior, IA, et al. “Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies.” The American journal of clinical nutrition 34.8 (1981): 1552-1561.

[18] Isaacs, CE, et al. “Antiviral and antibacterial lipids in human milk and infant formula feeds.” Archives of Disease in Childhood 65.8 (1990): 861-864.

[19] Available at: http://www.livestrong.com/article/446041-is-coconut-oil-good-for-frying-on-high-temperature-cooking/. Accessed on October 28, 2014.

[20] Eyres L, Sherpa N and Hendriks G. Avocado oil: a new edible oil from Australasia. Lipid Technol 2001;Vol 13, no 4:84-88.

[21] Swisher, Horton E. Avocado oil. J Am Oil Chem 65 (1988): 1705.

[22] Unlu, Nuray Z., et al. “Carotenoid absorption from salad and salsa by humans is enhanced by the addition of avocado or avocado oil.” The Journal of nutrition 135.3 (2005): 431-436.

[23] Watts GF, Lewis B, Brunt JNH, Lewis ES, Coltart DJ, Smith LDR, Mann JI and Swan AV. Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas’ Atherosclerosis Regression Study (STARS). Lancet 1992;339:563-569.

[24] Available at: https://theconsciouslife.com/omega-3-6-9-ratio-cooking-oils.htm. Accessed on October 28. 2014.

[25] Available at: http://www.vegkitchen.com/tips/avocado-oil-expeller-pressed-naturally-refined/attachment/smoke-point-chart/. Accessed on October 28, 2014.

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