Tag Archives: cardiovascular disease

Renowned evolutionary biologist Theodosius Dobzhansky said “nothing in biology makes sense except in the light of evolution.”[1] Throughout our evolution, we have lived in daily cycles of light and dark. These cycles have led to the development of natural circadian rhythms that impact many aspects of our health and vitality.

Circadian rhythms are triggered by the bright light stimulus in the morning and darkness in the evening. The hypothalamus area of the brain – specifically the suprachiasmatic nucleus (SCN) – is the master regulator, synchronising the body’s circadian clock based on information it receives from photoreceptors in the eyes in response to light [2]. The impacts of circadian rhythm are wide-reaching;

Disruption of the circadian clock can have a big impact on the body’s ability to function optimally. Jet lag – that feeling of fatigue, disorientation and mental sluggishness after travelling through multiple time zones – is a classic example [3-6]

Unfortunately, the negative effects can be more serious than just a little sluggishness. The incidence of workplace injuries and traffic accidents increases when the clocks move forward in the spring [7, 8].

Experts are just starting to uncover the many potential ripple effects of circadian dysfunction on our health: from heart disease [9, 10] and cognitive decline [11, 12], to blood sugar dysfunction and increased diabetes risk [13]; to changes in body-fat storage and breakdown [14-16], reduced liver, pancreatic, and cardiac and skeletal muscle function [17-25].

 

Late-Night Eating & Circadian Rhythm

Today, there are many ancestral circadian mismatches with modern life. Late-night eating may be one of the most glaring incongruous elements. We’re in the midst of a weight gain and obesity epidemic with 70% of adults over the age of 20 in America are overweight or obese and 50% of the population now classified as pre-diabetic or diabetic.[26-27] A body of research is appearing showing that late-night eating may be a significant contributor [27-29].

A 2014 study of overweight and obese diabetics investigated the impacts of a late-night snack on their requirement for supplemental insulin. Subjects were divided into carbohydrate, whey protein, casein, or placebo groups. All groups required significantly more insulin after all late-night snacks, though the protein snack did compare more favourably to the carbohydrate snack [30]. These results confirmed a 2003 study on late-night eating and diabetics. This earlier study showed consistently higher blood sugar levels when snacking late at night, regardless of the macronutrient composition of the meal [31].

Why is late-night eating potentially so bad for us? One possible explanation is our circadian rhythms may prevent us from effectively managing food eaten later at night. There is evidence showing the thermic effect of food is reduced in the evening, due to the circadian regulation of insulin sensitivity, meaning your blood sugar and insulin response to carbs at night is more exaggerated than during the day [32].

 

Solutions for A Modern Circadian Mismatch

Our Paleolithic ancestors would’ve rarely (if ever) eaten after dark. Yet in today’s modern world, the light emitted from iPads, laptops, TVs and mobile devices make it far easier to stay up later at night. This presents a circadian mismatch to our evolutionary biological clocks which translates into more opportunity (and likelihood) to eat. If you’re struggling with weight gain, chronically high blood sugar, pre-diabetes or diabetes then shifting your focus to “meal-timing” can be a simple and highly effective part of the solution to improving your health.

To support a healthy circadian clock, implement the following “meal-timing” strategy:

  • Avoid eating late at night – consider abstaining from all food after 6:00 or 7:00 pm or ditch your late-night snacking while on the couch and try sipping on a herbal tea instead
  • Go for an evening walk, do some light stretching, or take a relaxing bath.

 

In my experience as a clinician, I see major progress in clients who decide to abstain from food in the evening. Once they get through the first few nights, the cravings plummet and it becomes much easier to ingrain the new habit.

Supporting your circadian clock with meal-timing strategies can be an “easy win” to restoring health and vitality [33]. It’s simple and highly effective. 

 

References

1. Gerhart-Hines, Z. and M.A. Lazar, Circadian metabolism in the light of evolution. Endocr Rev, 2015. 36(3): p. 289-304.
2. Guler, A.D., et al., Melanopsin cells are the principal conduits for rod-cone input to non-image-forming vision. Nature, 2008. 453(7191): p. 102-5.
3. Tapp, W.N. and B.H. Natelson, Circadian rhythms and patterns of performance before and after simulated jet lag. Am J Physiol, 1989. 257(4 Pt 2): p. R796-803.
4. Leloup, J.C. and A. Goldbeter, Critical phase shifts slow down circadian clock recovery: implications for jet lag. J Theor Biol, 2013. 333: p. 47-57.
5. Comperatore, C.A. and G.P. Krueger, Circadian rhythm desynchronosis, jet lag, shift lag, and coping strategies. Occup Med, 1990. 5(2): p. 323-41.
6. Vosko, A.M., C.S. Colwell, and A.Y. Avidan, Jet lag syndrome: circadian organization, pathophysiology, and management strategies. Nat Sci Sleep, 2010. 2: p. 187-98.
7. Coren, S., Daylight savings time and traffic accidents. N Engl J Med, 1996. 334(14): p. 924.
8. Varughese, J. and R.P. Allen, Fatal accidents following changes in daylight savings time: the American experience. Sleep Medicine, 2001. 2(1): p. 31-36.
9. Maemura, K., [Circadian rhythm and ischemic heart disease]. Nihon Rinsho, 2013. 71(12): p. 2124-9.
10. Marchant, B., Circadian rhythms and ischaemic heart disease. Br J Hosp Med, 1996. 55(3): p. 139-43.
11. Gehrman, P., et al., The relationship between dementia severity and rest/activity circadian rhythms. Neuropsychiatr Dis Treat, 2005. 1(2): p. 155-63.
12. Ancoli-Israel, S., et al., Variations in circadian rhythms of activity, sleep, and light exposure related to dementia in nursing-home patients. Sleep, 1997. 20(1): p. 18-23.
13. Afsar, B., Disruption of circadian blood pressure, heart rate and the impact on glycemic control in type 1 diabetes. Diabetes Metab Syndr, 2015. 9(4): p. 359-63.
14. Cincotta, A.H., et al., Circadian neuroendocrine role in age-related changes in body fat stores and insulin sensitivity of the male Sprague-Dawley rat. Chronobiol Int, 1993. 10(4): p. 244-58.
15. Wang, L. and S. Liangpunsakul, Circadian clock control of hepatic lipid metabolism: role of small heterodimer partner (Shp). J Investig Med, 2016. 64(7): p. 1158-61.
16. Gnocchi, D., et al., Lipids around the Clock: Focus on Circadian Rhythms and Lipid Metabolism. Biology (Basel), 2015. 4(1): p. 104-32.
17. Gerhart Hines, Z., et al., The nuclear receptor Rev-erbα controls circadian thermogenic plasticity. Nature, 2013. 503(7476): p. 410-413.
18. Bookout, A.L., et al., FGF21 regulates metabolism and circadian behavior by acting on the nervous system. Nat Med, 2013. 19(9): p. 1147-52.
19. Shostak, A., J. Meyer-Kovac, and H. Oster, Circadian regulation of lipid mobilization in white adipose tissues. Diabetes, 2013. 62(7): p. 2195-203.
20. Boden, G., et al., Evidence for a circadian rhythm of insulin secretion. Am J Physiol, 1996. 271(2 Pt 1): p. E246-52.
21. Degaute, J.P., et al., Quantitative analysis of the 24-hour blood pressure and heart rate patterns in young men. Hypertension, 1991. 18(2): p. 199-210.
22. Zambon, A.C., et al., Time- and exercise-dependent gene regulation in human skeletal muscle. Genome Biol, 2003. 4(10): p. R61.
23. Carter, R., et al., Non-alcoholic fatty pancreas disease pathogenesis: a role for developmental programming and altered circadian rhythms. PLoS One, 2014. 9(3): p. e89505.
24. Kettner, N.M., et al., Circadian Homeostasis of Liver Metabolism Suppresses Hepatocarcinogenesis. Cancer Cell, 2016. 30(6): p. 909-924.
25. Zhou, D., et al., Evolving roles of circadian rhythms in liver homeostasis and pathology. Oncotarget, 2016. 7(8): p. 8625-39.
26. CDC: Center for Disease Control & Prevention. Retrieved from – https://www.cdc.gov/nchs/fastats/obesity-overweight.htm
27. Menke, A., et al., Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012. JAMA, 2015. 314(10): p. 1021-9.
28. Cleator, J., et al., Night eating syndrome: implications for severe obesity. Nutr Diabetes, 2012. 2: p. e44.
29. Gallant, A.R., J. Lundgren, and V. Drapeau, The night-eating syndrome and obesity. Obes Rev, 2012. 13(6): p. 528-36.
30. Colles, S.L., J.B. Dixon, and P.E. O’Brien, Night eating syndrome and nocturnal snacking: association with obesity, binge eating and psychological distress. International Journal of Obesity, 2007. 31(11): p. 1722-1730.
31. Kinsey, A.W., et al., Influence of night-time protein and carbohydrate intake on appetite and cardiometabolic risk in sedentary overweight and obese women. Br J Nutr, 2014. 112(3): p. 320-7.
32. Kalergis, M., et al., Impact of bedtime snack composition on prevention of nocturnal hypoglycemia in adults with type 1 diabetes undergoing intensive insulin management using lispro insulin before meals: a randomized, placebo-controlled, crossover trial. Diabetes Care, 2003. 26(1): p. 9-15.
33. Bo, S., et al., Is the timing of caloric intake associated with variation in diet-induced thermogenesis and in the metabolic pattern? A randomized cross-over study. Int J Obes (Lond), 2015. 39(12): p. 1689-95.
34. Mattson, M.P., et al., Meal frequency and timing in health and disease. Proc Natl Acad Sci U S A, 2014. 111(47): p. 16647-53.

 

 

 

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).

Grapefruits: The Best Boost for Your Arteries | The Paleo Diet

INTRODUCTION: HERE IS A GRAPEFRUIT

If you are a devout follower of Paleo, then you know that we encourage eating fruits such as grapefruit. In addition to being low in calories, it is also a great source of vitamin C, as well as vitamin A, vitamin B5, and vitamin B9.1 Furthermore grapefruit is packed with fiber, and phytonutrients like lycopene, limonoids and flavanones.2

Over the years, many scientific studies have shown the great health benefits, including decreasing cancerous growth3, and possibly being as effective in treating diabetes type II as metformin.4 An exceptional study just published in the American Journal of Clinical Nutrition provides great evidence regarding the benefits of grapefruit consumption on vascular function in postmenopausal women and decreasing the risk of arterial stiffness.5 In simpler terms, how drinking grapefruits can boost the arteries, and decrease the risk of developing cardiovascular diseases such as a myocardial infarction/heart attack, or a stroke.

OVERVIEW OF STUDY

Researchers recruited 48 healthy postmenopausal women who were between three to 10 years post menopause. These women were randomly assigned to drink 340 mL of grapefruit juice a day containing 210 mg naringenin glycosides (flavanones), or a matched control drink without flavanones for 6 months each. Then there was a two month washout period between beverages, before the participants were crossed over into the other group.

The most important end-point was the measurement of endothelial function in the brachial artery by means of flow-mediated dilation. Additionally, blood pressure, arterial stiffness, and endothelial function in the peripheral arterial bed were assessed as signs of vascular function. These measurements and blood collection for clinical biochemical markers were carried out in overnight-fasted subjects, pre and post the six month treatment periods.

The results showed a significant decrease in the carotid-femoral pulse wave velocity (PWV) after the consumption of grapefruit juice, at 7.36 m/s. On the other hand, it was 7.70 m/s after consumption of the matched control drink without flavanones. This PWV is seen as the gold standard for evaluating central arterial stiffness, and has a strong correlation with the development of the risk of cardiovascular disease6. The scientists estimate that the PWV reduction of -0.524 m/s is similar to about an absolute 5% risk reduction in cardiovascular disease.

WHAT ARE FLAVANONES?

Many people may be unaware of flavanones. These are compounds that are a subclass of flavonoids, and seen mainly in citrus fruits such as oranges and grapefruits.7 While an orange has the highest amounts of flavanones at 48 mg/100 g aglycones,8 a grapefruit has a total flavanone content (summed means) of 27 mg/100 g9. Lemons contain an overall flavanone content of 26 mg aglycones/100 g edible fruit or juice, while limes have 17 mg aglycones/100 g edible fruit or juice.10 Epidemiological studies showed and demonstrated the many benefits of flavanones including its anti-inflammatory and lipid-lowering properties.11 A previous study demonstrated the possibility of flavanones decreasing the risk of ischemic stroke in women by 17%.12

Well you may be wondering since oranges have a greater content of flavanones, would it not be easier to just drink up some orange juice instead? Well as we have always advocated, commercial juices frequently contain excess sugar, and while you may benefit from the decreased risk of cardiovascular disease, it would be unwise to do so at the expense of diabetes.

ARTERIAL STIFFNESS

As one ages, the aorta stiffens, a process that may be hastened by arterial hypertension.13 It results in a condition known as arteriosclerosis.14 So, if you have high blood pressure, you really should be eating your grapefruits and oranges. Arterial stiffness describes the decreased ability of the artery to swell up and contract as a result of any pressure changes.15 In addition, multiple studies have also shown the predictive significance of arterial stiffness (AS) in a range of populations as an independent predictor of cardiovascular morbidity and all-cause mortality.16

CONCLUSION

In closing, this recent study suggests that the consumption of grapefruit juice by middle aged post-menopausal women is beneficial for arterial stiffness. Given the earlier statement about the possibility of increased sugar in juices, my suggestion instead would be to eat grapefruit whole instead, as we recommend with other fruit and vegetables when following a Paleo diet. Moreover, careful chewing has been shown to stimulate the release of 2 intestinal peptides which decrease appetite and food intake.17 This indicates more benefits for you to actually eat a grapefruit, instead of drinking the juice.

 

REFERENCES

[1] Consumption of Clarified Grapefruit Juice Ameliorates High-Fat Diet Induced Insulin Resistance and Weight Gain in Mice. PLoS ONE 9(10): e108408. doi:10.1371/journal.pone.0108408

[2] Consumption of Clarified Grapefruit Juice Ameliorates High-Fat Diet Induced Insulin Resistance and Weight Gain in Mice. PLoS ONE 9(10): e108408. doi:10.1371/journal.pone.0108408

[3] Consumption of Clarified Grapefruit Juice Ameliorates High-Fat Diet Induced Insulin Resistance and Weight Gain in Mice. PLoS ONE 9(10): e108408. doi:10.1371/journal.pone.0108408

[4] Chudnovskiy R, Thompson A, Tharp K, Hellerstein M, Napoli JL, Stahl A (2014) Consumption of Clarified Grapefruit Juice Ameliorates High-Fat Diet Induced Insulin Resistance and Weight Gain in Mice. PLoS ONE 9(10): e108408. doi:10.1371/journal.pone.0108408

[5] Habauzit V, Verny MA, Milenkovic D, Barber-Chamoux N, Mazur A, Dubray C, Morand C.Flavanones protect from arterial stiffness in postmenopausal women consuming grapefruit juice for 6 mo: a randomized, controlled, crossover trial. Am J Clin Nutr. 2015 Jul;102(1):66-74. doi: 10.3945/ajcn.114.104646

[6] Cavalcante JL, Lima JC, Redheuil A, Al-Mallah MH. Aortic Stiffness: Current Understanding and Future Directions. J Am Coll Cardiol. 2011;57(14):1511-1522. doi:10.1016/j.jacc.2010.12.017.

[7] Peterson, J., Beecher, G., Bhagwat, S., Dwyer, J., Gebhardt, S., Haytowitz, D., & Holden, J. (2006). Flavanones in grapefruit, lemons, and limes: A compilation and review of the data from the analytical literature. Journal of Food Composition and Analysis, 19, S74–S80.

[8] Peterson, J., Beecher, G., Bhagwat, S., Dwyer, J., Gebhardt, S., Haytowitz, D., & Holden, J. (2006). Flavanones in grapefruit, lemons, and limes: A compilation and review of the data from the analytical literature. Journal of Food Composition and Analysis, 19, S74–S80.

[9] Peterson, J., Beecher, G., Bhagwat, S., Dwyer, J., Gebhardt, S., Haytowitz, D., & Holden, J. (2006). Flavanones in grapefruit, lemons, and limes: A compilation and review of the data from the analytical literature. Journal of Food Composition and Analysis, 19, S74–S80.

[10] Peterson, J., Beecher, G., Bhagwat, S., Dwyer, J., Gebhardt, S., Haytowitz, D., & Holden, J. (2006). Flavanones in grapefruit, lemons, and limes: A compilation and review of the data from the analytical literature. Journal of Food Composition and Analysis, 19, S74–S80.

[11] Peterson, J., Beecher, G., Bhagwat, S., Dwyer, J., Gebhardt, S., Haytowitz, D., & Holden, J. (2006). Flavanones in grapefruit, lemons, and limes: A compilation and review of the data from the analytical literature. Journal of Food Composition and Analysis, 19, S74–S80.

[12] Cassidy, A., Rimm, E., O’Reilly, E., Logroscino, G., Kay, C., Chiuve, S., & Rexrode, K. (2012). Dietary Flavonoids and Risk of Stroke in Women. Stroke, 43, 946-951. doi:10.1161/STROKEAHA.111.637835

[13] Cavalcante JL, Lima JC, Redheuil A, Al-Mallah MH. Aortic Stiffness: Current Understanding and Future Directions. J Am Coll Cardiol. 2011;57(14):1511-1522. doi:10.1016/j.jacc.2010.12.017.

[14] Cavalcante JL, Lima JC, Redheuil A, Al-Mallah MH. Aortic Stiffness: Current Understanding and Future Directions. J Am Coll Cardiol. 2011;57(14):1511-1522. doi:10.1016/j.jacc.2010.12.017.

[15] Cavalcante JL, Lima JC, Redheuil A, Al-Mallah MH. Aortic Stiffness: Current Understanding and Future Directions. J Am Coll Cardiol. 2011;57(14):1511-1522. doi:10.1016/j.jacc.2010.12.017.

[16] Cavalcante JL, Lima JC, Redheuil A, Al-Mallah MH. Aortic Stiffness: Current Understanding and Future Directions. J Am Coll Cardiol. 2011;57(14):1511-1522. doi:10.1016/j.jacc.2010.12.017.

[17] Keller, D. (2011, September 13). Thorough Chewing Raises Hormones Regulating Food Intake. Retrieved July 9, 2015, from Medscape: http://www.medscape.com/viewarticle/749504

Which Diet Best Supports Heart Health? | The Paleo Diet

“A healthy diet and lifestyle,” says the American Heart Association (AHA), “are your best weapons in the fight against heart disease.”1 But does the AHA’s recommended diet protect against heart disease better than other diets, particularly the Paleo diet?

Researchers from Eastern Michigan University (EMU) recently compared these two diets for a study published in Nutrition Research. They found that adherence to the Paleo diet for four months significantly decreases total cholesterol (TC), LDL cholesterol, and triglycerides, while increasing HDL cholesterol, compared to four months on the AHA’s recommended diet.

The AHA’s diet includes large amounts of whole grains and dairy, two food groups the Paleo diet, of course, eliminates. The AHA also discourages saturated fat, claiming, “Eating foods that contain saturated fats raises the level of cholesterol in your blood.”2 The current study, however, adds to a growing body of evidence suggesting saturated fat is heart healthy, whereas high-carbohydrate grain-based diets may worsen cardiovascular disease markers.

The EMU researchers recruited 10 men and 10 women between the ages of 40 and 62. Each had hypercholesterolemia (high cholesterol levels) and none were taking cholesterol-reducing medication. Each participant followed the AHA’s recommend diet for 4 months, followed by 4 months on the Paleo diet. Compared to baseline, TC decreased slightly (3%) following the AHA diet, followed by a “very large” 20% decrease from AHA to Paleo.3 Similarly, LDL reductions were “small” (3%) from baseline to AHA, followed by a “very large” 36% decrease from AHA to Paleo.

Weight loss occurred on both diets but was significantly better on the Paleo diet. For men, the AHA diet reduced mean body weight by 3.3 ± 2.7 kg, relative to baseline (P < .001), with an additional 10.4 ± 4.4 kg reduction following 4 months on the Paleo diet. For women, no significant weight reductions followed the AHA diet, but the Paleo diet resulted in significant 8.1 ± 5.9 kg reductions.

This study follows up on previous studies demonstrating improved lipid profiles based on Paleo diet adherence, including a 2009 study showing significant improvements after just 10 days on Paleo and another 2009 study showing significant improvements for type-2 diabetes patients following 3 months on Paleo. 4, 5 The current study, however, does have some limitations, which the researchers openly acknowledge, including a small sample size (20 participants) and the study’s racial homogeneity (predominantly white). Additionally, the study did not allow for order bias, meaning all participants first cycled through the AHA diet, followed by the Paleo diet.

Additionally, it would have also been interesting to see each diet’s impact on both small-particle and large-particle LDL. Measurements of total LDL can be misleading because small-particle LDL accumulates within the arterial walls, whereas large-particle LDL floats through the bloodstream and is generally considered benign.6 Saturated fat has been shown to change small-particle LDL into large-particle LDL.7 In this study, the Paleo diet decreased LDL cholesterol levels more than the AHA diet, but the study tells us nothing about changes in the small- and large-particle LDL.

The AHA’s recommended diet appears to be relatively ineffective for treating hypercholesterolemia. Besides encouraging an AHA-type diet, typical allopathic treatments for hypercholesterolemia often include statin drugs. Statins may reduce cholesterol favorably, but have numerous potential side effects, including myopathy, nausea, neuropathy, elevated liver enzymes, and increased risk of new-onset diabetes.8,9

With no risks and significant benefits, the Paleo diet seems to be the smartest approach to reversing hypercholesterolemia and generally improving heart health. You have nothing to lose and everything to gain going Paleo.

 

REFERENCES

[1] Healthy Eating. American Heart Association. Retrieved from http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/Healthy-Eating_UCM_310436_SubHomePage.jsp

[2] Saturated Fats. American Heart Association. Retrieved from http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/Saturated-Fats_UCM_301110_Article.jsp

[3] Pastore, RL, et al. (June 2015). Paleolithic nutrition improves plasma lipid concentrations of hypercholesterolemic adults to a greater extent than traditional heart-healthy dietary recommendations. Nutrition Research, 35(6). Retrieved from http://www.nrjournal.com/article/S0271-5317%2815%2900097-4/abstract

[4] Frassetto, LA, et al. (February 2009). Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. European Journal of Clinical Nutrition, 63. Retrieved from http://www.nature.com/ejcn/journal/v63/n8/full/ejcn20094a.html

[5] Jonsson, T, et al. (July 2009). Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovascular Diabetology, 8(35). Retrieved from http://www.cardiab.com/content/8/1/35

[6] Tribble, DL, et al. (April 1992). Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis, 93(3). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/1590824

[7] Campos, H, et al. (February 1992). Low density lipoprotein particle size and coronary artery disease. Arteriosclerosis and Thrombosis, 12(2). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/1543692#

[8] Zhang, H, et al. (April 2013). Discontinuation of Statins in Routine Care Settings: A Cohort Study. Annals of Internal Medicine, 158(7). Retrieved from http://annals.org/article.aspx?articleid=1671715

[9] Carter, AA, et al. (May 2013). Risk of incident diabetes among patients treated with statins: population based study. British Medical Journal, 346. Retrieved from http://www.bmj.com/content/346/bmj.f2610

Evolution and High Protein Diets Part 3 | The Paleo Diet

Did you miss Evolution and High Protein Diets Part 1? Click Here to Read It!

Did you miss Evolution and High Protein Diets Part 2? Click Here to Read It!

DIETARY PROTEIN: HEALTH AND WELL BEING

Establishing Cause and Effect between Diet and Disease

One of the challenges faced by nutritional scientists when they ultimately make recommendations regarding what we should and should not eat is to establish cause and effect between a dietary element and the subsequent development or prevention of disease. Some foods and some dietary habits promote good health whereas others promote disease.

No single procedure alone can establish cause and effect,65, 66 nor can any single study prove causality.67 Observational epidemiological studies can only show relationships among variables and are notorious for showing conflicting results68 and cannot provide decisive evidence by themselves either for or against specific hypotheses.69 For example increased animal protein has been associated with a decreased risk for coronary heart disease (CHD) in a large group of nurses (The Nurses Health Study),70 whereas exactly the opposite association was found for markers of CHD and meat consumption in people from rural China.71, 72 An analogy here may be appropriate to show you why observational epidemiological studies can only show relationships and not establish causality. In New York City, there is a strong association between the size of a structure fire and the number of fire trucks at the fire, but can we conclude that more fire trucks cause bigger fires?

In order to establish cause and effect between diet and disease, it takes more than just observational epidemiological evidence.69 There must also be what is referred to as “biological plausibility” in which evidence gathered from tissue, animal and short term human metabolic studies support causality.66 When observational epidemiological evidence is augmented by biological plausibility studies and confirmed by randomized controlled trials, the case for causality becomes ever more convincing. In regard to optimal amounts of dietary protein, the bulk of the evidence from tissue and animal studies and from human dietary interventions provides a compelling case for the therapeutic effects of high protein diets.

Dietary Protein and Cardiovascular Disease

One of the reasons why observational epidemiological studies yield contradictory results is because of the influence of confounding variables which cause confusion in the interpretation of the results because of the mixing of effects from two or more variables.68 For example, although some observational studies have shown a positive association between animal protein and cardiovascular disease (CVD), it is entirely possible that this association is spurious because the measurement of animal protein is confounded by another variable that is also linked to CVD.  Meat is a major source of animal protein in the U.S. diet,20 but it is also a major source of saturated fat.73 Because meat comes as an inseparable package of (protein + saturated fat), animal protein ingestion will be highly correlated to saturated fat, thereby making it difficult to disengage the atherogenic effect of saturated fat from that of animal protein. Accordingly, experimental studies are more useful to determine the true effect animal protein may have upon cardiovascular risk factors because they can be designed to isolate the protein effects from the saturated fat effects.

Sinclair and colleagues74 performed an experiment in which they fed 10 adults a low fat, lean beef-based diet for five weeks. Energy intake was kept constant over the five week study. Total blood cholesterol concentrations fell significantly within one week of commencing the diet, but rose as beef fat drippings were added in a stepwise manner in weeks four and five.  The authors concluded, “. . . it is the beef fat, not lean beef itself, that is associated with elevations in cholesterol concentrations.

Numerous short term human dietary interventions have demonstrated the therapeutic effect of lean, animal based protein upon blood lipid parameters. Wolfe and colleagues have shown that the isocaloric substitution of protein (23% energy) for carbohydrate in moderately hypercholesterolemic subjects resulted in significant decreases in total, LDL and VLDL cholesterol, and triglycerides while HDL cholesterol increased.75 Similar blood lipid changes have been observed in normal healthy subjects76 and in type II diabetic patients in conjunction with improvements in glucose and insulin metabolism.77, 78

A litany of more recent studies has confirmed that elevations in dietary protein have a beneficial effect upon blood lipid profiles.79-85 The mechanism or mechanisms of action of high protein diets upon blood lipid chemistry are not clear; however animal studies suggest that the beneficial effects are caused by their powerful inhibition of hepatic VLDL synthesis, perhaps by altering apoprotein synthesis and assembly in the liver.86

The relationship between protein intake and blood pressure has been comprehensively examined in observational population studies, and support the notion that higher protein intake can lower blood pressure.87-89 A substantial number of randomized controlled trials have demonstrated that higher dietary protein either from soy,90-92 mixed dietary sources85 or from lean red meat93 significantly lower blood pressure.

Dietary Protein and Insulin/Glucose Metabolism and Weight Regulation

In addition to reducing CVD risk by improving the blood lipid profile and reducing blood pressure, higher protein diets have been shown to improve insulin sensitivity and glycemic control79, 81, 84, 94-96 while promoting greater weight loss80, 83, 84, 97, 98 and improved long term sustained weight maintenance99, 100 than low fat high carbohydrate calorie restricted diets. The weight loss superiority of higher protein, calorie restricted diets over either calorie restricted (low fat/ high carbohydrate) diets or calorie restricted (high fat/low carbohydrate) appears to be caused by the greater satiety value of protein compared to either fat or carbohydrate.macronutrients (protein, fat, carbohydrate), protein causes the greatest release of a gut hormone (PYY) that reduces hunger103 while simultaneously improving central nervous system sensitivity to leptin,97 another hormone that controls appetite and body weight regulation.

Dietary Protein and Bone Health

One of the crucial issues regulating bone mineral health and integrity is calcium balance which represents the difference between the amount of dietary calcium which is absorbed and the amount of calcium leaving the body through the urine and feces. Figure 5 demonstrates two key points: 1) most (~75%) of dietary calcium is not absorbed, and 2) calcium absorption increases with decreasing dietary intakes and decreases with increasing dietary intakes.104

Evolution and High Protein Diets | The Paleo Diet

Figure 5.  Relation between Calcium Intake and Absorption

Because dietary protein has been frequently, but not always,105-108 shown to increase urinary calcium excretion, it is possible that long term ingestion of high protein diets could lead to accelerated loss of calcium from the bones thereby impairing bone health and integrity.

Without the concurrent measurement of dietary calcium absorption along with urinary calcium losses the net calcium balance cannot be known. Hence, the simple observation that dietary protein ingestion may increase urinary calcium losses tells us little or nothing about calcium balance. In evaluating the effect of high protein diets upon bone mineral health, it is therefore crucial to measure both urinary calcium excretion and intestinal absorption of calcium. In this regard, Pannemans and colleagues109 compared a low protein (12% energy) to a high protein diet (21% energy) in young and elderly subjects.  Both a higher urinary calcium excretion and a higher intestinal absorption of calcium were induced by the high protein diet, thus no negative calcium balance occurred.

A similar experiment confirmed that elevated dietary protein enhances calcium absorption and thereby counters the increased urinary excretion of calcium.110

Furthermore, a series of recent dietary interventions in humans has shown that high protein, meat based diets do not cause loss of calcium from the skeleton, but actually have a favorable effect upon it by lowering bone resorption105, 107,  111, 112 and may actually increase bone formation by dietary protein induced increases in IFG-1.105

Dietary Protein and Kidney Function

One of the most common misperceptions about high protein diets is that they can damage the kidneys of healthy normal individuals. This concept is known as the “Brenner Hypothesis”113 and suggests that increased dietary protein elevates the kidney’s filtration rate (GFR) which in turn alters the kidney’s structure (glomerulosclerosis) which then causes albumin to appear in the urine (microalbuminuria).  Although these series of steps represent the hypothesis Brenner proffered,113 his experiments actually showed an entirely different series of events. In reality, Brenner demonstrated that patients with pre-existing kidney disease had an elevated GFR, glomerulosclerosis and microalbuminuria and that by reducing dietary protein the GFR and microalbuminuria could be lowered.113 He further suggested that because elevated dietary protein increased the GFR in short term studies (< 2 weeks) of healthy normal subjects, protein was responsible for kidney damage. The problem with this interpretation is that markers of functional kidney damage in the normal subjects (microalbuminuria) were not demonstrated along with the elevations in GFR, nor were any long term studies (3-6 months) carried out to determine if the kidneys adapted to a higher protein intake.

The incidence of diabetic end stage kidney disease has increased steadily over the past three decades.114, 115 If dietary protein were responsible for causing kidney damage, then one might expect that dietary protein would have steadily increased during this same time interval. In fact, dietary proten significand female subjects.118 The high protein diet did not cause urinary albumin to increase. Additionally, the specific GFR, which is an expression of the filtration rate per unit kidney volume, did not change during the high protein diet, indicating that renal (kidney) adaptation occurred to the higher protein load.  The authors summarized, “We therefore conclude that a high dietary protein intake does not appear to have adverse effects on renal function in individuals without renal impairment.”

Dietary Protein and Cancer

Observational epidemiological studies frequently,119 but not always120 show that high animal protein diets may increase the risk for a variety of cancers, particularly colorectal cancer.121 Consequently, it might be expected that non-meat eating vegetarians would have a lower risk for these cancers. Paradoxically, this effect has not been consistently demonstrated.119 A proposed mechanism of action for the carcinogenic effect of meat consumption is the formation of toxic N-nitroso compounds (NOC) in the gut from heme iron in meat.122, 123 Short term human studies are in agreement that increased meat consumption increases NOC formation both in the lower122 and upper123 gastrointestinal tract. However, whether this situation translates into increased cancer risk is not known because to date, no randomized controlled trials of increased meat consumption in humans, using cancer diagnosis as an end point, have been conducted.

The meats and fish consumed by pre-agricultural humans were almost always fresh, whereas current western diets contain significant quantities of processed, salted meats and fish preserved with nitrites and nitrates. Processed meats contains 10 times more NOC (5.5 µmol/kg) than fresh meat (0.5 µmol/kg).124 Pre-agricultural humans consumed their fresh meats along with high intakes s of fresh fruits and vegetables estimated to be between 35-45% of total energy14 compared to 8.1% of total energy in the current U.S. diet.125 Increased fruit and vegetable consumption increases the fecal transit time so that NOC have less contact time with the colonic mucosa and therefore may reduce the carcinogenic risk.126 Hence, the context under which high meat consumption occurred in hunter-gatherers varied significantly from what occurs in westernized populations.

Animal based foods were almost always consumed fresh in conjunction with copious quantities of fresh fruits and vegetables.  Even when vegetable intake was low or absent in these peoples, there is little evidence for an association of high protein, animal based diets with colorectal cancer. Prior to western acculturation, the Inuit may have consumed more than 95% of their daily energy from animal and seafood,15 yet a comprehensive review examining virtually all historical and ethnographic data of these people prior to westernization was unable to document a single case of colorectal cancer.126 Should a high protein meat based diet initiate or promote colorectal cancer, then one might expect obligate carnivores such as cats to demonstrate high incidences of these malignancies.  In, fact the opposite is true, and the rate of gastrointestinal tract cancers is quite low in domestic cats.128 In summary the case for animal based, high protein diets causing colorectal cancer, within the context of pre-agricultural diets, is weak.

Dietary Protein and Muscle Protein Synthesis and Fatigue

For athletes and individuals engaging in regular exercise, an animal based, high protein diet may be ergogenic and facilitate improved performance because of the stimulatory effect of dietary branch chain amino acids (BCCA) upon muscle protein synthesis,129-131 particularly when they are consumed in the post exercise window.132, 133 Table 2 demonstrates that lean meats and fish are much richer sources of the branch chain amino acids (valine, leucine and isoleucine) than are plant foods. In addition to facilitating muscle synthesis during the post exercise recovery period, BCCA may also improve endurance performance by reducing perceived exertion and mental fatigue by reducing the synthesis of brain 5-hydroxytryptamine, a substance that may promote central fatigue.134

DIETARY PROTEIN: SUMMARY AND CONCLUSIONS

The evolutionary evidence indicates that so called “high protein diets” (20-30% total energy) and “very high protein diets” (30-40% total energy) actually represent the norm which conditioned the present day the human genome over more than 2 million years of evolutionary experience. The evolutionary template would predict that human health and well being will suffer when dietary intakes fall outside this range. Hence the current U.S. consumption of protein (15% total energy) may not optimally promote health and well being. There is now a large body of experimental evidence increasingly demonstrating that a higher intake of lean animal protein reduces the risk for cardiovascular disease, hypertension, dyslipidemia, obesity, insulin resistance, and osteoporosis while not impairing kidney function.

 

REFERENCES

Parts 1, 2, & 3

[1]. Bogert LJ, Briggs GM, Calloway DH. Nutrition and Physical Fitness, Ninth Edition. W.B. Sauders Company, Philadelphia, 1973.

[2] Dyerberg J, Bang HO. A hypothesis on the development of acute myocardial infarction in Greenlanders. Scand J Clin Lab Invest Suppl. 1982;161:7-13.

[3] Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL, Goff DV. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr. 1981 Mar;34(3):362-6.

[4] No authors listed. Position paper on trans fatty acids. ASCN/AIN Task Force on Trans Fatty Acids. American Society for Clinical Nutrition and American Institute of Nutrition. Am J Clin Nutr. 1996 May;63(5):663-70.

[5] National Academy of Sciences, Institute of Medicine. Letter Report on Dietary Reference Intakes for Trans Fatty Acids, 2002. http://www.iom.edu/CMS/5410.aspx.

[6]http://www.choosemyplate.gov/

[7] Willett WC, Stampfer MJ. Rebuilding the food pyramid. Sci Am. 2003 Jan;288(1):64-71

[8] Krauss RM, Eckel RH, Howard B, et al. Dietary Guidelines: revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation. 2000 Oct 31;102(18):2284-99.

[9] Blanck HM, Gillespie C, Serdula MK, Khan LK, Galusk DA, Ainsworth BE .Use of low-carbohydrate, high-protein diets among americans: correlates, duration, and weight loss. MedGenMed. 2006 Apr 5;8(2):5.

[10] Ornish D. Dr. Dean Ornish’s Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery. New York : Random House, 1990.

[11] Nesse RM, Stearns SC, Omenn GS. Medicine needs evolution. Science 2006;311:1071.

[12] Dobzhansky T. Am Biol Teacher. 1973 March; 35:125-129.

[13] Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, Brand-Miller .Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005 Feb;81(2):341-54.

[4] Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr. 2000 Mar;71(3):682-92.

[15] Cordain L, Eaton SB, Brand Miller J, Mann N, Hill K. The paradoxical nature of hunter-gatherer diets: Meat based, yet non-atherogenic. Eur J Clin Nutr 2002; 56 (suppl 1):S42-S52.

[16] Cordain L, Watkins BA, Mann NJ. Fatty acid composition and energy density of foods available to African hominids: evolutionary implications for human brain development. World Rev Nutr Diet 2001, 90:144-161.

[17] Bravata DM, Sanders L, Huang J, Krumholz HM, Olkin I, Gardner CD, Bravata DM. Efficacy and safety of low-carbohydrate diets: a systematic review.
JAMA. 2003 Apr 9;289(14):1837-50.

[18] St Jeor ST, Howard BV, Prewitt TE, Bovee V, Bazzarre T, Eckel RH et al.. Dietary protein and weight reduction: a statement for healthcare professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2001 Oct 9;104(15):1869-74.

[19] Wright JD, J Kennedy-Stephenson J, Wang CY, McDowell MA, Johnson CL, National Center for Health Statistics, CDC. Trends in intake of energy and macronutrients—United States, 1971-2000. JAMA. 2004;291:1193-1194.

[20] McDowell M, Briefel R, Alaimo K, et al. Energy and macronutrient intakes of persons ages 2 months and over in the United States: Third National Health and Nutrition Examination Survey, Phase 1, 1988–91. Washington, DC: US Government Printing Office, Vital and Health Statistics; 1994. CDC publication No. 255.

[21] Rudman D, DiFulco TJ, Galambos JT, Smith RB 3rd, Salam AA, Warren WD. Maximal rates of excretion and synthesis of urea in normal and cirrhotic subjects.J Clin Invest. 1973 Sep;52(9):2241-9.

[22] peth JD, Spielmann KA. Energy source, protein metabolism, and hunter-gatherer subsistence strategies. J Anthropological Archaeology 1983;2:1-31.

[23] Speth JD. Early hominid hunting and scavenging: the role of meat as an energy source. J Hum Evol 1989;18:329-43.

[24] Noli D, Avery G. Protein poisoning and coastal subsistence. J Archaeological Sci 1988;15:395-401.

[25] Lieb CW. The effects on human beings of a twelve months’ exclusive meat diet. JAMA 1929;93:20-22.

[26] Ogden CL, Fryar CD, Carroll MD, Flegal KM. Mean body weight, height and body mass index, United States 1960—2002 . Center for Disease Control. Advance Data from Vital and Health Statistics, No. 347, October 27, 2004.

[27] Oliver WJ, Cohen EL, Neel JV. Blood pressure, sodium intake, and sodium related hormones in the Yanomamo Indians, a “no-salt” culture. Circulation. 1975 Jul;52(1):146-51.

[28]Semaw S, Rogers MJ, Quade J, Renne PR, Butler RF, Dominguez-Rodrigo M, Stout D, Hart WS, Pickering T, Simpson SW. 2.6-Million-year-old stone tools and associated bones from OGS-6 and OGS-7, Gona, Afar, Ethiopia. J Hum Evol. 2003 Aug;45(2):169-77.

[29]Bunn, HT, Kroll EM. Systematic butchery by Plio-Pleistocene hominids at Olduvai Gorge, Tanzania. Curr Anthropol 1986;20:365–398.

[30]de Heinzelin J, Clark JD, White T, Hart W, Renne P, WoldeGabriel G, Beyene Y, Vrba E. Environment and behavior of 2.5-million-year-old Bouri hominids. Science. 1999 Apr 23;284(5414):625-9

[31]Asfaw B. White T, Lovejoy O, Latimer B, Simpson S, Suwa, G. Australopithecus garhi: A new species of early hominid from Ethiopia. Science 1999; 284, 629–635.

[32]Vekua A, Lordkipanidze D, Rightmire GP, Agusti J, Ferring R, Maisuradze G, Mouskhelishvili A, Nioradze M, De Leon MP, Tappen M, Tvalchrelidze M, Zollikofer C. A new skull of early Homo from Dmanisi, Georgia. Science. 2002 Jul 5;297(5578):85-9.

[32]Zhu RX, Potts R, Xie F. Hoffman KA, Deng CL, Shi CD, Pan YX, Wang HQ, Shi, RP, Wang YC, Shi GH, Wu NQ. New evidence on the earliest human presence at high northern latitudes in northeast Asia. Nature 2004; 431: 559–562.

[33]Aiello LC, Wheeler P. The expensive tissue hypothesis. Curr Anthropol 1995; 36:199–222.

[34]Leonard W.R, Robertson ML. Evolutionary perspectives on human nutrition: The influence of brain and body size on diet and metabolism. Am J Hum Biol 1994; 6: 77–88.

[35]Pawlosky R., Barnes A., Salem, N. Essential fatty acid metabolism in the feline: Relationship between liver and brain production of long-chain polyunsaturated fatty acids. J Lipid Res 1994;35: 2032–2040.

[36]Hussein N, Ah-Sing E, Wilkinson P, Leach C, Griffin BA, Millward DJ. Long-chain conversion of [13C] linoleic acid and alpha-linolenic acid in response to marked changes in their dietary intake in men. J Lipid Res. 2005 Feb;46(2):269-80.

[37]Sturman JA, Hepner GW, Hofmann AF, Thomas PJ. Metabolism of [35S] taurine in man. J Nutr. 1975 Sep;105(9):1206-14.

[38]Chesney RW, Helms RA, Christensen M, Budreau AM, Han X, Sturman JA. The role of taurine in infant nutrition. Adv Exp Med Biol. 1998;442:463-76.

[39]Laidlaw SA, Shultz TD, Cecchino JT, Kopple JD. Plasma and urine taurine levels in vegans. Am J Clin Nutr. 1988 Apr;47(4):660-3.

[40]Knopf K, Sturman JA, Armstrong M, Hayes KC. 1978. Taurine: An essential nutrient for the cat. J Nutr 1978;108: 773–778.

[41]MacDonald ML, Rogers QR, Morris JG. Nutrition of the domestic cat, a mammalian carnivore. Annu Rev Nutr 1984; 4: 521–562.

[42]Fam AG. Gout: excess calories, purines, and alcohol intake and beyond. Response to a urate-lowering diet. J Rheumatol. 2005 May;32(5):773-7.

[43]Matzkies F, Berg G, Madl H. The uricosuric action of protein in man. Adv Exp Med Biol 1980;122A:227-31.

[44]Loffler W. Grobner W, Medina R, Zollner N. Influence of dietary purines on pool size, turnover, and excretion of uric acid during balance conditions. Isotope studies using 15N-uric acid. Res Exp Med (Berl). 1982(2):113-123.

[45]Oda M, Satta Y, Takenaka O, Takahata N. Loss of urate oxidase activity in hominoids and its evolutionary implications. Mol Biol Evol. 2002 May; 19(5): 640-53.

[46]Abadeh S, Killacky J, Benboubetra M, Harrison R. Purification and partial characterization of xanthine oxidase from human milk. Biochim Biophys Acta. 1992 Jul 21;1117(1):25-32

[47]Xu P, LaVallee P, Hoidal JR. Repressed expression of the human xanthine oxidoreductase gene. E-box and TATA-like elements restrict ground state transcriptional activity. J Biol Chem. 2000 Feb 25;275(8):5918-26.

[48]Dessein PH, Shipton EA, Stanwix AE, Joffe BI, Ramokgadi J. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis. 2000 Jul;59(7):539-43.

[49]vTeleki G. The omnivorous chimpanzee. Sci Am 1973; 228: 33–42.

[50]Stanford CB. The hunting ecology of wild chimpanzees: Implications for the evolutionary ecology of Pliocene hominids. Am Anthropol 1996; 98: 96–113.

[51]Schoeninger MJ, Moore J, Sept JM. Subsistence strategies of two “savanna” chimpanzee populations: The stable isotope evidence. Am J Primatol 1999: 49: 297–314.

[52]van der Merwe NJ, Thackeray JF, Lee-Thorp JA, Luyt J. The carbon isotope ecology and diet of Australopithecus africanus at Sterkfontein, South Africa J Hum Evol 2003;44: 581–597.

[53]Lee-Thorp J, Thackeray JF, van der Merwe N. The hunters and the hunted revisited. J Hum Evol 2000; 39: 565–576.

[54]Sponheimer M, Lee-Thorp JA.. Differential resource utilization by extant great apes and australopithecines: Towards solving the C4 conundrum. Comp Biochem Physiol A 2003;136: 27–34.

[55]Sussman RW. Foraging patterns of nonhuman primates and the nature of food preferences in man. Fed Proc 1978;37: 55–60.

[56]Richards MP, Pettitt PB, Trinkaus E, Smith FH, Paunovic M, Karavanic, I. Neanderthal diet at Vindija and Neanderthal predation: The evidence from stable isotopes. Proc Natl Acad Sci 2000;97: 7663–7666.

[57]Bocherens H, Drucker DG, Billiou D, Patou-Mathis M, Vandermeersch B. Isotopic evidence for diet and subsistence pattern of the Saint-Cesaire I Neanderthal: review and use of a multi-source mixing model. J Hum Evol. 2005 Jul;49(1):71-87

[58]Balter V, Simon L. Diet and behavior of the Saint-Cesaire Neanderthal inferred from biogeochemical data inversion. J Hum Evol. 2006 Oct;51(4):329-38.

[59]Currat M, Excoffier L. Modern humans did not admix with Neanderthals during their range expansion into Europe. PLoS Biol. 2004 Dec;2(12):e421. Epub 2004 Nov 30

[60]Richards MP, Hedges REM, Jacobi R, Current, A, Stringer C. Focus: Gough’s Cave and Sun Hole Cave human stable isotope values indicate a high animal protein diet in the British Upper Palaeolithic. J Archaeol Sci 2000;27: 1–3.

[61]Gray JP. A corrected ethnographic atlas. World Cult J 1999;10: 24–85.

[62]Hayden B. Subsistence and ecological adaptations of modern hunter/gatherers. In: RSO Harding, RSO, Teleki G. (Eds.), Omnivorous Primates. Columbia University Press, New York, 1981, pp. 344–421.

[63]Kaplan H, Hill K, Lancaster J, Hurtado AM. A theory of human life history evolution: diet, intelligence, and longevity. Evol. Anthropol 2000;9:156–185.

[64]Kaplan H, Hill K, Lancaster J, Hurtado AM. A theory of human life history evolution: diet, intelligence, and longevity. Evol. Anthropol 2000;9:156–185.

[65]Sempos CT, Liu K, Ernst ND. Food and nutrient exposures: what to consider when evaluating epidemiologic evidence. Am J Clin Nutr. 1999 Jun;69(6):1330S-1338S.

[66]Potischman N, Weed DL. Causal criteria in nutritional epidemiology. Am J Clin Nutr. 1999 Jun;69(6):1309S-1314S.

[67]Freudenheim JL. Study design and hypothesis testing: issues in the evaluation of evidence from research in nutritional epidemiology. Am J Clin Nutr. 1999 Jun; 69(6): 1315S-1321S.

[68]Fraser GE. A search for truth in dietary epidemiology. Am J Clin Nutr. 2003 Sep;78(3 Suppl):521S-525S.

[69]Flegal KM. Evaluating epidemiologic evidence of the effects of food and nutrient exposures. Am J Clin Nutr. 1999 Jun;69(6):1339S-1344S.

[70]Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Speizer FE, Hennekens CH, Willett WC. Dietary protein and risk of ischemic heart disease in women. Am J Clin Nutr. 1999 Aug;70(2):221-7.

[71]Campbell TC, Junshi C. Diet and chronic degenerative diseases: perspectives from China. Am J Clin Nutr. 1994 May;59(5 Suppl):1153S-1161S.

[72]Campbell TC, Parpia B, Chen J. Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China study. Am J Cardiol. 1998 Nov 26;82(10B):18T-21T.

[73]Popkin BM. Where’s the fat? Trends in U.S. Diets 1965-1996. Prev Med 2001;32:245-54.

[75]Wolfe BM & Giovannetti PM (1991): Short term effects of substituting protein for carbohydrate in the diets of moderately hypercholesterolemic human subjects. Metabolism 40, 338-343.

[76]Wolfe BM & Piche LA (1999): Replacement of carbohydrate by protein in a conventional-fat diet reduces cholesterol and triglyceride concentrations in healthy normolipidemic subjects. Clin. Invest. Med. 22, 140-148.

[77]O’Dea K (1984): Marked improvement in carbohydrate and lipid metabolism in diabetic Australian Aborigines after temporary reversion to traditional lifestyle. Diabetes 33, 596-603.

[78]O’Dea K, Traianedes K, Ireland P, Niall M, Sadler J, Hopper J & DeLuise M (1989): The effects of diet differing in fat, carbohydrate, and fiber on carbohydrate and lipid metabolism in type II diabetes. J. Am. Diet. Assoc. 89, 1076-1086.

[79]Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, Christou DD. A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women. J Nutr. 2003 Feb;133(2):411-7.

[80]Noakes M, Keogh JB, Foster PR, Clifton PM. Effect of an energy-restricted, high-protein, low-fat diet relative to a conventional high-carbohydrate, low-fat diet on weight loss, body composition, nutritional status, and markers of cardiovascular health in obese women. Am J Clin Nutr. 2005 Jun;81(6):1298-306.

[81]Farnsworth E, Luscombe ND, Noakes M, Wittert G, Argyiou E, Clifton PM. Effect of a high-protein, energy-restricted diet on body composition, glycemic control, and lipid concentrations in overweight and obese hyperinsulinemic men and women. Am J Clin Nutr. 2003 Jul;78(1):31-9.

[82]Luscombe-Marsh ND, Noakes M, Wittert GA, Keogh JB, Foster P, Clifton PM. Carbohydrate-restricted diets high in either monounsaturated fat or protein are equally effective at promoting fat loss and improving blood lipids. Am J Clin Nutr. 2005 Apr;81(4):762-72

[83]Aude YW, Agatston AS, Lopez-Jimenez F, Lieberman EH, Marie Almon, Hansen M, Rojas G, Lamas GA, Hennekens CH. The national cholesterol education program diet vs a diet lower in carbohydrates and higher in protein and monounsaturated fat: a randomized trial. Arch Intern Med. 2004 Oct 25;164(19):2141-6.

[84]McAuley KA, Hopkins CM, Smith KJ, McLay RT, Williams SM, Taylor RW, Mann JI. Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese women. Diabetologia. 2005 Jan;48(1):8-16.

[85]Appel LJ, Sacks FM, Carey VJ, Obarzanek E, Swain JF, Miller ER 3rd, Conlin PR, Erlinger TP, Rosner BA, Laranjo NM, Charleston J, McCarron P, Bishop LM; OmniHeart Collaborative Research Group. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA. 2005 Nov 16;294(19):2455-64.

[86]Kalopissis, AD Griffaton G, Fau D. Inhibition of hepatic very low density lipoprotein secretion on obese Zucker rats adapted to a high protein diet. Metabolism 1995;44:19-29.

[87]Appel LJ. The effects of protein intake on blood pressure and cardiovascular disease. Curr Opin Lipidol. 2003 Feb;14(1):55-9. Review.

[89]Elliott P. Protein intake and blood pressure in cardiovascular disease. Proc Nutr Soc. 2003 May;62(2):495-504.

[90]He J, Whelton PK. Elevated systolic blood pressure as a risk factor for cardiovascular and renal disease. J Hypertens Suppl. 1999 Jun;17(2):S7-13.

[91]Burke V, Hodgson JM, Beilin LJ, Giangiulioi N, Rogers P, Puddey IB. Dietary protein and soluble fiber reduce ambulatory blood pressure in treated hypertensives. Hypertension. 2001 Oct;38(4):821-6.

[92]Washburn S, Burke GL, Morgan T, Anthony M. Effect of soy protein supplementation on serum lipoproteins, blood pressure, and menopausal symptoms in perimenopausal women. Menopause. 1999 Spring;6(1):7-13.

[93]He J, Gu D, Wu X, Chen J, Duan X, Chen J, Whelton PK. Effect of soybean protein on blood pressure: a randomized, controlled trial.Ann Intern Med. 2005 Jul 5;143(1):1-9.

[94]Hodgson JM, Burke V, Beilin LJ, Puddey IB. Partial substitution of carbohydrate intake with protein intake from lean red meat lowers blood pressure in hypertensive persons. Am J Clin Nutr. 2006 Apr;83(4):780-7

[95]Nuttall FQ, Gannon MC. The metabolic response to a high-protein, low-carbohydrate diet in men with type 2 diabetes mellitus. Metabolism. 2006 Feb;55(2):243-51.

[96]Nuttall FQ, Gannon MC. Metabolic response of people with type 2 diabetes to a high protein diet. Nutr Metab (Lond). 2004 Sep 13;1(1):6

[97]McAuley KA, Smith KJ, Taylor RW, McLay RT, Williams SM, Mann JI. Long-term effects of popular dietary approaches on weight loss and features of insulin resistance. Int J Obes (Lond). 2006 Feb;30(2):342-9.

[98]Weigle DS, Breen PA, Matthys CC, Callahan HS, Meeuws KE, Burden VR, Purnell JQ. A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. Am J Clin Nutr. 2005 Jul;82(1):41-8

[100]Due A, Toubro S, Skov AR, Astrup A. Effect of normal-fat diets, either medium or high in protein, on body weight in overweight subjects: a randomised 1-year trial. Int J Obes Relat Metab Disord. 2004 Oct;28(10):1283-90

[101]Westerterp-Plantenga MS, Lejeune MP, Nijs I, van Ooijen M, Kovacs EM. High protein intake sustains weight maintenance after body weight loss in humans. Int J Obes Relat Metab Disord. 2004 Jan;28(1):57-64.

[102]Lejeune MP, Kovacs EM, Westerterp-Plantenga MS. Additional protein intake limits weight regain after weight loss in humans. Br J Nutr. 2005 Feb;93(2):281-9.

[103]Porrini M, Santangelo A, Crovetti R, Riso P, Testolin G, Blundell JE. Reid M, Hetherington M. Relative effects of carbohydrates and protein on satiety — a review of methodology. Neurosci Biobehav Rev 1997 May;21(3):295-308

[104]Poppitt SD, McCormack D, Buffenstein R. Short-term effects of macronutrient preloads on appetite and energy intake in lean women. Physiol Behav 1998 Jun 1;64(3):279-85

[105]Batterham RL, Heffron H, Kapoor S, Chivers JE, Chandarana K, Herzog H, Le Roux CW, Thomas EL, Bell JD, Withers DJ. Critical role for peptide YY in protein-mediated satiation and body-weight regulation. Cell Metab. 2006 Sep;4(3):223-33.

[106]O’Brien KO, Abrams SA, Liang LK, Ellis KJ, Gagel RF. Increased efficiency of calcium absorption during short periods of inadequate calcium intake in girls. Am J Clin Nutr. 1996 Apr;63(4):579-83

[107]Dawson-Hughes B, Harris SS, Rasmussen H, Song L, Dallal GE. Effect of dietary protein supplements on calcium excretion in healthy older men and women. J Clin Endocrinol Metab. 2004 Mar;89(3):1169-73

[108]Spencer H, Kramer L, Osis D, Norris C. Effect of a high protein (meat) intake on calcium metabolism in man. Am J Clin Nutr. 1978 Dec;31(12):2167-80

[109]Roughead ZK, Johnson LK, Lykken GI, Hunt JR. Controlled high meat diets do not affect calcium retention or indices of bone status in healthy postmenopausal women. J Nutr. 2003 Apr;133(4):1020-6

[110]Arjmandi BH, Khalil DA, Smith BJ, Lucas EA, Juma S, Payton ME, Wild RA. Soy protein has a greater effect on bone in postmenopausal women not on hormone replacement therapy, as evidenced by reducing bone resorption and urinary calcium excretion. J Clin Endocrinol Metab. 2003 Mar;88(3):1048-54

[111]Pannemans DL, Schaafsma G, Westerterp KR. Calcium excretion, apparent calcium absorption and calcium balance in young and elderly subjects: influence of protein intake. Br J Nutr. 1997 May;77(5):721-9.

[112]Kerstetter JE, O’Brien KO, Insogna KL. Dietary protein affects intestinal calcium absorption. Am J Clin Nutr. 1998 Oct;68(4):859-65.

[113]Kerstetter JE, O’Brien KO, Caseria DM, Wall DE, Insogna KL. The impact of dietary protein on calcium absorption and kinetic measures of bone turnover in women. J Clin Endocrinol Metab. 2005 Jan;90(1):26-31.

[114]Kerstetter JE, Wall DE, O’Brien KO, Caseria DM, Insogna KL. Meat and soy protein affect calcium homeostasis in healthy women. J Nutr. 2006 Jul;136(7):1890-5

[115]Brenner BM, Meyer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease.N Engl J Med. 1982 Sep 9;307(11):652-9.

[116]Lippert J, Ritz E, Schwarzbeck A, Schneider P. The rising tide of endstage renal failure from diabetic nephropathy type II–an epidemiological analysis. Nephrol Dial Transplant. 1995;10(4):462-7.

[117]Ritz E, Rychlik I, Locatelli F, Halimi S. End-stage renal failure in type 2 diabetes: A medical catastrophe of worldwide dimensions. Am J Kidney Dis. 1999 Nov;34(5):795-808.

[118]Wrone EM, Carnethon MR, Palaniappan L, Fortmann SP; Third National Health and Nutrition Examination Survey. Association of dietary protein intake and microalbuminuria in healthy adults: Third National Health and Nutrition Examination Survey. Am J Kidney Dis. 2003 Mar;41(3):580-7.

[119]Johnson DW. Dietary protein restriction as a treatment for slowing chronic kidney disease progression: the case against. Nephrology. 2006 Feb;11(1):58-62.

[120]Skov AR, Toubro S, Bulow J, Krabbe K, Parving HH, Astrup A. Changes in renal function during weight loss induced by high vs low-protein low-fat diets in overweight subjects. Int J Obes Relat Metab Disord. 1999 Nov;23(11):1170-7.

[121]Bingham SA. High-meat diets and cancer risk. Proc Nutr Soc. 1999 May;58(2):243-8.

[122]Truswell AS. Meat consumption and cancer of the large bowel. Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S19-24.

[123]Larsson SC, Wolk A. Meat consumption and risk of colorectal cancer: A meta-analysis of prospective studies.Int J Cancer. 2006 Sep 21; [Epub ahead of print]

[124]Bingham SA, Hughes R, Cross AJ. Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response. J Nutr. 2002 Nov;132(11 Suppl):3522S-3525S

[125]Lunn JC, Kuhnle G, Mai V, Frankenfeld C, Shuker DE, Glen RC, Goodman JM, Pollock JR, Bingham SA. The effect of haem in red and processed meat on the endogenous formation of N-nitroso compounds in the upper gastrointestinal tract. Carcinogenesis. 2006 Oct 19; [Epub ahead of print].

[126]Haorah J, Zhou L, Wang X, Xu G, Mirvish SS. Determination of total N-nitroso compounds and their precursors in frankfurters, fresh meat, dried salted fish, sauces, tobacco, and tobacco smoke particulates. J Agric Food Chem. 2001 Dec;49(12):6068-78

[126]Gerrior S, Bente I. 2002. Nutrient Content of the U.S. Food Supply, 1909-99: A Summary Report. U.S.D.A, Center for Nutrition Policy and Promotion. Home Economics Research Report No. 55.

[127]Hughes R, Pollock JR, Bingham S. Effect of vegetables, tea, and soy on endogenous N-nitrosation, fecal ammonia, and fecal water genotoxicity during a high red meat diet in humans. Nutr Cancer. 2002;42(1):70-7.

[128]Stefansson V. Cancer: Disease of Civilization. Hill and Wang, New York, 1960.

[129]Patnaik AK, Liu SK, Johnson GF. Feline intestinal adenocarcinoma. A clinicopathologic study of 22 cases. Vet Pathol. 1976;13(1):1-10

[130]Anthony JC, Lang CH, Crozier SJ, Anthony TG, MacLean DA, Kimball SR, Jefferson LS. Contribution of insulin to the translational control of protein synthesis in skeletal muscle by leucine. Am J Physiol Endocrinol Metab. 2002;282:E1092-101.

[131]Layman DK. Role of leucine in protein metabolism during exercise and recovery. Can J Appl Physiol 2002;27:646-62.

[132]Rasmussen BB, Tipton KD, Miller SL, Wolf SE, Wolfe RR. An oral essential amino acid-carbohydrate supplement enhances muscle protein anabolism after resistance exercise.J Appl Physiol. 2000 Feb;88(2):386-92.

[133]Tipton KD, Rasmussen BB, Miller SL, Wolf SE, Owens-Stovall SK, Petrini BE, Wolfe RR. Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol Endocrinol Metab. 2001 Aug;281(2):E197-206.

[134]Levenhagen DK, Gresham JD, Carlson MG, Maron DJ, Borel MJ, Flakoll PJ. Postexercise nutrient intake timing in humans is critical to recovery of leg glucose and protein homeostasis. Am J Physiol Endocrinol Metab. 2001;280:E982-93.

[135]Blomstrand E. Amino acids and central fatigue. Amino Acids 2001;20:25-34.

Eliminating Hypertension with Coconut Oil and Exercise | The Paleo Diet

Would you believe saturated fat rich coconut oil could improve your cardiovascular health? It seems counter intuitive based upon common impressions of saturated fat being detrimental to our vascular system,1 however a new study indicates that the combination of coconut oil supplementation and exercise has been linked to reduced body weight, reduced blood pressure, improved baroreflex sensitivity, decreased lipid peroxidation, and reduced superoxide levels.2 These findings have the ability to help over 67 million people struggling with hypertension, who have blood pressure levels greater than 120/80 mm Hg3, increasing their risk of heart attacks, heart disease, strokes, vision issues and kidney disease.

The researchers used baroreflex sensitivity, a tool for the assessment of autonomic control of the cardiovascular system, to assess the impact coconut oil and exercise had on their subjects’ health, independently and together. Baroreceptors, located in the carotid sinus and in the aortic arch, adjust the pressure changes in the arterial wall to maintain homeostasis with parasympathetic responses.4 Cardiovascular diseases are often accompanied by an impairment of baroreflex mechanisms, and a reduction in the baroreflex control of heart rate has been reported in hypertension, coronary artery disease, myocardial infarction, and heart failure.5

Further, elevated blood pressure corresponds to both the release of free fatty acids into the blood and muscle fibers6 as well as to oxidative stress, an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants.7 These factors promote inflammatory processes such as atherosclerosis8 and lead to heart and blood vessel disorders, atherosclerosis, heart failure, heart attack and inflammatory diseases. Coconut oil and exercise showed the combination of the two led to a decrease in oxidative stress, which correlates with better endothelial-dependent relaxation of the aorta and significantly lower (20 mm Hg) blood pressure.9

How can this new research help you?

Hunter-gatherers avoided the many modern diseases that plague us today. The Paleo lifestyle, including the dietary and exercise prescriptions, can assist you in lowering blood pressures to healthy levels, especially with the regular addition of coconut oil into your dietary regime.

Dietary changes are usually prescribed prior to medication as a method to lower blood pressure levels into a safe range. The Paleo Diet eliminates processed foods, salt, and is high in anti-inflammatory Omega-3 fatty acids.10

Numerous studies provide clear evidence of the positive effects of exercise on lowering blood pressure values to a healthy range.11 People who are inactive typically have higher blood pressure than those who exercise regularly, and inactivity is a major risk factor for cardiovascular disease.12

It is possible to reduce your risk for hypertension with lifestyle choices alone. Blood pressure tends to rise with age, so it’s important to monitor it annually with your doctor. The long-term health benefits by making long-lasting lifestyle changes by adopting a Paleo Diet will follow.

 

REFERENCES

[1] Beegom, Raheena, and Ram B. Singh. “Association of higher saturated fat intake with higher risk of hypertension in an urban population of Trivandrum in South India.” International journal of cardiology 58.1 (1997): 63-70.

[2] Alves, Naiane FB, et al. “Coconut oil supplementation and physical exercise improves baroreflex sensitivity and oxidative stress in hypertensive rats.”Applied Physiology, Nutrition, and Metabolism 40.999 (2015): 1-8.

[3] Available at: http://hyper.ahajournals.org/site/misc/StmtGuidelines.xhtml. Accessed on February 25, 2014.

[4] La Rovere, Maria Teresa, Gian Domenico Pinna, and Grzegorz Raczak. “Baroreflex sensitivity: measurement and clinical implications.” Annals of Noninvasive Electrocardiology 13.2 (2008): 191-207.

[5] Eckberg DL, Sleight P. Human Baroreflexes in Health and Disease. In: EckbergDL, SleightP, (eds): Oxford , Clarendon Press, 1992

[6] Wang, Hui, et al. “Role of oxidative stress in elevated blood pressure induced by high free fatty acids.” Hypertension Research 32.2 (2009): 152-158.

[7] Halliwell, Barry. “Biochemistry of oxidative stress.” Biochemical Society Transactions 35.5 (2007): 1147-1150.

[8]  Wu, Lingyun, et al. “Dietary approach to attenuate oxidative stress, hypertension, and inflammation in the cardiovascular system.” Proceedings of the National Academy of Sciences of the United States of America 101.18 (2004): 7094-7099.

[9] Ibid.

[10] Weaver, Kelly L., et al. “Effect of dietary fatty acids on inflammatory gene expression in healthy humans.” Journal of Biological Chemistry 284.23 (2009): 15400-15407.

[11] Available at: http://www.unm.edu/~lkravitz/Article%20folder/hypertension.html. Accessed on February 26, 2015.

[12] Whelton, Seamus P., et al. “Effect of aerobic exercise on blood pressure: a meta-analysis of randomized, controlled trials.” Annals of internal medicine136.7 (2002): 493-503.

 

US Government Poised to Drop Cholesterol Warnings? | The Paleo Diet

The notion that dietary cholesterol, (cholesterol that occurs naturally within food), promotes cardiovascular disease has been a central tenet of the US government’s dietary recommendations for the past 50 years, including their Food Guide Pyramid (retired in 2005), MyPyramid (retired in 2011), and their current MyPlate configuration. Soon, however, the government may finally change its course, aligning itself with decades of scientific research showing that dietary cholesterol neither increases serum (blood) cholesterol levels nor increases risks for cardiovascular disease.

This surprising revelation broke when the Washington Times reported that the highly influential Dietary Guidelines Advisory Committee (DGAC), the group responsible for providing the scientific basis for official US dietary guidelines, is poised to reverse its longstanding warnings against eggs, shrimp, various animal fats, and other foods rich in dietary cholesterol.1

Such a reversal would be highly impactful and significant considering that official dietary guidelines affect school lunch programs and other institutional menu planning, while also directly influencing the eating habits of millions of Americans.

The DGAC convenes once every five years to update and adjust, if necessary, their recommendations. According to the Washington Post, at the panel’s final meeting in December, they decided to withdraw their dietary cholesterol warnings. “A person with direct knowledge of the proceedings,” the Post reports, “said the cholesterol finding would make it to the group’s final report, which is due within weeks.”2 In the current status and trend recap following December’s meeting the DGAC notes, “Cholesterol is not considered a nutrient of concern for overconsumption.” Read more here.

Members of the DGAC are not commenting publically until their report is published and submitted to the Department of Health and Human Services and the Department of Agriculture. Those agencies are not required to act upon the DGAC’s recommendations, but experts speaking with the Post report, “major deviations are not common.”

Let’s face it. The US government’s dietary recommendations have flown in the face of published nutritional science for far too long. It can’t, however, go on like this indefinitely. Eventually, the weight of the science coupled with shifts of thinking among scientists, nutrition experts, and consumers will nudge the government toward scientifically sound recommendations, as opposed to recommendations that serve the interests of food manufacturers and large agricultural conglomerates.

The campaign against dietary cholesterol dates back to 1961, when the American Heart Association (AHA) began warning against overconsumption. The AHA currently recommends no more than 300 mg daily. Eggs contain 185 mg of cholesterol, which means for decades past the AHA (and the US government by extension) has been taking the position that eating more than one daily egg is dangerous.

Even the infamous Dr. Ancel Keys, the progenitor of the lipid hypothesis of coronary heart disease, acknowledged as early as 1953 that dietary cholesterol doesn’t increase blood cholesterol and thus (according to his lipid hypothesis) doesn’t drive heart disease. Keys wrote in the American Journal of Public Health, “Repeated careful dietary surveys on large numbers of persons in whom blood cholesterol was measured consistently fail to disclose a relationship between the cholesterol in the diet and in the serum.”3

The Paleo Diet strongly encourages the DGAC to reverse its longstanding antagonism against healthy foods like eggs, beef, and shrimp, which contain relatively high amounts of dietary cholesterol. We further encourage the relevant governmental agencies to act upon the DGAC’s anticipated reversal, thereby definitively ending the ridiculous and entirely unscientific war against dietary cholesterol, an important and beneficial nutrient.

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] Whoriskey, P. (February 10, 2015). The U.S. government is poised to withdraw longstanding warnings about cholesterol. The Washington Post. Retrieved from http://www.washingtonpost.com/blogs/wonkblog/wp/2015/02/10/feds-poised-to-withdraw-longstanding-warnings-about-dietary-cholesterol/?tid=sm_fb

[2] Ibid.

[3] Keys, A. (November 1953). Prediction and Possible Prevention. American Journal of Public Health and the Nation’s Health, 43(11). Retrieved from http://ajph.aphapublications.org/doi/abs/10.2105/AJPH.43.11.1399

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.

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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