top of page

How Do You Decide If a Diet Is Healthy?

There is no such thing as a “best” diet.




Ah nutrition, the minor, straightforward, non-controversial, never-going-to-offend-or-tick-anyone-off topic. Let me preface with what this article will not be. It will not be a series of recommendations and arguments for or against specific dietary approaches, followed by a closing recommendation of a single strategy. Why? That is a waste of time.

There is no such thing as a one-size-fits-all diet. It doesn’t exist. There are so many complexities and variables regarding the success of a strategy or what is deemed “healthy.” Furthermore, many of the health markers are grossly misunderstood, such as cholesterol. (set aside some time and read all 9 parts of the Peter Attai series on cholesterol) I will use a couple of the more common dietary approaches — veganism or plant-based diet, time-restricted feeding, paleo, and ketogenic —to showcase the complexity of measuring health and the common fallacies of interpreting research. Ultimately, the goal is to help you make more informed dietary decisions through your own research and asking dieticians and physicians the right questions.

This is not medical advice. I am not a registered dietician. As stated, this article is meant to help you in your future research and understanding the information you read and hear. I will share my dietary strategy as full disclosure and attempt to remain unbiased. The following should not be interpreted as advice on which dietary strategies to employ. Consult with a registered dietician.

Let’s jump in.

Diet vs. Diet



There is a common misconception around the word diet. While dieting or a diet can certainly be a short-term plan to achieve a particular goal, a diet also refers to your common eating habits. Unfortunately, magazines and TV commercials have most people focused on the former definition. This creates a problem. Instead of eating well regularly, many people eat what they want then attempt a quick fix while holding their nose through a series of meals, or skipping meals altogether. Exercise is often approached in the same way. This is neither sustainable nor enjoyable.


Instead, adopting a healthy lifestyle and eating habits can help with any nutrition goal you have. Whether your goals are weight loss, muscle gain, athletic performance, improved lipid profile, lower blood pressure, clearer skin, or more energy, consistent dietary habits can make or break the goals. Crash dieting is not sustainable. Most individuals regain the weight plus an additional 10% within a year of completing the diet. What I am advocating for is a lifestyle change.


But which approach should you choose? Furthermore, if the goal is healthy eating, are you doomed to a life of eating rabbit food and cardboard? I can’t answer the first question but I can provide tools and information to help you make an informed decision. The answer to the second question is a resounding no.


Some individuals reading this may think the answer is simple, that by switching over to a vegan lifestyle or a ketogenic diet, all health complications will be solved and everyone will be fit enough to compete in the CrossFit Games. Unfortunately, there is no gold standard of nutrition and likely never will be due to the complexity of nutrition and our bodies. Our genetics influence our responses to a diet.


Also, in attempting to maximize one goal, such as muscle gain, we may cause harm in other areas through excessive consumption or specific foods or malnutrition through a lack of variety. You have to decide what is important to you.


How I currently eat (subject to change)

Allow me to start with full disclosure of my dietary approach. I have taken on many different strategies with one of the more recent being predominantly plant-based. Currently, I limit my eating window to 6–8 hours (intermittent fasting) with high fat and low carbohydrate intake. I have entered ketosis, but I am not regularly tracking my ketone levels.



While I predominantly focus on consuming meat from high-quality sources — such as wild-caught salmon or grass-fed beef — and avoid refined sugars, I will indulge in a robust grain-fed prime porterhouse from my favorite local steakhouse and white chocolate cheesecake on special occasions.


My body handles those foods well, they are infrequently consumed, and I enjoy them immensely. The key is I have built-in wiggle room to handle the occasional splurge. I am not competing in bodybuilding competitions. If I was, the adherence would be higher.

I am more satisfied with my current diet, achieve greater exercise performance, have improved body composition, and better sleep quality, than past dietary approaches. This does not mean a strictly plant-based diet is generally inferior. It means a high-fat, low-carbohydrate, short feeding window diet works well for me.


There is a substantial amount of evidence that supports a low carb or ketogenic diet for producing very favorable nutritional biomarkers and lipid levels. (source) There are equally favorable results for a fully plant-based, or vegan, lifestyle. (source) The key is avoiding tunnel vision and absolutes, as they are dangerous in the field of nutrition.



I encourage you to track your own dietary strategies — specifically write them down — and how they affect your mood, sleep, and physical and mental performance. If you are seeking a dramatic change in your diet, consult your physician, and get blood work. Even the simple act of tracking is a powerful exercise to gain a better understanding of your dietary strategies, your motivations behind food choices — taste, performance, weight, culture, cost, ease to cook or obtain — and your understanding of the impact food has on your lifestyle.


Anecdotal evidence plays a role, but it is still low on the evidence hierarchy.

“There are three kinds of lies: lies, damned lies, and statistics.” — Mark Twain

The China Study is one of the most well-known nutrition studies in the world, and rightfully so due to its size and scope. The study highlighted positive correlations between animal protein intake and development of cardiovascular disease, diabetes, and cancer; conversely, the data showed a negative correlation with the same diagnoses and people consuming plant-based diets. The problem? The lack of control.


Traditional western diets are riddled with high amounts of refined sugar, saturated and trans-fat, salt, and excessive calories. Singling out the cheese and animal meat is insufficient.

Without controlling the vast number of variables and prospectively analyzing multiple data sets, we cannot begin to determine causation. Furthermore, we see similar rates of low mortality and disease in Greenland Eskimos with roughly 70% of their diet coming from animal fat. (source) Complicating the evidence further, more recent studies suggest that a primary influencer of their response may be genetic, which allows their bodies to better process the fat and are protected against harmful effects.


Adding to this theory, recently Greenlanders have started to ‘modernize’ their diet by reducing fat intake and increasing carbohydrate intake. As the diet has modernized, the incidence of diabetes has increased.


Again, causation cannot be drawn but it leads to additional questions about which components of the diet are harmful. There is potential that they have a poor tolerance to increases in glucose and fructose and would benefit from a return to a high-fat diet, even saturated fat, but we are not sure. Nutritional research does not lend itself to hard facts and absolutes.


As stated earlier, tunnel vision can be dangerous in the world of nutrition, especially when it is combined with confirmation bias and epidemiologic research. For example, several large prospective cohorts have drawn similar conclusions as the China Study. (source, source, source) Further analysis revealed the following were associated with increased red & processed meat consumption:

  • Decreased exercise frequency and duration

  • Increased BMI

  • Increased smoking

  • Increased prevalence of diabetes

  • Lower (not a typo) cholesterol levels

  • Increased total caloric intake

  • Increased alcohol intake

This leads to a couple of questions. Is it possible that the elevated BMI, diabetes, low levels of cholesterol (we need cholesterol), or a combination caused the increased mortality rates and not the red meat?


It is very possible the red meat caused the development of those conditions; however, an association is not a cause and effect relationship. Furthermore, is it possible the poor exercise habits, smoking, increased caloric intake, increased alcohol intake or some combination caused the increased mortality rates? Perhaps they even caused elevated BMI, diabetes, and low levels of cholesterol alone.


Red and processed meat cannot be treated as a homogenous and consistent variable. We must consider all that is potentially consumed with the meat (the buns, the fries, the sodas, the sauces, etc.), the source of the meat (wild-caught, foraging, grass-fed), and the cooking methodology (low vs. high heat, fried, baked, etc.). Lastly, we can layer on additional lifestyle habits, such as sleep and stress levels.


Let’s flip the script and look at sugar. A vegan diet will be naturally high in fruits and vegetables. What happens if I focus on the sugar components? Sugar consumption is linked to the same dramatic rise in obesity, cancer, and heart disease, in addition to Alzheimer’s disease.


Consumption of fructose, which is the sugar found in fruit and fruit juice, may be of greater concern due to its linkage to visceral adiposity (i.e. fatty liver disease) and hypertension in rodent studies. (source) The “natural” part of sugar does not make it healthy; sugar is sugar. I have no issue with remaining strict in a diet; but does this mean we should avoid sugars at all costs? A proponent of a ketogenic diet may propose such a strategy.


If the goal is to achieve natural ketosis, then yes, you typically need to consume less than 30–50 g of carbohydrates a day and potentially layer on some level of fasting.


However, it does not mean sugar, and fructose specifically, is the root of all evil. In fact, recent evidence in humans suggests that preliminary evidence in rodents has led to a misunderstanding of the dose-response to fructose, meaning extreme amounts need to be consumed by humans to see the same negative effects. (source)


Once again, more data is needed. Furthermore, focusing on a single nutrient ignores all the other health benefits (fiber, vitamins, phytochemicals).




Defining ‘Healthy’

Many consider nutrition to be a ‘soft’ science. As we have started to explore, the ability to boil down an effect to specific causes is nigh impossible. The volume of variables that modulate an individual’s response to the consumption of certain foods is substantial.


Furthermore, it is difficult to encompass all possible benefits of a diet within a specific dietary approach. The specific goals you are trying to obtain along with the pros and cons of each dietary choice should be weighed.


For example, if someone’s cultural background involves the consumption of animal-based products, and they have many family recipes that are meaningful that also contain animal-based products, a friend or colleague suggesting a vegan diet will lead to a very short conversation. It is important to recognize life is full of trade-off; nutrition is not an exception.


The volume of markers for health is staggering. Here is a sample of all the ways in which a dietary response may be deemed “healthy”:

  • General goals: Weight loss, weight maintenance, hypertrophy, body fat %

  • Specific markers: cholesterol levels (HDL, LDL, TGs), c-reactive protein, resting glucose, A1C, omega-3 and omega-6 fatty acid levels

  • Hormonal control: testosterone, estrogen, cortisol, leptin, ghrelin, IGF-1, insulin

  • Vitamin/mineral levels: Calcium, B12, iron, thiamin, zinc, A, C, D, K

This is not a comprehensive list, but it highlights the difficulty in defining “healthy” food. Furthermore, dietary choices can have a substantial impact on psychological health. If someone is miserable and feels their diet is a chore, not only will the adherence be poor, but it may negate potential benefits.


If your goal is to maximize muscle hypertrophy (build muscle), the protein demands will be higher than strictly necessary for optimal metabolic function. While this can be more difficult to achieve with a plant-based or vegan diet, the amount of protein consumed in the paleo diet is often excessive.



Studies demonstrate that we maximize our therapeutic effect from protein around 1.7-2.2 g/kg of body weight. (source) Evidence suggests excessive protein intake may worsen insulin sensitivity and lead to insulin resistance. (source) More is not always better.


If you want to achieve and maintain a body fat percentage under 8%, you often will need to be in a hypocaloric state which can lead to the chronically altered secretion of testosterone, cortisol, leptin, and ghrelin (similar to sleep deprivation). (source) These hormonal alterations are detrimental to your ability to heal from injury.


If you have difficulty with caloric control, intermittent fasting, or time-restricted feeding may be a great option for you, as the research demonstrates it may improve satiety leading to fewer calories consumed. (source)


Additionally, exercising in a fasted state can improve fat oxidation (you burn more fat). However, studies also indicate acute exercise performance in the fasted state may worsen performance, although there are conflicting results. We are unable to develop a one-size-fits-all diet that checks all the boxes for optimizing “health”.


Nutrition myths

There are many other nutritional myths that can be covered, and new evidence may come to light tomorrow which flies in the face of most of the information presented in this article. This brings me to the robustness of the research.


The absence of evidence does not equal evidence of absence. This applies to all fields of research, but I will focus on nutrition. The fact the epidemiologic studies are flawed— one can argue that is redundant — does not mean meat is out of the woods.


Richard Feynman hit the nail on the head when stating, “Scientific knowledge is a body of statements of varying degrees of uncertainty/certainty — some most unsure, some nearly sure, none absolutely certain.” Through data aggregation, we refine our hypothesis. Absolute statements are dangerous in any field, nutrition chief among them.


I have only scratched the surface and that is intentional. Nutrition cannot be covered with a quick conversation and a couple of recommendations. I haven’t even covered the detrimental aspects of poor nutrition yet. Like I said earlier, the effects of dietary choices extend far beyond aesthetics. To close this article, I will focus on the conditions most prevalent and concerning, affecting a large proportion of people.


The scale is the least of your concerns

Metabolic syndrome is a cluster of conditions — obesity, hypertension, dyslipidemia, and elevated fasting glucose — that increase an individual’s risk for diabetes and cardiovascular complications. To make matters worse, musculoskeletal diseases can lead to the worsening of metabolic syndrome.


One of the primary complications of metabolic syndrome is impaired muscle integrity, which consists of persistent muscle loss, intramuscular fat accumulation, and connective tissue deposition. Degradation of our muscular system is a problem, as muscle is responsible for the majority of total body glucose utilization, which when impaired leads to insulin resistance.


Strength and power are also the primary determinants of health regarding functional mobility and reducing fall risks. Additional complications from metabolic syndrome, such as increased inflammation, are related to the presence of excessive adipose tissue (fat).

This leads to increased risk for future injury and reduces the body’s healing capacity. What other lovely consequences does metabolic syndrome bring to the party? Tendon damage decreased bone mineral density, and osteoarthritis are a couple of others.


I could go on about the impact on muscle quality, the activity of satellite cell activity, recruitment of macrophages and fibroblasts, and the elevation of inflammatory mediators, but I think the point is clear: metabolic syndrome and the associated conditions are detrimental to health.


In general, diets that promote inflammation are high in refined starches, sugar, saturated and trans-fats, and low in omega-3 fatty acids, natural antioxidants, and fiber. For those ready cry foul on the dangers of fructose and animal sources of omega-3 fatty acids, you are more than welcome to avoid fruits and/or fish. I firmly plant those in the “healthy” column as the pros outweigh the cons, however, as with many areas of health, arguments can be made on both sides and encourage you to dive deeper into each topic.



Higher fruit and vegetable intakes are associated with lower oxidative stress and inflammation, likely due to the presence of dietary fiber, salicylic acid, antioxidants, and other goodies within. The addition of antioxidants or vegetables may limit or even reverse pro-inflammatory responses to meals high in saturated fat.


At the end of the day, there is no one size fits all diet. There are many potential benefits to a vegetarian or vegan diet, time-restricted feeding, a ketogenic diet, and many strategies in between. You can employ a combination and don’t need to adhere to a strict ‘school of thought’ and your responses will be significantly impacted by genetics, exercise, sleep, stress, gender, and age. As stated before, you can also follow these diets and while consuming “unhealthy” foods as well.


Addressing the elephant in the room

To close, it is worth noting the impact of taste and pleasure. Many individuals associate taste with health. The tastier a food is the less healthy it is and vice versa. Unfortunately, this leads many people to make unhealthy food choices and is one of the first counterarguments to suggestions for dietary changes. True, there are potential benefits from enjoying your food and the experience.


Experimental studies from animal and human models have shown that foods high in calories, fat, and sugar can lead to pain relief, possibly by modulating the endogenous opioid system and reducing activation of brain regions associated with pain. The key is an individual assessment of the cost-benefit.


People without comorbidities, good looking lipid profiles, appropriate hormonal levels, and healthy body composition have more wiggle room and will tolerate “unhealthy” foods. The body is more resilient and the negative effects of glucose, free radicals, and inflammation will be transient. We must assess the long- term impact of diets consistently high in calories, saturated and trans-fat, and sugar and understand the limitations of the protective effect of pleasure, even if some anecdotal reports are impressive.


Food choices are personal. This is not a license to down a full pizza or KFC $5 Fill-Ups with regularity. Aesthetics and weight are only part of the health equation. It is also a mistake to view this in a binary light. A diet is not simply classified as ‘healthy’ or ‘unhealthy,’ as there are many gradations. I can sample every dessert on the menu on my birthday or enjoy half the buffalo chicken dip when my diet is on point every other day of the week and I exercise regularly. You have to keep your goals in mind.


There is no secret society that will take your vegan membership card if you occasionally enjoy a cookie made with butter. You can still hang out with your keto friends and read the keto blogs if you decide to order home fries at brunch. Diets are complex and food should be enjoyed. We all should educate ourselves to better understand the impact food has on our bodies and not stress about pigeon holding ourselves to specific “lifestyles.”


References

  1. Bazinet RP, Chu MW. Omega-6 polyunsaturated fatty acids: is a broad cholesterol-lowering health claim appropriate? CMAJ 2014;186(6):434-9 doi: 10.1503/cmaj.130253[published Online First: Epub Date]|.

  2. Craig WJ. Health effects of vegan diets. Am J Clin Nutr 2009;89(5):1627S-33S doi: 10.3945/ajcn.2009.26736N[published Online First: Epub Date]|.

  3. Cederberg H, Stancakova A, Kuusisto J, Laakso M, Smith U. Family history of type 2 diabetes increases the risk of both obesity and its complications: is type 2 diabetes a disease of inappropriate lipid storage? J Intern Med 2015;277(5):540-51 doi: 10.1111/joim.12289[published Online First: Epub Date]|.

  4. Bang HO, Dyerberg J, Nielsen AB. Plasma lipid and lipoprotein pattern in Greenlandic West-coast Eskimos. Lancet 1971;1(7710):1143-5 doi: 10.1016/s0140-6736(71)91658-8[published Online First: Epub Date]|.

  5. Zheng Y, Li Y, Satija A, et al. Association of changes in red meat consumption with total and cause specific mortality among US women and men: two prospective cohort studies. BMJ 2019;365:l2110 doi: 10.1136/bmj.l2110[published Online First: Epub Date]|.

  6. Wang X, Lin X, Ouyang YY, et al. Red and processed meat consumption and mortality: dose-response meta-analysis of prospective cohort studies. Public Health Nutr 2016;19(5):893-905 doi: 10.1017/S1368980015002062[published Online First: Epub Date]|.

  7. Pan A, Sun Q, Bernstein AM, et al. Red meat consumption and mortality: results from 2 prospective cohort studies. Arch Intern Med 2012;172(7):555-63 doi: 10.1001/archinternmed.2011.2287[published Online First: Epub Date]|.

  8. Hannou SA, Haslam DE, McKeown NM, Herman MA. Fructose metabolism and metabolic disease. J Clin Invest 2018;128(2):545-55 doi: 10.1172/JCI96702[published Online First: Epub Date]|.

  9. Rizkalla SW. Health implications of fructose consumption: A review of recent data. Nutr Metab (Lond) 2010;7:82 doi: 10.1186/1743-7075-7-82[published Online First: Epub Date]|.

  10. van Buul VJ, Tappy L, Brouns FJ. Misconceptions about fructose-containing sugars and their role in the obesity epidemic. Nutr Res Rev 2014;27(1):119-30 doi: 10.1017/S0954422414000067[published Online First: Epub Date]|.

  11. Jager R, Kerksick CM, Campbell BI, et al. International Society of Sports Nutrition Position Stand: protein and exercise. J Int Soc Sports Nutr 2017;14:20 doi: 10.1186/s12970-017-0177-8[published Online First: Epub Date]|.

  12. Rietman A, Schwarz J, Tome D, Kok FJ, Mensink M. High dietary protein intake, reducing or eliciting insulin resistance? Eur J Clin Nutr 2014;68(9):973-9 doi: 10.1038/ejcn.2014.123[published Online First: Epub Date]|.

  13. Maestu J, Eliakim A, Jurimae J, Valter I, Jurimae T. Anabolic and catabolic hormones and energy balance of the male bodybuilders during the preparation for the competition. J Strength Cond Res 2010;24(4):1074-81 doi: 10.1519/JSC.0b013e3181cb6fd3[published Online First: Epub Date]|.

  14. Cangemi R, Friedmann AJ, Holloszy JO, Fontana L. Long-term effects of calorie restriction on serum sex-hormone concentrations in men. Aging Cell 2010;9(2):236-42 doi: 10.1111/j.1474-9726.2010.00553.x[published Online First: Epub Date]|.

  15. Ganesan K, Habboush Y, Sultan S. Intermittent Fasting: The Choice for a Healthier Lifestyle. Cureus 2018;10(7):e2947 doi: 10.7759/cureus.2947[published Online First: Epub Date]|.

  16. Vieira AF, Costa RR, Macedo RC, Coconcelli L, Kruel LF. Effects of aerobic exercise performed in fasted v. fed state on fat and carbohydrate metabolism in adults: a systematic review and meta-analysis. Br J Nutr 2016;116(7):1153-64 doi: 10.1017/S0007114516003160[published Online First: Epub Date]|.

  17. Zouhal H, Saeidi A, Salhi A, et al. Exercise Training and Fasting: Current Insights. Open Access J Sports Med 2020;11:1-28 doi: 10.2147/OAJSM.S224919[published Online First: Epub Date]|.

  18. Moro T, Tinsley G, Bianco A, et al. Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males. J Transl Med 2016;14(1):290 doi: 10.1186/s12967-016-1044-0[published Online First: Epub Date]|.

  19. Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature 2012;482(7383):27-9 doi: 10.1038/482027a[published Online First: Epub Date]|.

  20. Liska D, Mah E, Brisbois T, Barrios PL, Baker LB, Spriet LL. Narrative Review of Hydration and Selected Health Outcomes in the General Population. Nutrients 2019;11(1) doi: 10.3390/nu11010070[published Online First: Epub Date]|.

  21. Marklund M, Wu JHY, Imamura F, et al. Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality. Circulation 2019;139(21):2422-36 doi: 10.1161/CIRCULATIONAHA.118.038908[published Online First: Epub Date]|.

  22. Gurzell EA, Wiesinger JA, Morkam C, Hemmrich S, Harris WS, Fenton JI. Is the omega-3 index a valid marker of intestinal membrane phospholipid EPA+DHA content? Prostaglandins Leukot Essent Fatty Acids 2014;91(3):87-96 doi: 10.1016/j.plefa.2014.04.001[published Online First: Epub Date]|.

  23. Harris WS, Sands SA, Windsor SL, et al. Omega-3 fatty acids in cardiac biopsies from heart transplantation patients: correlation with erythrocytes and response to supplementation. Circulation 2004;110(12):1645-9 doi: 10.1161/01.CIR.0000142292.10048.B2[published Online First: Epub Date]|.

  24. Fenton JI, Gurzell EA, Davidson EA, Harris WS. Red blood cell PUFAs reflect the phospholipid PUFA composition of major organs. Prostaglandins Leukot Essent Fatty Acids 2016;112:12-23 doi: 10.1016/j.plefa.2016.06.004[published Online First: Epub Date]|.

  25. Harris WS, Tintle NL, Etherton MR, Vasan RS. Erythrocyte long-chain omega-3 fatty acid levels are inversely associated with mortality and with incident cardiovascular disease: The Framingham Heart Study. J Clin Lipidol 2018;12(3):718-27 e6 doi: 10.1016/j.jacl.2018.02.010[published Online First: Epub Date]|.

  26. Lee TH, Hoover RL, Williams JD, et al. Effect of dietary enrichment with eicosapentaenoic and docosahexaenoic acids on in vitro neutrophil and monocyte leukotriene generation and neutrophil function. N Engl J Med 1985;312(19):1217-24 doi: 10.1056/NEJM198505093121903[published Online First: Epub Date]|.

  27. Phillipson BE, Rothrock DW, Connor WE, Harris WS, Illingworth DR. Reduction of plasma lipids, lipoproteins, and apoproteins by dietary fish oils in patients with hypertriglyceridemia. N Engl J Med 1985;312(19):1210-6 doi: 10.1056/NEJM198505093121902[published Online First: Epub Date]|.

  28. Harris WS. Fish oils and plasma lipid and lipoprotein metabolism in humans: a critical review. J Lipid Res 1989;30(6):785-807

  29. Wanders AJ, Zock PL, Brouwer IA. Trans Fat Intake and Its Dietary Sources in General Populations Worldwide: A Systematic Review. Nutrients 2017;9(8) doi: 10.3390/nu9080840[published Online First: Epub Date]|.

  30. Dhaka V, Gulia N, Ahlawat KS, Khatkar BS. Trans fats-sources, health risks and alternative approach - A review. J Food Sci Technol 2011;48(5):534-41 doi: 10.1007/s13197-010-0225-8[published Online First: Epub Date]|.

  31. Iqbal MP. Trans fatty acids - A risk factor for cardiovascular disease. Pak J Med Sci 2014;30(1):194-7 doi: 10.12669/pjms.301.4525[published Online First: Epub Date]|.

  32. Anderson KE. Comparison of fatty acid, cholesterol, and vitamin A and E composition in eggs from hens housed in conventional cage and range production facilities. Poult Sci 2011;90(7):1600-8 doi: 10.3382/ps.2010-01289[published Online First: Epub Date]|.

  33. Ponnampalam EN, Mann NJ, Sinclair AJ. Effect of feeding systems on omega-3 fatty acids, conjugated linoleic acid and trans fatty acids in Australian beef cuts: potential impact on human health. Asia Pac J Clin Nutr 2006;15(1):21-9

  34. Daley CA, Abbott A, Doyle PS, Nader GA, Larson S. A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef. Nutr J 2010;9:10 doi: 10.1186/1475-2891-9-10[published Online First: Epub Date]|.

  35. Provenza FD, Kronberg SL, Gregorini P. Is Grassfed Meat and Dairy Better for Human and Environmental Health? Front Nutr 2019;6:26 doi: 10.3389/fnut.2019.00026[published Online First: Epub Date]|.

  36. Orlich MJ, Singh PN, Sabate J, et al. Vegetarian dietary patterns and mortality in Adventist Health Study 2. JAMA Intern Med 2013;173(13):1230-8 doi: 10.1001/jamainternmed.2013.6473[published Online First: Epub Date]|.

  37. Huang T, Yang B, Zheng J, Li G, Wahlqvist ML, Li D. Cardiovascular disease mortality and cancer incidence in vegetarians: a meta-analysis and systematic review. Ann Nutr Metab 2012;60(4):233-40 doi: 10.1159/000337301[published Online First: Epub Date]|.

  38. Haghighatdoost F, Bellissimo N, Totosy de Zepetnek JO, Rouhani MH. Association of vegetarian diet with inflammatory biomarkers: a systematic review and meta-analysis of observational studies. Public Health Nutr 2017;20(15):2713-21 doi: 10.1017/S1368980017001768[published Online First: Epub Date]|.

  39. Chaix A, Manoogian ENC, Melkani GC, Panda S. Time-Restricted Eating to Prevent and Manage Chronic Metabolic Diseases. Annu Rev Nutr 2019;39:291-315 doi: 10.1146/annurev-nutr-082018-124320[published Online First: Epub Date]|.

  40. Rynders CA, Thomas EA, Zaman A, Pan Z, Catenacci VA, Melanson EL. Effectiveness of Intermittent Fasting and Time-Restricted Feeding Compared to Continuous Energy Restriction for Weight Loss. Nutrients 2019;11(10) doi: 10.3390/nu11102442[published Online First: Epub Date]|.

  41. Chaix A, Zarrinpar A, Miu P, Panda S. Time-restricted feeding is a preventative and therapeutic intervention against diverse nutritional challenges. Cell Metab 2014;20(6):991-1005 doi: 10.1016/j.cmet.2014.11.001[published Online First: Epub Date]|.

  42. Longo VD, Panda S. Fasting, Circadian Rhythms, and Time-Restricted Feeding in Healthy Lifespan. Cell Metab 2016;23(6):1048-59 doi: 10.1016/j.cmet.2016.06.001[published Online First: Epub Date]|.

  43. Kosinski C, Jornayvaz FR. Effects of Ketogenic Diets on Cardiovascular Risk Factors: Evidence from Animal and Human Studies. Nutrients 2017;9(5) doi: 10.3390/nu9050517[published Online First: Epub Date]|.

  44. Ludwig DS. The Ketogenic Diet: Evidence for Optimism but High-Quality Research Needed. J Nutr 2019 doi: 10.1093/jn/nxz308[published Online First: Epub Date]|.

  45. Boison D. New insights into the mechanisms of the ketogenic diet. Curr Opin Neurol 2017;30(2):187-92 doi: 10.1097/WCO.0000000000000432[published Online First: Epub Date]|.

댓글


bottom of page