The Vegan Diet for Longevity and Anti-Aging: Part 1

by

If you doubt the anti-aging effects of a diet composed strictly of nutrient-packed whole plant foods, then you should check out Bernando Lapallo, a lifetime raw vegan who lived to 114.

<

Longevity and aging is a huge industry these days. People all over the world are getting together in communities to swap ideas and experiment to various protocols, sharing their results, etc. Diet has always been at the core of this endeavor so I thought I’d write a bit about the vegan diet in the context of longevity and health.

Longevity Vs. Aging

Keep in mind that the terms longevity and anti-aging are often used interchangeably. Longevity really just refers to lifespan. Anything that successfully slowed the aging process or staved off disease would result in increased longevity all else equal. Aging is a process whereby our bodies become more susceptible to chronic diseases.

Here are the definitions by Roger B. McDonald, et al. Definitions of the two terms vary, but I think this is a helpful distinction.1

Aging: the progressive, event-dependent decline in the ability to maintain biochemical/physiological function.

Longevity: the length of the life span independent of the biological aging process.

The Vegan Diet and Longevity

When done correctly it appears, that the vegan diet does promote longevity. In regards to studies on health-conscious populations (Oxford Vegetarian Society Study, Adventist Studies, etc.), Pramil N. Singh wrote in Vegetarian Nutrition Volume 3, “a significant reduction in risk (for all-cause mortality) for very low meat intake persists even after controlling for a number of important predictors of longevity (smoking, alcohol use, physical activity, education, body mass index).”2

When examining the many benefits associated with plant-based diets, you can either focus on the exclusion of meat or the healthy whole plant foods that replace the meat. Pramil N Singh was able to control for a number of healthy behaviors that may bias the positive effects of low meat consumptions towards protection. However, the data at hand was considered insufficient to determine whether the protective effects were due to the elimination of meat vs. the inclusion of whole plant foods.

But, whatever the exact reasons may be, the take-home message is that vegetarian eating patterns are associated with greater longevity.

The Vegan Diet and Aging

Now, the above pertains to longevity in terms of lifespan. The study of antiaging focuses on mechanisms more so than epidemiological data regarding life expectancy. Specifically, it studies mechanisms that are potentially responsible for the human body becomes less functional over time and more susceptible to disease. It is highly theoretical at this point and much less straightforward. It seems that there are many ways in which a healthy whole food vegan diet may be anti-aging thus promoting longevity.

In What Ways Is the Vegan Diet Anti-Aging?

A well-planned vegan diet can help you maintain good health—to slow the process by which our bodies become more susceptible to disease over time.

As you’ll see, oxidative stress is the common denominator in all of the theories of aging, and a healthy vegan diet can help you hit that problem from different angles.

  1. It helps you avoid excessive energy consumption—calorie restriction is key to longevity.
  2. It helps you avoid certain deleterious food components that may cause oxidative stress.
  3. It provides food components that are potentially protective. This includes foods that may prevent oxidative stress (antioxidants), and calorie restriction “mimetics”—compounds that are thought to potentially mimic the longevity-promoting effects of calorie restriction.

A Few Theories of Aging

1. Dietary Restriction (DR)

It’s been proven that dietary restriction (DR) without malnutrition prolongs life in a diverse range of organisms. Dietary restriction is simply a restriction of some component in the diet. As for which aspect of the diet that one could benefit from restricting, that remains the subject of debate. The two areas of restriction with the most scientific consensus are calories and protein.

Calorie Restriction (CR)

This is the setting of calories at some level slightly less than what would be needed for daily maintenance needs.

Keep in mind that caloric restriction (CR) and dietary restriction (DR) are often (but not always) used interchangeably. I found this distinction helpful and will be using it in this article.

Restriction of Certain Nutrients

Although it is generally believed that increased longevity with dietary restriction arises from eating fewer calories, there is an increasing body of evidence indicating that restriction of certain nutrients, rather than calories per se, is responsible for increased life expectancy.3-12

Methionine Restriction

Some scientists believe that restricting proteins that are characteristically high in methionine (animal proteins) may be what’s really going on with benefits seen from protein restriction. I.e. less protein overall will mean less methionine all else equal.

The Ratio of Protein to Non-Protein Energy

Those who get most of their energy from foods higher in carbs/lower in protein would be expected to benefit if this mechanism were valid.

Keep in mind that while protein restriction has gained a lot of attention in recent times, the balance of opinion in this area is that CR, not PR, is responsible for the extension in lifespan seen in mammals thus far.13,14


2. The Use of Mimetics

Mimetics are certain nutrients found in fruits and vegetables, such as resveratrol, that are thought to promote longevity in the same way that calorie restriction does. They seem to trigger the same anti-aging processes. I’ll be covering this in depth in part two.

Anti-aging Properties of the Vegan Diet

Now, let’s take a closer look at the various aspects of plant-based diets that may lead to a longer life. Keep in mind that it’s all theoretical at this point.

1. Lower Caloric Density

As we’ve seen, caloric restriction is the main mechanism thought to account for the effect of certain diets on longevity. A healthy whole food vegan diet is high in volume/bulk and low in calories making it the perfect diet for eating as little as possible while remaining satiated.

Now, let’s cover some of the popular theories as to how CR can result in a greater lifespan.

Decreased Oxidative Damage

When tissues undergo oxidative damage, the process leaves behind biomarkers that accumulate in the tissues. These biomarkers include broken DNA strands, protein carbonyls, and oxidized lipid membranes, etc. Not important.

There are many studies that have demonstrated that CR reduces the concentration of these biomarkers.15-17

Researchers began by comparing older tissues with younger tissues to get a baseline for the number of biomarkers that should be accumulated by a certain age—because age is simply a proxy for how much time a given tissue has had to undergo oxidation.

With that baseline in mind, they put various rodents under CR conditions and found that restriction of calories resulted in less oxidative damage than what would be expected at a given age.

So, basically, they concluded that CR conditions induce a slower rate of tissue accrual of oxidative damage and thus contributes to the beneficial effect of CR on longevity.

Improved Mitochondrial Function

There’s some overlap here for sure, but this pertains to ROS in the mitochondria. It’s significant because while there are many sites within cells where ROS are generated, the mitochondria produce the majority of it during normal metabolism.18

Several studies have established that, at least in the tissues from rodent species, the major cause of reduced ROS when calories are restricted, comes from a decrease in the rate of free radical generation.19,16,20-22

It should be noted that this has only been demonstrated in isolated mitochondria or cells in vitro, and thus probably under non-physiological conditions.

2. Vegan Diets Have a High Carbohydrate to Protein Ratio

You might wonder how it is that scientists could know for sure whether it’s calorie restriction or the restriction of certain nutrients that are responsible for the effect of low-calorie diets on longevity. It’s not exactly easy to separate the effects of nutrients and calories.

Researchers really wanted to know the answer, and as a result certain technology has emerged that can help disaggregate some of these variables. There’s something known as the Geometric Framework (GF) that provides a way to disentangle the influences of nutrients vs. calories.23-27

I won’t bore you with the details—in other words, I have no idea how it works. Just know that three studies on insects have used this technology to demonstrate that caloric restriction is not the primary factor behind the life-extending benefits of dietary restriction.

Instead, the carbohydrate/protein ratio was the primary factor implicated in the diet-longevity connection.10,11,28

While CR is thought to be the primary factor, there is no doubt that specific nutrients have some level of impact on longevity, and the protein/non-protein energy balance is becoming a primary area of focus.

Why? What is it about a low protein/non-protein ratio that could be beneficial?

Decreased Mitochondrial ROS Production

Remember oxidative phosphorylation from high school biology class? The Krebs Cycle and electron transport chain, and all that jazz. It’s the processes that our cells/mitochondria use to take the food we’ve been eating and turn it into energy.

I’m very thankful for these processes because if not for them I wouldn’t be alive writing this article right now. But, when you break down macronutrients for energy it requires oxidation. Hence, oxidative phosphorylation. As important as this oxidative process is, it’s not special when it comes to the generation of reactive oxygen species (ROS).

When we break down food for fuel, we’re generating all kinds of free radicals which can damage DNA.

Anyway, it may just be that protein restriction—even absent calorie restriction—results in less ROS production, and by extension, results in less DNA damage over time. At least it seems to be the case with our furry cousins.29,6

Oxidative Modification of Proteins

Protein oxidative modification, or simply protein oxidation, is a class of protein posttranslational modifications—changes that can take place in the structure of a protein after it’s been made. They are caused by reactions between amino acid residues and ROS.

Many researchers believe the observed decrease in the rate of aging via protein restriction may in part be due to decreases in the level of oxidative modification that DNA and protein undergo.6

Insulin/IGF and TOR  Pathways

In recent times, something called the nutrient-sensing TOR pathway has been implicated as playing a role in the regulation of lifespan. TOR itself is an enzyme that regulates (via phosphorylation) a ton of different proteins

The pathway in which TOR regulates these proteins is responsive to specific nutrients.

Anyway, there are various relationships between insulin and IGF-1 (which we’ve talked about in other articles), and the TOR pathways, many of which involve the aging process.30-32

Nitrogen Breakdown Products

When the body breaks down protein, not only is it costly, but it produces nitrogenous waste products that have toxic effects. High protein intake may lead to an excess of these breakdown products which over the long-term wouldn’t be good for longevity.33,34

A Counter-Point: The Protein Leverage Effect

It’s important to note that there is a way in which low protein diets could have a negative effect on longevity. Not that low protein diets are linked to shorter life expectancy, but mechanistically it makes sense to many researchers that there could be an effect.

The idea is that protein intake, being more strongly regulated than carbohydrate and fat consumption, may result in an appetite that drives overeating which, of course, causes obesity and metabolic disorders.35,36

This is very theoretical (read: unproven), but then again, all of this stuff is so it should be mentioned.

Summary of Protein/Non-Protein Ratios

Again, it’s important to note that the consensus is still with calorie restriction. But, studies such as these show that the subject warrants further investigation.

Also note that in the event that low protein to non-protein ratios prove to promote longevity, a whole food vegan diet has you covered in this area. You really have to go out of your way to get a high protein to carbohydrate ratio when consuming a 100% plant-based diet.

3. Methionine Restriction

Plant proteins are generally low in methionine which may be a good thing. Many studies have shown methionine restriction to extend lifespan in rodents.3

It’s important to note that observed effects could simply be a roundabout way in which CR improves longevity.

For example, with methionine restriction, there’s an associated decrease in plasma glucose and insulin concentrations that.37

For this reason, it could be that impaired glucose metabolism via methionine restriction may result in energy restriction.

4. Plant-Based Diets Are Abundant in CR Mimetics

I’ll cover this in depth in Part 2 of this series. For now, just know that there are plant compounds known as CR mimetics. These are molecules in plants that activate similar pathways as calorie restriction in the promotion of longevity.38

These compounds are often pigments, such as anthocyanins, a compound I’ve touched on briefly before.

Anyway, if you’re interested what these compounds are, how they work, and how it is they could mimic some of the effects of fasting, then you’re going to want to stay tuned for Part 2 of the series on the vegan diet, longevity, and anti-aging.

References

  1. Roger B. McDonald, Rodney C. Ruhe. Aging and Longevity: Why Knowing the Difference Is Important to Nutrition Research. Nutrients. 2011;3(3):274–282.
  2. Vegetarian Nutrition Rosemary Ratzin-Turner-Joan Sabaté – Crc Press – 2001
  3. Zimmerman, J. A., Malloy, V., Krajcik, R. and Orentreich, N., 2003. Nutritional control of aging. Exp Gerontol 38, 47–52.
  4. Mair, W., Piper, M. D. W. and Partridge, L., 2005. Calories do not explain extension of life span by dietary restriction in Drosophila. PLoS Biol 3, 1305–1311.
  5. Piper, M. D. W., Mair, W. and Partridge, L., 2005. Counting the calories: the role of specific nutrients in extension of life span by food restriction. J Gerontol A Biol Sci Med Sci 60, 549–555.
  6. Ayala, V., Naudi, A., Sanz, A., Caro, P., Portero-Otin, M., Barja, G. and Pamplona, R., 2007. Dietary protein restriction decreases oxidative protein damage, peroxidizability index, and mitochondrial complex I content in rat liver. J Gerontol A Biol Sci Med Sci 62, 352–360.
  7. Hulbert, A. J., Pamplona, R., Buffenstein, R. and Buttemer,W. A., 2007. Life and death: Metabolic rate, membrane composition, and life span of animals. Physiol Rev 87, 1175–1213.
  8. Carey, J. R., Harshman, L. G., Liedo, P., Müller, H.-G., Wang, J.-L. and Zhang, Z., 2008. Longevity-fertility trade-offs in the tephritid fruit fly, Anastrepha ludens, across dietaryrestriction gradients. Aging Cell 7, 470–477.
  9. Hulbert, A. J., 2008. The links between membrane composition, metabolic rate and lifespan. Comp Biochem Physiol A Mol Integr Physiol 150, 196–203.
  10. Lee, K. P., Simpson, S. J., Clissold, F. J., Brooks, R., Ballard, J. W., Taylor, P. W., Soran, N. and Raubenheimer, D., 2008. Lifespan and reproduction in Drosophila: new insights from nutritional geometry. PNAS 105, 2498–2503.
  11. Maklakov, A. A., Simpson, S. J., Zajitschek, F., Hall, M., Dessman, J., Clissold, F., Raubenheimer, D., Bonduriansky, R. and Brooks, R. C., 2008. Sex-specific fitness effects of nutrient intake on reproduction and lifespan. Curr Biol 18, 1062–1066.
  12. Dussutour, A. and Simpson, S. J., 2009. Communal nutrition in ants. Curr Biol 19, 740–744 .
  13. Weindruch, R. and Walford, R. L., 1988. The Retardation of Aging and Disease by Dietary Restriction. Charles C Thomas, Springfield, IL.
  14. Masoro, E. J., 2006. Caloric restriction and aging: controversial issues. J Gerontol A Biol Sci Med Sci 61, 14–19.
  15. Yu, B. P., 1996. Aging and oxidative stress: modulation by dietary restriction. Free Radic Biol Med 21, 651–668.
  16. Merry, B. J., 2000. Calorie restriction and age-related oxidative stress. In Toussaint, O., Osiewacz, H. D., Lithgow, G. J. and Brack, C. (eds), Molecular and Cellular Gerontology Vol. 908. New York Academy of Sciences, New York, pp. 180–198.
  17. Hamilton, M. L., Van Remmen, H., Drake, J. A., Yang, H., Guo, Z. M., Kewitt, K., Walter, C. A. and Richardson, A., 2001. Does oxidative damage to DNA increase with age? Proc Natl Acad Sci 98, 10469–10474.
  18. Beckman, K. B. and Ames, B. N., 1998. The free radical theory of aging matures. Physiol Rev 78, 547–581.
  19. Sohal, R. S., Ku, H. H., Agarwal, S., Forster, M. J. and Lal, H., 1994. Oxidative damage, mitochondrial oxidant generation and antioxidant defenses during aging and in response to food restriction in the mouse. Mech Ageing Dev 74, 121–133.
  20. Merry, B. J., 2002. Molecular mechanisms linking calorie restriction and longevity. Int J Biochem Cell B 34, 1340–1354.
  21. Merry, B. J., 2004. Oxidative stress and mitochondrial function with ageing – the effects of calorie restriction. Aging Cell 3, 7–12.
  22. Sanz, A., Pamplona, R. and Barja, G., 2006. Is the mitochondrial free radical theory of aging intact? Antioxid Redox Signal 8, 582–599.
  23. Simpson, S. J. and Raubenheimer, D., 2007. Caloric restriction and aging revisited: the need for a geometric analysis of the nutritional bases of aging. J Gerontol A Biol Sci Med Sci 62, 707–713.
  24. Raubenheimer, D. and Simpson, S. J., 1993. The geometry of compensatory feeding in the locust. Anim Behav 45, 953–964.
  25. Simpson, S. J. and Raubenheimer, D., 1993. A multi-level analysis of feeding behaviour: the geometry of nutritional decisions. Philos Trans R Soc Lond B Biol Sci 342, 381–402.
  26. Raubenheimer, D. and Simpson, S. J., 1997. Integrative models of nutrient balancing: application to insects and vertebrates. Nutr Res Rev 10, 151–179.
  27. Simpson, S. J., Sibly, R. M., Lee, K. P., Behmer, S. T. and Raubenheimer, D., 2004. Optimal foraging when regulating intake of multiple nutrients. Anim Behav 68, 1299–1311.
  28. Fanson, B. G.,Weldon, C.W., Perez-Staples, D., Simpson, S. J. and Taylor, P.W., 2009. Nutrients, not caloric restriction, extend lifespan in Queensland fruit flies (Bactrocera tryoni). Aging Cell 8, 514–523.
  29. Sanz, A., Caro, P. and Barja, G., 2004. Protein restriction without strong caloric restriction decreases mitochondrial oxygen radical production and oxidative DNA damage in rat liver. J Bioenerg Biomembr 36, 545–552.
  30. Kapahi, P. and Zid, B. M., 2004. TOR pathway: linking nutrient sensing to life span. SAGE KE 36, pe34.
  31. Kapahi, P., Zid, B. M., Harper, T., Koslover, D., Sapin, V. and Benzer, S., 2004. Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway. Curr Biol 14, 885–890.
  32. Powers, R. W. I. I. I., Kaeberlein, M., Caldwell, S. D., Kennedy, B. K. and Fields, S., 2009. Extension of chronological life span in yeast by decreased TOR pathway signaling. Gene Dev 20, 174–184.
  33. Sara A, Sofia B, Sepideh B, et al. Parsing the life-shortening effects of dietary protein: effects of individual amino acids. Proc Biol Sci. 2017;11; 284(1846):20162052.
  34. Wright P. 1995. Review nitrogen excretion: three end products, many physiological roles. J. Exp. Biol. 281, 273–281.
  35. Simpson, S. J. and Raubenheimer, D., 2005. Obesity: the protein leverage hypothesis. Obesity Rev 6, 133–142.
  36. Sørensen, A., Mayntz, D., Raubenheimer, D. and Simpson, S. J., 2008. Protein-leverage in mice: the geometry of macronutrient balancing and consequences for fat deposition. Obesity 16, 566–571.
  37. Miller, R. A., Buehner, G., Chang, Y., Harper, J. M., Sigler, R. and Smith-Wheelock, M., 2005. Methionine-deficient diet extends mouse lifespan, slows immune and lens aging, alters glucose, T4, IGF-I and insulin levels, and increases hepatocyte MIF levels and stress resistance. Aging Cell 4, 119–125.
  38. Howitz, K. T., Bitterman, K. J., Cohen, H. Y., Lamming, D. W., Lavu, S., Wood, J. G., Zipkin, R. E., Chung, P., Kisielewski, A., Zhang, L. L., Scherer, B. and Sinclair, D. A., 2003. Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan. Nature 425, 191–196.