Finding the fountain of youth is part of the dream, isn’t it?
Stopping or reversing the effects of aging for a younger appearance, stronger body, more energy, better health, etc. Who wouldn’t want that?!
This is why there is always a new pill or powder or makeup or diet that promises to give us some portion of this dream. Sadly, that promise is almost always just clever marketing. But what if I told you there are things you can do, starting today, that can help you in reducing your body age? This includes looking and feeling younger (or even better than you might remember). I’m talking about:
It’s of course important to first state that none of this will magically happen overnight. BUT, when you consistently put the following strategies into play, you can slow down the aging process.
#1 Lift weights. It may sound simple and you may not see the correlation but I promise there is one. Lifting weights can be one of the best ways to increase your health span and improve your quality of life. In fact, muscle strength is one of the strongest predictors of how long and how well you will live.
It shocks me how many people are still to this day afraid of lifting weights but the fact is, regular resistance training can help maintain muscle and bone mass as you get older. Not only that but it can also boost mood, improve cognitive function, protect against injuries, and improve the overall quality of life. Lifting weights doesn’t mean you have to lift like a bodybuilder to reap the rewards. You just need resistance so whether that means you are lifting heavy or just using your own body weight, it doesn’t matter. You will see benefits.
#2 Incorporate Cardio. We’re talking about health here so you had to know that cardio was going to be on the list. But, normally it’s talked about just in the sense of your cardiovascular health but I want to discuss it in the sense of improving the health of your mitochondria. If you’re looking for anti-aging benefits then aerobic exercise should be at the top of your list.
Regular aerobic exercise stimulates a process called mitochondrial biogenesis, which means increasing the size and number of mitochondria. Basically this means that while resistance training increases muscle size and strength, one of the key physiological adaptations to regular aerobic exercise is an increase in mitochondria number and improvement in mitochondrial function.
I’m aware that cardio is not everyone’s favorite part of exercising so the good news is that you don’t have to spend hours doing it. You can go for long runs if that’s your thing but shorter bouts of high-intensity interval training will also do the trick.
As an added bonus, in a recent study published in the European Heart Journal, researchers from Germany found that both traditional endurance training and high-intensity interval training led to a two- to three-fold in activity of an enzyme called telomerase, which prevents the shortening of telomeres. (4) In simple terms, aerobic exercise led to increased telomere length, literally turning back the clock on the participants’ body age.
For most people, a good rule of thumb is to do 2 – 3 cardio sessions (either traditional endurance exercise, interval training, or a combination of the two) each week.
#3 Incorporate fasting. Fasting is a favorite tool of mine for many reasons and its anti-aging benefits is just one of them. Intermittent fasting—and especially time-restricted feeding (TRF)—is one of the most popular health and wellness trends and for good reasons. As I’ve discussed in many other blogs, intermittent fasting is linked to a robust array of health benefits, and one of its most attractive features is that it only specifies when you eat and doesn’t necessarily restrict what or how much. In other words, intermittent fasting (IF) can be paired with any pattern of eating (e.g., Paleo, Mediterranean, Low FODMAP) that suits your fancy.
Among the myriad of purported benefits of IF is that it may offer anti-aging properties. In fact, Dr. Valter Longo, one of the leading IF researchers (whose particularly IF specialty is fasting-mimicking diets or FMD for short), wrote a book titled The Longevity Diet, which suggests a clear tie between IF and longevity.
For example, Dr. Longo’s research has revealed that FMD, which entails following a low-calorie, low-protein diet for a 5-day period during a monthly cycle, significantly reduces biomarkers for aging, increases regeneration markers, and promotes optimal healthspan in humans. (5,6)
Part of the reason that IF may flex its anti-aging muscle is through caloric restriction (CR), arguably one of the most effective tools to reduce your body age. A fairly robust body of research has shown that CR reliably extends lifespan, and this can be traced back, at least in part, to improvements in mitochondria size, number, and function.
IF has been shown to up-regulate a process called autophagy, which essentially involves “cleaning up” cellular garbage, including damaged mitochondria, and while the relationship is complex, autophagy appears to have a selective role (positive) on cellular senescence. (10) As an added benefit, whereas CR typically results in the loss of calorie-burning lean muscle, IF promotes fat loss while retaining valuable lean mass, which is arguably one of the most overlooked variables for living a long, healthy life. (7,11)
#4 Get outside. Yes, it’s that simple. Get out from being the computer, and from under the fluorescent lights and out into nature and the bright sunlight. Believe it or not, one of the simplest ways to reduce your body age is to spend more time in nature. Of course, when most people think about being outside, they think about sun exposure, which, of course, leads to vitamin D. After all, it’s called the “sunshine vitamin” for a reason; that said, vitamin D is actually a hormone, and nearly every tissue in the body has a vitamin D receptor, highlighting its far-reaching array of benefits.
As we all know, too much AND not enough sunlight can be potentially harmful. Avoiding sun exposure is a major risk factor for all-cause mortality—as much as a 2-fold higher mortality rate. There’s also an inverse relationship between vitamin D levels (i.e., lower levels = higher risk/incidence) and breast cancer, colorectal cancer, bladder cancer, cardiovascular disease, metabolic syndrome, type 2 diabetes, Alzheimer’s disease (and all forms of dementia), autoimmune conditions (e.g., multiple sclerosis, psoriasis), liver disease, and macular degeneration to name a few. (12) Of course, these are just associations; however, they do suggest some intriguing relationships.
On the flip side, the irony is that longer-living sun-seekers are at a greater risk of skin cancer; HOWEVER, sun exposure is related to better skin cancer outcomes. Considering that nonmelanoma skin cancer is associated with many thousands or tens of thousands of cumulative hours of lifetime sun exposure, the risks of inadequate sun exposure are more concerning for most people. However, sunburns are associated with a substantially increased risk (about double) of melanoma and nonmelanoma skin cancer. The WORST-case scenario is the person who doesn’t get much sun exposure, but when s/he does, s/he gets sunburned.
But it’s not just about vitamin D (although that’s obviously important). Connecting with nature—such as through forest bathing, grounding (i.e., walking barefoot in the grass), gardening, or simply soaking up your natural surroundings—can have tremendous whole-body benefits, such as: (13, 14, 15, 16)
#5 Get more sleep. Want a surefire way to fast forward the hands-on your body clock and accelerate your body age? Don’t get enough sleep. That’s right, yet another benefit of restorative sleep is reducing your body age.
Research has shown a linear association between sleep duration, sleep quality, and telomere length. In other words, lack of sleep is directly associated with shorter telomere length and cellular aging. For example, in a study published in the journal PLoS One, researchers from the United Kingdom found that men who slept 5 or fewer hours per night had 6% shorter telomere lengths than men who slept at least 7 hours. (19)
So, here’s yet another reason to put a priority on sleep, and when it comes to improving the restorative quality of sleep, there are three factors to consider: timing (when you go to bed), intensity, and duration (how long you’re in bed). The best way to capitalize on all three components is to improve your sleep hygiene and reset your circadian rhythms.
For many people, one of the most important steps you can take to improve your sleep timing, intensity, and duration is to get in bed earlier.
#6 Cut the crap (i.e., added sugar and refined grains). Pretty much regardless of your health and wellness goal, if you want to get better, you’re pretty much playing with house money if you bet that cutting our added sugar and refined grains will be one of the steps to get you there.
When it comes to reducing your body age, there are several factors at play. For starters, glycemic control (i.e., blood sugar management) seems to be one of the most important health biomarkers to monitor as research shows that a measurement called HbA1c, which stands for glycated (or glycosylated) hemoglobin, is a key predictor of mortality (which is a scientific term for “death”).
Basically, HbA1c is a robust biomarker of the preceding 2 – 3 months’ average blood glucose level. In other words, it’s a relatively long-term measure of one’s blood glucose control (i.e., glycemic control). (20) What’s even more interesting is that HbA1c predicts mortality independently of fasting blood glucose, which is a more commonly tested biomarker. (21,22)
In addition to HbA1c, glycemic variability (think swings or fluctuations in blood sugar) is an extremely important player when it comes to glycemic control. Poor glycemic balance (think spikes in blood sugar after a meal followed by a rapid drop) is directly related to poor mood states, crappy energy levels, and subsequent poor food choices. (23)
What’s more, poor glycemic control is one of the primary variables contributing to mitochondrial dysfunction. (24) At least part of the disrupting effect of poor glycemic control can likely be traced to advanced glycation end-products (AGEs). AGEs, which are “glycotoxins” that can be produced during cooking (e.g., grilling, broiling, frying) and also be formed inside the body (typically in line with poor glycemic control, or high blood sugar), increase free radical formation, increase oxidative stress, and promote inflammation.
Along those lines, AGEs been implicated in mitochondrial dysfunction, and if that wasn’t enough, mitochondrial dysfunction is thought to exacerbate the production of AGEs, “fueling the fire” so to speak. (25–28) AGEs…that’s a pretty appropriate acronym, don’t you think? Not surprisingly, poor glycemic control has been linked to shortened telomere length. (29)
Moral of the story: If you want to reduce your body age, cut out the junk food that’s made with added sugars and refined grains. I’m talking about so-called foods and drinks like sugar-sweetened beverages (like soda, fruit juice, and fruit-flavored drinks), sugar, candy, cakes, cookies, muffins, pies, desserts, sweetened yogurt, ice cream, pastries, ready-to-eat cereals, granola bars, sauces, dressings, and the like.
Instead, focus on eating more whole foods (fruits are completely fine, by the way). The bonus of eating more colorful veggies and fruits is, of course, younger, healthier-looking skin.
It all boils down to moving more, moving often, and moving in a variety of ways. We need to eat primarily real food, ditch the junk, and experiment with going long periods without eating. Get outside and connect with nature.
If you’re consistently taking care of business with these anti-aging strategies, then you’re in really good shape.
But, we’re all human so if you’re not—and don’t feel bad if that’s you—then consider starting with one area at a time. Never try to make too many changes at once. Once you’ve figured out one for a few weeks, then consider adding another and before you know it, you’ll be feeling better than ever.
1. Latorre E, Torregrossa R, Wood ME, Whiteman M, Harries LW. Mitochondria-targeted hydrogen sulfide attenuates endothelial senescence by selective induction of splicing factors HNRNPD and SRSF2. Aging. 2018 Jul 19;10(7):1666–81.
2. Bernadotte A, Mikhelson VM, Spivak IM. Markers of cellular senescence. Telomere shortening as a marker of cellular senescence. Aging. 2016 Jan 23;8(1):3–11.
3. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013 Jun 6;153(6):1194–217.
4. Werner CM, Hecksteden A, Morsch A, Zundler J, Wegmann M, Kratzsch J, et al. Differential effects of endurance, interval, and resistance training on telomerase activity and telomere length in a randomized, controlled study. Eur Heart J. 2019 Jan 1;40(1):34–46.
5. Longo VD, Panda S. Fasting, Circadian Rhythms, and Time-Restricted Feeding in Healthy Lifespan. Cell Metab. 2016 Jun 14;23(6):1048–59.
6. Brandhorst S, Choi IY, Wei M, Cheng CW, Sedrakyan S, Navarrete G, et al. A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan. Cell Metab. 2015 Jul;22(1):86–99.
7. Mattson MP, Longo VD, Harvie M. Impact of intermittent fasting on health and disease processes. Ageing Res Rev. 2017 Oct;39:46–58.
8. Anton SD, Moehl K, Donahoo WT, Marosi K, Lee SA, Mainous AG, et al. Flipping the Metabolic Switch: Understanding and Applying the Health Benefits of Fasting: Flipping the Metabolic Switch. Obesity. 2018 Feb;26(2):254–68.
9. Jornayvaz FR, Shulman GI. Regulation of mitochondrial biogenesis. Essays Biochem [Internet]. 2010 [cited 2017 Sep 13];47. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3883043/
10. Kwon Y, Kim JW, Jeoung JA, Kim M-S, Kang C. Autophagy Is Pro-Senescence When Seen in Close-Up, but Anti-Senescence in Long-Shot. Mol Cells. 2017 Sep 30;40(9):607–12.
11. Mattson MP. Challenging Oneself Intermittently to Improve Health. Dose-Response. 2014 Oct 20;12(4):600–18.
12. Hoel DG, Berwick M, de Gruijl FR, Holick MF. The risks and benefits of sun exposure 2016. Dermatoendocrinol [Internet]. 2016 Oct 19 [cited 2018 Jul 27];8(1). Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5129901/
13. Stothard ER, McHill AW, Depner CM, Birks BR, Moehlman TM, Ritchie HK, et al. Circadian Entrainment to the Natural Light-Dark Cycle across Seasons and the Weekend. Curr Biol. 2017 Feb 20;27(4):508–13.
14. Keniger LE, Gaston KJ, Irvine KN, Fuller RA. What are the benefits of interacting with nature? Int J Environ Res Public Health. 2013 Mar 6;10(3):913–35.
15. Buckley RC, Westaway D, Brough P. Social Mechanisms to Get People Outdoors: Bimodal Distribution of Interest in Nature? Front Public Health [Internet]. 2016 [cited 2019 Jan 7];4. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5108769/
16. Ideno Y, Hayashi K, Abe Y, Ueda K, Iso H, Noda M, et al. Blood pressure-lowering effect of Shinrin-yoku (Forest bathing): a systematic review and meta-analysis. BMC Complement Altern Med [Internet]. 2017 Aug 16 [cited 2019 Jan 7];17. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5559777/
17. Holt-Lunstad J, Smith TB, Baker M, Harris T, Stephenson D. Loneliness and social isolation as risk factors for mortality: a meta-analytic review. Perspect Psychol Sci J Assoc Psychol Sci. 2015 Mar;10(2):227–37.
18. Carroll JE, Diez Roux AV, Fitzpatrick AL, Seeman T. Low Social Support Is Associated With Shorter Leukocyte Telomere Length in Late Life: Multi-Ethnic Study of Atherosclerosis (MESA). Psychosom Med [Internet]. 2013 Feb [cited 2019 Jan 4];75(2). Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3881963/
19. Jackowska M, Hamer M, Carvalho LA, Erusalimsky JD, Butcher L, Steptoe A. Short sleep duration is associated with shorter telomere length in healthy men: findings from the Whitehall II cohort study. PloS One. 2012;7(10):e47292.
20. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2010 Jan;33 Suppl 1:S62-69.
21. Silbernagel G, Grammer TB, Winkelmann BR, Boehm BO, März W. Glycated Hemoglobin Predicts All-Cause, Cardiovascular, and Cancer Mortality in People Without a History of Diabetes Undergoing Coronary Angiography. Diabetes Care. 2011 Jun 1;34(6):1355–61.
22. Bancks MP, Odegaard AO, Pankow JS, Koh W-P, Yuan J-M, Gross MD, et al. Glycated Hemoglobin and All-Cause and Cause-Specific Mortality in Singaporean Chinese Without Diagnosed Diabetes: The Singapore Chinese Health Study. Diabetes Care. 2014 Dec;37(12):3180–7.
23. Penckofer S, Quinn L, Byrn M, Ferrans C, Miller M, Strange P. Does Glycemic Variability Impact Mood and Quality of Life? Diabetes Technol Ther. 2012 Apr;14(4):303–10.
24. Dassanayaka S, Readnower RD, Salabei JK, Long BW, Aird AL, Zheng Y-T, et al. High glucose induces mitochondrial dysfunction independently of protein O-GlcNAcylation. Biochem J. 2015 Apr 1;467(1):115–26.
25. Nowotny K, Jung T, Höhn A, Weber D, Grune T. Advanced Glycation End Products and Oxidative Stress in Type 2 Diabetes Mellitus. Biomolecules. 2015 Mar 16;5(1):194–222.
26. Sayej WN, Knight III PR, Guo WA, Mullan B, Ohtake PJ, Davidson BA, et al. Advanced Glycation End Products Induce Obesity and Hepatosteatosis in CD-1 Wild-Type Mice [Internet]. BioMed Research International. 2016 [cited 2017 Sep 15]. Available from: https://www.hindawi.com/journals/bmri/2016/7867852/
27. Wang X, Yu S, Wang C-Y, Wang Y, Liu H-X, Cui Y, et al. Advanced glycation end products induce oxidative stress and mitochondrial dysfunction in SH-SY5Y cells. In Vitro Cell Dev Biol Anim. 2015 Feb;51(2):204–9.
28. Ward MS, Fortheringham AK, Cooper ME, Forbes JM. Targeting advanced glycation endproducts and mitochondrial dysfunction in cardiovascular disease. Curr Opin Pharmacol. 2013 Aug;13(4):654–61.
29. Wang J, Dong X, Cao L, Sun Y, Qiu Y, Zhang Y, et al. Association between telomere length and diabetes mellitus: A meta-analysis. J Int Med Res. 2016 Dec;44(6):1156–73.
30. Farzaneh-Far R, Lin J, Epel ES, Harris WS, Blackburn EH, Whooley MA. Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease. JAMA. 2010 Jan 20;303(3):250–7.
31. Farzaneh-Far R, Lin J, Epel E, Lapham K, Blackburn E, Whooley MA. Telomere length trajectory and its determinants in persons with coronary artery disease: longitudinal findings from the heart and soul study. PloS One. 2010;5(1):e8612.
32. Kiecolt-Glaser JK, Epel ES, Belury MA, Andridge R, Lin J, Glaser R, et al. Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial. Brain Behav Immun. 2013 Feb;28:16–24.
33. Steptoe A, Kivimäki M. Stress and cardiovascular disease. Nat Rev Cardiol. 2012 Jun;9(6):360–70.
34. Rosmond R. Stress induced disturbances of the HPA axis: a pathway to Type 2 diabetes? Med Sci Monit Int Med J Exp Clin Res. 2003 Feb;9(2):RA35-39.
35. Randolph SA. The Power of Gratitude. Workplace Health Saf. 2017 Mar 1;65(3):144–144.