Chronic illnesses are a feature of advancing years. Many theories have been put forth as to why this is the case and these theories often are in conflict, yet there is a surprising degree of agreement on at least one point: the health and longevity of at least 50 percent of the adult population are primarily related to dietary practices. Often the culprit is referred to as the “Western” diet and lifestyle pattern, meaning a shift towards increased consumption of red meat, animal fats and sugar at the expense of foods high in fiber and in conjunction with sedentary habits.1 As an example of the latter, suburbs in America increasing are built without sidewalks, let alone access to stores or post offices within walking distance. Even many metropolitan centers, such as Los Angeles, may have few resources that can be reached without either a car or some form of public transportation. As a result of dietary changes and exercise habits, presently 69 percent of those aged 20 years and older in the United States are either overweight or obese with fully 35.1 percent being obese.2

Telomeres, DNA, Aging and Diet—Nutritional Solutions?

The development of many age-related chronic diseases and aging itself are related to the health of the DNA (deoxyribonucleic acid) found in the chromosomes of cells and the length of chromosome caps, known as telomeres, that protect against damage to DNA. Telomere health, in turn, is dependent on other cellular components that modulate telomere function and length. Telomere malfunctioning leads to conditions such as vascular aging and atherosclerosis. Inappropriate diet is one factor that can lead to telomere dysfunction. A study in the current issue of Cell Reports using a special animal model elucidates some of the ways in which this takes place.3 Essentially, this is a model of how wrong and/or excessive dietary habits lead to aging. A positive outcome of the study is the finding that alpha lipoic acid (ALA) can reverse this process of disruption and thus prevent or at least ameliorate the accelerated aging and chronic diseases which otherwise result in this model.

The study begins with a standard approach taken in many laboratories, which is to work with animals that have been bred to lack certain functional metabolic pathways leading to what are termed “knockout” animals, in this case, knockout mice. The scientists wanted to examine the role(s) of peroxisome proliferator-activated receptors (PPARs) in the regulation of telomeres. The PPARs are a group of nuclear receptor proteins that function as regulators of the expression of genes, the cellular blueprints found in the nuclei of cells. For the purposes of the study, animals were used whose genes lead to one functioning PPAR being “knocked out” by inactivation or deletion. This particular PPAR, peroxisome proliferator-activated receptor ã coactivator-1á (PGC-1á), was demonstrated to be important for the activation of telomeres and their regulation of aging and prevention of DNA damage. Significantly, the damage done by disruption of PGC-1á was not direct, but rather was mainly due to the downregulation of an enzyme known as telomerase reverse transcriptase (TERT).

Several practical implications might be drawn from this study. First, dietary factors can greatly increase the rate of aging and the development of chronic diseases. The study used mice and this model has limitations for drawing parallels with human dietary practices, in part because mice do not naturally consume diets with significant percentages of fats, hence compared with humans, mice have underactive enzymes utilized for dealing with fats (desaturation enzymes, for instance), and so forth. Nevertheless, the point remains that unbalanced diets play an important role in aging. Second, the researchers demonstrated convincingly that ALA rectifies at least some of the major consequences of diet-induced telomere dysfunction, including reducing the vascular aging, atherosclerosis and damage to DNA. Third, it may be possible to use other nutritional items with roles in the body that complement, overlap or parallel those of ALA to achieve similar benefits. For example, the combination of L-carnitine and ALA or CoQ10 (either as ubquinol or ubiquinone) may prove especially useful in reversing damage to the mitochondria.

Although ALA and, more generally, L-carnitine taken in conjunction with ALA or CoQ10, may improve “health span,” these nutrients have not been shown to increase lifespan per se.4 Another approach to be considered either as an alternative or in addition such supplements is the proper use of calorie restriction mimetics. To date, caloric restriction practiced properly remains the only proven method for promoting an actual increase in lifespan. Possible caloric restriction mimetics include –(-)hydroxycitrate5 (also anti-inflammatory and protective of the mitochondria)6,7 bitter melon8 and rock lotus.9

Fat versus Sugar in the Diet
It should be admitted that there is no true consensus as to the culprits on the dietary side. Over the last decade, the longstanding strictures against animal fats increasingly have come under attack with a grudging acceptance that refined carbohydrates and sugars (especially fructose) along with a reduced intake of fiber explain much of the Western dietary problem. The animal fat component of the dietary theory was called into question as long ago as the Hammond Report,10 which was showcased in the 1964 Surgeon General’s official statement on smoking. In 2015, major reviews have appeared indicating that no randomized controlled trials supported the introduction of dietary fat guidelines in 1977 and 1983.11 Moreover, “saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes,” albeit the evidence for this conclusion is somewhat “heterogeneous with methodological limitations.”12 More surprising still, some saturated fats, such as those found in full fat dairy (particularly cream, high-fat fermented milk and cheese), reduce, for instance, the rate of developing diabetes.13 What about all those animal studies? For one thing, rodent models for fat consumption turn out to be misleading for humans in various ways and sometimes even for the animals.14 In light of current evidence, the US Department of Agriculture and Department of Health and Human Services lifted guidelines on cholesterol and total dietary fat in 2015.

(See also the comments on nutrients necessary for the proper metabolism of saturated fats in the September 2015 issue of this magazine in the article “Beyond Synergy—the Entourage Effect in Nutrition and Herbalism.”) http://totalhealthmagazine.com/Herbal-Medicine/Beyond-Synergy%E2%80%94the-Entourage-Effect-in-Nutrition-Herbalism.html

Opposing the “fat” hypothesis camp is what might be called the “sugar” hypothesis camp. To these researchers, the Western diet introduced altered components involving mainly “1) glycemic load, 2) fatty acid composition [i.e., reduce omega-3 fatty acids], 3) macronutrient composition, 4) micronutrient density, 5) acid-base balance, 6) sodium-potassium ratio, and 7) fiber content.”15 A study published in 2014 is but one of an increasing chorus of studies supporting this position and found that even 15 percent added sugars in the diet (the amount found in one average 20 ounce soft drink per day) increased cardiovascular disease by 38 percent compared with ingestion of less than 10 percent added sugars.16 Another study, this one from 2015, demonstrated that changing to a diet sufficiently rich in non-digestible carbohydrates induced significant weight loss and reduced inflammation in obese children and even in children with genetic obesity.17 Similar results have been found with radical reductions in caloric and carbohydrate intake in obese and diabetic adults. Finally, something to ponder is the argument of one set of researchers that diets high in carbohydrates, especially fructose, but relatively low in fat and cholesterol are contributory to Alzheimer’s disease.

Beyond Fat and Sugar
In the early 1960s, the Canadian philosopher Marshall McLuhan coined the phrase, “the medium is the message,” by which he meant that the medium by which information is sent (print, radio, television) is not neutral; the medium has an impact on how the message is perceived. It turns out that something similar is true of nutrition. Nutrients are more than the macronutrients carbohydrates, fat and protein. Likewise, nutrients are more than the sum of micronutrients (vitamin C, iron, etc.) or even these plus phytonutrients. As French gastronomy would have it, the “presentation” is important. Two variations on this theme have been researched with surprising results.

First, there is the issue of the processing of food. As one observer has put it, The most important factor now, when considering food, nutrition and public health, is not nutrients, and is not foods, so much as what is done to foodstuffs and the nutrients originally contained in them, before they are purchased and consumed. That is to say, the big issue is food processing – or, to be more precise, the nature, extent and purpose of processing, and what happens to food and to us as a result of processing. Specifically, the public health issue is ‘ultra-processing’, as defined here. This is my basic proposal.…Such products are made at distance as separate items that are trucked in, assembled, and made ready-to-heat and—to-eat…19

In a later paper looking at Canada, one of the world’s wealthiest and best educated nations, the finding was that “[o]nly the 20 % lowest consumers of ultra-processed products (who consumed 33·2 % of energy from these products) were anywhere near reaching all nutrient goals for the prevention of obesity and chronic non-communicable diseases.”20 Moreover, an examination of trends in Canada from 1938 to 2011 determined that the “share of ready-to-consume products rose from 28.7% to 61.7%, and the increase was especially noteworthy for those that were ultra-processed.”21 Unprocessed or minimally processed foods steadily were replaced by processed foods over this period. Using a model based on the dietary habits of the United Kingdom, simply cutting in half the foods eaten that are processed and ultra-processed with no other changes in diet or exercise habits would reduce cardiovascular disease deaths by approximately 35 percent.22

After the issue of food processing and ultraprocessing, there is a second (and related) approach to diet that goes beyond the issues of fat and sugar. It is no secret that, especially in America, snacking is the national pastime. Snacks make up approximately 27 percent of the calories consumed by children in the US.23 Researchers at the University of North Carolina at Chapel Hill decided to look at the issue of the Western diet with what they termed the “cafeteria” diet.24 This cafeteria diet contained a variety of human snacking foods, e.g., high-salt, high-fat, low-fiber, energy dense foods such as cookies, chips and processed meats. The researchers started with an animal model (keep in mind the earlier comments as to how rodents respond excessively to fats compared to humans) with male Wistar rats fed a standard chow diet (SC), a low-fat diet (LFD), a high-fat diet (HFD) or a cafeteria diet (CAF). Just to be clear, these diets were

  • SC = standard chow with 12 percent calories from fat (porcine fat and linoleic acid)
  • LFD = standard chow with more carbohydrate, but only 10 percent calories from fat (lard and soybean oil)
  • HFD = standard chow with less carbohydrate and 45 percent calories from fat (more lard)
  • CAF = ad libitum three human snack foods (cookies, cereals, cheese, processed meats, crackers, etc.) rotated daily plus ad libitum SC; total fat as a percent of diet was similar to the HFD

The results of this ten-week trial were surprising. For starters, the HFD group reduced food intake by about 10 percent such that all the rats in groups SC, LFD and HFD consumed about 100 calories per day per rat. The CAF rats, in contrast, increased caloric consumption by about 30 percent more than the SC and LFD groups and 40 percent more than the HFD group. In line with these data, at ten weeks the SC group was the lightest, the CAF group had gained almost twice as much weight, and both the LFD and HFD groups were intermediate to the first two and overall closer to the SC group in weight gain.

To be sure, the CAF diet was high in fat. It also was high in sodium, saturated fatty acid, trans-fatty acids, and cholesterol but low in fiber and micronutrients such as vitamin A and calcium. The LFD turned out to be less healthful for Wistar rats than did the SC diet and the HFD was somewhat less healthful in this animal model than either the SC or LFD versions. However, the really damaging dietary effects were found in the CAF group. The cafeteria diet induced high blood sugar, insulin resistance, increased fat mass with inflammation, liver dysfunction with inflammation, and significant damage to the pancreatic islets. The researchers’ own conclusion is:

In sum, the CAF provided a robust model of human metabolic syndrome compared to traditional lard-based HFD, creating a phenotype of exaggerated obesity with glucose intolerance and inflammation.

(Note that this trial did not contain a high-sugar arm; experiments by others have demonstrated that an increased intake of simple sugars rapidly induces elevations in blood pressure and a number of other disturbances in rodents just as in humans.)

Conclusion
It turns out, just as one might expect, a bad diet and poor exercise habits can significantly increase metabolic factors linked to aging and chronic diseases. Fortunately, it also seems to be the case that at least some of the damage done by a bad diet can be undone if caught in time, the right supplements are adopted, and the bad diet and habits are corrected. One catch is that the usual suspects in terms of diet may not be the right suspects and/or may not be acting alone. After 60 years of demonization, the negative role of saturated fat in the diet is in question (although not the need for more omega-3 fatty acids, which is a different issue) and the emphasis has shifted to added sugars, in particular, fructose. At the same time, new avenues of research have begun to emphasize that there is more to the problem than the fat/carbohydrate duality or even the fat/ sugar duality. Processed and ultra-processed foods in general increasingly are the hallmarks of the Western diet. Relatedly, the modern culture of “snacking” based on high-salt, high-fat, lowfiber, refined carbohydrate energy dense foods such as cookies, chips and processed meats can be shown to seriously distort the metabolism in the direction of obesity, insulin resistance and inflammation, i.e., the metabolic syndrome.

What is to be done? A start would be to eat less processed food, more fiber, somewhat less carbohydrate, more omega-3 fatty acids, more fresh and locally-grown foods, more fruit and vegetables to increase potassium intake and less of anything containing salt. Home-cooked should replace take-out whenever possible, a practice that would be good for families in general through more time for the members eating meals together. Simple changes can yield some pretty hefty benefits.

  1. Boaz NT. Evolving health: the origins of illness and how the modern world is making us sick. Wiley, 2002.
  2. Centers for Disease Control and Prevention data for 2011–2012.
  3. Xiong S, Patrushev N, Forouzandeh F, Hilenski L, Alexander RW. PGC-1ev Modulates Telomere Function and DNA Damage in Protecting against Aging-Related Chronic Diseases. Cell Rep. 2015 Sep 1;12(9):1391–9.
  4. Lee CK, Pugh TD, Klopp RG, Edwards J, Allison DB, Weindruch R, Prolla TA. The impact of alpha-lipoic acid, coenzyme Q10 and caloric restriction on life span and gene expression patterns in mice. Free Radic Biol Med. 2004 Apr 15;36(8):1043–57.
  5. Madeo F, Pietrocola F, Eisenberg T, Kroemer G. Caloric restriction mimetics: towards a molecular definition. Nat Rev Drug Discov. 2014 Oct;13(10):727–40.
  6. Nisha VM, Priyanka A, Anusree SS, Raghu KG. (-)-Hydroxycitric acid attenuates endoplasmic reticulum stress-mediated alterations in 3T3-L1 adipocytes by protecting mitochondria and downregulating inflammatory markers. Free Radic Res. 2014 Nov;48(11):1386–96.
  7. United States Patent 8,394,856 (-)-Hydroxycitric acid for controlling inflammation
  8. Going Wild with Bitter Melon for Blood Sugar Support. Total Health August 2011.
  9. Uncovering the Longevity Secrets of the rock lotus. Total Health October 2010.
  10. Morowitz HJ. Hiding in the Hammond Report. Hospital Practice. August,1975:35 and 39.
  11. de Souza RJ, Mente A, Maroleanu A, Cozma AI, Ha V, Kishibe T, Uleryk E, Budylowski P, Schünemann H, Beyene J, Anand SS. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ. 2015 Aug 11;351:h3978.
  12. Harcombe Z, Baker JS, Cooper SM, Davies B, Sculthorpe N, DiNicolantonio JJ, Grace F. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart. 2015 Jan 29;2(1):e000196.
  13. Ericson U, Hellstrand S, Brunkwall L, Schulz CA, Sonestedt E, Wallström P, Gullberg B, Wirfält E, Orho-Melander M. Food sources of fat may clarify the inconsistent role of dietary fat intake for incidence of type 2 diabetes. Am J Clin Nutr. 2015 May;101(5):1065-80.
  14. Tallman DL, Noto AD, Taylor CG. Low and high fat diets inconsistently induce obesity in C57BL/6J mice and obesity compromises n-3 fatty acid status. Lipids. 2009 Jul;44(7):577–80.
  15. Cordain L1, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, Brand-Miller J. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005 Feb;81(2):341–54.
  16. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med. 2014 Apr;174(4):516–24.
  17. Chenhong Zhang, Aihua Yin, Hongde Li, Ruirui Wang, et al. Dietary Modulation of Gut Microbiota Contributes to Alleviation of Both Genetic and Simple Obesity in Children. EBioMedicine. 2015 August;2, 8: 968–984.
  18. Seneff S, Wainwright G, Mascitelli L. Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet. Eur J Intern Med. 2011 Apr;22(2):134–40.
  19. Monteiro C. The big issue is ultra-processing. ‘Carbs’: The answer. [Commentary]/World Nutrition. 2011 Februrary;2(2):86–97.
  20. Moubarac JC, Martins AP, Claro RM, Levy RB, Cannon G, Monteiro CA. Consumption of ultra-processed foods and likely impact on human health. Evidence from Canada. Public Health Nutr. 2013 Dec;16(12):2240-8.
  21. Moubarac JC, Batal M, Martins AP, Claro R, Levy RB, Cannon G, Monteiro C. Processed and ultra-processed food products: consumption trends in Canada from 1938 to 2011. Can J Diet Pract Res. 2014 Spring;75(1):15–21.
  22. Moreira PV, Baraldi LG, Moubarac JC, Monteiro CA, Newton A, Capewell S, O’Flaherty M. Comparing different policy scenarios to reduce the consumption of ultraprocessed foods in UK: impact on cardiovascular disease mortality using a modelling approach. PLoS One. 2015 Feb 13;10(2):e0118353.
  23. Piernas C, Popkin BM. Trends in snacking among U.S. children. Health Aff (Millwood) 2010;29:398–404.
  24. Sampey BP, Vanhoose AM, Winfield HM, Freemerman AJ, Muehlbauer MJ, Fueger PT, Newgard CB, Makowski L. Cafeteria diet is a robust model of human metabolic syndrome with liver and adipose inflammation: comparison to high-fat diet. Obesity (Silver Spring). 2011 Jun;19(6):1109–17.