Noncaloric Sweeteners: What’s the Rub??

avoid-artificial-sweeteners

 

Happy December, ceiling fans 🙂 In September, I wrote a post reviewing Fat Chance, a book by Dr. Robert Lustig, that discusses the root causes of obesity and Metabolic Syndrome. The review caught the eye of Dr. Lustig’s business partner at the Institute for Responsible Nutrition, and we had a great exchange over the past couple of months. This was very exciting and a big deal for me! He asked me to write a guest post on their website, and coincidentally enough, it is about a topic that I’ve been meaning to explore for quite some time: Noncaloric sweeteners.

The blue, yellow, and pink rectangular packets are a visual staple on tables at American restaurants. Sweet’N Low, Equal, Splenda, and Stevia (with a new, green seat at the table) are alternatives to sugar that our country has adopted with open arms. I question, do they actually work in thwarting weight gain without sacrificing sweetness? Are they safe? Please check out my interesting and eye-opening post on their site here, or you can check it out below (They left out a few key graphs and figures). Either way, I appreciate your support, as always!

 


 

It is well known and undisputed that the increased consumption of sugar, in all its variations, has contributed to the ever-growing prevalence of obesity and metabolic syndrome over the past fifty-plus years. Once the exception, metabolic dysregulation and its related symptoms have now etched themselves as the rule in our global health picture. As a result, the industries involved in treating, rectifying, and capitalizing on this problem and its associated costs are estimated to be in the tens of billions of dollars.

 

Weight loss programs, pharmaceuticals, exercise techniques, surgical procedures, nutritional supplements, and diet products targeted to consumers and physicians permeate the media, literature, and our everyday vernacular. Rife among these countless products and initiatives designed as quick-fix remedies to lower blood sugar, boost weight loss, increase insulin sensitivity (and the like) are noncaloric artificial sweeteners (NAS).

 

NAS are commonly deemed as a safe and beneficial solution for weight loss, given their low caloric content, stunted insulin response, and reduced costs for use in commercial products. Yet, their surge in promotion, production, and consumption over the past twenty to thirty years has not done the average American’s waistline any favors. In fact, the opposite has occurred. So, what’s the rub??

 

type 3 diabetes

 

Before I try to tackle this question, I would like to point out that there truly is not enough clinical research or epidemiological data out there to definitively conclude whether to label NAS as “good” or “bad” in comparison to sugar. Many of the studies that promote their safety and benefits for weight loss are industry-funded. Unbiased, evidence-based research is sparse. Further, the FDA’s approval of their portioned use in foods doesn’t really account for the surplus amounts of these substances most consumers actually ingest due to their ubiquity and our nation’s appetite.

 

All being said, my hope for this post is to illuminate two rather different mechanisms through which NAS can disrupt metabolic function and perhaps further negate the weight problems they were created to fix. The significant kind of weight gain that plagues many in our society is not just a matter of caloric indulgence; it is an overall reflection and byproduct of the inner workings of one’s body and health gone awry. Because of this, I would like to draw some attention away from the mouth, and focus instead on two different areas that NAS can considerably affect: the brain and the gut … and as a result, one’s clothing size.

 

Many of us, when we have just sampled a delicious dessert, have said, “Oh my goodness, this must be so bad for you.” Simply put, this is our body’s innate ability to determine the caloric contents of what we eat based on its sweet taste.

 

As a result of a sweet taste and our brain and body’s calibration of its caloric estimation, an assembly line of biochemical reactions occurs that determines how our body then regulates the caloric energy we have just received. Our metabolism revs up like an engine because it has fuel to burn. Our brain also tells us to stop eating (or drinking) because it received a negative feedback message that our body has enough energy to accomplish what it needs to.1,2

 

Now, if something were to disrupt this communication – like, keeping the sweet taste in tact but omitting the calories – don’t you think the body and brain would get a little confused? That nice give-and-take balance is thrown off; the sweet taste registers, but there are no calories, nutrients, or fuel to burn and utilize. It’s sort of like the boy who cried wolf. What a gyp! A predictive relationship, such as the sweet taste, caloric estimation, and metabolic adjustment is based upon a specific cue followed by a specific outcome. The relationship becomes progressively weaker when either the cue or the outcome occurs alone. In the case of NAS, the sweet taste occurs alone without the calories to produce a proper outcome.1,2

 

In a 2008 study1, Susan Swithers, the leading scientist on noncaloric sweeteners, successfully demonstrated this predictive relationship with sweet tastes and what ensues metabolically when it is disrupted by NAS. In a normal, healthy rat, they ingest a form of glucose, the sweet taste signals the imminent arrival of nutrients and calories into the gut where they will be broken down and used for energy. When the nutrients in the food are absorbed in the gut, their core body temperature rises, and the rats become more active to utilize and burn the energy provided by the calories. She found that, “impairing the ability of sweetness to predict the arrival of energy in the gut accurately reduced the efficient utilization of that energy,”1 thereby weakening the feedback loop to the brain in order produce satiation.

 

rats and artificial diabetes

 

In Swithers’ study, two separate groups of rats were fed yogurt; one was sweetened with glucose, the other with saccharin (Sweet’N Low). It was found that those who were fed the saccharin had increased overall caloric intake (despite saccharin being noncaloric), greater weight gain, increased body fat, and lowered temperature change (reflecting a lowered metabolic rate) when other caloric foods were introduced.

 

As we know, a normal diet doesn’t consist solely of NAS or zero calories; one is bound to encounter calories and glucose at some point. This study revealed that, with the presence of NAS in the diet, the aforementioned predictive relationship is no longer tightly regulated, and when one eats or drinks anything with calories going forward, the body doesn’t quite know what to do with itself. In response, it cannot find its satiety point, stores fat, and does not burn energy as efficiently.

 

graph1

 

graph2

As you can see, it’s not to say that sugar is by any means an innocent bystander. This study, however, effectively shows that NAS are certainly not a magic bullet for weight loss either. In fact, they fare worse on almost all accounts.1

 

While Swithers’ research indicates that NAS do not have much influence on glucose homeostasis, a 2014 study3 by Suez et al. discovered a secondary route through which these noncaloric sweeteners do affect our glucose metabolism – via our microbiome.

 

Most of the noncaloric sweeteners fail to elicit an insulin response because, well, they go right through us. They slide through our GI system without being absorbed into the gut. Through their transit, though brief, they interact with our glorious microbiome and the intestinal bacteria colonies residing there, which we are learning play integral roles in regulating multiple physiological processes.3 This groundbreaking study went on to research how NAS may directly impact the microbiome, and as a result, the many processes to which it is intimately connected, including glucose metabolism.

 

microbiome-cartoon

 

In a set of experiments, Suez et al. monitored the glucose tolerance of mice ingesting water sweetened with aspartame (Equal, NutraSweet), saccharin, and sucralose (Splenda). At week 11 of this experiment, the NAS-mice had developed marked glucose intolerance compared to those ingesting sucrose, glucose, and plain water.

 

To determine whether their glucose intolerance was specifically induced by changes to their microbiome, antibiotics were administered to address their cultured dysbiosis. Lo and behold, once their dysbiosis was eradicated by the antibiotics, their glucose tolerance returned to healthy curves, despite the mice maintaining their NAS-laden diets. Further, the researchers took a fecal transplant from the dysbiotic guts of these mice and placed them into healthy germ-free mice. Six days after the transfer, glucose intolerance ensued in the recipients, illustrating a clear relationship between NAS use, resultant dysbiosis, and causative metabolic dysregulation.3 To note, saccharin-consuming mice displayed considerable dysbiosis, engendering the most significant changes in microbial overgrowth.

 

The researchers then went on to confirm the same effects in humans. Following seven healthy volunteers who do not consume NAS, the researchers asked the participants to ingest the upper limits of the FDA-approved daily allowance of saccharin for one week. Through monitoring glucose measurements, researchers found that the participants developed poorer glycemic responses compared to controls. Most importantly, there were significant changes to their microbiome composition after NAS ingestion.

 

To determine whether the dysbiotic changes to their microbiome caused their metabolic changes, fecal transplants from Day 1 and Day 7 of the trial of the NAS-participants and controls were placed into healthy germ-free mice. Day 7 transplants induced significant glucose intolerance in the mice compared to Day 1. However, both Day 1 and Day 7 transplants from controls had no effect on the mice’s glucose tolerance.

 

This study showcased that, in both mice and humans, increased incidence of glucose intolerance was mediated by modulation of the composition and function of their gut microbiota.3 As we know, one’s glucose tolerance plays a significant and direct role in their risk for developing obesity and metabolic syndrome.

 

As Suez nicely put it, NAS are “enhancing the exact epidemic they themselves intended to fight.”3

 

gut rx to artificial sweeteners

 

As I mentioned before, but it doesn’t hurt to reiterate, this is not a post recommending sugar consumption over NAS. Minimal to no amounts of both should be consumed in efforts to lose weight and restore metabolic and hormonal communication. However, I hope these studies revealed that a calorie certainly is not just a calorie, and this notion of weight management is antiquated at best. There are multiple players in the game and multiple avenues by which one can treat and improve such derangements. NAS add insult to injury by impairing multiple systems simultaneously.

 

A balanced diet, rich with wholesome, unprocessed, nutrient-dense foods will eliminate the need for sugars and the artificial sweeteners that were created to replace them. Once you’ve made the switch, you will find out that life without both of them is, well, a whole lot sweeter.

 

If you would like a heads-up for when I write a future follow-up post to this one, detailing the most relevant research on all of the sweeteners out there (including Stevia, Lo Han Guo, and sugar alcohols) and their effects on our body, please fill out the subscription link on this page.

 

Thanks for reading!

 

 

References

 

  1. Swithers, S.E.; Davidson, T.L. A Role for Sweet Taste: Predictive Relations in Energy Regulation by Rats. Behavioral Neuroscience 2008, 122, 161-173.
  2. Swithers, S.E. Artificial Sweeteners produce the counterintuitive effect of inducing metabolic derangements. Trends in Endocrinology and Metabolism 2013, 24, 431-441.
  3. Suez J, Korem T, Zeevi D, et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature 2014, 514, 181-188.

 

 

The Global Obesity and Metabolic Syndrome Pandemic: What’s At the Root??

Fat Chance Cover

 

Hi everyone, Happy Labor Day weekend! Almost two months ago in one of my classes, we were assigned to read and analyze a diet/health book, write a research paper on it along with our analysis, and create a video communicating our findings. This turned out to be one of my favorite assignments in my program so far because there are countless books, blogs, and even journal articles published that go unquestioned. Both the public and physicians sometimes take the findings and advice and run with them without a second thought, dramatically adjusting their diets and lifestyles based upon what is shared. As a future practitioner who will undoubtedly have patients whose physical and mental health are negatively affected by the dogma put forth in such writing, a large part of my success in treating them will rely upon being able to effectively communicate why they feel the way they do, and why they need to shift their beliefs and try something new.

 

As part of any review, one needs to look at the background of the author (their credentials, affiliations, is there a financial angle, etc.), the science behind the central theory of the book, if the author uses peer-reviewed scientific references to back up their claims, and if there is other supporting research outside of what the author cites to further substantiate their advice. There are much more in-depth ways to evaluate journal articles, but there’s no need to delve into them on this post. The video explanation was a little difficult for me but I enjoyed it; we were only given ten minutes to effectively summarize our findings, and it was challenging to recall the complicated science and communicate it in a way so that everyone can absorb it. You can watch my video and read my written review below, and let me know what you think!!!

 

 

Dr. Robert Lustig, the author of Fat Chance, boasts an impressive résumé that has prepared him to effectively articulate and drive home the biochemical principles at the root of the global obesity pandemic. Earning his undergraduate degree from MIT and medical school training from Cornell University, along with many years spent working at St. Jude’s hospital treating children with hypothalamic disorders, Lustig is a neuroendocrinologist and an expert on metabolic disease.

 

Further, he has taught at the University of Wisconsin, University of Tennessee, and currently at the University of California San Francisco as a Professor of Pediatrics in Endocrinology. To boot, he has authored over 85 peer-reviewed articles. This distinguished amalgam of experience not only makes his work credible, but, given his teaching and writing experience, he is well-equipped to simplify complex biochemical pathways so the “layperson” can understand the dynamics of obesity and Metabolic Syndrome (MS).

 

The inception of his work in metabolic disease occurred while witnessing children become acceleratedly obese following damage to their hypothalamus as a result of diminished leptin signaling. Part of successful treatment for these children relied upon pharmaceutically-induced suppression of insulin secretion, causing them to become more active, eat less, and lose weight. Years later, this framework transcended to obese individuals without any form of hypothalamic disorder or damage, who Lustig treated successfully.1

 

Appropriately, the central theory of his book rests on debunking the world’s notion that obesity is a personal responsibility caused by eating too much and not exercising enough. To Lustig, a calorie is not a calorie. Biochemistry influences these behaviors and, without altering it, one can never improve their health. Referencing over 300 peer-reviewed scientific studies and books to support his theory (seven of which are his own work), along with clinical anecdotes of his patients woven through each chapter, Lustig is not pushing any fluff or conjecture upon the reader. Specifically, he expounds upon the “battle royale” between the Ancel Keys2 and John Yudkin3 studies, claiming Keys as the wrongful victor and how these findings incorrectly influenced our society to avoid dietary fat. Sugar, as Yudkin cited, is “pure, white, and deadly,” and the true villain in this story.

 

Lustig attributes the prevalence of metabolic disturbances today to the increased quantity and decreased quality of our food and beverage supply, specifically four main items: trans fats, branched-chain amino acids (BCAAs), alcohol, and most notably, fructose. He also emphasizes that fiber has all but been eliminated from most Americans’ diets. Cut the sugar, boost the fiber, and exercise; this is the central theory behind Fat Chance and on solving the global obesity and MS pandemic. In the next paragraphs, I will explain the biochemistry involved in arriving at this metabolic cul-de-sac and how his simplified recommendations can navigate one’s body out on to Easy Street.

 

parker

 

Our hormones control our behavior. Many women (and men!) can attest to this if they have ever experienced or witnessed uncontrollable mood swings prior to or during menses. For the health picture Lustig is describing, insulin and leptin are the two key players, and the hypothalamus is the conduit, specifically the vagus nerve.

 

Insulin is our energy storage hormone. When we consume carbohydrate-containing meals, our blood glucose elevates, and the pancreas secretes insulin to escort the glucose into the cells for energy, store the protein into our muscles, and fats as triglycerides. The more insulin pumping, the more fat storing.4 Leptin is a protein made and released by our fat cells that communicates with the hypothalamus regarding our satiety, fat storage amount, and nutrient metabolism.5 This messaging is part of our biochemistry and, in turn, influences our behavior.

 

In a normal, healthy individual, they eat, insulin rises, and energy goes to their fat cells. Leptin senses that their fat cells are energized, reports back to the hypothalamus and says, “We’re fed and happy, we don’t need anymore, so let’s start to do work and burn this energy.”6 The hypothalamus then tells the pancreas to stop pumping insulin by reducing our appetite so we don’t take in any more food. Insulin is leptin’s antagonist;7 when insulin levels are chronically high, the hypothalamus only sees this message. Leptin cannot get the hypothalamus’ attention, so the hypothalamus misses the memo, continuing to tell our body, “I didn’t hear you’re full or fat yet. In fact, it seems like you’re starving. Don’t burn anything, don’t do anything, and store all the fat you can because you need to survive!”8

 

Lustig reiterates that chronically high insulin levels are a result of increased consumption of fructose, trans fats, and alcohol, and its effects on our mitochondria. As the interpretation of Ancel Keys’ study led to the reduction of dietary fat in our food supply, increased amounts of sweetener were incorporated in order to make things palatable. This led to greater amounts of sucrose (50% glucose, 50% fructose) and high fructose corn syrup (55% fructose, 45% glucose) dominating nearly every manufactured food in our supermarkets.

 

Glucose metabolism is insulin-dependent and is metabolized by all organs, including the brain, for energy. What is left is then sent to the liver for glycogen formation. Fructose, on the other hand, goes straight to the mitochondria of our hepatocytes. Further, our liver requires three times as much energy to metabolize fructose, depleting our ATP stores. Similarly, four times as many calories of alcohol reach the liver versus that of glucose, which heads straight the mitochondria as well.9 To compound things further, trans fats, synthetic fats created to preserve shelf life and stability of processed foods, cannot be broken down by our mitochondria.10 In addition, taste and expiration dates were favored at the expense of fiber in our processed foods. Fiber inhibits the rate of flux of nutrients from our intestines to our bloodstream; the onslaught of these stresses to the mitochondria is decreased when our food contains it. Without it, our mitochondria must work harder and faster, and as a result, become overwhelmed and inefficient.11,12 With this lethal combination, our liver enzymes are overactive, inflammation and insulin resistance develop, and our leptin signaling becomes disrupted. We get sick or fat, or both.

 

bybyetransfats_590_417

 

Eating is a pleasurable experience, no doubt. When we eat something we love, dopamine is released, and we experience pleasure.13 Both leptin and insulin, when they rise, cue the brain to stop releasing dopamine and clear it out of the synapses where it is active, respectively.14,15 However, in metabolic syndrome, where one is hyperinsulinemic and thereby blocking leptin signaling, the brain once again misses the memo to shut down all parts of this reaction. As a result, eating continually triggers the same feeling of reward – not easily thwarted – and one keeps eating and eating.

 

By avoiding sugar and increasing fiber, we avoid these consequences and allow our mitochondria to get back on track. By adding exercise to the equation, one builds muscle and new mitochondria, decreases visceral fat, improves insulin levels and sensitivity, and reignites proper communication between leptin and the hypothalamus.16,17 Exercise also increases the rate of our Krebs cycle – all of which burns energy and fats faster and more efficiently. We become healthier, skinnier, or both.

 

xigKbqB6T

 

Most of Lustig’s references cover the most relevant and comprehensive studies and literature that exist on the topic of MS. I found additional supporting research that backs up the science he so eloquently supplies along with his traditional remedy of diet and lifestyle change. Four studies discuss increased fructose consumption as a causative factor in metabolic syndrome,18-20 which is significantly hastened by the removal of fiber from the diet.21 Two studies emphasize the risk heavy alcohol consumption poses on development of MS,22 differing in severity by alcohol type.23 One study highlights the improvement of metabolic syndrome scores in those with T2DM and MS as a result of combined aerobic exercise and strength training.24 Again, there are countless studies that confirm Lustig’s “theory,” as it is hard science.

 

Slightly off topic, I found a study that showed a significant correlation between decreased marital satisfaction of women and their risk for developing MS as a result. Interestingly, the same was not reflected for men.25

 

As for my opinion, I would not categorize Fat Chance as a “diet book,” by any means; it is a sound scientific explanation of metabolic disease, and Lustig does a superior job of communicating where we have gone wrong. Ironically, where this book does lack a punch and where he loses his credibility is in the actual dietary recommendations section. He provides general practices: avoid sugar (specifically fructose), eat more fiber, eat real food, etc. He also provides a “red, yellow, and green” status system for foods that should be consumed sparingly, three to five times a week, and everyday, respectively. This yellow status column introduced my first bone to pick with Lustig.

 

Many items on the yellow list are processed, pro-inflammatory, refined foods. Kashi? Cheerios?! Canola oil? Egg beaters? Salami??? Lunch meats? He also red-lists nutritious foods like coconut oil and palm oil without any reasoning to explain their place on the list. Oddly, he also places diet drinks and noncaloric sweeteners on the “limbo list,” which I assume means that the jury is still out on these. This disappointed me, as a 2008 study26 shows that noncaloric sweeteners disrupt innate physiological responses to glucose and further compound factors leading to MS. Perhaps his strict science background relating to biochemistry limits his knowledge to the insulinogenic properties of food at the expense of other effects these types of food have on our overall health. The book can only cover so much, though. And, to his credit, his green list is ripe with grassfed meats, pastured eggs and poultry, wild fish, whole grains, fruits and vegetables, and organic dairy.

 

The other bones I have to pick with the author involve his negative views on BCAAs and his take on micronutrient supplements.

 

Lustig explained that BCAAs (the essential amino acids valine, leucine, and isoleucine), when in excess, head straight to our hepatocytes’ mitochondria to be burned for energy and lead to fat synthesis. He also cited a study that correlated those with MS having higher levels of these amino acids in their bloodstream.27 This is correlation and not causation, though. In my research, I have found that plasma levels of BCAAs fluctuate to meet demands of different metabolic pathways.28,29 In skeletal muscle, BCAAs are transaminated to ketoacids, which are then broken down and oxidized by the branched-chain ketoacid dehydrogenase enzyme (BCKD) to eventually feed into the Krebs cycle for energy production. Increased insulin levels, which are a hallmark of obesity and MS, inhibit BCKD activity.29 Metabolic acidosis, which is seen in tandem with the catabolic states characteristic of obesity and insulin resistance,30 also inhibits BCKD.28 Depression of the enzyme’s activity minimizes complete BCAA oxidation, causing them to accumulate in the blood, thus being one rationale as to why plasma levels are elevated in these states.28,29

 

Furthermore, a study31 by Macotela et. al on rats with Metabolic Syndrome fed a high fat diet for eight weeks responded to doubling of dietary leucine alone, reversing their metabolic abnormalities and upregulating their insulin sensitivity. This being said, I would remove BCAAs from the list of culprits, as their plasma elevations are a downstream effect, and can even be beneficial to the system.

 

As for micronutrient supplements, Lustig says on page 156, “Micronutrients matter – the biochemistry says so – except they don’t work when provided as supplements in clinical trials. . . And nutritional supplements can’t reverse that which has previously been destroyed.” As a clinical nutritionist in training, I beg to differ.

 

Chromium is known for its role in insulin sensitization. When insulin is secreted, it rushes to receptors on the cell like a lock-and-key to transport glucose out of the blood and into the cells. The insulin receptor, tyrosine kinase, is dependent upon chromium for activation and functionality, in order to allow for insulin to unlock the cell and import glucose. Without chromium, this sensitization is lost and insulin resistance can occur.28 Understandably, those deficient in this nutrient would have decreased insulin sensitivity. In fact, a 2011 study32 revealed that the worse one’s insulin resistance is, the greater amount of chromium they excrete in their urine, further compounding its low circulation. It was shown that this chromium dumping occurs well before development of T2DM, and supplementation with the nutrient could prevent its further progression.

 

Furthermore, a 2013 study33 was performed on women with polycystic ovarian syndrome (PCOS) comparing the effects of chromium picolinate and Metformin, a pharmaceutical used to increase insulin sensitivity. After three months of treatment, chromium picolinate significantly decreased fasting blood sugar along with fasting insulin levels, thus revealing increased insulin sensitivity. Chromium was also better tolerated than the Metformin.

 

I agree that supplementation is not a magic bullet, but it could certainly boost metabolic pathways and is a clinically proven beneficial adjunct to a comprehensive treatment plan.

 

Refreshingly, Lustig dedicates 42 pages at the end of the book to public health policy, government, and political involvement in our food supply and their onus in our current mess. He discusses the health insurance industry and the need for sugar intake to be treated the same way smoking was or else we will not be successful in overcoming this health crisis. This was extremely encouraging to hear from an esteemed medical doctor, as most seem to avoid these hot button topics all together.

 

murray-budget-2

 

As a practitioner, I would not recommend this book for all of my clients; it was extremely enjoyable for me because I am familiar with anatomy, physiology, and advanced biochemistry. For the client who comes in who has no clue about anything and just wants to lose weight, this would be way over their heads. However, I would definitely recommend this for “technical” personality types. Clients who inquire about details and scientific research, ask why and how about everything, and who need to see facts and understand things in order to initiate behavior would benefit immensely from Lustig’s explanations. For anyone I recommend this book to, however, I would tell them to skip over the dietary recommendations section. Or, I would need to feel confident in their understanding of my beliefs on food quality and nutrition prior to them reading it.

 

The best part of the book, in my opinion, is Lustig’s tone. He manages to get heavy and difficult messages across to the reader, but keeps things light and provides hope and a means to change things for the better – for everyone – not just for oneself. After all, he stresses that this is not about personal responsibility anymore; it is a public health crisis. He also has a whip-sharp wit and sarcasm, which surprised me for a San Franciscan. It all made sense, though, when I researched his biography; he’s from Brooklyn. 🙂

 

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Enjoy the holiday weekend! Thanks for reading!

 

 

References

  1. Lustig RH, Greenway F, Velasquez-Mieyer P, et al. A multicenter, randomized, double-blind, placebo-controlled, dose-finding trial of a long-acting formulation of octreotide in promoting weight loss in obese adults with insulin hypersecretion. International Journal of Obesity. 2005;30(2):331-341.
  2. Keys A, Aravanis C. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. Cambridge, Mass: Harvard University Press; 1980.
  3. Yudkin J. Pure, White and Deadly: How Sugar Is Killing Us and What We Can Do to Stop It. London: Davis-Poynter; 1972.
  4. Lustig RH. Pediatric Endocrine Disorders of Energy Balance. Reviews in Endocrine and Metabolic Disorders. 2005;6(4):245-260.
  5. Flier JS. What’s in a Name? In Search of Leptin’s Physiologic Role. Journal of Clinical Endocrinology & Metabolism. 1998;83(5):1407-1413.
  6. Leibel RL. The Role of Leptin in the Control of Body Weight. Nutrition Reviews. 2002;60(10):15-19.
  7. Lustig RH. Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics. Nature Clinical Practice Endocrinology & Metabolism. 2006;2(8):447-458.
  8. Leibel RL. Changes in Energy Expenditure Resulting from Altered Body Weight. New England Journal of Medicine. 1995;333(6):399-399.
  9. Lustig RH. Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanol. Journal of the American Dietetic Association. 2010;110(9):1307-1321.
  10. Tetri LH, Basaranoglu M, Brunt EM, Yerian LM, Neuschwander-Tetri BA. Severe NAFLD with hepatic necroinflammatory changes in mice fed trans fats and a high-fructose corn syrup equivalent. AJP: Gastrointestinal and Liver Physiology. 2008;295(5).
  11. Post RE, Mainous AG, King DE, Simpson KN. Dietary Fiber for the Treatment of Type 2 Diabetes Mellitus: A Meta-Analysis. The Journal of the American Board of Family Medicine. 2012;25(1):16-23.
  12. Levine R. Monosaccharides in Health and Disease. Annual Review of Nutrition. 1986;6(1):211-224.
  13. Carr K., Tsimberg Y, Berman Y, Yamamoto N. Evidence of increased dopamine receptor signaling in food-restricted rats. Neuroscience. 2003;119(4):1157-1167.
  14. Farooqi IS, Bullmore E, Keogh J, Gillard J, O’Rahilly S, Fletcher PC. Leptin Regulates Striatal Regions and Human Eating Behavior. Science. 2007;317(5843):1355-1355.
  15. Carvelli L, MorĂłn JA, Kahlig KM, et al. PI 3-kinase regulation of dopamine uptake. Journal of Neurochemistry. 2002;81(4):859-869.
  16. Little JP, Safdar A, Benton CR, Wright DC. Skeletal muscle and beyond: the role of exercise as a mediator of systemic mitochondrial biogenesis. Applied Physiology, Nutrition, and Metabolism. 2011;36(5):598-607.
  17. Bajpeyi S, Tanner CJ, Slentz CA, et al. Effect of exercise intensity and volume on persistence of insulin sensitivity during training cessation. Journal of Applied Physiology. 2009;106(4):1079-1085.
  18. Das UN. Sucrose, fructose, glucose, and their link to metabolic syndrome and cancer. Nutrition. 2015;31(1):249-257.
  19. Kelishadi R, Mansourian M, Heidari-Beni M. Association of fructose consumption and components of metabolic syndrome in human studies: A systematic review and meta-analysis. Nutrition. 2014;30(5):503-510.
  20. Shapiro A, Mu W, Roncal C, Cheng K-Y, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. AJP: Regulatory, Integrative and Comparative Physiology. 2008;295(5).
  21. Amin F, Gilani AH. Fiber-free white flour with fructose offers a better model of metabolic syndrome. Lipids in Health and Disease. 2013;12(1).
  22. Sun K, Ren M, Liu D, Wang C, Yang C, Yan L. Alcohol consumption and risk of metabolic syndrome: A meta-analysis of prospective studies. Clinical Nutrition. 2014;33(4):596-602.
  23. Chen C-C, Lin W-Y, Li C-I, et al. The association of alcohol consumption with metabolic syndrome and its individual components: the Taichung community health study. Nutrition Research. 2012;32(1):24-29.
  24. Earnest CP, Johannsen NM, Swift DL, et al. Aerobic and Strength Training in Concomitant Metabolic Syndrome and Type 2 Diabetes. Medicine & Science in Sports & Exercise. 2014;46(7):1293-1301.
  25. Whisman MA, Uebelacker LA. A longitudinal investigation of marital adjustment as a risk factor for metabolic syndrome. Health Psychology. 2012;31(1):80-86.
  26. Swithers SE, Davidson TL. A role for sweet taste: Calorie predictive relations in energy regulation by rats. Behavioral Neuroscience. 2008;122(1):161-173
  27. Newgard CB, An J, Bain JR, et al. A Branched-Chain Amino Acid-Related Metabolic Signature that Differentiates Obese and Lean Humans and Contributes to Insulin Resistance. Cell Metabolism. 2009;9(4):311-326.
  28. Lord RS, Bralley A. Laboratory Evaluations for Integrative and Functional Medicine. Revised 2nd Edition. Duluth, GA: Genova Diagnostics; 2012.
  29. Adams SH. Emerging Perspectives on Essential Amino Acid Metabolism in Obesity and the Insulin-Resistant State. Advances in Nutrition. 2011;2(6):445-456.
  30. Korte MS, Koolhaas JM, Wingfield JC, McEwen BS. The Darwinian concept of stress: benefits of allostasis and costs of allostatic load and the trade-offs in health and disease. Neuroscience & Biobehavioral Reviews. 2005;29(1):3-38.
  31. Macotela Y, Emanuelli B, BĂĄng AM, et al. Dietary Leucine – An Environmental Modifier of Insulin Resistance Acting on Multiple Levels of Metabolism. PLoS ONE. 2011;6(6):1-13.
  32. Bahijri SM, Alissa EM. Increased insulin resistance is associated with increased urinary excretion of chromium in non-diabetic, normotensive Saudi adults. Journal of Clinical Biochemistry and Nutrition. 2011;49(3):164-168.
  33. Amooee S, Parsanezhad ME, Shirazi MR, Alborzi S, Samsami A. Metformin versus chromium picolinate in clomiphene citrate-resistant patients with PCOS: A double-blind randomized clinical trial. Iran J Reprod Med. 2013;11(8):611-618.

 

Does Fructose Make You Fat?

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Have you ever seen the commercial sponsored by the Corn Refiners Association claiming that there is nothing wrong with high fructose corn syrup? That it’s “just sugar” and your body can’t tell the difference? If you haven’t, check it out below. I laughed out loud the first time I saw it air during prime time television. Unfortunately, this is the type of media messaging that is accessed and absorbed by American viewers, particularly adolescents and mothers. It is strategic and smart marketing on their behalf, because the next time these consumers are at the grocery store and happen to glance at the ingredients on a product, they’ll most likely remember, “Oh yeah, high fructose corn syrup isn’t even bad for you. It’s just sugar.” How terribly wrong.

 

 

There has been a lot of back and forth between fructose being bad and good for you. Personally, I try not to villainize any food group, macro or micronutrient. But, I recently gained some insight into how fructose is metabolized in the body in my biochemistry of nutrition class. When I say fructose, I don’t want you to think I’m referring to a piece of fruit here and there, a breakfast smoothie, or having a plethora of seasonal watermelon in the summer. This is naturally occurring fructose and these levels can be handled by metabolic pathways in healthy individuals. Rather, I’m talking about the American population loading up on sugar-laden candies, sodas, breakfast cereals, and many processed foods that contain high fructose corn syrup. THIS is when you run into trouble. Quite frankly, this is the reason why our country’s obesity rate is rising by the day.

 

In this commercial, the mom wandering around in a corn maze (??) is basically saying that sugar is sugar – it doesn’t matter what form it’s in – the body recognizes it all as the same thing. Well, this is loosely true. It’s sort of like saying a Ferrari is the same thing as a Chrysler Sebring; both can be convertibles, have four wheels, and get you from point A to point B. See my point? This lady/actress and Michael Scott are most likely good friends.

 

So, what’s false about this commercial??

Well, there are many different types of sugar that exist. Let’s start out with the basics and then I will show you how high fructose corn syrup is linked to them. Glucose is our body’s (and brain’s!) main, most easily metabolized, and preferred carbohydrate fuel source. It is a monosaccharide, which is the most basic sugar/carbohydrate form that exists. As such, glucose can be metabolized by any cell in the body. The other monosaccharides are fructose and galactose. Glucose, fructose, and galactose all have a chemical formula of C6H12O6, which is about as far as their similarities go. The difference lies in the placement of the carbon, hydrogen, and oxygen bonds in their structures, as can be seen in the diagram below. Your body is picky, it knows the difference between these sugars very well, contrary to what the corn refiners say:

 

carbon structure

Now, one of the main reasons we ingest glucose, or any food for that matter, is to break it down in order to utilize its caloric energy or store it for later on. In chemistry terms, “energy” is basically referred to as ATP, or adenosine triphosphate. Ring any bells??

 

So, you have a nice bowl of pasta for dinner. What happens? Glucose is released from the carbohydrates, it raises your blood sugar, your brain registers this, and insulin is secreted to get the glucose out of the bloodstream and into the cells where it can be burned, in this scenario. Once in the cells, it enters glycolysis, which ends in the formation of pyruvate. Pyruvate makes its way to the Krebs cycle, and eventually yields a total of 36 ATP – aka energy for your body to use as it sees fit. This mechanism is highly complex and works extremely efficiently since regulating blood sugar is integral to our homeostasis.

 

Why, then, would our body have two separate pathways to breakdown fructose and galactose if the one I just discussed for glucose works so well? It doesn’t.

Fructose and galactose undergo short reactions to rearrange their structures in order for them to enter glycolysis just like glucose. This saves the body a lot of energy. One of the ways fructose undergoes this type of rearranging can be seen in the below diagram. When fructose enters the liver, it requires a bit of effort to get it into glycolysis, into which glucose would normally slip so easily. (Warning – I have no graphic design talent):

 

fructose metabolism diagram 2

 

As you can see, fructose eventually needs to be converted to glyceraldehyde-3-phosphate. This is accomplished by adding a phosphate. Where does this phosphate come from? The P in ATP!

 

Translation: It costs your body energy every time you ingest a molecule of fructose.

Now, the sugar we ingest – what form is it in? Cane sugar, also known as table sugar or sucrose, is 50% glucose and 50% fructose. Not that bad. This is also naturally occurring. High fructose corn syrup, on the other hand, is a man-made sweetener and preservative that has chemically altered the glucose in corn starch to become fructose, resulting in a super sweet and palatable end product. Is corn a fruit? Not the last time I checked. Hmm … Anyway, as a result, HFCS is 55% fructose and 45% glucose. In your body, this translates to a lot more fructose that needs to be broken down.

 

Unlike glucose, which can be processed in all cells of the body, fructose can only be metabolized in the liver. In a previous post, I emphasized how overburdened the liver is on a daily basis with its metabolic duties. So, if you are inundating your body with fructose on top of everything else, you will really be depleting the liver of its energy stores. If you and your liver are energy deficient (which is very common), the glyceraldehyde seen in the diagram will stand alone, phosphate-less, and be unable to enter glycolysis.

 

Where does this leftover glyceraldehyde go? It stores itself in the adipose, or fat tissue … You gain weight.

 heavy bird in tree

What is also interesting is when you ingest glucose, it provides a “satiety” signal to the brain. This signal assists insulin in getting the glucose out of your blood and into the cells. Fructose, on the other hand, is not used by the brain for fuel. Therefore, it never gets there to provide that same message of, “I ate, that was delicious, I’m satisfied, you can put down the fork now.” Moreover, the transporter that pushes fructose out of the blood and into the cells is not insulin dependent. Consequently, your tissues can’t really absorb and process the fructose as readily. Once the fructose is able to get in the cell, if in excess, it will react to form components of triglycerides more readily than glucose would. Sorry to break it to you, but there’s always excess fructose floating around when you’re consuming high fructose corn syrup. Which means, you’ll usually be forming triglycerides, which are fat stores.

 

In addition to not stimulating insulin, fructose fails to stimulate leptin hormone production. Leptin is the key hormone that regulates your hunger signals. If it’s not working, you will always feel hungry, never feel satisfied, and your body will hold onto the weight because your brain is telling it that you haven’t really eaten, so why burn it? Our bodies are very smart and protective of our survival. So, you can see how a diet high in fructose over a long period of time can throw off your sugar metabolism and appetite, right? This is a recipe for consistent weight gain and insulin resistance –> diabetes –> obesity!

 

So, yeah, I would have to disagree with that commercial. Shame on them.

 

Peace of mind starts on your plate – or in the produce section, in this case. Not in a Pepsi can.

If there’s one thing you can remove from your diet as a first step toward breaking that ceiling, slimming your waistline, and lowering your risk for diabetes and obesity – get rid of the high fructose corn syrup.

 

Happy Holidays!!

 

 

Research cited: Ferder, L.; Ferder, M.D.; Inserra, F. The Role of High Fructose Corn Syrup in Metabolic Syndrome and Hypertension. Current Hypertension Reports, 2010, 12, 105-112.

 

Why Djokovic Is My 2014 US Open Hopeful – Yes, This Is Still A Health Blog

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US Open, Flushing, New York. September 2014.

 

My pick for any Grand Slam is easily and always my boyfriend, Rafael Nadal. However, since he pulled out of the tournament this year due to a wrist injury, I had to feel out the other competitors to see who I wanted to get behind.

 

It was an absolutely gorgeous day at the Billie Jean King National Tennis Center yesterday. I walked around the grounds in Flushing to check out some of the rising young junior talent on the side courts, as well as the mature veterans battle it out in Arthur Ashe during the Quarterfinals.

 

Aside from the heart they bled out on the courts, I couldn’t help but gape in wonderment at their physiques, energy, and stamina in the sticky NYC heat and the blaring sunlight that reflected a blue tint on their faces from the court surface . . . as I sat there a sweaty mess debating if it was too far of a walk to get the $7 Evian face mist to keep me from falling into heat stroke.

 

So, with the Murray v. Djokovic match taking place later that night, and with Novak having just won Wimbledon, I admit I was rooting for Murray to advance to the Semis. However, once the second tie-breaker was done and seeing Djokovic wipe the court with Murray in the third and fourth sets, I have set my sights on a new man – Nole!

 

You don’t have to be a tennis fan to be truly amazed at his performance and conditioning. However, if you were watching the same match five years ago, the outcome probably would have been different. Why? Because Djokovic wasn’t gluten-free!

 

You ask, how does being gluten-free have anything to do with tennis? Well, prior to changing his diet and eliminating gluten-containing foods, Novak thought his career and success were fleeting. He didn’t even think he belonged on the same court as his opponents. He was plagued constantly by chest pain, stomach spasms, asthma, injuries, and fatigue. He could not depend on his body to provide the consistent, healthy performance for which he tirelessly trained. Just as he was rising to the top of his game, symptoms that anyone would attribute to physical exhaustion and the stress and rigor of a professional athlete’s lifestyle would pull him right back down. But, those factors weren’t the cause – gluten was.

 

In his book, Serve to Win: The 14-Day Gluten-Free Plan for Physical and Mental Excellence, Djokovic explained, “There was something about me that was broken, unhealthy, unfit. Some called it allergies, some called it asthma, some just called it being out of shape, but no matter what we called it, no one knew how to fix it.”

 

Sound familiar? In fact, most people suffer with symptoms like this for years without a doctor even thinking to look at food intolerances or digestive issues. Luckily, mainstream practitioners are even catching on and accepting this as truth today.

 

So, why would avoiding gluten (or other allergens) make such a difference in his tennis game? Or in anyone’s health? Let me break it down for you.

 

Did you know that 80% of your immune system resides in your gut? Eighty percent. That’s a lot, no? You have what are called Peyer’s patches, which are small regions of lymphatic tissue, that are woven throughout the lining of the small intestine. They form an integral part of the immune system by monitoring the food that comes through your digestive system for any harmful bacteria. Say if you eat some produce that inevitably has bacteria on it from the soil, or a piece of chicken that is not 100% fresh, Peyer’s patches will sense this and trigger the immune system to create pathogen-specific antibodies to target that bacteria and kill it before it can go anywhere in the body outside of the gut and make you very sick.

 

Now, how does a food intolerance occur? Well, the diet most Americans (and I guess, Serbians) eat tremendously damages the lining of the small intestine in which the Peyer’s patches do their work. Normally, when the lining is healthy, smooth and in tact, nothing slips through the cracks and reaches the patches other than microscopic bacteria.

 

However, with a damaged gut… gaps, holes, and tears start to develop and then pieces of digested food can slip down to the patches. Once this happens – Game, Set, Match: Allergen.

 

Your immune system then starts making antibodies that are now food-specific (remember, they are supposed to be pathogen-specific). Your body now sees that particular food protein in the same way it saw that harmful bacteria riding down on that piece of spinach. So, if you eat this food regularly, your immune system thinks it constantly needs to make antibodies. It then doesn’t know which end is up and starts to not only attack the food, but healthy tissues that were minding their own business, as well. This leads to systemic inflammation – something I’m sure athletes and their trainers do not want for themselves. In Nole’s case, inflammation manifested itself in the forms of asthma, sinus issues, fatigue, constant injuries, and terrible mood swings on the court.

 

By avoiding the perpetrators, Peyer’s patches can take a breather, and you can allow your gut and immune system to relax, heal, and do their normal jobs correctly – not work overtime or fulfill someone else’s responsibilities. See, everybody should have a mandatory two week vacation – not just people in Finance.

 

So, in essence, if you let your gut heal completely (which can take up to two years), and then adapt to an ideal diet, you should be able to eat those foods again. In essence. You should know by now that things aren’t ever this simple.

 

There are other things that irritate and damage the gut lining aside from gluten and other allergens: sugar, stress, alcohol, artificial sweeteners, pollutants in tap water, preservatives, unhealthy oils, heavy metals, grains, unsoaked/unsprouted seeds and nuts, excessive amounts of starches, too much fiber, lack of sleep, eating in an unrelaxed state of mind, etc. The list goes on.

 

This is why it is so important to adopt a consistently healthy, balanced, varied, clean diet so that you are not bombarding your body with things that it has to work hard to overcome. If you give it the fuel it needs to a greater extent than the things that will damage it, you tip the scales in good health’s favor.

 

If you are thinking of doing an elimination diet, here are my recommendations:

First and foremost, work with an experienced health practitioner who specializes in this. I wouldn’t try it on your own, as you could be missing a link. Naturopaths, Chiropractors, and Clinical Nutritionists are your best bet. They also have access to the best types of allergy tests that your insurance can cover and will capture everything you need to know before you get started.

Avoid the foods to which you are highly allergic completely, 100%, for a few months. Then ask yourself if you are noticing a difference after about four months. Any difference is progress in the right direction.

Avoid common irritants (gluten, dairy, corn, soy, peanuts) as much as you can during this time as well. If they’re not on your high allergen list, it’s okay if you slip up on occasion. You will definitely notice a difference with this step.

Rebuild your gut lining through fermented foods (kombucha, kimchi, sauerkraut, kefir), bone broths, and gut-building supplements that a practitioner could recommend. I wouldn’t go out and buy any probiotic or glycine, etc. in a health food store. It could be unnecessary and a waste of money if you don’t know what to target. Practitioners also have access to the most effective, cleanest supplements.

Maintain a healthy diet and stress level as much as you can. You don’t have to be nuts or stringent about it, but it should be a lifestyle choice. You will undoubtedly notice a long-term difference with this step.

 

And until Rafa’s back, LET’S GO NOLE!!!

 

Thanks for reading. Please feel free to message me if you want to hear more or less about topics I’m covering – I’m open to suggestions!

 

 

Orthorexia Nervosa – Huh?

In my first blog post, I detailed the extreme measures I took to improve my diet in an effort to reclaim my health. To be clear – I didn’t just make a few tweaks here and there. I wasn’t just avoiding gluten and dairy. I didn’t just cut out alcohol for a few months. I didn’t do a few juice cleanses and call it a day. I changed everything I knew on how to nourish myself and stuck to it for eighteen months with a vigilance I didn’t even know I had in me. It was a long term, devout commitment to something I knew would pay off – or at least had faith that it would, anyway.

 

Like any commitment – be it a job, relationship, marriage, investment, or pet – it took work. And, the more I put into it, the stricter I was with the quality of food I consumed, the quicker my health improved and life was back on track. This, my friends, is what Pavlov termed positive reinforcement. I was hook, line and sinker with no desire to cheat, flirt, or even take an innocent glance in the opposite direction.

 

What originally felt like positive reinforcement, however, eventually instilled a sense of fear within me. I began to wonder, “What if I don’t keep this going? What if I slip up? What if that had dairy in it? What if I’m not getting the right ratio of Omega 3s to Omega 6s? Oh no, those blueberries weren’t organic. Did that Lara Bar have too many carbs for this late in the day? Will that cause my symptoms to return?”

 

Exhausting. Crazy. Familiar???

 

I knew, for sure, that having my symptoms return was absolutely not an option for me if I was able to control it. For some people, though, having control over something you fear can turn into an unhealthy obsession. So, like most relationships that aren’t meant to be, the pendulum began to swing from hot-and-heavy and honeymoon-phase to trouble-in-paradise and me questioning if it was really worth it or necessary to be this committed to something that was affecting my happiness.

 

Well, here’s what I’ve learned.

 

There’s having a healthy diet. And then there’s being unhealthy about having a healthy diet. It’s a fine line.

With the flurry of information from ill-informed people that’s accessible on the internet these days, knowledge is no longer power, it’s paralysis.

 

I remember being at a barbecue over Labor Day weekend a couple of years ago and not “being able” to eat or drink anything there besides water and fruit salad because I was worried about the quality of the food, the types of oils it was cooked in, and what its allergens might do to me. Mind you, barbecues at the Jersey Shore are something you go to with a completely empty stomach – crab sauce, burgers, chips and dip, steamers, cocktails, cannolis. You get it. Truth be told, I was doing more damage to my body and immune system by a) not eating food with needed calories when it was in front of me, and b) worrying so much about the negative repercussions it could possibly have on my health.

 

It’s a fact that we are primal beings. We have the same genetic makeup as the first Homo sapiens on the planet. Way back then, their lives revolved around finding food, finding safety, and reproducing. The main form of stress they endured was famine. As their bodies evolved to survive this type of adversity, it learned to slow down their metabolism, store fat, and shut down reproductive function so they wouldn’t lose body fat (warmth), and wouldn’t have to nourish a baby in their womb while not having the fuel to healthily do so.

 

Stress is stress is stress is stress. The body does not know the difference between the various negative forms, but it reacts the same way to all of them. These days, people place this same degree of stress on themselves when they diet, when they exercise too much, when they don’t sleep enough, and most importantly, when they live in constant fear and worry. The version of constant fear I wrote about today is termed orthorexia nervosa.

 

BUT! What if you have an autoimmune condition? There really are antibodies that are produced in your body which attack various organ systems when you consume proteins to which your immune system is reactive. Luckily, there are other ways to address your immune symptoms through modalities outside of diet, which I plan to delve into in due time.

 

What I do know is that happiness and relaxation are paramount to calming down your immune system along with any sort of inflammation in your body. Fear and stress … are not.

 

So, chances are that the GMO-laden, canola-oil fried, preservative-filled, hydrogenated tortilla chips that all of your friends are enjoying with their guacamole and sugar-filled, liver-taxing margaritas won’t hurt you any worse than being afraid of eating them will. Go ahead, indulge. Your belly, heart, leptin levels, sanity, and most importantly – your dinner date, will be thankful.

 

In the meantime, stay tuned for posts on other ways to help your immune system as the grass continues to grow here.