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, Morón 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, Bång 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.

 

Oxytocin: The Love Hormone

oxytocin_molecule

 

 

Happy Valentine’s Day, ceiling fans! In the spirit of a holiday blazoned with romance, I thought it best to provide a post on an essential hormone we produce that not only makes you feel all kinds of rosy inside, but is a cornerstone to our health and happiness as well, especially when it comes to relationships.

 

As the title of this post lends itself, I’m referring to oxytocin. Although not widely known or commonly talked about in the mainstream media, significant amounts of research have highlighted its many benefits in our body, including recent implications in weight loss.

 

So, let’s get to it, shall we?

 

In mammals, oxytocin is a hormone released from the pituitary gland to trigger muscle contractions during labor and delivery and to release milk during lactation. While these are its principal responsibilities, oxytocin also functions as a neuropeptide, which is a small compound that acts locally within the brain on a specific pathway. The particular pathway oxytocin interacts with is the reward and reinforcement system fueled by the neurotransmitter dopamine. This is part of the same neurocircuitry that recreational drugs, like cocaine and heroine, act upon to evoke sensations of euphoria and addiction – both of which are also common emotions felt on the rollercoaster ride of romantic relationships.

 

Research has shown that a female prairie vole promptly becomes attached to the nearest male suitor when her brain is suffused with oxytocin, ultimately leading to her choice in a monogamous pair bonding that will last for her entire life. The same type of behavior can be observed in humans; during intercourse, surges of oxytocin are released, which help establish a deeper connection and attachment to one’s partner, even if you weren’t necessarily interested in them prior to having sex. (I think everyone’s twenties should be starting to make a little more sense to them right now). Further, dopamine receptors light up when looking at pictures of a loved one.

 

oxytocin copy

 

Similarly, in male prairie voles, a hormone called vasopressin, which is intimately related to oxytocin, “stimulates pair bonding, aggression towards potential rivals, and paternal instincts, such as grooming offspring in the nest.”1 In fact, a gene that regulates vasopressin receptors in the brain determines the likelihood of a male bonding with a female vole.

 

Correspondingly, in humans, this same gene (AVPR1A) is linked to one’s ability to bond and have a healthy, fulfilling relationship. Mutational variants in this gene result in men being twice as likely to remain unmarried. On top of this, those men who are married and have a polymorphism of this gene are twice as likely to report crises in their marriages and have spouses who are dissatisfied, in comparison to men who carry an intact version of this gene.

 

I bet there would have been a lot more funding for the Human Genome Project had it been known that genetic screenings for a good husband may exist.

 

Aside from its heavy influence on bonding abilities, oxytocin also plays a big role in one’s ability to trust. Trust permeates everything in our world – from our choices in political candidates, business transactions, social attachments, and even our sense that our daily life and universe are unfolding as they should. A double-blind placebo-controlled study was conducted to administer nasal spray containing oxytocin to participants in a role-playing game. Participants played the role of either an investor or trustee, investing money to a trustee who could either take all of their investment and run, or split half of it with the investor – the latter resulting in a higher yield for both parties. Those who were administered oxytocin contributed a significantly higher amount of monetary investment than those who received a placebo, exhibiting a greater level of trust in others when participating in risk-taking behavior. If there are any hedge fund managers browsing this website, linking up with a biochemist may be in your best interest!

 

 

Back to bonding, have any of you ever noticed that you involuntarily lost weight at the beginning of falling in love with someone?

 

Or maybe you maintained your weight or even shed a few pounds despite overindulging on a romantic vacation? Well, oxytocin was to thank. In the past few years, new studies performed on obese rats have shown the link between oxytocin and weight loss. The obese rats, independent of the types of diets they were on, reduced their food intake and sustained consistent weight loss when administered regular doses of oxytocin. This occurred in spite of no energy expenditure (exercise) on the rat’s behalf, to boot. Moreover, the rats that were obese as a result of their genes (meaning they were leptin-resistant), lost as much weight as the rats who were obese as a result of force-feeding. This shows that oxytocin may circumvent leptin resistance, a growing problem in our society, proving to be a possible effective treatment in genetically inherited metabolic syndromes like type II diabetes and obesity.

 

 

So, how can one boost their oxytocin production? Here are some easy and natural ways:

 

  1. Physical Contact – this is a biggie! Hug, kiss, hold hands, snuggle, have sex – you get it.
  2. Be Charitable – Do something nice for someone who needs it. Take your friend out to dinner or give belongings that mean something to you away to charity. These acts all trigger a cascade of reactions in your brain that help facilitate oxytocin release.
  3. Walk! – Research has shown that taking a walk is more beneficial and health-boosting than running and working out for some individuals. More importantly, get outdoors and smell the fresh air. Walking meetings have grown in popularity in the corporate world, and it seems like this may be a great way to establish a relationship with a client.
  4. Listen to soothing music
  5. Indulge in comfort food – and don’t think twice about it. Even better, share it with someone.
  6. Surround yourself with animals and pet them – this is my favorite. Whenever I hear my dog snorting her way up the stairs to my room, I instantly feel warm inside. Therapy dogs are frequently taken to hospitals and nursing homes for the numerous health benefits they provide.
  7. Sing and dance
  8. Say, “I love you” out loud to someone you care about. No texts.
  9. Deep breathing, yoga, and meditation
  10. I also heard that clicking the “like” button on this blog post boosts your oxytocin levels, so you can test it out here. 😉

 

Of course oxytocin is not the only factor, or hormone for that matter, involved in love. But, it’s an interesting component! As you know, we are primal beings. Chances are back when we were cavemen, those who had healthy oxytocin function bonded and created strong nuclear families, which helped propel them through harsh conditions to survive and evolve. There was no match.com or “types” one was attracted to back then; there were simply primal attractions and a need to procreate, preferably with one worthy and healthy mate.

 

So, the next time you have an indescribable connection with someone, or witness the effortlessness with which some couples interact, hopefully after reading this post you’ll have a newfound understanding of what having “chemistry” really means. It is, in essence, good chemistry.

 

hearts1

 

Thanks again for reading!

 

…And a very happy one to my blue-eyed valentine <3

 

 

References:

 

  1. Young, L.J. Love: Neuroscience reveals all. Nature, 2009, 457, 148.
  2. Blevins, J.E.; Ho, J.M. Role of oxytocin signaling in the regulation of body weight. Reviews in Endocrine and Metabolic Disorders, 2013, 14, 311-329.
  3. De Boer, A.; Van Buel, E.M.; Ter Horst, G.J. Love is more than just a kiss: A neurobiological perspective on love and affection. Neuroscience, 2012, 201, 114-124.
  4. Kosfeld, M.; Heinrichs, M.; Zak, P.J.; Fischbacher, U.; Fehr, E. Oxytocin increases trust in humans. Nature, 2005, 435, 673.
  5. Morton, G.J.; Thatcher, B.J.; Reidelberger, R.D.; Ogimoto, K; Wolden-Hanson, T.; Baskin, D.G.; Schwartz, M.W.; Blevins, J.E. Peripheral oxytocin suppresses food intake and causes weight loss in diet-induced obese rats. American Journal of Physiology – Endocrinology and Metabolism, 2012, 302, E134-E144.
  6. Scheelea, D.; Willea, A.; Kendrick, K.M.; Stoffel-Wagnerd, B.; Becker, B.; Gunturkune, O.; Maiera, W.; Hurlemanna, R. Oxytocin enhances brain reward system responses in men viewing the face of their female partner. PNAS, 2013, 110, 20308-20313