Some research shows that the use of artificial sweeteners is associated with a modest weight loss (2).

Other research shows that the use of artificial sweeteners is associated with weight gain (3,4, 5, 6, 7, 8).

Everyone says they are right (9).

Just that, besides weight loss or weight gain, the use of artificial sweeteners is also associated with:

1. glucose intolerance induced by dysbiosis (10,11, 12, 13, 14)
2. diabetes (15, 16, 17, 18, 19, 20, 21)
3. cardiovascular disease (22, 23, 24, 25, 26)

And also, starting 2012 artificial sweeteners are recognised as environmental contaminants (27, 28, 29).

So, don’t worry = no sugar?

References

(1) Shankar, Padmini, Suman Ahuja, and Krishnan Sriram. “Non-nutritive sweeteners: review and update.” Nutrition 29.11 (2013): 1293-1299).

(2) Miller, Paige E., and Vanessa Perez. “Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies.” The American journal of clinical nutrition 100.3 (2014): 765-777.

(3) Fowler, Sharon PG, Ken Williams, and Helen P. Hazuda. “Diet soda intake is associated with long‐term increases in waist circumference in a biethnic cohort of older adults: The San Antonio longitudinal study of aging.” Journal of the American Geriatrics Society 63.4 (2015): 708-715.

(4) Pliego-Rivero, F. Bernardo, et al. “The Non-Caloric Sweeteners Aspartame, Sucralose and Stevia sp. Induce Specific but Differential Responses to Compartmentalized Adipose Tissue Accumulation.” The FASEB Journal 31.1 Supplement (2017): 639-46.

(5) Polyák, Éva, et al. “Effects of artificial sweeteners on body weight, food and drink intake.” Acta Physiologica Hungarica 97.4 (2010): 401-407.

(6) Meni, Allison C. Sylvetsky, Susan E. Swithers, and Kristina I. Rother. “Positive association between artificially sweetened beverage consumption and incidence of diabetes.” Diabetologia 58.10 (2015): 2455-2456.

(7) Yang Qing. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. The Yale journal of biology and medicine, 2010, 83.2: 101.

(8) Simon, Becky R., et al. “Artificial sweeteners stimulate adipogenesis and suppress lipolysis independently of sweet taste receptors.” Journal of Biological Chemistry 288.45 (2013): 32475-32489.

(9) Mandrioli, Daniele, Cristin E. Kearns, and Lisa A. Bero. “Relationship between research outcomes and risk of bias, study sponsorship, and author financial conflicts of interest in reviews of the effects of artificially sweetened beverages on weight outcomes: a systematic review of reviews.” PloS one 11.9 (2016): e0162198.

(10) Bokulich, Nicholas A., and Martin J. Blaser. “A bitter aftertaste: unintended effects of artificial sweeteners on the gut microbiome.” Cell metabolism 20.5 (2014): 701-703.

(11) Suez, J., Korem, T., Zeevi, D., Zilberman-Schapira, G., Thaiss, C. A., Maza, O., … & Kuperman, Y. (2014). Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature, 514(7521), 181-186.

(12) Nettleton, Jodi E., Raylene A. Reimer, and Jane Shearer. “Reshaping the gut microbiota: Impact of low calorie sweeteners and the link to insulin resistance?.” Physiology & behavior 164 (2016): 488-493.

(13) Pepino, M. Yanina. “Metabolic effects of non-nutritive sweeteners.” Physiology & behavior 152 (2015): 450-455.

(14) Swithers, Susan E. “Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements.” Trends in Endocrinology & Metabolism 24.9 (2013): 431-441.

(15) Nettleton, Jennifer A., et al. “Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA).” Diabetes care 32.4 (2009): 688-694.

(16) Fagherazzi, Guy, et al. “Consumption of artificially and sugar-sweetened beverages and incident type 2 diabetes in the Etude Epidémiologique auprès des femmes de la Mutuelle Générale de l’Education Nationale–European Prospective Investigation into Cancer and Nutrition cohort.” The American journal of clinical nutrition 97.3 (2013): 517-523.

(17) Greenwood, D. C., et al. “Association between sugar-sweetened and artificially sweetened soft drinks and type 2 diabetes: systematic review and dose–response meta-analysis of prospective studies.” British Journal of Nutrition 112.05 (2014): 725-734.

(18) Yarmolinsky, James, et al. “Artificially Sweetened Beverage Consumption Is Positively Associated with Newly Diagnosed Diabetes in Normal-Weight but Not in Overweight or Obese Brazilian Adults.” The Journal of nutrition 146.2 (2016): 290-297.

(19) Fagherazzi, Guy, et al. “Chronic Consumption of Artificial Sweetener in Packets or Tablets and Type 2 Diabetes Risk: Evidence from the E3N-European Prospective Investigation into Cancer and Nutrition Study.” Annals of Nutrition and Metabolism 70.1 (2017): 51-58.

(20) Meni, Allison C. Sylvetsky, Susan E. Swithers, and Kristina I. Rother. “Positive association between artificially sweetened beverage consumption and incidence of diabetes.” Diabetologia 58.10 (2015): 2455-2456.

(21) Hoffmann, Brian R., and Andrew S. Greene. “Mechanisms of Vascular Endothelial Dysfunction: The Problem with Sugar and Artificial Sweeteners.” The FASEB Journal 31.1 Supplement (2017): 853-9.

(22) Cheungpasitporn, Wisit, et al. “Sugar and artificially sweetened soda consumption linked to hypertension: a systematic review and meta-analysis.” Clinical and Experimental Hypertension 37.7 (2015): 587-593.

(23) Narain, Aditya, C. S. Kwok, and M. A. Mamas. “Soft drinks and sweetened beverages and the risk of cardiovascular disease and mortality: a systematic review and meta‐analysis.” International journal of clinical practice 70.10 (2016): 791-805.

(24) Wersching, Heike, Hannah Gardener, and Ralph L. Sacco. “Sugar-Sweetened and Artificially Sweetened Beverages in Relation to Stroke and Dementia.” (2017): 1129-1131.

(25) Gardener, Hannah, et al. “Diet soft drink consumption is associated with an increased risk of vascular events in the Northern Manhattan Study.” Journal of general internal medicine 27.9 (2012): 1120-1126.

(26) J., Beiser, A. S., Aparicio, H. J., Satizabal, C. L., Vasan, R. S., … & Jacques, P. F. (2017). Sugar-and Artificially Sweetened Beverages and the Risks of Incident Stroke and Dementia. Stroke, STROKEAHA-116.

(27) Scheurer, Marco, Heinz-J. Brauch, and Frank T. Lange. “Analysis and occurrence of seven artificial sweeteners in German waste water and surface water and in soil aquifer treatment (SAT).” Analytical and bioanalytical chemistry 394.6 (2009): 1585-1594.

(28) Sang, Ziye, et al. “Evaluating the environmental impact of artificial sweeteners: a study of their distributions, photodegradation and toxicities.” Water research 52 (2014): 260-274.

(29) Lange, F. T., Scheurer, M., & Brauch, H. J. (2012). Artificial sweeteners—a recently recognized class of emerging environmental contaminants: a review. Analytical and Bioanalytical Chemistry, 403(9), 2503-2518.

Articolul Don’t worry = No sugar? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

• They know that gluten can cause allergie or intolerance.
• They know gluten makes them gain weight.
• They know that.
• They know that..
• They know that…

From whom do they know all that?

From people with gluten sensitivities, of course.

And the direct feedback of a person with gluten sensitivity feels extremely valuable for someone who wish to know about gluten side effects. Just that it varies widely from one person to other persons asked for this feedback (1).

And yes, we all would expect this feedback to be:

• negative from patients with celiac disease;
• and somehow improved from people following a gluten-free diet because they think they have gluten intolerance (2).

The fact that someone has the discipline to respect a gluten-free diet is exceptional, just not necessarily healthy (3,4).

On the other hand, people know for sure that running is necessarily healthy.

• They know that it improves cardio-vascular health because it’s said that you won’t have a stroke if you run a marathon (5,6,7).
• They know that it helps with weight loss (8).
• They know that it improves blood lipids profile by increasing HDL-cholesterol level (9).
• They know that it ameliorates depression (10).
• And they suppose that it improves runners immunity (11).

From whom do they know all that?

From runners, of course.

And the direct feedback of a runner feels extremely valuable for someone who wish to know about running side effects. Just that it varies widely from one person to other persons asked for this feedback (12).

And yes, we all would expect this feedback to be:

• positive from short and medium distance runners (after learning to breathe properly). Because if we’d ask, some people would not run even to catch a bus that comes every hour. The next one will come.
• and somehow less positive from runners just ending a marathon or an ultramarathon when – although mentally everything is extraordinary – physically things can be less extraordinary (13).

The fact that someone has the discipline, mental, respiratory and muscular capacity to run a marathon or an ultramarathon is exceptional, just not necessarily healthy.

Without the proper nutrition, long and unltra-long distance running can be unhealthy at least in terms of gastrointestinal, cardiovascular and osteo-articular heath (but I will write two separate articles about the last two).

And yes, anyone can decide for himself that my opinion is pointless and keep running for as long as he can without talking with a gastroenterologist or with a sports nutritionist despite digestive symptoms felt during running.

Just that my opinion is not grounded on personal experience. I run with a 6-7′ per km a maximum of 10-15 km per week, and I feel fine. Also, I know many people that run more than that, and that run marathons and ultra-marathons, and they feel fine. My opinion is not grounded on their running experience either.

My opinion is grounded on studies on runners who experienced symptoms from digestive discomfort to digestive hemorrhage durring long distance running events (14).  Because if a behavior/ medication/ supplement is beneficiary for 70 people – this may seem as pretty conclusive for people leaving with a health problem, thus many would extrapolate that behavior/ medication/ supplement as a solution for their own problem.

But what if they are 70 out of a 1,000 people, and that same behavior/ medication/ supplement had no effect or was harmfull for the last 930? If you’d have no problem maybe you’d mostly consider the theoretical implications.

But if you do have digestive symptoms while running, let’s see what studies are saying.

Many long distance runners present digestive symptoms like:

• gastroesophageal reflux (15)
• vomiting, diarrhea, abdominal cramping (16)
• and even digestive bleeding (17).

Thus, because of the fact that gastrointestinal discomfort felt by these runners mimics gluten intolerance symtoms, it has emerged the assumption that a gluten-free diet is beneficial for runners (18).

But a gluten-free diet for an endurance sport seems diametrically opposite of the pasta party concept, right?

Thus, besides the supposed gluten sensitivity, what might other digestive symptoms’ causes be in people that actually experience them only when running?

Long distance running can generate:

• sympathetic nervous system hyperactivity – which inhibits intestinal mucosal cells’ ability to secrete enzymes, causing an inability to digest dissacharides – further transported to the colon where they are fermented by local bacteria (19);
• intestinal dehydration – which increases intestinal absorbability for partially undigested nutrients – causing allergic like reactions like bloating, abdominal cramping, blood in faeces during the sport event – but in runners who have no problem what so ever eating gluten rich foods when they don’t run (20,21);
• intestinal vasoconstriction – which decreases liquids intestinal absorbability during running – especially for water either without/ with a carbohydrates and electrolytes content inappropriate for that athlete – which can cause diarrhea (22).

So, is the gluten-free diet beneficial for long-distance runners?

Yes if the runner has celiac disease or gluten intolerance also when he/ she does not run.

And no if the digestiv discomfort happens only when running because the above mentioned causes does not magically dissapear if we take out gluten for the runner’s diet.

Because they are caused by the sympathetic nervous system (responsable for fight or flight reactions) and by dehydration (if the runner does not properly hydrate according with his own health and training status during that particular run) – during long distance running digestive symptoms will keep happening even on a gluten-free diet (23).

As a general rule – without proper sports nutrition – the higher the effort, the higher both the intestinal ischemia and the intestinal permeability, thus the higher the digestive symptoms.  And, sadly, this type of simptomps don’t occur only in runners, but also in  cyclists, swimmers, triathletes and other athletes involved in endurance sports.

So what can they do to avoid digestive symptoms during sports events?

A. Before the sports event:

1. 1 month before: hydration traing – done repeatedly before the event with the exact same sports drink that will be used during the sports event;
2. 1 week before: eating high quality foods, as natural and as simplest cooked possible: proteins, carbohydrates, fibres and flavonoids supplying foods ± high quality omega-3 fats at every meal (high quality proteins and carbohydrates are mutually reinforcing);
3. 1 1/2 – 2 hours before: take the meal before the event, and then just focus on hydration (proper hydration before the sports event is essential for effective hydration during the event);
4. avoid evitarea antiinflammatory medication just before the event (24).

B. During the sports event:

1. The most important thing not to do during a sports event is to start something new: untested sports drink, new running shoes, miracle supplements. Just keep business as usual and you’ll have a better chance for success;
2. Hydrate regularly with low quantity of sports drinks appropriate for your body, running style and performance – again: use those you trained with repeatedly before the event;
3. Avoid solid foods – which need more time for gastric emptying – and replace them with gels and semi-liquid foods containing electrolytes, amino acids and dextrose (25);
4. Drink water with your gels, and alternate gels with sports drinks to restore blood volume decreased through dehydration (maintaining blood volume protects your heart and maintains your performance during sports events)
5. Avoid caffeine and anti-inflammatory medication if you experienced digestive symptoms in other sports events;
6. However, if digestive symptoms still occur, decrease intensity until they diminish or remediate.

Of course this plan might not suit gastro-intestinal pathology, thus realy pay attention to your gut while running. If you feel ill – better stop and see a medical doctor.

And yes – it is far easier to eliminate complete categories of foods than to follow the above plan, but it surely is easier than to counteract the impact of a gluten-free diet on endurance sports performance.

If you are a runner with digestive discomfort while running, please read the following references.

(1) Capannolo, A., et al. “Non-Celiac Gluten Sensitivity among Patients Perceiving Gluten-Related Symptoms.” Digestion 92.1 (2015): 8-13.

(2) Newman, Kaylee. “Excluding Gluten in a Healthy Collegiate Runner.” Journal of Sports Medicine and Allied Health Sciences: Official Journal of the Ohio Athletic Trainers Association 1.1 (2015): 19.

(3) De Palma, Giada, et al. “Effects of a gluten-free diet on gut microbiota and immune function in healthy adult human subjects.” British journal of nutrition102.08 (2009): 1154-1160.

(4) Mariani, Paolo, et al. “The gluten-free diet: a nutritional risk factor for adolescents with celiac disease?.” Journal of pediatric gastroenterology and nutrition 27.5 (1998): 519-523.

(5) Noakes, TIMOTHY D. “Heart disease in marathon runners: a review.” Medicine and science in sports and exercise19.3 (1987): 187-194.

(6)La Gerche, André, et al. “Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes.” European heart journal (2011): ehr397.

(7) Herrmann, Markus, et al. “Post-race kinetics of cardiac troponin T and I and N-terminal pro-brain natriuretic peptide in marathon runners.” Clinical chemistry49.5 (2003): 831-834.

(8) Tremblay, Angelo, Jean-Pierre Després, and Claude Bouchard. “Adipose tissue characteristics of ex-obese long-distance runners.” International journal of obesity 8.6 (1983): 641-648.

(9) Olchawa, Beata, et al. “Physical fitness and reverse cholesterol transport.”Arteriosclerosis, thrombosis, and vascular biology 24.6 (2004): 1087-1091.

(10) Leedy, M. Gail. “Commitment to distance running: Coping mechanism or addiction?.” Journal of Sport Behavior23.3 (2000): 255.

(11) Nieman, David C. “Marathon training and immune function.” Sports Medicine37.4-5 (2007): 412-415.

(12) Neilan, Tomas G., et al. “Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon.” Circulation114.22 (2006): 2325-2333.

(13) Mann, Nirmal S., and Sital Singh. “Runners’ Diarrhea: Systematic Evaluation of 1184 Cases with Meta-Analysis.” International Medical Journal 22.1 (2015).

(14) 94 de studii despre efectele gastrointestinale ale alergatului: http://www.uptodate.com/contents/gastrointestinal-disorders-in-athletes

(15) Parmelee-Peters, Katrina, and James L. Moeller. “Gastroesophageal reflux in athletes.” Current sports medicine reports 3.2 (2004): 107-111.

(16) Mann, Nirmal S., and Sital Singh. “Runners’ Diarrhea: Systematic Evaluation of 1184 Cases with Meta-Analysis.” International Medical Journal 22.1 (2015).

(17) McCabe III, Marshall E., et al. “Gastrointestinal blood loss associated with running a marathon.” Digestive diseases and sciences 31.11 (1986): 1229-1232.

(18) Lis, Dana, et al. “No Effects of a Short-Term Gluten-free Diet on Performance in Nonceliac Athletes.”

(19) Ter Steege, R. W. F., and J. J. Kolkman. “Review article: the pathophysiology and management of gastrointestinal symptoms during physical exercise, and the role of splanchnic blood flow.” Alimentary pharmacology & therapeutics35.5 (2012): 516-528.

(20) Øktedalen, O., et al. “Changes in the gastrointestinal mucosa after long-distance running.” Scandinavian journal of gastroenterology 27.4 (1992): 270-274.

(21) Parmelee-Peters, Katrina, and James L. Moeller. “Gastroesophageal reflux in athletes.” Current sports medicine reports 3.2 (2004): 107-111.

(22) ten Haaf, Dominique SM, et al. “Nutritional indicators for gastrointestinal symptoms in female runners: the ‘Marikenloop study’.” BMJ open 4.8 (2014): e005780.

(23) Lis, D. M. “Gluten-Free Diet May Not Boost Athletic Performance: A new study shows no difference in performance or reduction of GI symptoms when cyclists cut out gluten.” (2015).

(24) Küster, Michael, et al. “Consumption of analgesics before a marathon and the incidence of cardiovascular, gastrointestinal and renal problems: a cohort study.” BMJ open 3.4 (2013): e002090.

(25) Murray, Robert. “The effects of consuming carbohydrate-electrolyte beverages on gastric emptying and fluid absorption during and following exercise.” Sports Medicine 4.5 (1987): 322-351.

Articolul Is the gluten-free diet beneficial for runners? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

– Do you want to lose weight?

– For really, really, real, do you really want to?

Maybe you still want to, maybe you gave up, maybe you’re during a time when everything’s smooth and perfect between you and your body. Or maybe you got to the conclusion that you will never like your body because you like to eat a lot. And diets look like a calvary… from what you heard from others. Unnecessary torment, plus that who loves you loves you exactly the way you are and that people should love you for your inner beauty. True?

– Still, do you want to lose weight?
– And, if you want to, do you want it a little or do you want it a lot?

Many people consider this a rhetorical question.

“Of course I want to lose weight! Everybody wants to lose weight!”.

However, statistically, in a maximum of 2 years from the beginning of a diet, most people regain all the weight they lost during the diet and, also statistically, many start again to diet – the same or a new, more convenient or maybe more drastic one.

Therefore, if you do not ask yourself this question before you start (or even before you quit) and you do not find a sufficiently clear and specific answer, when the going will get tough, you will continue to behave automatically as you did before you prematurely decide that you want to lose weight.

When you risk assuming that you want to and just rush into a diet, you also assume the solution is somewhere outside of you:
– in the stratosphere,
– in conjunction between Mars and Uranus presented in the morning at the horoscope,
– in magical ingredients,
– in teas, pills or drugs that “increase” your metabolism,
– in avoiding one or another category of nutrients,
– in counting calories, glycemic indexes… and so on.

It’s just that metabolism is neither the abstract thing you regulate by drinking tea, nor the only thing to regulate when it comes to long-term fat loss.

Even if you only want to lose weight and you do not care what you lose as long as you lose something, metabolism is still not an abstract concept.

Simplistically, metabolism is not something meant to help you lose or gain weight, but a series of biochemical reactions designed to serve your internal organs to survive:

1. when you eat too little (by not feeding muscles and by actually burning muscle proteins as a source of nutrients for your internal organs when you starve yourself), and
2. when you eat too much (by not feeding muscles  and by transforming the excessive food intake into fat).

In the absence of starvation or overeating, your metabolism nourishes quietly the internal organs, then the active muscle cells and then – if anything remains – the adipose tissue.

The only variable in the metabolism that can be increased or decreased is the amount of active muscle mass – the only metabolic aspect able to save you, and the only part without any metabolic protection.

Fat has an army of adipokines as personal protection, army able to hit you where it hurts harder: in the hunger centre of your hypothalamus.

The reason I said that metabolism is neither abstract nor the only thing essential for weight losing is that – in the absence of a disease – these biochemical reactions cannot be controlled behaviourally, they happen for the good of the internal organs anyway you behave.

Weight loss is just a consequence of your behavior in response to a bodily or mental state generated by a trigger.

And your behavior is controlled by unconscious areas in your brain – designed to help you survive, not to lose weight – unconscious areas that work hand-in-hand with the army of adipokine secreted by fatty tissue.

You can ignore try to ignore your physical and mental state – because you supposedly want to lose weight – by typing a Copy/ Paste diet over your eating behaviour and hoping that this time you will finally reach the desired results.

You can fight with yourself, you can try to avoid the triggers, avoid social events and ignore when you are invited to business meals or stop visiting friends.

But when there is a trigger that generates a bodily or mental state that leads you to a fattening behaviour and you just give Copy / Paste over one link of this chain, you get:

– sleeping disorders,
– stress,
– decrease of immunity,
– decreased metabolism
– and increased percentages of body and visceral fa

+/- weight loss by dehydration and muscle mass loss.

If you just assume you want to lose weight, you’ll be pleased: the atrophied muscles temporarily fit into smaller size clothing.

Just that the smaller size clothing phase happens only until the army generated by your fat will take control of you by lowering your ability to perceive satiety and pleasure, and by sharpening your perception of the foods you like to such an extent that you’ll not be able to focus on anything but the need to eat.

If you really, really, really want to lose weight, you need to understand both how metabolism works and the external triggers that drives you to behave in a way that is not align with your body image goals.

Articolul The Copy/Paste Diet apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

In this article, I don’t just want to talk about Dukan diet, but about ketogenic diets with very low carb intake in general (taking into account that the ones promoted to be the most effective are those with a carb intake between 30-50g per day and with a moderate to low protein intake).

The meta-analyses of most studies show that even though they can have different results on the short term, different diets pretty much have the same results over the long term: such a metabolic inflexibility that can make even/ or especially someone ketogenic adapted to gain a lot of weight if they slip outside the diet.

Ketogenic diets rely on the assumption that if you take the carbs out of your diet, you lose weight. And, on the scale, you do.

But the main question you should ask yourself before starting is:

How long do you think you can keep a ketogenic diet by the book?

Because no matter how contradictory the studies results might be when it comes to ketogenic diets long term health consequences, and no matter the disputes between the pro- and the con- part’s arguments – even those on the pro part who understand what happens within the body after the ketogenic adaptation agree that this type of diet must be followed exactly as it is due to the fact that any mistake can make you as fat as you were/ fatter in no time (1).

Dukan diet, Atkins diet – or the new high fat low/ moderate protein and very low carb ketogenic diet – are amazingly effective for total body weight loss from day one: you literally see your weight disappearing, pound by pound.

But despite this extremely easy to monetize magic efficiency, on the inside you accelerate the mechanism that cause fat gain with every single pound lost on the scale because the fat is not completely burned, but moved from the fat tissue to your blood, your inner organs and your muscle.

I know for sure that you know – from the first moment you considered starting a ketogenic diet – that you will regain the lost weight if or when you’ll stop following it. Which: yes,  in the end happens with any diet if you fall off the wagon.

Maybe you don’t care about it now, maybe you just want to be slim for your 10 years reunion with your high school or college classmates. Or maybe you’re tired of counting calories or of following glycemic index charts that vary so much that you don’t know what to think anymore.(2)

You’re just fat and wish for a real solution: one on which you can actually see results in your mirror.

And, I also know that you’re going to stick your teeth into it to stick to this diet as long as you’ll can. But the weight regain you’ll see in the same mirror after you’ll fall off your ketogenic diet will not be generated by the fact that you reintroduced carb, but by metabolic consequences of the fact that you eliminated them in the first place.

To lose fat, you must take the fatty acids out of the fat tissue, transport them to the muscle cells, introduce them through the muscle’s membranes, introduce them through the mitochondria’s membranes, couple it with oxaloacetate and “burn” it inside the Krebs cycle.And we have two sources of oxaloacetate: carbs or amino acids – both low as intake in the ketogenic diet. Without oxaloacetate you don’t burn fat, you just take it out of the fat tissue and deposit it elsewhere in your body.(3)

This incomplete catabolism of fatty acids – that happens when you go too low in your quest against carbs and proteins:

• aggravates or generates insulin resistance,(4)
• stimulates muscles autophagy to supply the liver cells with proteins during the diet,(5)
• decreases the active muscle cell number and it increases the fat cells size and number by transforming pre-adipocytes into adipocytes.(6)

At first you’ll lose weight, then you’ll have this shell egg fragile body weight, and then you’ll see in the mirror what’s happening inside your body. Although you only gain weight after the ketogenic diet, the fat gain is generated during the diet.(7)

If you ever wondered “why can’t I lose weight?” or “how can I lose weight?” or ” how can I maintain the weight loss?” or other contemporaneous questions like this one, the answer is that insulin is like a bodyguard that blocks your access to your fat. But it is not the big fat bored bodyguard that spends he’s day doing nothing for his paycheck. Insulin is like this super-fit, agile, highly trained Bruce Lee – the employee you want to fire, after you’ve drained him with too much workload. Ketogenic diets puts this Bruce Lee out of work, giving you the craved access to your fat.

On the paper, if you take out the carbs, you can burn the fat because oxaloacetate can be made from proteins too (either directly or through the pyruvate way).

But there are 3 mains issues with this approach, issues that seeds fat gain from day 1 you start the Dukan diet:

1. You can gain fat from proteins also.

The human body cannot store proteins, but it can transform proteins in fat if you overeat them. You can store carbs as glycogen, you can store pretty much infinite amounts of fat, but you cannot store proteins.

After eating proteins, we use them:

• to repair what’s to repair
• to build up what’s to build up
• to secrete what’s to secrete
• to make some energy (if carbs or ketones are not around, some amino acids can directly enter the Krebs cycle without oxaloacetate help)
• to make ketones (other amino acids can be transformed into ketones to be used instead of proteins for energy) or
• to make fatty acids (while other amino acids will be transformed into pyruvate and acetyl-CoA, respectively into malonil-CoA, and then into fatty acids).(8)

This is how a hyper-proteic meal unbalanced by a moderate carb intake and regular physical exercise can also lead to weight gain through de novo lipogenesis from proteins. Proteins are the most important nutrients when it comes to weight loss, muscle maintainance or muscle  and performance gains. And despite the fact that protein sysntesis platous at about ± 30g protein intake/ meal, the protein intake can further impact total protein banace by cedreasing protein breakdown. But the protein intake per se is not enough.

Besides the fact that high fat ketogenic diets can generate leptin resistance directly and insulin resistance indirectly (by decreasing the sarcolemic expression of GLUT 4 in skeletal muscle cells), it is true that ketones can ensure the survival of most body cells.

And I wrote “most” because some human cells do not have mitochondria so they function only on anaerobe glycolysis (erythrocytes), and because the other human cells cannot use ketones for energy (hepatocytes). For erythrocytes, glucagon’s gluconeogenesis saves the day.  But gluconeogenesis costs ATP, so it does not start unless the blood sugar becomes too low or unless the protein intake is high but not too high.

And the “not too high” part can mainly be balanced by a regular, smart and intensive physical exercise.

Sedentariness and fat loss don’t coexist.

2. Dukan diet decreases weight only by dehydration.

The adaptive mechanism you use to survive ketogenic diets – gluconeogenesis – consumes ATP, which means it won’t happen if you start eating too little due to a “ketogenic” disgust of eating.(9)

Also, the muscle cells do not have glucagon receptors, so they won’t benefit from this mechanism even if you eat enough.

It is true that in the beginning, the ketogenic diets can decrease muscle’s insulin resistance due to the decrease carb intake. But, in time, it gets back up again for two simple reasons: proteins call back Bruce Lee, and glucagon will give him a raise to forgive you.

Even if you would completely take carbs out of your diet, the excessive intake of proteins stimulate both glucagon and insulin secretion. Moreover, glucagon per se stimulates insulin secretion.

And the new fatty acids made by de novo lipogenesis will compete for membrane access inside the muscle cells with any newly-made-glucose-by-liver-gluconeogenesis, increasing or generating insulin resistance if you did not have it before the diet (~20% of visibly “fat” people don’t have insulin resistance, and ~40% of currently “slim” people have it. And I wrote “visibly” cause in my practice I saw quite a few slim people with body fat percentages ranging from 35-40).

So:

• your skeletal muscle cells won’t be fed with the newly made glucose – becoming increasingly closed for glucose through a decrease muscles’ membrane expression of the GLUT4,(10)
• and their proteins will be literally used to feed the liver cells – which cannot feed on ketones because they don’t have the enzyme that can transform ketones back to acetyl-CoA  and introduce them into TCA to make energy (in Romanian is called “tioforaza,” but I don’t know its name in English).

3. Through insulin resistance and muscle autophagy, ketogenic diets can generate adipocyte hyperplazia.

The adipocytes’ size and number starts to increase – while you lose weight on the scale through water loss – because they received the “food” that should have been delivered to muscle cells.(11)

The weight loss you see on the scale is dehydration doubled by redistributing fat throughout your body and by increasing your fat cells number by transforming pre-adipocytes into adipocytes.

Image Source: Lippincott, Biochimie Ilustrata, P.C. Champe, R.A. Harvey, D.R. Ferrier

During the ketogenic diet you can mainly:

• take out the fat from the adipose tissue and ectopically deposit it in other areas of your body,(12)
• and increase the fat cells number.(13)

During ketogenic diets fat burn starts but mainly remains incomplete.(14)

Yes you’ll weigh less, yes you’ll wear smaller size clothes, but you will do it by “burning” your muscles not your fat. And, in time, you’ll start gaining more and more weight by eating less and less food because your ghrelin will stay low as you diet.(15)

The problem with Dukan diet, or with any ketogenic diet for that matter, is not if you will fall off, but when.

It’s like willingly hanging yourself off a cliff holding on to your will.

And you will not fall off due to a lack of will, but because from the day you have started this metabolic madness an entire army of hormones is fighting you to stop destroying yourself.

Ketones are symbols of starvation and ketogenesis is a metabolic red flag that calls to action this army of hormones to fight your destructive behavior.

But the steeply increased fatty acids level in your blood – either coming from the little lipolysis that took place when Bruce Lee gathered this army, or from the eaten food – will stimulate leptin (yes, the satiety hormone).

In English, after some time on the ketogenic diet you’ll feel sick to your stomach even when thinking about meat.

And because leptin acts also in the hippocampus, this disgust will be memorized deep inside your brain to try to prevent future ketogenic diets attempts.(16)

But too much leptin will deregulate your appetite to such an extent that you get to a point when you’ll only dream donuts while eating increasingly less ketogenic food or more processed “look alike carbs” ketogenic food.

No amount of will can pay in a single day the price of a pound of fat.

If you are a strong person, with too much will power for your wellbeing, this army of hormones will try to save you from:

• osteoporosis,(17)
• kidney stones,(18) and from
• other nephropathies,(19)

Or from other side effects long term ketogenic diets might have.

I do not want to talk about these side effects because people who start ketogenic diets think they have the luxury to postpone taking care of their health till after they lose weight. If you are one of these people, just remember that your insulin is like a metabolic Bruce Lee – it is far better to have him as a friend.

You’ll lose total body weight for sure on Dukan diet.

But you’ll do this by cannibalizing your muscles to feed your liver, by depositing fat inside your muscles, in your blood, or in your kidneys, and by increasing your fat cells size and number.

Before Dukan diet everyone knew you were fat.

After the diet, for a while, you’ll be the only one knowing it by living with your new fragile weight.

Then it will be your doctors turn to find out.

References

(1) Pagoto, Sherry L., and Bradley M. Appelhans. “A call for an end to the diet debates.” JAMA 310.7 (2013): 687-688.
(2) Wolever, T. M. “The glycemic index.” World review of nutrition and dietetics 62 (1989): 120-185.
(3) Unger, Roger H. “Minireview: weapons of lean body mass destruction: the role of ectopic lipids in the metabolic syndrome.” Endocrinology 144.12 (2003): 5159-5165.
(4) Yki-Järvinen, Hannele. “Ectopic fat accumulation: an important cause of insulin resistance in humans.” Journal of the Royal Society of Medicine 95.Suppl 42 (2002): 39.
(5) Kim, Kook Hwan, and Myung-Shik Lee. “Autophagy as a crosstalk mediator of metabolic organs in regulation of energy metabolism.” Reviews in Endocrine and Metabolic Disorders 15.1 (2014): 11-20.
(6) Ochner, Christopher N., et al. “Biological mechanisms that promote weight regain following weight loss in obese humans.” Physiology & behavior 120 (2013): 106-113.
(7) MacLean, Paul S., et al. “Biology’s response to dieting: the impetus for weight regain.” American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301.3 (2011): R581-R600.
(8) Grantham, James P., et al. “Modern diet and metabolic variance-a recipe for disaster?.” Nutrition journal 13.1 (2014): 15.
(9) Feinman, R.D.; Fine, E.J. Nonequilibrium thermodynamics and energy efficiency in weight loss diets. Theor. Biol. Med. Model. 2007, 4, doi:10.1186/1742-4682-4-27.
(10) Ellenbroek, Johanne H., et al. “Long-term ketogenic diet causes glucose intolerance and reduced β-and α-cell mass but no weight loss in mice.” American Journal of Physiology-Endocrinology and Metabolism 306.5 (2014): E552-E558.
(11) Koves, Timothy R., et al. “Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance.” Cell metabolism 7.1 (2008): 45-56.
(12) Garbow, Joel R., et al. “Hepatic steatosis, inflammation, and ER stress in mice maintained long term on a very low-carbohydrate ketogenic diet.” American Journal of Physiology-Gastrointestinal and Liver Physiology 300.6 (2011): G956-G967.
(13)Tchoukalova, Yourka D., et al. “Regional differences in cellular mechanisms of adipose tissue gain with overfeeding.” Proceedings of the National Academy of Sciences 107.42 (2010): 18226-18231.
(14) Koves, Timothy R., et al. “Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance.” Cell metabolism 7.1 (2008): 45-56.
(15) Arner, Erik, et al. “Adipocyte turnover: relevance to human adipose tissue morphology.” Diabetes 59.1 (2010): 105-109.
(16) Balietti, Marta, et al. “Ketogenic diets cause opposing changes in synaptic morphology in CA1 hippocampus and dentate gyrus of late-adult rats.” Rejuvenation research 11.3 (2008): 631-640.
(17) Hawkes, Colin Patrick, and Michael A. Levine. “Ketotic Hypercalcemia: A Case Series and Description of a Novel Entity.” The Journal of Clinical Endocrinology & Metabolism 99.5 (2014): 1531-1536.
(18) KIELB, STEPHANIE, et al. “Nephrolithiasis associated with the ketogenic diet.” The journal of Urology 164.2 (2000): 464-466.
(19) De Vries, Aiko PJ, et al. “Fatty kidney: emerging role of ectopic lipid in obesity-related renal disease.” The Lancet Diabetes & Endocrinology 2.5 (2014): 417-426.

Articolul Dukan Diet – the simplest way to gain fat apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.