Really! I saw with my own eyes how they cooked together during a Christmas TV show some potatoes with turkey meat that looked so absolutely marvellous that one could eat the TV.

Probably neither my mother nor Jamie’s mother had heard of Montignac or of the gastric juice diluting in the stomach if you drink water while you eat, still apparently some of us grew up with this combination sold as pure heresy by so many self-declared Google University graduates.

And I write “apparently some of us” because, although I think we all grew up with potatoes and meat, nowadays it looks like some started to argue their parents for not knowing basic things like the one stating potato should not be eaten together with meat. Their parents messed up the metabolism they are trying so hard to fix by finally consuming the protein and the carbohydrate separately and by drinking water at least half an hour after eating to not dilute the juice.

– What juice?

– One, that one, why do you need to ask?!

Digestion of potato starch begins in the mouth, under the action of salivary amylase, stops in the stomach and restarts in the small intestine, under the action of pancreatic amylase, no matter what other foods you eat at that meal.

Digestion of the fat from the butter and milk used to cook mashed potatoes begins in the stomach and mainly takes place in the small intestine, under the action of pancreatic lipase after being emulsified by bile salts, no matter what other foods you eat at that meal.

Digestion of meat proteins begins in the stomach and takes place in the small intestine under the action of pancreatic proteases, no matter what other foods you eat at that meal.

And no matter what you eat at that meal, the main thing that happens to food within the stomach is mechanical digestion because the stomach works just like a blender, mixing very well all the gastric content.

The idea that some things are digested earlier and others later, or that some things do not digest well because you have combined them with something can be a good subject for a glass of wine chat when you’re imagination runs low, but the stomach digestion result is gastric chyme – a homogeneous semi-liquid mixture of nutrients, less than 0.5 mm in diameter, which is gradually eliminated as small amounts through the pylorus canal in the small intestine.

The main role of the stomach is mechanical digestion.

Nothing rots or ferments in the stomach, because these two processes can only be performed by bacteria, and there are no bacteria in the stomach.

Or, if you painfully feel that in your own and personal stomach are some bacteria, you are warmly invited to the gastroenterologist for a Helicobacter pylori test and proper treatment.

And for God’s sake, if one could dilute the gastric juice by drinking water while eating, no one would even need omeprazole.

And if you’re experiencing bloating after eating, avoid eating too much and please don’t nibble in between meals. No fruit snacks, no coffee, gum or other nibbling, because such behaviour disrupts satiety hormones secretion, influencing metabolism and digestive motility.

The glucose, fructose, galactose, fatty acids and amino acids are the result of the intestinal – not gastric –digestion. And intestinal digestion is the same for all pancreas owners.

– So, did my mother and Jamie’s mother ate potatoes and meat at the same meal because they knew they have a pancreas = internal organ secreting amylase, lipase, and proteases (enzymes perfectly capable to digest any food combination – and even the pancreas itself in case of an acute pancreatitis for example)?

– Nope, I do not think they knew all this.

They probably ate potatoes and meat at the same meal and fed as with such delicious foods because, after such a meals we all felt good.

P.S. To all pseudo-nutritionists out there or to people who believe that the entire world’s gastronomy is completely fucked up I cordially recommend reading Illustrated Biochemistry. It helps weed out the non-sense.

Articolul Potatoes + meat = LOVE apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

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.

I will explain why you keep failing of your diet.

Picture this:

You hold a donut in your hand and you die to eat it. It smells so good!

You feel frustration building in your mind.

You don’t want to eat it.

You should not eat it.

The past week you tried so hard to follow your diet and you even went to gym as planned.

The mere thought of wanting to eat this doughnut scratches your brains out.

And here is why you’ll probably allow yourself to eat it:

1. You rely on diets.

Each time you fall of your diet you promise to start again tomorrow – the diet, the sports or any other invented dieting f. word so that you can peacefully eat this donut.

The heck with it, this is just a donut…

But to even mental this thought you rely on diets.

Diets are here to save the day when you become emotionally hijacked, and you asume starting one again as the price you’ll pay tomorrow for satisfying your crave today.

But this is why you’ll actually going to eat this donut:

2. Your amygdala (survival nervous center) is overstimulated by the stress in your life. 

Amygdala is essential for decoding emotions, especially those recognized by the hippocampus as threats.

It is highly connected with all autonomic structures meant to keep us alive.

And one of the way it adapts us to stress is by commanding beta-endorphins’ secretion – natural anestesics secreted by our neurons to dull pain. Sadly though, the side effect is a decreased ability to perceive pleasure.

3. Nucleus accumbens (pleasure nervous center) is anesthetized both by stress released beta-endorphins and by intermittent access to dopamine triggers.

The reward value of foods you refuse to eat despite wanting them so bad increases as your ability to perceive pleasure decreases with each overeating episode.

And we compensate a decreased ability to perceive pleasure with an increased consumption of the very food we deny ourselves.

4. Papez circuit (the main mechanism that connects emotional expression with memory) expects you to feel the same amount of pleasure you felt when you ate other donuts. 

Because of this circuit, each time you will eat foods that impacts your nucleus accumbens (in English: “that you like”) you will unconsciously compare the pleasure you feel today with the pleasure you once felt when eating the same foods.

But because of stress and intermittent access to those foods, your ability to perceive pleasure will be naturally diminished.

Thus neurophysiologically, the more you will resist the stronger the urge to it that donut and the more donuts you will eat.

And yes you are right: if you just eat this donut you might get a bit fatter simply because anything we eat regardless of physiological hunger – either the healthiest fruit or the unhealthiest donut – impacts our metabolism and might deregulate appetite hormones secretion indirectly (through deregulating incretins) or directly through insulin resistance (which is among the main obesity causes, along with dysbiosis, dyslipidemia, and leptin resistance).

Thus, if resisting to eat “fattening” foods is potentially more fattening than actually eating them, how can you eat them without gaining fat?

1. To eat anything you want you must first associate eating with physiological hunger.

And to be able to wait enough to only eat when hungry you must hold the promise that you’ll satisfy your cravings when hungry.

It is said that we make our choices either out of fear, or out of trust.

And while rulled by stress and deprivation your choice comes from your fear hyjacked amygdala, not by your conscious brain.

Under stress, the difference between eating what you want when hungry and eating what you want regardless of hunger being biologically similar with the difference between smoothly stopping your car at the red light or abruptly stopping it into a roadside tree.

2. No matter how good that food is, you must respect satiety. 

And you can’t really perceive satiety if your mind is on Facebook.

To avoid weight gain you must respect satiety, and to perceive satiety clues you must savour your food without doing other things while eating.

3. Even if it’s the best donut ever and you just want to eat it, it should come after eating proteins and a salad.

Yes I know this kind’av ruins the whole concept of rebellious eating, but this is the whole point: overeating comes as a mutiny. 

So learn to transform cravings into everyday pleasures by taking rebellion out of satisfying them.

The fibers in that salad will do some damage control in your gut, while the proteins will do some damage control in your blood.

And yes you read that right: to eat donuts or cake or brownies or whatever you like, you should combine them with enough proteins. And if you are a fan of separatists diets  and eat proteins at separate meals than carbohydrates – because supposedly proteins take X time and Y enzymes to digest and carbs Z and Y – then simply take a piece of steak, some baked potato, a peach or an apple, and a tomato salad and put them in a blender.

Press the button, wait, and then look at the perfect puree – perfectly similar with the one blended by your very stomach that retropulsivly pushes away from your pilor back to more blending any morsel of food bigger than 2 mm.

Do you actually think that your pancreas enzymes will have any issue digesting any part of that puree?

Or that the pancreatic enzymes will say – Geez, this is a carb, I must first digest proteins?

Pancreas secretes peptidases for proteins barely touched by gastric peptidases, amylases for uncooked amidin – also barely touched until your gut because salivary amylase only begins carbohydrates digestion – and lipases for fats that, unless you’re a newborn, weren’t touched either until your gut.

And pancreatic enzymes are so efficient that they can even “digest” the pancreas cells (in pathologic situations, of course).

This confusion regarding sepparating carbohydrates and proteins within the same meal or eating fruits between meals  is completely missing from your pancreas able to properly digest mixed meals and to skyrocket insulin secretion when fed only with carbs for some magical unbiological reasons.

We all know thin people that can eat huge amounts of foods without gaining one gram of fat, so maybe the concept of eating “more” is less fattenting than eating “wrong”.

Each time you just have a snack (which actually is just another fancy way of sneaking in some food in the absence of hunger) you potentially gain more fat than when eating a complete meal when hungry.

Let me write this again:

When eating less without hunger you gain more weight than when eating more when hungry.

Pretty unfair right?

And the bloating blamed on eating fruits with meals does not happen in your stomach but in your colon and it does not happen because you ate fruits with your meal or because fruits need other digestion times or enzymes for digestion than proteins food sources or other vegetables.

Bloating has a million causes: maybe you eat too much raw food, maybe this is the way you somatize stress because you overstimulated amygdala impacted your pilor and intestinal motility in such a way that too much undigested food particles get to your colon.

Or maybe you have an irritable bowel syndrome, also masivly aggravated by stress.

As long as you do not understand how your body and mind play you obese, you’ll be a leaf in the weight loss industry’s wind.

This confusion is the basis of this industry profits.

Today 1.5 billion people are overweight, 1 billion are chronic dieters and 0.5 billion are obese. And the weight loss industry expects these numbers to double.

Today 40 million children are obese and the weight loss industry expects this number to soon grow to 70 million.

There is no confusion, we know digestive system physiology and eating behavior neurophysiology since long ago.

This is about money: according to an analysis made by businesswire.com – Weight Management Market by Services, Supplements, Diet, Equipment and Devices: Global Analysis and Forecast 2007-2015 – the weight loss industry profits was 385.1 billion dolars in 2010 and they expect a 650.9 billion dolars in 2015. 

No confusion, just money.

Articolul Why you keep falling of your diet? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

It is much or less accepted because hunger is associated with dieting.

It is what scares people people when even considering to start a diet to lose their increasing weight accumulated on body parts they wish they could somehow hide.

It is the price dieters feel they pay in exchange for a barbeque with friends.

It is what makes dieters feel virtous on an extremely restrictive diet.

And yes: it is purely biologic.

But hunger biology is connected with diets deregulating the secretion of a hormone secreted by the very fat tissue they’re trying to get rid of: leptin.

This fat tissue is not the inactive hassle most think they carry along for nothing, but a tissue with extremely important implications in most aspects related to health: cardiovascular function, immunity, reproduction, memory, general behavior and eating behavior – just to name a few.

There are many hormones involved in apetite control, but leptin is one of the most important links between the fat tissue and being hungry on a diet. And this can be pretty annowing to understand because leptin is actually a satiety hormone – and overweight and obese people have more leptin than thin people (who actually have more ghrelin – the appetite hormone).

Ghrelin is secreted by the stomach and duodenum, and through blood it reaches the hunger nervous centru in hypothalamus and commands you to eat. Because of this tiny effect, people trying to lose weight would like ghrelin vanished from the face of the earth – and sadly they get their wish come true as they actually secrete far less ghrelin than they would actually need to have a healthy appetite.

On the other hand, leptin – the satiety hormone secreted by the fat tissue – reaches the satiety nervous center in the hypothalamus and commands you to stop eating. This happens even in people who never felt satiety in their life, the only difference between people with or without a disturbed appetite being that the hypothalamus of those with the disturbed one is deaf to leptin’s commands (leptin resistance).

These people’s increased fat tissue secrete more and more leptin which sadly does not translate into more and more satiety, but into more and more loss of satiety with each episode of eating past satiation. And losing this satiety clue is not the only consequence.

Leptin resistance directly cause/ or it aggravates insulin resistance = the very reason you feel hungry when going on diets that rigidly set rules about when and how much to eat, rules that usually are completely dissociated from your physiological hunger and satiety sensations.

To paint this simply, one insulin facilitates the glucose entrance in the muscle and adipose tissues, blood sugar goes down and you get hungry again. But a body flowded with ton of insulin literaly shuts down glucose entrance in these tissues (at first in the muscle tissue, and if you insist also in the adipose tissue – which is a sad reality we can passed down to children born from parents with adipose tissue isulin resistance decribed in chapter 5 of my second book: Nutrition Guide for Mums).

During hyperinsulinemia, the skeletal muscle starves despite eating.

The more you decrease your insulin sensitivity, the more you:

• decrease your skeletal muscle, thus your metabolism,
• increase your body fat percentage,
• deregulate your appetite =
  • paradoxal hunger very soon after eating
  • incontrolable cravings for sweet and fatty foods – cravings that once satisfied increase leptin resistance further and the cycle starts back again growing in a spiral of diets, hunger, cravings and binges extremely hard to get out of.

The first signes of insulin resistance – physical signs like hirsutism, hyperkeratosis on hands and feets, dry elbows or knees, or cracked heels – are rarely recognized as a sign of metabolic disorders by untrained eyes.

If ignored, they progress to decreased fertility, low immunity, dyslipidemia, increased aggressivity, decreased ability to cope with stress, decreased adaptability or impaired memory – all sad consequnces of refusing to respect satiety signals sent to your mind by your older, wiser hypothalamus.

As I explained above, despite what most would expect, overweight and obese people secrete more satiety hormones and less appetite hormones than thin people.

But once disrespected, satiety becomes harder and harder to hear.

So stop eating when you feel satiety no matter how little you ate, or how good the food is.

Disrespecting satiety is much more expensive than most afford to pay because the price ain’t money, the price is health.

Articolul Why you feel hungry when you are on a diet? 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.

– What is the most important part of your car?  

You may be wondering what your car has to do with my nutrition, but if you play in.

Let me start: the experience with the people I work with everyday has shown me that nutrition is much easier to understand when comparing learning to drive your car to learning to drive your body.

Most of the ideas we still have today about weight loss are on the market for about 100 years: calories, glycemic index, miraculous food combinations, ketogenic diets, dehydration, starvation. And for 100 years the world is getting… bigger and bigger.

So maybe we need to understand the mechanisms behind the fattening and not blindly pursue other people’s solutions, frequently efficient only on the short run.

Now it’s your turn:

– So? What is the most important part of your car?

Most of the drivers I asked this question said the engine. If you have the same opinion, please take a state-of-the-art engine and drive it home in a car without a windshield.

A personal example of this was when I left my son in the car for a few minutes and he inserted all the coins he found in the door of my car into the CD part of the radio… Nothing compared to a long road without radio, news, discussions or even some ads. Trust me, on a long drive home with a bored child in the car, most of us would even miss the radio.

Returning to nutrition, is absolutely essential to know your goal:

• weight loss
• physical performance
• increased immunity
• improved fertility
• vitality
• improved health

Power is the engine. It’s just that, unfortunately, there are plenty of other non-food factors that can keep you from getting where you want to be, stress and sleep being on the top of the list.

In my workshops and my books I present in detail the mechanisms by which stress affects us metabolically, psychologically and behaviorally, as well as some of the solutions in find efficient for metabolic self-control during stress. In this article I want to explain a little bit about sleep.

If your sleep is not good, it is as if you want to go to work with your handbrake pulled: you might ruin the engine, you’ll get nowhere and you will get angry.

– And what does quality sleep mean?

Most of the people I asked (and I often ask) think that “quality sleep” actually means a quantity: if you sleep 6-8 hours, then it’s ok.

– But what do you do if you sleep 9 hours and still wake up tired?

– Or 10?

Biologically, the same thing happens in your body just like when you only slept for 3 hours because you turned on all your sides until you fell asleep and you woke up 5 times over night.

1. Metabolic: You will compensate the lack of effective sleep with increased cortisol secretion because you lose REM sleep – ie the most restful part of the sleep cycle – during times of high stressful events. And cortisol fattens like hell.
2. Psychological: You will be more irritable, more impulsive, harder to get along with others (because, due to fatigue, you have decreased empathy and assertiveness). And studies show that irritability increases the secretion of hydrochloric acid and ghrelin – a hunger hormone secreted by your stomach as a compensatory mechanism to keep you off a gastric ulcer. Depending on their type of personality, some people get fatter during stressful times, some get ulcers.
3. Behavioural: You will do too many of the activities you do not need and too few of the ones that do you do need (because, due to lack of quality sleep, you will have the tendency to either do a thousand things at a time or to not care of everything. And also due to increasing fatigue you will probably skip sports, which will paradoxically make you even more tired than you already are).

And, also depending on the personality type, you might completely ignore any common sense nutrition – the most important part of your “car” – and you might try to survive on smocking, caffeine, HFCS and TF (in English: coffee, soft drinks and fast food) to make your day more tolerable.

The absolute best nutrition plan is trashed down the toilet by a low quality sleep, so – if you recognize yourself in the pattern above – please read the “Stress” part of „The Old Chocolate Diet“.

Articolul What is the most important part of your car? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

1. Metabolic effects of weight loss thermotherapy

The basic concept behind the apparent efficacy of weight loss thermotherapy is the physiological adaptation to either cold or heat. So implicitly, weight loss thermotherapy contains procedures that expose the body to abrupt temperature changes.

Besides the apparent fast weight loss, this type of procedures have the following side effects:

1.1. Appetite hormones deregulation

From the neurophysiological point of view, the first problem is that the nervous centers responsible for thermic regulation are located in the hypothalamus, very close to the nervous centers of hunger and satiety.

Cold is perceived near the hunger centre, and  heat next to the satiety one.

For this reason, people who still behave physiologically (such as small children, adults who are not on a diet or people who do not eat compulsively) have a natural tendency to eat more in the winter and less in the summer.

But this natural tendency can be intensified by the abrupt temperature changes induced by weight loss thermotherapy procedures. Thus, even if it theoretically stimulates brown fat tissue, “cold” thermotherapy ( and the many exotically-weird types of wrapping) indirectly stimulates NPY and AgRP secretory neurons in the arcuate nucleus of the hypothalamus – thus increasing the perception of hunger.

Such procedures do not increase metabolism because heat generation in adults is generated by muscle contraction, not by mitochondrial activity in brown adipocytes (1).

On the other hand, “hot” thermotherapy (classical sauna or various new types of sauna “in the weight loss capsule”) indirectly stimulates POMC and CART secreting neurons from the same hypothalamic nucleus, generating satiety and lowering metabolism in order not to produces even more heat through muscle contraction.

However, these indirect stimuli – either for the hunger or for the satiety nervous centres – generate sensations that may not coincide with the blood glucose levels, thus these fakery hunger or satiety are associated with a disturbed appetite (2).

This paves the foundation for leptin resistance (3,4). Thus, by regularly practicing weight loss thermotherapy procedures you risk perceiving less and less satiety, while becoming quasi-continuously hungry (5).

1.2. Metabolic decrease

The second problem, apart from the disturbed appetite, is that the weight loss generated by these procedures is only apparent, the decrease in total weight being obtained either by dehydration or by muscle catabolism (6).

The easy to maintain long-term weight loss involves lowering the percentage of fat, not dehydration or the decreasing of the percentage of active striated muscle mass.

Thermotherapy procedures can lead to some detoxification through sweat or some muscle contraction through tremor, not to fat loss.

Replacing regular physical exercise and proper nutrition with weight loss thermotherapy and crash diets leads to dyslipidemia and insulin resistance, not to fat loss:

• dyslipidemia aggravates leptin resistance (7),
• leptin stimulates insulin secretion
• and hyperinsulinism decreases the percentage of active muscle mass by blocking glucose entrance through these muscles’ membrane – which is gradually manifested by gaining weight while eating less and less (8).

1.3. Insulin resistance

The third problem – besides disturbed appetite and metabolic decrease though dehydration and muscle catabolism – is the potential under-eating that a person who wants to lose weight quickly can get while on weight loss thermotherapy.

In the case of cold thermotherapy, the feeling of hunger increases due to the indirect stimulation of the cold perception center, amplifying the physical hunger generated throughout the day by the physiological blood glucose decrease.

If starvation is part of the prescribed diet, and the person who does the weight loss thermotherapy does not eat, despite the perception of gastric hunger (9), lipolysis is initiated in the adipose tissue with the delivery of fatty acids to the muscle tissue for energy.

But if this person does not practice regular sports, the percentage of active muscle mass will be low and the amount of glycogen stored within these sedentary cells will be low as well. This is physiologically aggravated as the person is more sedentary and older  and it is called sarcopenic obesity (10).

Thus, theAcetyl-Co derived from the beta-oxidation of the fat delivered to these muscles cannot be introduced into the Krebs cycle due to the fact that these cells contain insufficient oxaloacetate.

Consequently, either muscle protein catabolism occurs to make the oxaloacetate , or dyslipidemia occurs with elevated blood LDL-cholesterol levels and triglycerides, eventually doubled by depositing some of these triglycerides inside the liver or inside the muscle cell (similar to that of an Argentinian beef steak) (11).

In order to obtain long-term fat loss, we have to practice sports regularly to avoid leptin resistance, insulin resistance and dyslipidemia and to avoid excessive or inadequate carbohydrate intake.

And in the case of hot electrotherapy procedures applied without proper nutrition, all that can be lost is water ± your metabolism down the toilet (12).

Lipolysis is not activated because it is too hot, but vasodilatation will lead to dehydration by increased water loss. Dehydration can overstimulate the satiety nervous centre (13).

As with dietary starvation in people who practice cold thermotherapy procedures, people who practice hot thermotherapy procedures can involuntarily eat too little because of the over-stimulated satiety centre.

Insulin resistance does not occur only when overeating,  but also when undereating – being a protective mechanism meant to keep the internal organs and the brain alive when nutrients availability is too low.

And, just as with hot thermotherapy procedures, fat loss stops due to insulin resistance, together with a gradual increase in fat deposition inside muscle, blood, liver, and even kidneys (14).

Of course, dehydration has an absolutely immediate weight loss effect by lowering the total body weight.

Just that the weight loss obtained through thermotherapy is associated with metabolic decrease, while that obtained through regular physical exercises (especially anaerobic) and proper nutrition is associated with an improved metabolism (15).

2. Metabolic effects of weight loss electrotherapy

Unlike weight loss thermotherapy, there is a little more science behind the combination of electrotherapy and fat loss. It’s just that electrotherapy is aimed at physical therapy for people with disabilities, not for weight loss. And even in these people, electrotherapy is just an adjuvant to the overall recovery treatment, the basis being medical physical exercise.

2.1. Metabolic effects of cavitation by ultrasound

One of the most expensive passive-non-invasive weight loss procedures is ultrasound cavitation.

Ultrasounds are extremely powerful waves – very useful in physical therapy – that are able to break adipocytes and eliminate the triglycerides stored whithin them.

But as with dyslipidemia obtained as a consequence of thermotherapy, moving fat from the fat tissue into the blood generates leptin resistance (generating decreased satiety and increased food cravings) and insulin resistance (generating decreased metabolism that will get you fattened while eating less and less ).

The difference is that in the case of cavitation dyslipidemia is much more pronounced, and leptin disorder can have serious health implications long-term.

Thus, since leptin does not only regulate satiety but also immunity, fertility, osteogenesis, cellular apoptosis and memory, the regular occurrence of massive dyslipidemia produced by repeated cavitation procedures increases the risk of:

• Weight gain ⁽¹⁶⁾
• Polycystic ovary and anovulatory infertility ⁽¹⁷⁾
• Osteoporosis ⁽¹⁸⁾
• Cancer (especially estrogenic ones) ⁽¹⁹⁾
• Alzheimer ⁽²⁰⁾

And, of course, because of the increased amount of fat that floods the striated muscle cells, insulin resistance also occurs alongside the consequent metabolic decline, adding liver or kidney steatosis (21, 22), cardiovascular disease (23), and type 2 diabetes (24) to the picture of the risks of such abrupt dyslipidemia as the one caused by cavitation.

Unfortunately for your long-term health and body image, on the outside of your body the short term effect is sudden weight loss, and the long term side effects are not immediately visible.

2. 2. Metabolic effects of muscle electrostimulation

A cheaper and less harmful form of weight loss electrotherapy is muscle stimulation.

Also coming from physical therapy, electrostimulation is a passive form of muscle contraction, designed to help atrophic or paralysed muscles gain back their former functions. Muscle electrostimulation mimics resistance exercise, generating an anaerobic metabolic adaptation.

Just that, if 0 represents the force of a paralyzed muscle and 5 represents the force of a healthy muscle, electrotherapy without physical therapy cannot increase muscle force over 2 (a force that is not enough to perform anti-gravitational movements) (25).

Muscle electrostimulation is just an adjuvant to physical therapy, medical physical exercise being the basis. So even people with disabilities have to move or to be moved in order to increase strength and muscle tone.

Moreover, anabolism generates nutrient anabolism, not nutrient catabolism.

Anaerobic sports may increase the percentage of active striated muscle mass, increasing metabolism (mainly by increasing the energy consumed per 24 hours for tonic muscle contraction) (26).

Fat loss is achieved by practicing aerobic exercise (cardio type) with a sufficiently high intensity (or interval training – HIIT – the most effective form of physical exercise for weight loss) (27).

So, if in the weight loss equation (= healthy eating + cardio + anaerobic) we replace only the anaerobic exercise part with muscle electrostimulation, healthy eating and proper cardio should still be done regularly to actually lose fat (28).

Weight loss electrostimulation per se – either in the absence of aerobic exercise, either in the presence of starvation diets or in the presence of continuously mindless eating, leads to fat gain, not to fat loss even while the total body weight temporarily decreases (29,30).

Conclusion

Healthy weight loss is fat loss, optimally paralleled with increased active muscle mass that will help you easily maintain your hard earned results long-term.

Fast weight loss gimmicks are fattening in the long run.

Quoted studies

(1) Ravussin, Yann et al. “Effect of intermittent cold exposure on brown fat activation, obesity, and energy homeostasis in mice.” PloS one 9.1 (2014): e85876.

(2) Eccles, R. et al. “Cold pleasure. Why we like ice drinks, ice-lollies and ice cream.” Appetite 71 (2013): 357-360.

(3) Crujeiras, Ana B. et al. “Weight regain after a diet-induced loss is predicted by higher baseline leptin and lower ghrelin plasma levels.” Journal of Clinical Endocrinology & Metabolism 95.11 (2010): 5037-5044.

(4) Schwartz, Michael W. et al. “Specificity of leptin action on elevated blood glucose levels and hypothalamic neuropeptide Y gene expression in ob/ob mice.” Diabetes 45.4 (1996): 531-535.

(5) Münzberg, H. et al. “Leptin receptor action and mechanisms of leptin resistance.” Cellular and Molecular Life Sciences 62.6 (2005): 642-652.

(6) Steen, Suzanne Nelson, Robert A. Oppliger, and Kelly D. Brownell. “Metabolic effects of repeated weight loss and regain in adolescent wrestlers.” Jama 260.1 (1988): 47-50.

(7) Kaur, Kawaljit, Sharda Sidhu, and Gurcharan Kaur. “Association between leptin and lipid profile among women.” Annual Review & Research in Biology 4.5 (2014).

(8) Yoshino, Jun, et al. “Diurnal Variation in Insulin Sensitivity of Glucose Metabolism Is Associated With Diurnal Variations in Whole-Body and Cellular Fatty Acid Metabolism in Metabolically Normal Women.” The Journal of Clinical Endocrinology & Metabolism (2014).

(9) Ciampolini, Mario et al. “Sustained self-regulation of energy intake: Initial hunger is associated with low pre-meal blood glucose and prevents energy accumulation.” Manuscript submitted for publication March 2009 (2008).

(10) Roubenoff, Ronenn. “Sarcopenic obesity: the confluence of two epidemics.” Obesity research 12.6 (2004): 887-888.

(11) Pan, D.A. et al. Skeletal muscle triglyceride levels are inversely related to insulin action. Diabetes, 1997, 46.6: 983-988.

(12) Cheuvront, Samuel N. et al. Water-deficit equation: systematic analysis and improvement. The American journal of clinical nutrition, 2013, 97.1: 79-85.

(13) Hamilton, C.L. Interactions of food intake and temperature regulation in the rat. Journal of comparative and physiological psychology, 1963, 56.3: 476.

(14) Montani, Jean-Pierre et al. “Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases.” International Journal of Obesity 28 (2004): S58-S65.

(15) Holloszy, John O. Exercise-induced increase in muscle insulin sensitivity. Journal of Applied Physiology, 2005, 99.1: 338-343.

(16) Torres‐Andrade, Rodrigo et al. “The increase in body weight induced by lack of methyl CpG binding protein‐2 is associated with altered leptin signalling in the hypothalamus.” Experimental physiology (2014).

(17) Messinis, Ioannis E. et al. “Polycystic ovaries and obesity.” Best Practice & Research Clinical Obstetrics & Gynaecology (2014).

(18) Upadhyay, Jagriti, Olivia M. Farr, and Christos S. Mantzoros. “The role of leptin in regulating bone metabolism.” Metabolism (2014).

(19) Pan, Haitao, Jiao Guo, and Zhengquan Su. “Advances in understanding the interrelations between leptin resistance and obesity.” Physiology & behavior 130 (2014): 157-169.

(20) Bonda, David J. et al. “Dysregulation of leptin signaling in Alzheimer disease: evidence for neuronal leptin resistance.” Journal of neurochemistry 128.1 (2014): 162-172.

(21) Birkenfeld, Andreas L., and Gerald I. Shulman. “Nonalcoholic fatty liver disease, hepatic insulin resistance, and type 2 diabetes.” Hepatology 59.2 (2014): 713-723.

(22) 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.

(23) Shulman, Gerald I. “Ectopic Fat in Insulin Resistance, Dyslipidemia, and Cardiometabolic Disease.” New England Journal of Medicine 371.12 (2014): 1131-1141.

(24) Gastaldelli, Amalia. Role of beta-cell dysfunction, ectopic fat accumulation and insulin resistance in the pathogenesis of type 2 diabetes mellitus. Diabetes research and clinical practice 93 (2011): S60-S65.

(25) Doucet, Barbara M., Lam, Amy, Griffin, Lisa. Neuromuscular electrical stimulation for skeletal muscle function. The Yale journal of biology and medicine, 2012, 85.2: 201.

(26) Hunter, Gary R. et al. Resistance training increases total energy expenditure and free-living physical activity in older adults. Journal of Applied Physiology 89.3 (2000): 977-984.

(27) Shiraev, Tim, and Gabriella Barclay. Evidence based exercise: Clinical benefits of high intensity interval training. Australian family physician 41.12 (2012): 960.

(28) Watanabe, Kohei, Yoshiki Taniguchi, and Toshio Moritani. Metabolic and cardiovascular responses during voluntary pedaling exercise with electrical muscle stimulation. European journal of applied physiology (2014): 1-7.

(29) Carpenter, Catherine L. et al. Body Fat and Body-Mass Index among a Multiethnic Sample of College-Age Men and Women. Journal of obesity, 2013, 2013.

(30) Mauriège, P. et al. Weight loss and regain in obese individuals: A link with adipose tissue metabolism indices?. Journal of physiology and biochemistry, 2013, 1-9.

Articolul Fast weight loss gimmicks 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.

I’ll explain Top 3 factors that contribute to weight gain during holiday.

First of all, I would like to point out that yes, you have read correctly: there are some factors that make you gain weight on holiday, not the food itself.

And yes, I know that chocolate has saturated fats and that pizza or Sicilian pasta have a glycemic index as high as the Trajan’s Column. Still, the bio avocado fattens as much as the most delicious tart if you eat it mindlessly.

So let me explain to you how the conjuncture factors – and not the food itself – fatten you every time, whether it is an ultra all inclusive holiday in Antalya, a city break in Rome or a Christmas in Vienna.

Then I’ll introduce 3 effective solutions that, when properly applied every day, prevent fattening on holiday because it solves these 3 factors just before you actually go on holiday.

Now, before I begin, I would like to mention that if you are 30 years old, you have a lot of abdominal fat, you work from morning till night, you eat all kinds of nonsense food and you are on the verge of depression, probably by applying these 3 solutions, your life and body image will only begin to improve if you’ll start using the information below.

Your metabolism is low, you probably have insulin resistance, disturbed appetite, and dopaminergic receptors in free fall.

It happens.

But the only difference between you and better you is YOU.

So, if you do not apply these 3 solutions at least now, that you are home, without a world of culinary temptations, then we are wasting time together.

And probably this article will not help you because the unapplied information has zero value.

But if you’re tired of keeping infinite diets and then getting more weight with each holiday, then apply the solutions every day for 21 days (yes, just as you know it takes you to form a new reflex). You’ll be delighted with the result!

So, here are the main factors that make you gain weight on holiday:

1. diversity
2. uncertainty
3. legitimacy

Most of us are overcome when we see a sea of food, which looks beautiful, fresh and smells heavenly. It is absolutely normal! As normal as the fact that most men marry beautiful women dressed in white.

Solution no. 1 so you do not get fat on holiday is: THE MOTHER-IN-LAW.

Yeah, you read correctly – and I do not ask you to take her with you on the holiday, but to behave as if you were the mother of one of those men who had entered the blind week, a real mother-in-law, with super airs and whims.

Basically, before you eat anything, you have to choose 2-3 foods you would give an absolute 10 out of 10 for wearing, showing and make-up. Maximum artistic impression!

In order not to get fat on holiday or on Christmas or visiting or elsewhere you’ll face food mountains, you have to have super airs and whims, and act more pretentious than a mother-in-law.

So choose only those dishes you really like and enjoy each piece with the greatest excitement, without fear or regret.

Solution no. 2 so that you do not get fat on holiday is: YOUR RIGHT FIST.

Most girls’ fathers have two fears:

1. That their girl will find someone and get married.
2. That their girl will not find someone and get married.

So is eating on holiday:

1. what do you do if the food is delicious?
2. what do you do if the food is not delicious?

No matter how good or bad is food on holiday, so as not to get fat on that holiday, you have to face this dilemma with determination.

So, you apply the mother-in-law method and choose 2-3 of the best dishes available, savour piece by piece and promise to eat at the next table other 2-3 dishes of the ones that tempted you.

Seriously: 2-3, not more, as your stomach is not a car trunk. If you want to not gain weight during the holiday, the food you put in there should not push your liver for more room inside your abdomen.

Your fasting stomach has ~ the size of the right fist and. So, to feel the optimal moment of satiety, no meal should exceed 2-3 portions, each of the size of your right fist.

Solution no. 3 so that you do not get fat on holiday is: YOUR HUNGER SENSATION.

It is your right to to eat the most delicious meals.

It is perfectly legitimate!

I do it when I’m not on vacation, absolutely every day.

Just that nibbling mindlessly on this or that when you are not hungry gets you fattened on whatever you eat, be it healthy nuts or fried potato chips.

It does not matter how little calories you consume, what glycemic index, what glycemic load or how you combine the foods. If you are not hungry and nibble: bye, bye silhouette.

You can perceive hunger at the head of the chest, with the same degree of intensity as pee feeling, that is:

• 0 if you do not need to eat,
• 1 if you feel like eating, but you can still wait, and
• 2 if you are just as hungry how hard are you to pee.

So, to not to get fat on your lovely holiday:

1. be pretentious as a mother-in-law
2. think like bride’s father and
3. go to the bathroom before you wet your pants.

1. eat only foods that you’d grade a 10 out of 10
2. limit yourself to 2-3 dishes, each of the size of your right fist,
3. wait for you to get hungry before you eat anything.

Applying these 3 solutions, you will not gain weight in any holiday in your life, but you can even slim while you are on holiday. All you have to do is apply them consistently.

To  our health!

Articolul Top 3 factors that contribute to holiday weight gain & what to do about them apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Now seriously: which foods are fattening and which ones are not fattening?! 

Women usually do not ask, they think they already know and go on the principle that they are drinking beer today and dieting tomorrow. Or Monday. 

Still, the question remains: does the beer gain weight or not?

Leaving aside simplistic assumptions about calories or glycemic indices calculated on other bellies than yours, let’s see together what happens to beer after it passes through the mouth.

There are probably a lot of beer recipes, but they all contain the same main ingredients: water, yeast, malt and hops, with a maximum of 5-7% alcohol.

• Many types of water, more or less mineral or carbonated, are used, but almost all beer has the same ~ 90% water content.
• There are hundreds of kinds of beer yeast, but they are all produced by the same fungus, Saccharomyces cerevisiae.
• The malt is made of more or less roasted barley, but with the same initial content of ~ 70% starch.
• And hops is the natural preservative that gives the same bitter taste that real fans are looking for in every glass of cold beer.

Of course, I talk about serious beers – untamed neither with “identical natural” flavors, nor with artificial sweeteners, nor with HFCS (high fructose corn syrup), beers for masculine men, not for women on the lemonade diet. 

So, if we put aside water, yeast and hops –which, although good, in themselves, do not bring anything from which the body can make fat – the only nutritional intake from beer that actually can make you fat is the malt’s starch that is mostly transformed by Saccharomyces cerevisiae into alcohol. 

So, the legitimate question would be not “if the beer makes us gain weight”, but “if alcohol gets fat”, because a bottle or can of 500 ml of beer contains on average as much alcohol as a glass of 200 ml of dry wine (to compare serious beers with serious wine).

Before we talk about the ability of alcohol itself to increase or not the percentage of body fat, I would also like to mention the impact of beers with lower or no alcohol content. Such beers contain “fried” starch – that is attackable by salivary amylase (assuming, of course, that they did not add any other “sugars”).

However, because we do not chew beer – the impact of salivary amylase is minimal, having a time of action equal to the actual time the beer spent in the mouth –, from the contained starch can be obtained only some maltose and malto-oligosaccharides.

In the stomach, salivary amylase is inactivated when the pH falls below 4, and in the 5-10 minutes when the beer is there, neither maltose nor malto-oligogazaride have any digestion.

Further, in the small intestine, pancreatic amylase continues to break malto-oligosaccharides to maltose, and disaccharidases secreted by the small intestinal mucosal cells biochemically rupture each maltose molecule into two glucose molecules.

Due to the intestinal absorption mechanisms of glucose, if beer is drunk apart from a full meal, no matter how little glucose would result from the metabolism of the beer, it will be completely absorbed. On the other hand, if the beer is consumed as part of a complete meal – along with a salad and barbecue, for example – the amount of glucose actually absorbed after beer metabolism can vary.

So no. 1: strictly from the point of view of minimising metabolic impact to avoid fattening, beer should be consumed at mealtimes and not between meals.

Another thing we have to take into consideration is that people with irritable bowel syndrome, gastric hyperacidity, or intestinal dysbiosis – caused by either a recent diarrhea or antibiotic, NSAIDS or prescription drugs for heartburn may suffer from temporary disaccharidase insufficiency. 

Therefore, because only the monosaccharides (glucose, fructose, galactose) can be absorbed through the small intestinal mucosa, the undigested disaccharides in the small intestine reach the large intestine where they can cause osmotic diarrhea and / or fermentation, bloating, abdominal cramps and flatulence.

If you suffer from an irritable bowel or if you simply bloat often, I have written this special article for you: Simple solutions for people with irritable bowel.

Further, insulin causes the absorbed glucose to be converted in the liver:

• in glycogen stores – in the happy case when glycogen stores of the liver are not already full
• in acetyl-CoA – from which it follows:

– energy – if glycogen stores are full and the level of ATP in the hepatic cell is low
– or fat – if the glycogen stores are full and the ATP level is sufficient

Unlike the easy concept of “calories” – ATP can not be “increased” or “stored” because, if it is enough, processes that could further increase ATP are stopped, being replaced by the processes that form energy deposits: either carbohydrates (glycogen) or fat.

But because the storage of glycogen is strictly limited in quantity, and the fat storage is not, the fat deposits will increase:

• in internal organs (especially in the liver and kidneys),
• in the blood – increasing blood level of triglycerides,
• and in adipose tissue.

So no. 2: one beer does not make you gain weight, but the more you drink, the greater the chance of gaining weight.

Now let’s get back to beers with 5-7% alcohol. They do not contain much starch, the alcohol being the only ingredient with fattening potential.

Alcohol does not require “digestion”, about 20% of alcohol is directly absorbed through the stomach mucosa, the rest being absorbed in the small intestine. After absorption, as in the case of glucose, liver passage is obligatory, the liver being the headquarter of alcohol metabolism.

All well and beautiful, except that, during the metabolism of alcohol – from ethanol to acetaldehyde, to acetic acid and, then, to acetyl-CoA –, the cell accumulates a too large amount of NADH.

(Strictly for understanding this article, all you need to know about NADH is that its accumulation in the cell stops acetyl-Coa from entering the Krebs cycle from which you could have obtained, for example, 12 ATPs per molecule of alcohol or 36 ATPs per molecule of glucose.

The NADH build-up generated by too high alcohol consumption leave the cells in anaerobic glycolysis, from which you only get 2 ATPs and a headache directly proportional to the consumed amount of alcohol).

The real problem with the consumption of alcoholic beverages (among which, if you exaggerate with the amount, you can also include the beer) is not only the blocking of the Krebs cycle, but also the blocking of gluconeogenesis (synthesis of glucose de novo inside the body). 

Of course, the 25 ml of alcohol in a 500 ml beer bottle will not impact these metabolic processes for too long. 

But if the alcohol consumed is higher, the body will go into hypoglycemia, which it will not be able to correct until you eat because gluconeogenesis does not work. 

To survive until you feed it, your body will use glycogen stores in the liver and / or will begin the adipose tissue lipolysis.

However, this lipolysis does not mean weight loss, the full burning of fatty acids in the Krebs cycle means weight loss.

Lipolysis means just moving the fat from the fatty tissue to the blood and then into the muscle – a factor generating insulin resistance, at a rate directly proportional to the number of beers or other alcoholic beverages consumed per unit of time. And the insulin resistance causes a lot of fat. And if we add to this resistance and the fact that alcohol generates dezinhibition, we can expect an uninhibited food consumption alongside an uninhibited alcohol consumption.

So no. 3: One or two beers a day will not make you fat, but more might.

Articolul Does drinking beer makes you gain weight? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

To start, let’s define exactly what is used to sweeten light or “sugar-free” soda drinks and what is used to sweeten normal or cola “with sugars”.

“Normal” soda drinks do not contain actual sugar – which is biochemically a disaccharide called sucrose, consisting of glucose + fructose, biochemically bound to each other – but High Fructose Corn Syrup (abbreviated to HFCS) – which is basically a mixture of the same two monosaccharides but unbound to each other and the fructose to glucose proportion in the made-up mixture is quite different from the one in natural sugar.

Light soda contains a lot of chemicals that are mostly inedible, among which aspartame, acesulfame potassium (Ace K) and sucralose (Splenda). However, despite the fact that aspartame is so controversial that it was removed from the market temporarily in some “civilized” countries, it is actually the most commonly used artificial sweetener in the world.

So, when we compare the metabolic impact of normal soda drinks with light soda drinks, we mainly actually compare the metabolic impact of HFCS to aspartame.

Aspartame is an artificial sweetener – also named in European Union countries E951 – used for sweetening “light”, “zero”, “diet” or other “sugar-free” soda drinks.

Although it is sweet, aspartame is not a carbohydrate but a protein.

After consumption, aspartame is broken down in the small intestine – under the action of peptidases produced by the small intestine cells – into methanol, phenylalanine and aspartic acid. Thus, the health risks potentially associated with aspartame frequent intake may be due to:

• methanol and its metabolites toxicity – with carcinogenic potential
• increased plasma levels of phenylalanine and aspartic acid – which are potentially harmful for the brain normal function
• increased norepinephrine and dopamine catecholamine concentrations – with addictive potential

However, aspartame is declared “safe for human consumption” in over 130 countries at doses below 40 mg/ day per kg of body weight.

But since these seemingly informative numbers means nothing to the average human, let’s see an illustrative example:

• a can of 330 ml of light soda drink contains about 200 mg of aspartame
• a 70 kg adult can theoretically consume a maximum of 2.800 mg of aspartame per day,
• that is: about 14 cans of 330 ml light soda drinks – and of course, most people keep their soda drinking way below this level.

However, aspartame is also found in many other drinks, foods, drugs and chewing gums – the total daily aspartame intake being almost impossible to estimate as “safe” or “unsafe”.

We can say that no one drinks 14 cans of soda per day, so it’s safe.

And we can say that we actually don’t know all the aspartame intake from other food and drinks, thus it isn’t safe.

But we just don’t really know.

Despite the legal reinsurance that EFSA (European Food Safety Authority) has given us on December 10, 2013, there are many studies conducted by other scientists demonstrating the following consequences of aspartame intake:

• weight gain (3)
• increased risk of diabetes (4)
• increased risk of multiple myeloma, non-Hodgkin’s lymphoma and leukemia (5,6)
• increased risk of cardiovascular disease (7)
• disordered appetite (8)
• migraines, depression and irritability (9)

On the other hand, HCFS is a kind of artificial fructose, called in the European Union countries and HFCS-55, used mainly for the sweetening of normal soda drinks – which actually can also be called “sugar-free” because they also contain no actual sugar.

Sugar is a disaccharide composed of a molecule of glucose biochemically linked to a molecule of fructose. The disaccharidases secreted by the small intestinal mucosa are required for sugar to be digested into glucose and fructose and further absorbed into the blood.

HFCS is a mixture of individual monosaccharides – the same glucose and fructose, but as they come biochemically separated the body doesn’t have to contribute to their digestion and intestinal absorption in any way. Thus HCFS is extremely absorbable even when the intestinal mucosa is inflamed, unlike sugar that requires the integrity of the mucosa intestinal for digestion and absorption.

After the fast absorption, the glucose from the HFCS mixture generates an insulin secretion spike followed by reactive hypoglycemia, and the contained fructose is converted inside the liver directly into VLDL fat that will be deposited locally.

Thus, as studies after studies continue to show, consumption of HFCS sweetened soda drinks leads to:

• weight gain (10)
• hepatic steatosis (11)
• increased risk of kidney disease (12)
• increased risk of cardiovascular disease (13)
• decreased perception of satiety (14)
• decreased perception of pleasure (15)
• increased hunger and appetite (16)

In addition, if we take into account that all the enzymes and hormones involved in digestion are secreted long before these beverages actually reach the digestive system, it is clear that both of these aspartame sweetened or HFCS sweetened soda drink variants have an impact on the secretion of digestive enzymes, incretins and insulin, both types leaving the body “high and dry”.

Neither cola light type drinks nor normal cola type drinks provide the body with the real sugar usable as a source of energy, but with synthetic chemicals whose consumption generates de novo lipogenesis.

De novo lipogenesis translates to gradual weight gain, dyslipidemia, liver and kidney steatosis, and a disordered appetite built up on a gradually increasing craving that will make you want to consume them daily.

When one decides whether to consume normal soda drinks or light soda drinks, what one decides is actually just where he or she wants to deposit the fat formed de novo – inside the body – the mechanisms leading to increased fat deposits happening after the consumption both types (17).

Of course, you can continue to “don’t worry, no sugar” and drink them “just for the taste of it”, but keep in mind that you are doing it on your increasing fat.

Quoted studies

(1) “Scientific Opinion on the re-evaluation of aspartame (E 951) as a food additive”. EFSA Journal 11 (12): 263. 10 December 2013. doi:10.2903/j.efsa.2013.3496.

(2) http://www.efsa.europa.eu/en/press/news/131210.htm

(3) Fowler, Sharon P. et al. “Fueling the Obesity Epidemic? Artificially Sweetened Beverage Use and Long‐term Weight Gain.” Obesity 16.8 (2008): 1894-1900.

(4) Sakurai, Masaru et al. “Sugar-sweetened beverage and diet soda consumption and the 7-year risk for type 2 diabetes mellitus in middle-aged Japanese men.” European journal of nutrition 53.1 (2014): 251-258.

(5) Belpoggi, Fiorella et al. “Results of Long‐Term Carcinogenicity Bioassay on Sprague‐Dawley Rats Exposed to Aspartame Administered in Feed.” Annals of the New York Academy of Sciences 1076.1 (2006): 559-577.

(6) Aune, Dagfinn. “Soft drinks, aspartame, and the risk of cancer and cardiovascular disease.” The American journal of clinical nutrition 96.6 (2012): 1249-1251.

(7) Dhingra, Ravi et al. “Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community.” Circulation 116.5 (2007): 480-488.

(8) Qing Yang. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. The Yale Journal of Biology and Medicine. June 2010.

(9) Lindseth, Glenda N. et al. “Neurobehavioral Effects of Aspartame Consumption.” Research in nursing & health 37.3 (2014): 185-193.

(10) Basciano, Heather, Lisa Federico, and Khosrow Adeli. “Fructose, insulin resistance, and metabolic dyslipidemia.” Nutrition & metabolism 2.1 (2005): 5.

(11) Collison, Kate S. et al. “Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and HFCS‐55.” Obesity 17.11 (2009): 2003-2013.

(12) Johnson, Richard J., L. Gabriela Sanchez-Lozada, and Takahiko Nakagawa. “The effect of fructose on renal biology and disease.” Journal of the American Society of Nephrology 21.12 (2010): 2036-2039.

(13) Tappy, Luc et al. “Fructose and metabolic diseases: new findings, new questions.” Nutrition 26.11 (2010): 1044-1049.

(14) Dekker, Mark J. et al. “Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome.” American Journal of Physiology-Endocrinology and Metabolism 299.5 (2010): E685-E694.

(15) Cameron, Jameason D., and Éric Doucet. “Reinforcement and food hedonics: a look at how energy deprivation impacts food reward.” Handbook of Behavior, Food and Nutrition. Springer New York, 2011. 2285-2305.

(16) Bellisle, F., and A. Drewnowski. “Intense sweeteners, energy intake and the control of body weight.” European Journal of Clinical Nutrition 61.6 (2007): 691-700.

(17) Feijó Fde M, Ballard CR, Foletto KC, Batista BA, Neves AM, Ribeiro MF, Bertoluci MC. Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. Appetite. January 2013. doi: 10.1016/j.appet.2012.10.009.

Articolul What is the metabolic difference between cola light and normal cola? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Sport is very important in weight loss, but by sport we only maintain the results from our eating behaviour.

Sedentariness is a basic cause of the fattening, but we cannot lose weight only by making sport.

Studies that have tried to prove that more physical activity helps losing weight failed to show efficacy, at least for two reasons:

• more sport means more hunger, that most don’t knows how to control properly
• and, of course, more sport means that you’ll have to do more and more to see any results because of the physical adaptation of the body to each of your training session

Although many studies have tried to show that the link between hunger and sport does not exist, let’s be serious!

– How many people did a serious hour of cycling, tae-bo or step aerobics without wanting to temporarily move to the refrigerator?

Of course, it is a fantasy that passes after the first banana, but it is so common that researchers who claim that sport actually decreases the hunger feeling probably did not do too much sports themselves in their lives.

Because we feel hunger after exercise, maintaining optimal competition weight is sometimes more difficult than the training itself.

Athletes who practice sports with weight categories (boxing, judo, weightlifting) or those from sports with “artistic impression” (skating, dancing or even swimming) – in which the body of the athlete is practically visible, as the actual sports clothing cannot hide any extra pounds – can certify the fact that doing more sports does nothing to help them losing weight, increasing both their hunger and their aversion to the scale.

Of course, there are many who think that these athletes eat more than they need, putting their performance in jeopardy either because they do not know how to eat properly, or because they do not have enough will to eat properly.

But many of these many, pointing to the straw in the eyes of performance athletes who are struggling to maintain their optimal competition body weight, carry a huge beam with themselves, often being overweight and sedentary, but with a big big mouth.

Insulin resistance is the reason why I do not recommend more sport and the reason why these athletes get fatter despite the huge amount of physical exercise they do on a daily basis – and I will explain it below.

A sedentary muscle cells cannot feed on glucose because the membrane of an unused skeletal muscle cell is kept impermeable for nutrients. Maybe we can debate the idea if the social aid works or not at the society level, but the human body does not feed cells that don’t work.

When you seriously do sports (that is, at least to cannot check your Facebook account while you are sitting on a plank position…), the body starts to open capillaries in areas of unused muscle cells, they get some nutrients, start to contract asynchronously to those you use regularly and you start to tremble.

To start to tremble, the muscle cells you usually use should be oxygen-free, ie the effort you make must be intense enough.

And because the fat used until then in the low and medium intensity effort can no longer be burned in the absence of oxygen, the body starts to use glycogen (glucose being the only one that can be burned without oxygen, but with an 18 times smaller efficacy than in the presence of oxygen).

You are gasping for air, with tired oxygen-free abruptly awaken muscle cells, but if you resist and continue, you start to tremble and feed these several newly active muscle cells – temporarily.

If you keep the discipline up and gradually start to do this regularly, the body will feed them regularly and your metabolism will gradually increase. But you cannot lose weight only by this metabolic increase which is quite tiny. What this gives you is a metabolic flexibility that will allow some room for now and then exceptions allowing you to eat a bit more while weighing the same. The reverse – metabolic decrease – meaning that you start weighing more and more while eating less, and this can happen even in professional athletes.

That’s why we need intelligent trainers and nutritionist who know what they are talking about and who, if possible, have heard of malonil-Coa in their lives. As if they haven’t heard of this little thing, they do not know how you – or them for that matter – could lose weight without some form of obvious or hidden starvation, quoting and selling “personalized” diets copied from Dr. Google.

Returning to performance athletes and amateur athletes, their active muscle cells are many, and their brain knows this, because it needs to feed them daily.

When doing regular sports, the membranes of an increasing number of muscle cells will be kept permeable to glucose even in the presence of fatty acids, because those cells work and consume everything they receive by making glycogen deposits and burning all the incoming fats. This parallels the intensity and amount of physical effort made by the athlete.

When the level of effort decreases, there is a metabolic inertia: the muscular cells that aren’t working today still receive the same amount of fatty acids they received and burned yesterday, when they were working. But today these cells rest, and the metabolic reactions that should have burned these fatty acids do not happen in the absence of physical effort, thus are deposited in the cells.

This is why, the higher the physical effort you make on a regular basis, the more care you must have with your food when your decrease the physical effort level.

This is why, many athletes gain weight after competitions, and this is why amateur athletes have to choose very carefully the level of sport they can maintain on the long run. Because, if they do not chose it carefully and train chaotically, the membrane permeability of their muscle cells will decrease much more than that of sedentary people simply because an athlete is delivering much more fat to the muscle on a daily basis.

A performance athlete who eats chaotically endangers his performance, and one who closely adapts his diet to the level of effort increases his chances of optimal performance. And the trainers or amateurs athletes can get the same consequences if they do not adapt their diet in the days without physical effort.

In sedentary people, a sudden intake of fatty acids in the muscle cell makes their membranes impermeable, lowering their active muscle cells percentage because the delivered fat is being stored in muscle cells without the much needed muscle contraction.

When these former active muscle cells become full of fatty acids (with the marbled appearance of a piece of beef flooded with fat), they begin to have dyslipidemia, the fat being “stored” further in the blood and – if they insist – in the liver.

Please mind that the many weight loss electrotherapy procedures available today actually create more metabolic problems than they solves, and if you do chose such “shortcuts” instead of or on top of working out, you should really consider a consultation to a qualified nutritionist to not throw your metabolism down the trash can.

Researchers recommend for maintaining weight (attention, “for maintaining weight”, not for losing weight!) between 250 and 350 minutes of sports per week – that is an average of 50 minutes a day.

And “the dogs bark while the bear keeps on moving”: that is, most people couldn’t care less about the researchers recommendations related to anything that is not a priority, and therefore the vast majority becoming increasingly sedentary and, of course, fatter and fatter.

People are not more sedentary because they are stupid, but because they are so stressed, tired, busy to prioritise their time at least to walk their dog (if they have one), much less to do sports – before or after work, take the children to school, film and/or park, to went to visit their parents or to go to an art exhibition. There are so many things to do and so little time.

Still, you will never “find” the time for anything, if you want time you must “make” it.

And if you would make the time to regularly do physical activity you would be less fatigued, you would increase your resistance to stress, counteract some of the harmful effects of smoking, increase your level of focus and discipline which would help you gradually become less busy thanks to the increased efficacy,  and keep you away from cardiovascular disease, diabetes, Alzheimer’s or cardiovascular disease.

However, this sport drudgery would not help you lose weight by itself, whatever it is. It would help you keep the results you achieve by eating properly.

By weight loss efficiency:

1. the best combination is: right nutrition + right sports
2. followed by: right nutrition without sports
3. then followed by: right sports without nutrition

Because of insulin resistance and increasing hunger sensation after sports, chaotic sport practice can have more damaging consequences than sedentariness.

In my first book, “5 Gears Diet”, I detailed how we can do sports in order to lose weight effectively, and I did that because, as I said above, people who do sports without a correct plan have more problems in maintaining their weight than those who do less or none.

Instead of a marathon of hours of mindless sports, it is more efficient to practice a shorter but smarter training actually build up and thought over by someone qualified in sports, and then simply do something else with your life besides going to the gym.

Or you can continue to do two or three consecutive hours of sports the same day, hoping that you will burn more calories and that you will lose weight faster, while everything you gain will be the a harder and harder ability to maintain your body weight.

Sport is good for health, but less and more intense is a thousand times more effective than more and idly.

Articolul Why I do not recommend too much sport for weight loss? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.