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.

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.

From a metabolic point a view, being pregnant means decreased muscle insulin sensitivity to redirect glucose to feed the fetus. This physiological pregnancy insulin resistance is the reason weight gain during pregnancy seems to happen even after drinking water, as its direct effect is a decreased metabolism for the mother. As you might know, metabolism it is not something that we can increase by drinking tea. Any tea. Metabolism is the energy required by the internal organs and brain, plus the energy needed for thermoregulation, plus the energy needed for digesting food, plus the energy needed by the contracting skeletal muscle cell to maintain tonus. The only metabolic factor that can be increased or decreased without pathology is this number of skeletal muscle cells that contract 24/7.

Pregnancy does not equal gaining body fat, but gaining body weight. This is true up to about 9 kg gestational weight increase, above which we start to talk about fat gain. At first, pregnant women do not gain weight by eating too much but by physiological metabolic decrease due to insulin resistance, which can healthily generate a gestational weight gain of about 9 to 15 kg. Above this value, we stop talking about a healthy gestational weight gain, and the “unhealthy” reverse refers to the fetus, not to the mother. Sadly, many mothers gain far too much weight during pregnancy, way above the recommended gestational weight gain range, risking both to remain overweight after birth, and to increase the child’s risk of developing a bucket full of diseases among which obesity is the less dangerous one. The child of a mother who gained too much during pregnancy has an increased risk of metabolic syndrome, (8) obesity, (9) and eating disorders (10) because the fetus develops insulin resistance while in the womb. (11)

In many maternities, newborns are fed on a schedule. Once home, the new mom must decide two things: if she will breastfeed her baby, and if she will demand feed him (or her) or feed him on a schedule. The first decision is widely debated and most mothers do their best to breastfeed their newborns. Yet, from a public health point of view, we mostly do not address the second decision even though demand feeding children of mothers who gained too much weight during pregnancy can balance their metabolic adaptations to the mother’s gestational eating behavior. (12)

When a pregnant woman overeats the fetus overeats, increasing the adipose cells number and decreasing the muscle mitochondria number he will be born with. (13) The thrifty genes hypothesis can be explained as a fetal insulin resistance’s side effect. Because of the reactive increased fetal insulinemia – reactive to the huge amount of nutrients the fetus receives due to the mother’s increased insulin resistance – glucose cannot enter through skeletal muscles’ GLUT4 membrane transporters and it’s redirected either towards the fetal adipose tissue causing macrosomia, (14) either towards the liver where it is transformed into fatty acids that can potentially clog placental vessels causing the child to be born with a weight below his gestational age. (15) So, it is not the birth weight of the newborn, but the gestational weight gain that can tell us something about the newborn’s metabolism. An insulin resistant fetus will genetically adapt by coding thrifty genes that will help his starving muscular cells survive his mother’s overeating. Scientists knew this survival mechanism from children of diabetic mothers, but studies on infantile obesity etiology link the thrifty genes hypothesis to children of mothers who gained too much weight during pregnancy also. (16) Scientists hypothesize that these children are born with a normal number of skeletal muscle cells, but with fewer mitochondria, and with a higher number of adipose fat cells = an innate low metabolism. This innate low metabolism can be aggravated by feeding the newborn regardless of his hunger, on a tight meal schedule, and it can be balanced by demand feeding. (17)

We know that adipose hyperplasia mostly happens up to one year of age if newborns are overfed, regardless of their hunger and satiation, increasing their obesity risk for life. (18) Such a behavior is also more prevalent in overweight, obese or eating disorder affected parents, which further increase the child obesity risk. However, eating without hunger or past satiation – either when we are talking about fetuses, newborns, adolescents or grandparents – has more risks than just gaining weight, due to the satiety hormone, leptin. Leptin is secreted by the fat tissue, and it inhibits the hunger neurons within the arcuate nucleus from the hypothalamus. It is responsible for the lack of hunger we experience during night sleep (based on an insulin – melatonin interaction), and for the long term control of satiety. More fat tissue, means more leptin, but – and this is a huge but – the hypothalamus’s becomes leptin resistance exactly as the muscle cell become insulin resistance. And during pregnancy even the placenta secrete leptin, so a fetus of a mother who overeats during pregnancy will be born both insulin resistant and with a degree of leptin insensitivity. Insulin resistance means increased obesity risk, and leptin resistance means a huge number of other risks.

Now, besides leptin, there are other satiety hormones of which I want to mention two: CCK (colecistokinin), and PYY (polypeptide Y). CCK is secreted when special cells within the small intestine’s lining come in contact with lipids, and it generates short term satiety. For meals constituted of “milk” only, replacing natural, whole fat milk with degreased types of milk or with low fat vegetal versions of “milk” can deregulate CCK secretion, causing infant hyperphagia. (19) PYY is secreted when other special cells within ileum and colon lining come into contact with digestion products, and it generates satiety between meals. Snacking can deregulate PYY and cause an insulin secretion spike if it happens too soon after a full meal. (20) It is true that there are no black and white solutions when it comes to preventing or treating children’s obesity, but snacking can potentially do more harm than good for a child born insulin resistant, and with a higher body fat percentage that will secrete a higher amount of leptin. (21) And this higher amount of leptin will not translate in higher satiety, but in lesser as the arcuate nucleus of the hypothalamus adapts to the leptin flood by becoming leptin resistant.

The fetus’ hypothalamus can become leptin resistant during pregnancy if the mother overeats to the point of highly increasing her body fat percentage, while decreasing her insulin and leptin sensitivity. (22) The newborn of an insulin and leptin resistant mother can also become leptin resistant during his first year of life – “eating well” enough to sooth parents and grandparents worries – if he is fed regardless of his hunger and satiation. He will mostly grow well, but what if he’ll grow too “well?” The World Health Organization scientists predict that 30 million children more than today will become overweight or obese in the next 10 years, and the children born insulin and leptin resistant fed regardless of their hunger and/ or satiation will be a huge part of them. Moreover, leptin – the main satiety hormone – does not regulate only satiety. It regulates cellular replication, differentiation and apoptosis – potentially linking obesity with the cancer risk. (23) It stimulates the release of gonadotropin hormones (GNRH), which will command the release of the lutein hormone (LH) – linking leptin resistance with PCOS and infertility. (24) Optimal leptin secretion, along with STH and GNRH secretions, is also essential for puberty onset when the body is ready, and not before. (25) The same leptin is essential for fetal brain development, learning capacity and memory. (26) And the same leptin is crucial for innate and acquired immunity, fetal leptin resistance being linked with thyme atrophy or with a decreased function of the macrophage cells. (27) So, when the pregnant mother overeats and gain too much weight during pregnancy and/ or when she feeds her children regardless of their hunger and satiation, she unknowingly risk to disturb all this leptin regulated systems, obesity being the smaller risk of all. (28)

It is true that a meal schedule is easier to apply and more emotionally comfortable than demand feeding newborns. But a meal schedule can only regulate ghrelin, (29) while the other hormones involved in regulating appetite are more sensitive to blood sugar than to the emptiness of the stomach – which can coincide or not with a blood sugar decreased enough to stimulate the hunger center. (30) The energy needs of different bodies are different from day to day, but the newborn bodies’ needs differ far more than others as a newborn almost triples his weight in the first year of life. Predicting his food needs based on other newborn needs, without considering his unique metabolism, can undernourish or overnourish this particular child generating or aggravating insulin and leptin resistance. (31) And then we see he’s fat, and/ or that he has a low immunity, and/ or that his gonads are not properly developed, and/ or that he’s brain abilities are not what we’ve expected, and/ or that he has a cancer risk – all in the name of the soothing feeling we have as parents when we know a child “ate well.”

Feeding any child regardless of his hunger and satiation puts him at these risks, but a child born from a mother who overate during pregnancy is much more at risk for developing metabolic complications than the children born by mothers who stayed within the recommended gestational weight gain range. Demand feeding can balance their innate low metabolism and increase their leptin sensitivity, (32) being the best chance we got to reverse this increasing infantile obesity trend that we, almost hopelessly, witness today.

By Diana Artene, PT, ND, MSN.

References

1. World Health Organization, Comission on Ending Childhood Obesity, http://www.who.int/dietphysicalactivity/end-childhood-obesity/en/
2. Rosenbloom, Arlan L., et al. “Type 2 diabetes mellitus in the child and adolescent.” Pediatric diabetes 9.5 (2008): 512-526.
3. Weiss, Ram, et al. “Obesity and the metabolic syndrome in children and adolescents.” New England Journal of Medicine 350.23 (2004): 2362-2374.
4. Tie, Hong-Tao, et al. “Risk of childhood overweight or obesity associated with excessive weight gain during pregnancy: a meta-analysis.” Archives of gynecology and obstetrics 289.2 (2014): 247-257.
5. Whitaker, Robert C. “Predicting preschooler obesity at birth: the role of maternal obesity in early pregnancy.” Pediatrics 114.1 (2004): e29-e36.
6. Ehrenthal, Deborah B., Cynthia S. Minkovitz, and Donna M. Strobino. “Maternal Obesity, Gestational Weight Gain, and Childhood Growth in the First Year of Life.” Obesity During Pregnancy in Clinical Practice. Springer London, 2014. 229-256.
7. Baughcum, Amy E., et al. “Maternal feeding practices and childhood obesity: a focus group study of low-income mothers.” Archives of Pediatrics & Adolescent Medicine 152.10 (1998): 1010-1014.
8. Plagemann, Andreas. “Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity.” Physiology & behavior 86.5 (2005): 661-668.
9. Mamun, A. A., and M. Mannan. “Gestational weight gain in relation to offspring obesity over the life course: a systematic review and bias‐adjusted meta‐analysis.” Obesity Reviews (2014).
10. Favaro, Angela, Elena Tenconi, and Paolo Santonastaso. “Perinatal factors and the risk of developing anorexia nervosa and bulimia nervosa.” Archives of General Psychiatry 63.1 (2006): 82-88.
11. Catalano, Patrick M., et al. “Fetuses of obese mothers develop insulin resistance in utero.” Diabetes care 32.6 (2009): 1076-1080.
12. Nicholas, Lisa M., et al. “Maternal obesity or weight loss around conception impacts hepatic fatty acid metabolism in the offspring.” Obesity (2014).
13. Hillier, Teresa A., et al. “Excess gestational weight gain: modifying fetal macrosomia risk associated with maternal glucose.” Obstetrics & Gynecology112.5 (2008): 1007-1014.
14. Hillier, Teresa A., et al. “Excess gestational weight gain: modifying fetal macrosomia risk associated with maternal glucose.” Obstetrics & Gynecology112.5 (2008): 1007-1014.
15. Hattersley, Andrew T., and John E. Tooke. “The fetal insulin hypothesis: an alternative explanation of the association of low birth weight with diabetes and vascular disease.” The Lancet 353.9166 (1999): 1789-1792.
16. Groop, Leif C., and Tiinamaija Tuomi. “Non-insulin-dependent diabetes mellitus-a collision between thrifty genes and an affluent society.” Annals of medicine29.1 (1997): 37-53.
17. Ciampolini, Mario, et al. “Interruption of scheduled, automatic feeding and reduction of excess energy intake in toddlers.” International journal of general medicine 6 (2012): 39-47.
18. Shukla, A., et al. “Infantile overnutrition in the first year of life: a field study in Dudley, Worcestershire.” British medical journal 4.5839 (1972): 507.
19. Plagemann, Andreas, et al. “Reduction of cholecystokinin-8S-neurons in the paraventricular hypothalamic nucleus of neonatally overfed weanling rats.”Neuroscience letters 258.1 (1998): 13-16.
20. Chen, XiaFang, et al. “Correlations of circulating peptide YY and ghrelin with body weight, rate of weight gain, and time required to achieve the recommended daily intake in preterm infants.” Brazilian Journal of Medical and Biological Research 45.7 (2012): 656-664.
21. Blundell, John E. “Perspective on the central control of appetite.” Obesity 14.S7 (2006): 160S-163S.
22. Férézou-Viala, Jacqueline, et al. “Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring.” American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293.3 (2007): R1056-R1062.
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