The question is why?

Permanent weight loss is actually a two-step process. There is a short-term and a long-term (time dependent) problem. This resistance to weight loss represents homeostasis. The hypothalamic region of the brain determines the Body Set Weight (BSW). This is our fat ‘thermostat’. Insulin acts here to set BSW higher. In the short term, we can use various diets to bring our actual body weight down. However, once below the BSW, the body activates mechanisms to regain that weight. This resistance to weight loss was first demonstrated by Drs. Leibel and Hirsch in 1984. Obese persons that had lost weight require fewer calories. Their metabolism had slowed dramatically. The body is actively resisting long-term weight loss. This widely known fact has been both proven scientifically and empirically.

Imagine that you set your house thermostat low, and you are cold. You plug in a small electric heater. Soon, the house starts to warm up. Any brand of electric heater seems to work. All heaters work. This is the short-term solution to the problem. After a while, the thermostat senses that the temperature has gone up. So it turns on the air conditioning to bring the temperature back down. Eventually, after a seesaw battle, the house always wins. The temperature eventually drifts down and we are cold again. This is the long-term problem. All heaters fail. The problem is homeostasis. While we have adjusted the temperature, we have not adjusted the thermostat.

Now, let’s put this into obesity terms. High insulin levels set the BSW ‘thermostat’ at a weight that is too high. Now we decide to lose weight. Following any reasonable diet reduces weight in the short term. This is the quick fix – just like the electric heater. What happens in the long term?

The problem of insulin resistance (time dependent factors) has not been addressed. The insulin resistance keeps insulin high. The BSW is still set at a very high level. The body responds to the weight loss by raising the body weight back up. Hormonal signals of hunger are increased, compelling us to eat. If that doesn’t work, total energy expenditure (TEE) is reduced. This was exactly the experience of the participants in the Minnesota Starvation Experiment. As metabolism decreases, it becomes harder and harder to lose weight. Eventually, after a seesaw battle, the BSW wins. The end result is all too familiar – weight regain. The problem is homeostasis.

So, there are actually two separate questions to lasting weight loss. There is both a short-term and a long-term question. The short-term question is “What to Eat”. The longer-term problem is why all diets fail. This is the problem of insulin resistance and resetting the BSW. This question revolves around “When to Eat”.  While these two questions are related, they must both be addressed to develop a comprehensive solution to obesity.

Dr Nasr Al-Jafari is a Dubai-based Family Medicine Consultant and Functional Medicine Practitioner. He graduated from The University of Nottingham and completed his consultant training at The University of Manchester, UK. He has pioneered the use of obesity theory in the UAE for weight loss and type 2 diabetes reversal at DNA Health Medical Center where he is Medical Director.

Well, no wonder dietary changes didn’t make any difference. That wasn’t their problem. It was the cortisol/ stress pathway all along.

If I’m honest – these problems are harder to fix. While there are time tested ways of reducing stress and cortisol levels, most patients simply do not take our advice to look into mindfulness/mediation/prayer/yoga/acupuncture/religion/massage.

‘People come to a diet clinic and get advice on how to meditate. They look at me like I have two heads!’

There is, however, good evidence that things such as mindfulness mediation can have an effect on weight loss.

At the University of California, San Francisco, a trial was done with mindfulness meditation and showed that they could reduce cortisol levels. This is no surprise since meditation has been done for thousands of years as a stress relieving method. This decrease in cortisol was closely paralleled by a decrease in abdominal fat.

The important thing to know about it is that meditation does not change the actual stressor. For example, suppose your boss is driving you crazy. You will be under a lot of stress. Meditation won’t change that one bit. What it will change is your body’s response to the stress. In the end, that is what is important. By decreasing the cortisol response, there is a decrease in abdominal fat. Your boss is still the jerk he was before. You have only changed your body’s response to this stressor.

One final thought about stress relief. It’s always a little amazing to me how far organized religion is ahead of the game. Think about the practices they preach. Prayer (similar to meditation). Belief in a higher power/ confession (stress relief). Weekly ceremonies, like mass (sense of community and continuity – important for stress relief). Small group session (friendship and sense of belonging – stress relief). Fasting. Yes, fasting. All of these practices that are so important for good health have been established thousands of years ago.

Dr Nasr Al-Jafari is a Dubai-based Family Medicine Consultant and Functional Medicine Practitioner. He graduated from The University of Nottingham and completed his consultant training at The University of Manchester, UK. He has pioneered the use of obesity theory in the UAE for weight loss and type 2 diabetes reversal at DNA Health Medical Center where he is Medical Director.

Do calories cause obesity? Yes, partially.

Does sugar cause obesity? Yes, partially.

Does sleep protect us from obesity? Yes, partially.

Does insulin resistance cause obesity?   Yes, partially.

Does stress cause obesity? Yes, partially.

‘All these factors converge on several hormonal pathways that lead to weight gain’

Virtually all diseases of the human body are multifactorial. Consider cardiovascular disease. Family history, age, gender, smoking, diabetes, high blood pressure, and lack of physical activity all influence the development of cardiovascular disease.

Obesity is also a multi-factorial disease. We should not expect any different. What is required is a framework, a structure, a coherent theory to understand how all these factors fit together. Too often, our current model of obesity assumes that there is only one single true cause, and that all others are pretenders to the throne.

‘There are endless debates about the true king. Too many calories cause obesity. No, too many carbohydrates. No, too much saturated fat. No, too much red meat. No, too much processed foods. No, too much high fat dairy. No, too much wheat. No, too much sugar. No, too much highly palatable foods. No, eating out. It goes on and on. They are all partially correct’

So, the Low Calorie believers disparage the Low Carbohydrate people. The Low Carbohydrate movement ridicules the Vegans. The Vegans mock the Paleo supporters. The Paleo followers deride the Low-fat devotees. All diets work, in the short term, because they all address a different aspect of the disease. But none of them work for very long, because none of them address the totality of the disease. Without this critical understanding of the multifactorial nature of obesity, we are doomed to this endless cycle of blame.

Similarly, most dietary trials are fatally flawed by this tunnel vision. The various trials comparing low carbohydrate to the low-calorie diets have all asked the wrong question. These two diets are not mutually exclusive. What if both are true? Then there will be similar weight loss on both sides. Low carb diets lower insulin. Lowering insulin levels reduces obesity. However, all foods raise insulin to some degree. Since refined carbohydrates often make up 50% or more of the Standard American Diet, low calorie diets generally reduce carbohydrates as well. So low calorie diets, by restricting the total amount of foods, still work to lower insulin levels. Both will work.

In a randomized study of four different diets, despite differences in carbohydrate, fat and protein content, weight loss was the same.  Maximum weight loss occurred at six months, with gradual regain thereafter. A 2014 meta-analysis of dietary trials reached much the same conclusion.

“Weight loss differences between individual diets were minimal”

Sure, sometimes one diet comes off as slightly better than another. The difference is often less than one kg and often fades by a year.

We’ve done Low Calories Low Fat. We’ve done high protein diets.  We’ve done cabbage soup diets. We’ve done high protein diet. None of them worked!

‘All these diets address only a single factor in a multi-factorial disease.  Further, they completely ignore the question of “When to Eat” as well as the time dependent factors of obesity’

Sometimes these results are interpreted as the belief that everything can be eaten in moderation. This does not even begin to address the complexity of weight gain in the human subject. It is essentially a cop-out answer. It is a deliberate attempt to evade the hard work of searching for dietary truths. For example, should we eat broccoli in the same moderation as ice cream? Obviously not. Should we drink milk in the same moderation as sugar sweetened beverages? Obviously not. The long-recognized truth is that certain foods must be severely restricted. This would include sugar sweetened beverages and candy, for instance. Other foods do not need to be reduced in any way – kale or broccoli, for instance.  Other foods, may be best taken in moderation – animal meat.

Others have erroneously concluded that ‘it is all about the calories’. Actually, it is nothing of the sort. Calories are only a single factor in the multifactorial disease that is obesity. It seems to be a default answer, but it has already been shown to be disastrously incorrect. After all, caloric reduction has proved itself a dismal failure over the last 50 years. Low calories diets have been tried again and again. It failed every single time.

There are other answers that are not really answers. These include, ‘There is no best diet’ or ‘Choose the diet that suits you’ or ‘The best diet is one you can follow”.

‘If supposed experts in nutrition and disease don’t know the right diet, how are you supposed to?’

This is intellectual laziness at its very worst, revealing a stunning lack of imagination about the problem of obesity. Does this mean that following the Standard American Diet is the best diet for me, because it is the one I can follow? Does this mean I can eat a diet of sugared cereals and pizza? Obviously not. ‘Experts’ who are too mentally sluggish in the quest for truth reach for the facile and incorrect answer that ‘All diets are equal’.

‘This pure intellectual laziness is unacceptable. We don’t need another ‘expert’ give us the lame-duck answer “All diets work. Do whatever you want”.’

Most diets attack a single part of the problem at a time. But why is it necessary to address one facet at a time? A multi-faceted approach is needed to address the multidimensional problem of obesity. Rather than targeting a single point in the obesity cascade, we need multiple targets and treatments. But the Low Carbohydrate proponents don’t want to hear about calories, meat, or insulin resistance. For them, it is all about carbohydrate restriction. But all foods, even low carbohydrate ones contribute to rising insulin levels. The Low Calorie devotees don’t want to hear about carbohydrates, sugars, meats, or dairy. For them, it is all about caloric restriction. You can eat ice cream for dinner if it has the same number of calories as a large salad. We don’t need to choose sides. Rather than compare a dietary strategy of low calorie versus low carbohydrate, why can’t we do both? There is no reason.

Dr Nasr Al-Jafari is a Dubai-based Family Medicine Consultant and Functional Medicine Practitioner. He graduated from The University of Nottingham and completed his consultant training at The University of Manchester, UK. He has pioneered the use of obesity theory in the UAE for weight loss and type 2 diabetes reversal at DNA Health Medical Center where he is Medical Director.

One of the major causes of chronic stress and obesity is sleep deprivation.

Studies have shown a relation between short sleep duration and excess weight, with less than 7 hours being the general the cut-off. The Quebec Family Study suggested an increased risk of 27% with shorter sleep duration. A 13-year prospective study even suggested that every extra hour of sleep was associated with a 50% reduction in risk of obesity. A one-year prospective study showed that sleeping less than 5 hours per night was associated with a 91% increase risk of obesity. Sleeping 5-6 hours was associated with at 50% increased risk. A meta-analysis of 696 studies published in 2008 showed that short sleep duration increased the risk of obesity by 55% in adults and 89% in children.

‘For every hour of sleep deprivation, BMI rose by 0.35 kg/m2’

But if the calories in-calories out model of weight loss held true, then how could this be? Sleeping less should increase energy expenditure since any activity used more calories than sleep. However, the opposite is true. Again, disproving the calorie theory of weight loss.

Interestingly, sleeping more than 8 hours per night may also increase risk of obesity. The Western New York Health Study also found that sleeping 6-8 hours per night was associated with the lowest risk of obesity. ‘Excessive’ sleeping over 8 hours increased the risk by 60% but too little sleep (<6 hours) tripled the risk of obesity.

Mechanisms

Sleep deprivation is a potent stressor and thus stimulates cortisol, which in turn raises blood sugars, resulting in high insulin levels. Cortisol also activates the sympathetic nervous system.

Sleep deprivation causes increased cortisol levels and sympathetic tone.

In one study Sleep deprivation resulted in 37-45% higher cortisol levels by the next evening. Glucose use by the brain decreases during sleep deprivation and likely contributes to the mental fogginess that we all experience. This can be measured by positron emission tomography (PET). Restriction of sleep to 4 hours in healthy volunteers resulted in a 40% decrease in glucose tolerance. The glucose response to breakfast was, in fact, high enough to classify these previously normal individuals as having pre-diabetes. Cortisol increased close to 20%.

Other studies have confirmed that it is possible to induce insulin resistance in normal volunteers simply with sleep restriction to four hours per night, even with a single night. After 6 days of sleep restriction, there was a 50% decrease in insulin sensitivity. In a Japanese study, shortened sleep duration increased risk of type 2 Diabetes.

Both leptin and ghrelin, key hormones in the control of body fatness and appetite show a circadian rhythm and are disrupted by sleep disturbance. Leptin rises slightly during sleep and ghrelin, the hunger hormone, tends to fall. Thus, hunger is suppressed despite maintenance of the fasting during sleep. The Wisconsin Sleep Cohort Study demonstrated the effects of sleep duration on these important hormones.  The Quebec Family study also found that short sleep duration was associated with higher body weight, decreased leptin and increased ghrelin.

Leptin increases steadily with more sleep. Higher leptin levels regulate body fat downwards making thinner. Ghrelin, the hunger hormone, steadily falls with more sleep. Lower ghrelin causes less hunger. Sleep deprivation results in higher ghrelin and hunger. Sleep deprivation of only 4 hours for two nights increased ghrelin by 28% and reduced leptin by 18% with accompanying increased hunger and appetite. Who can deny the ‘late-night munchies’?

Sleep deprivation clearly will undermine weight loss efforts. Adequate sleep is not only essential for restoring brain function, but also to prevent the metabolic consequences of high cortisol and insulin resistance. Interestingly, sleep deprivation under low stress conditions does not decrease leptin or increase hunger. This suggests that it is not the sleep loss per se that is harmful, but the activation of the stress hormones and hunger mechanisms. Getting enough good sleep is essential to any weight loss plan.

‘Sleep deprivation causes stress. Bottom line.’

But stress may also cause sleep deprivation. Increased cortisol often causes insomnia due to activation of the sympathetic ‘fight or flight’ system. This is a classic vicious cycle.

An interesting natural experiment on sleep deprivation occurred in South Korea. A 10 pm curfew was enforced on late-night tutoring schools. Subsequent studies estimated that each 1 hour increase in sleep duration lead to a 0.56 kg.m2 reduction in BMI and a 4.3% reduction in obesity in the affected grades.

There are several keys to good sleep hygiene, none that involve the use of medications. These disturb the normal sleep architecture, the pattern of REM and non-REM sleep.

Effective ways to improve sleep include:

1. Sleep in complete darkness
2. Keep regular sleeping hours
3. Keep bedroom slightly cool
4. 7-9 hours a night
5. Sleep in loose fitting clothes
6. See the light first thing in the morning
7. No TV in bedroom
8. Mindfulness/deep breathing exercises/meditation

Dr Nasr Al-Jafari is a Dubai-based Family Medicine Consultant and Functional Medicine Practitioner. He graduated from The University of Nottingham and completed his consultant training at The University of Manchester, UK. He has pioneered the use of obesity theory in the UAE for weight loss and type 2 diabetes reversal at DNA Health Medical Center where he is Medical Director.

The bottom line – Cortisol makes you fat….and both insulin and cortisol play a key role in carbohydrate metabolism – not coincidently.

Cortisol is otherwise known as our stress hormone.   It coordinates the ‘flight or fight response’ along the sympathetic nervous system. Not surprisingly, cortisol is produced in response to stress. In Palaeolithic times, this was often a physical stress, such a being chased by a predator. The release of cortisol was essential in preparing us to fight or flight.

Cortisol has many roles

1. Increases alertness and decreases the need for sleep.
2. Glucose availability is substantially enhanced, providing the energy for muscles.
3. All available energy is directed towards surviving the coming stressful period. Non-essential metabolic activities are curtailed.
4. Growth, digestion and other long-term issues are temporarily restricted.
5. Proteins are broken down and converted to glucose. In the fasted state, cortisol has several mechanisms to increase glucose in the body.

Vigorous physical exertion – fight or flight – soon followed using up the abundant supply of glucose. Shortly thereafter, when the danger had past, the cortisol levels decreased again back to low levels. The body is well adapted to the short-term increase in cortisol and glucose.

Cortisol’s effect on insulin

At first glance cortisol and insulin appear have opposite effects. Insulin is a storage hormone. Under high insulin levels, the body stores energy in the form of glycogen and fat. Cortisol, on the other hand prepares the body for action. This moves energy out of stores and into readily available forms such as glucose. With short-term physical stress, insulin and cortisol play opposite roles. This situation is quite different for long-term psychological stress.

In modern times, chronic, non-physical stressors increase cortisol

For example, problems at work, martial issues, sleep deprivation and arguments with children are all serious stressors, but fundamentally also do not result in vigorous physical exertion afterwards – therefore blood glucose remains elevated. Under conditions of chronic stress, glucose levels remain high. There is no vigorous physical exertion to burn off the glucose, and there is no resolution to the stressor. The blood glucose can remain chronically elevated.  This long-term elevation in glucose can trigger the release of insulin. Chronically elevated cortisol leads to increased insulin. This has been demonstrated in several studies.

One particular study demonstrated that cortisol increases with self-perceived stress levels. This stress-related increase in cortisol showed consistent strong relationship to both increased glucose and increased insulin levels. Since insulin is the major driver of obesity, it should be no surprise that it was also related to both BMI and abdominal obesity.

The same is true when using synthetic cortisol. Volunteers were given 50mg cortisol 4 x daily over 5 days. Insulin levels rose 36% from baseline. Another study showed that the use of prednisone increases glucose levels by 6.5% and insulin levels by 20%. Over time, insulin resistance also develops mainly at the hepatic level. There is a direct dose-response relationship between cortisol and insulin. For every unit of free cortisol increase, insulin increased by 9.7 mU/I.

Long-term use of prednisone may lead to an insulin resistant state or full-blown diabetes. The increased insulin resistance seen in type 2 diabetes leads to elevated insulin levels. Even five years after the cure of Cushing’s disease, the elevated insulin levels persist. This is likely related to the insulin resistance syndrome that has developed.

Cortisol produces insulin resistance in skeletal muscle by interfering in the insulin-signaling network. These interfere with insulin action after it binds the insulin receptor. In addition, muscles release amino acids for conversion to glucose, further increasing insulin resistance. Adiponectin, secreted by fat cells, which normally increase insulin sensitivity, are suppressed by glucocorticoids.

Multiple studies show that increasing cortisol confirms this insulin resistance.

If cortisol raises insulin, then reducing cortisol should reduce insulin. We find this situation in transplant patients who are maintained on synthetic cortisol for years or decades as part of their anti-rejection medications. Weaning off the prednisone resulted 25% drop in plasma insulin. This translated to a 6.0% weight loss and a 7.7% decrease in waist girth.

Does excess cortisol, from long-term psychological stress lead to weight gain?

Certainly, anecdotal evidence seems to suggest that stress leads to obesity. But there are certain disease states characterized by excessive cortisol production?  Yes – this is called Cushing’s disease or Cushing’s syndrome.  The hallmark of this disease is weight gain.

Many patients complain that they gain weight no matter how little they eat and no matter how much they exercise.

However, this effect is also seen even within the normal population. In a random sample from North Glasgow, Scotland, cortisol excretion rates were strongly correlated to Body Mass Index (BMI) and waist measurements. Higher cortisol levels were seen in heavier people. Cortisol related weight gain particularly deposits fat in the abdomen, which results in an increased waist/hip ratio (WHR).

Other measures of cortisol confirm the association with abdominal obesity. People with higher urinary cortisol excretion have higher waist to hip ratios. People with higher cortisol in the saliva have increased BMI and waist/hip ratio. In other words, there is substantial evidence that chronic cortisol stimulation increases both insulin and obesity. Long-term exposure to cortisol in the body may be measured by scalp hair analysis. In a study comparing obese patients to normal weight, researchers found elevated levels of scalp hair cortisol.

What about the opposite?

If high cortisol causes weight gain, then low cortisol levels should cause weight loss. This exact situation exists in the case of Addison’s disease – also known as adrenal insufficiency. The hallmark of Addison’s disease is weight loss. In large case series, 97% of patients exhibit weight loss. Cortisol levels went down. People lost weight.

The fact that is undeniable is that excess cortisol causes weight gain. By extension, stress causes weight gain. This is something that many people have intuitively understood despite the lack of rigorous evidence. It certainly makes sense. Much more sense than calories causing weight gain.

Reducing stress is difficult, but vitally important. Stress relief is an active process. There are many time-tested methods of stress relief. These include mindfulness meditation, yoga, massage therapy, and exercise. Studies on mindfulness intervention were able to use yoga, guided meditations, and group discussion to successfully reduce cortisol and abdominal fat.

Dr Nasr Al-Jafari is a Dubai-based Family Medicine Consultant and Functional Medicine Practitioner. He graduated from The University of Nottingham and completed his consultant training at The University of Manchester, UK. He has pioneered the use of obesity theory in the UAE for weight loss and type 2 diabetes reversal at DNA Health Medical Center where he is Medical Director

‘After 50 years of desperate, intense research, guess how many studies prove its effectiveness? How about zero? That’s right, Zero.’

The only reason we think the ‘caloric reduction’ is effective is because it’s been repeated so often.

This mirrors many other in-grained unscientific and disproven beliefs

1. Eat 5-a-day
2. Dietary cholesterol causes cardiovascular disease
3. Salt causes high blood pressure

No, the key to successful weight loss is to control your body’s ‘thermostat’ – the body set weight (BSW). A room thermostat is set to your desired room temperature and in the summer, when the outside temperature is hot, it turns on the air conditioning. In the winter, it detects the temperature is too cold, and turns on the heat. Your house stays at the perfect temperature despite wildly varying outside conditions.

In our bodies, we have the BSW, also called an appestat or obesistat, essentially a thermostat for body fatness. Some people believe we are designed to eat everything in front of our face and now that food is so easily available, we have no choice but to gain weight. This is false and completely ignores normal human physiology.

Instead, we have multiple overlapping powerful satiety mechanisms to stop eating. We have stretch receptors in our stomach to signal when it is too full. We have powerful satiety hormones such as peptide YY and cholecystokinin that stop us from eating.

From an evolutionary standpoint, these satiety mechanism makes a lot of sense. Our body is designed to stay within certain body fat parameters. If you are too skinny, you will die during the hard times (winter). If you are too fat, you will not be able to catch food, and you might just get eaten yourself. Wild animals almost never become obese to the point of being unable to function normally. Where are the morbidly obese Lions? Monkeys? Fish? When food is plentiful, numbers of animals increase. You don’t get a few morbidly obese giraffes. You get thousands of relatively normal sized giraffes!

The BSW sets an ideal body fatness that it defends just like our house thermostat. If we are too skinny, we try to gain weight. If we are too fat, we try to lose weight. The clearest experimental demonstration of this was done by Dr. Rudy Leibel in 1995. In this experiment he took volunteers, and overfed them to make them gain 10% more weight. Then he returned them to their regular weight, and then to 10% or 20% weight loss. At each point, he measured the basal metabolic rate (BMR), or how much energy (calories) the body is expending. After 10% weight gain, the body burns about 500 calories more per day compared to baseline. As the body returns to it’s original weight, so does the metabolic rate. After 10% weight loss, the body burns about 300 calories per day less.

The body tries very hard to maintain its BSW in the original position, acting just like our house thermostat. This directly contradicts the ridiculous Calories In/ Calories Out viewpoint that hold that simply eating too many calories causes body fatness without regard to the BSW or satiety hormones or pretty much any other physiologic signalling. If you deliberately overeat, your body tries to burn it off.

Calories’ is not a physiologic notion, as we’ve previously discussed. Our body has no ‘calorie’ receptors and does not know how many calories we eat or don’t eat. Over the past several centuries, we’ve decoded many of the human metabolic pathways. Do you see ‘calories’ mentioned ANYWHERE in this complex diagram? A calorie of carbohydrate is metabolised entirely differently from fat or protein. So why pretend they are the same? It’s like saying that humans and a tree trunk share the same physiology because we both weigh the same and would produce the same heat if burned in a calorimeter. Believing this totally ridiculous notion is a big part of why we’re losing the war on obesity.

‘This notion of ‘A calorie is a calorie’ is mostly pushed by processed food companies trying to convince you that it is fine to swap 100 calories of avocado for Coke in terms of weight gain. You’d have to be pretty dense to believe it. For food companies, the calories model is like Santa Claus. As long as they keep people believing, its a gift that keeps on giving.’

Take artificial sweeteners. It has no calories, so we can fool our taste buds, but can we fool our appestat? Not at all. How many people do you know have lost weight by switching to sweeteners? If all we had to do to lose weight was eat fake sugar and fake fat and no calories, we’d all be eating Olestra and Stevia and lose weight. There would be no obesity crisis. There would be no type 2 diabetes crisis. But there is.

Why ‘Caloric Reduction’ does not work

Suppose our house thermostat is set to 72F degrees, but we now want to be at 70F. Ignoring the thermostat, we turn on the portable air conditioner in. At first, the temperature drops to 70F but then the thermostat turns up the heat to return the room to 72F. We don’t like that, so we put a second and third air conditioner in. In response, the thermostat turns the heat on full blast. We continually fighting against ourselves in an ultimately futile attempt. Well, that didn’t work. What is a simpler solution? Turn down the thermostat.

This is analogous to reducing calories to lose weight because it completely ignores the BSW. Suppose our BSW is set at 200 pounds, but we want to weigh 170 pounds. Conventional advice tells us to cut 500 calories per day to lose 1 pound per week. Initially weight goes down to 185 pounds, but then our appestat kicks in to make us gain weight. We become hungrier and basal metabolism slows in order to regain the weight. So we try even harder by cutting more calories. But our body responds by further slowing our metabolism. We continually fight against ourselves in an ultimately futile attempt to lose weight. Well, that didn’t work. What is a simpler solution? Turn down the appestat or BSW. How to do that? Read on.

The Body Weight ‘Thermostat’

So how does our appestat work? Recall that obesity is a disease caused by excessive insulin, not excessive calories. It is a hormonal imbalance, not a caloric one. Insulin signals our body to store food energy in the form of body fat. When we fast, and insulin goes down, we burn some of that stored energy and this is why we don’t die in our sleep every night. Yes, we are able to survive without stuffing muffins in our mouths every 2 hours.

A thermostat works on a negative feedback loop. If the temperature is too low, the thermostat turns on the heat until it gets to the proper temperature and then it stops. The body also uses a negative feedback loop in the BSW. Excessive insulin leads an increase in the size of fat cells. They produce more of the hormone leptin which travels to the brain and signals that ‘we’re too fat’. Appetite decreases, we stop eating, and this lowers insulin. This signals our body to start burning fat instead of eating and storing it and returns us to our original, desired BSW.

This feedback loop keeps our weight relatively stable despite wide fluctuations in calorie intake and calorie expenditures day after day, week after week and year after year. After all, most people become obese by gaining 1-2 pounds per year. Over 40 years, this can add up. Assume that 1 pound of body fat is roughly 3500 calories. In a year, we might eat 2000 cal/day times 365 days = 730,000 calories. To gain 1 pound a year (3500 calories), we would need to accurately match calorie intake and expenditure to a 99.5% accuracy rate. That’s impossible. I have maintained an even weight since grade school, but I have no idea how many calories I eat and how many I expend. How do I maintain a 100% accuracy rate? Clearly, I could not do this through conscious regulation of my food intake/ exercise. No, body fat is regulated by a feedback mechanism – the BSW ‘thermostat’.

‘Obesity is therefore not a caloric balance problem, but rather the gradual increase in the BSW thermostat (appestat) over time.’

Obesity

The BSW is created by the balance of insulin effect versus leptin effect, just as the thermostat is regulated by the balance of heat versus cooling. In those who are obese, we know that insulin effect has prevailed over leptin effect. For example, if we inject exogenous insulin, we gain fat because we have tilted the balance towards insulin. In normal human obesity, this could be due to a number of reasons, but eating foods high in refined grains, eating frequently, eating lots of sugar (causes hepatic insulin resistance directly) are all culprits in keeping insulin levels high despite leptin’s best efforts to curb appetite to lower insulin. If insulin is extremely low, as in type 1 diabetes, the body loses weight continuously no matter how many calories are eaten.

The battle royale for the BSW is Insulin vs. Leptin. One is trying to make us gain fat, the other is trying to lose fat. If leptin wins, then we are able to reduce appetite and/ or increase basal metabolic rates sufficiently to burn off the excess calories being eaten. This is exactly what we saw in Rudy Leibel’s study of deliberate weight gain.

If you are obese, it’s because insulin prevailed over leptin. As the fat cells stay over-filled, they produce more and more leptin in an attempt to fight insulin. However, the root problem of hyperinsulinemia has not been solved (eating too much sugar, too many refined carbohydrates, eating constantly), so insulin also continues to march higher. And persistent high levels of hormones result in resistance. Eventually, persistent, high levels of leptin cause leptin resistance.

Leptin resistance is virtually universal in common obesity. With leptin down and out, insulin is now unopposed to cause weight gain. The insulin vs leptin battle has been lost, and the BSW thermostat is reset upwards.

So, what’s the answer? Suppose we use the standard dietary advice of cutting dietary fat, reducing calories but eating lots of carbohydrates and eating 6 or 7 times per day. Since dietary fat has little insulin effect, this caloric reduction strategy has not reduced insulin effect and makes no difference to this Insulin vs. Leptin battle. Yes, you can cut calories, but no, you didn’t reduce insulin’s effect. The BSW is unaffected and our bodies desperately try to regain the lost weight. This is precisely the dietary advice given over the last 40 years that has failed so spectacularly. Eating frequently means constant stimulation of insulin, which is also detrimental to weight loss efforts.

The key to combating obesity, then is to help in the Insulin vs Leptin fight by lowering insulin. Everything depends upon it. Leptin is already maxed out. The only thing left is to lower insulin. How to do that? Well, that’s exactly what we address at the DNA Health Center Weight Program.

Dr Nasr Al-Jafari is a Dubai-based Family Medicine Consultant and Functional Medicine Practitioner. He graduated from The University of Nottingham and completed his consultant training at The University of Manchester, UK. He has pioneered the use of obesity theory in the UAE for weight loss and type 2 diabetes reversal at DNA Health Medical Center where he is Medical Director.

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