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Ending the yo-yo diet syndrome

MagazineJuly 2014 (Vol. 25 Issue 4)Ending the yo-yo diet syndrome

It's not calories-it's your 'fat hormones'that may be keeping you fat, says Lynne McTaggart

It's not calories-it's your 'fat hormones' that may be keeping you fat, says Lynne McTaggart. Here's how to balance them forever

Several years ago, a team of Spanish doctors assembled a group of 105 overweight men and women in their 20s and 30s, and put them all on an eight-week calorie-restricted diet. At first it looked like the diet was working. The members of the group lost, on average, around 5 per cent of their body weight, which meant that anyone weighing about 12 stone (168 pounds) lost about 9 pounds. So far, so good.

Four months later, the researchers rounded up the participants again to see if the weight had stayed off, but were dismayed to learn that a large number of the study participants had put back on all the weight they'd lost. When the doctors investigated further, one important clue emerged as to why so many of them had suffered this yo-yo effect. It wasn't that the study group were diet cheats. In fact, it didn't,strictly speaking, have much to do with the food they ate. Their bodies were no longer recognizing the quality of what they were eating. Their hormonal 'fat thermostats' were turned on full blast, but malfunctioning, no longer sending the brain the right information about food.1

In those who'd gained back their weight, the Spanish team discovered higher levels of a hormone called 'leptin' and lower levels of another hormone called 'ghrelin', leading the researchers to conclude that these 'appetite-related' hormones may play an important role in weight regain after dieting.

New-found hormones

Both hormones, discovered only in the 1990s, are agents that regulate appetite and fat levels. Leptin-made in our stored fat cells, or 'adipose tissues'-is, in fact, a protein hormone that circulates through

the bloodstream to signal the brain about your body's level of fuel and whether it's providing an adequate amount of energy.

When you finish a meal, leptin is released from your fat stores and enters your bloodstream, eventually making its way to your brain to deliver the message that you're full and now have a certain amount of energy available.

In effect, rather than a thermostat, leptin might more properly be called an 'adipostat'-a fat regulator. It keeps your brain clued in as to whether you are hungry and how much fat is currently in your body, much like the gauge in your car lets you know how much petrol you have left in the tank.

As Robert H. Lustig, professor of paediatrics at the University of California at San Francisco and obesity expert, puts it, leptin isn't a fat hormone, it's a 'starvation hormone', made to let the brain know when we need to eat more. When leptin levels rise, your appetite tails off and you feel full. Your metabolic rate also increases. Your brain thinks you have enough food and fat to go about your normal bodily business. This, in turn, returns leptin levels back to normal. At that point, food loses its appeal and doesn't taste as good, which helps to indicate that you've had enough.

This process also sets your body's metabolism to normal, allowing you to eat normal amounts of food, and clearing the path for the body to undergo complex and energy-hungry processes like puberty and pregnancy.

When you go on a diet and lose fat, you naturally produce less circulating leptin. As a consequence, when your levels of leptin fall below a certain amount, your brain thinks you're starving and launches a number of initiatives to bring about a return to energy homeostasis (balance). One of the most basic of these actions is stimulation of the vagus nerve-the nerve that runs from the brain to the abdomen and governs energy storage-which will cause your appetite to increase.

While dieting, we often have too little circulating leptin. In one small-scale study, researchers using functional magnetic resonance imaging (fMRI) demonstrated that obese volunteers who'd lost 10 per cent of their body weight also showed changes in neural activity all over the brain in response to visual food cues, indicating a state of leptin deficiency.2

Leptin also regulates the rate at which fat is broken down. As leptin levels rise, your fat metabolic rate increases. When you diet and your leptin levels fall, so does the metabolic rate. This is often why dieters reach a plateau in their weight loss: the body thinks it's starving and goes on a kind of emergency alert, slowing down all physiological processes to maximize what energy it has left.

Leptin's opposite number

Besides leptin, another important hormone for fat regulation is an agent that goes by the strange name of 'ghrelin'. This gastric amino-acid peptide stimulates the secretion of growth hormone and increases the amount of fat in the body, hence its name; 'ghre' is an Indo-European prefix for the word 'grow', and presumably was chosen by its Japanese discoverers because of its role as a growth-hormone-releasing peptide.

Produced primarily in the cells lining the stomach, ghrelin is leptin's opposite number: levels of this hormone increase before meals and decrease after meals. Ghrelin affects a receptor in the pituitary-the so-called master gland of the body sitting at the base of the brain near the hypothalamus-and controls secretion of growth hormone from the anterior lobe of the pituitary to stimulate growth.

While ghrelin stimulates the release of growth hormone by acting directly on the pituitary, it also affects the various parts of the nervous system within the hypothalamus involved in appetite control. It seems to be centrally involved in the regulation of energy in the body. Indeed, the higher our levels of ghrelin, the hungrier we feel. Ghrelin levels peak before meals and plummet afterwards.

Although scientists have been using growth hormone for 25 years now, ghrelin was only discovered in the late 1990s. In one animal study, ghrelin injected into rats rapidly stimulated their feeding behaviour and increased their body weight.3 And although a series of laboratory studies have been carried out, and we know that ghrelin plays a major part in growth regulation by stimulating feeding and growth-hormone release, there are still a number of outstanding questions about its precise role in appetite control.4

In one small-scale clinical study, the researchers used a crossover design. In this case, they first gave intravenous infusions of ghrelin to nine healthy volunteers and asked them to select food from a buffet.

The experiment was then repeated but, this time, they administered an intravenous infusion of saline, or salt water. The results showed that the volunteers clearly consumed more food when given ghrelin rather than salt water, and also scored higher on appetite tests. 5

Scientists have also observed that chronically obese people have far lower levels of ghrelin than those who are of normal weight. Also, levels of ghrelin appear to be linked to circadian rhythms-which are faulty in obese people.6 Chronic sleep deprivation increases the production of ghrelin and so also stimulates the appetite.

Sleep your way to a normal fat thermostat

As a society, we're not only fatter than ever-in 2011, 35 per cent of American adults were obese, up from 30 per cent or less over the previous decade, while in the UK, the average rate was 25 per cent, up from 22 per cent in 2001-but we're also getting a good deal less sleep. The percentage of young adults who get eight to nearly nine hours of sleep per night has been cut nearly in half from 1960 to 2001-from 40.9 per cent to 23.5 per cent in the US. Other evidence has shown that not getting enough sleep affects blood levels of both leptin and ghrelin, as well as hunger and appetite levels in men.1

Those two pairs of factors are now thought to be related, according to recent Canadian research. A six-year study from Quebec of 323 men and 417 women, aged 21 to 64 years, showed that the less sleep obtained every night, the higher the fat indices and lower the levels of leptin. Those who reported getting seven to eight hours of sleep had significantly higher levels of leptin and lower fat indices than those who'd only managed to get five to six hours of sleep every night.

The researchers concluded that short sleep durations result in an increased risk of being overweight because of lower leptin levels than expected by fat mass alone. Also, there may even be an optimal number of sleeping hours at which body weight is regulated and maintained.2

This suggests that getting an optimal amount of sleep (seven to eight hours-no more, no less) does more than keep you alert; it also helps you regulate your weight.

In fact, there appears to be a subtle and possibly even competitive interplay between ghrelin and leptin in the regulation of appetite. For example, in the rat experiment mentioned above, the injected ghrelin also blocked the reduction of feeding behaviour induced
by leptin.3

Leptin resistance

Overweight people like those in the Spanish study who regained their weight loss have a problem that's referred to as 'leptin resistance'. Similar to 'insulin resistance' in type 2 diabetics, where the pancreas produces large amounts of insulin that the body can no longer deal with properly, leptin resistance occurs when increased levels of circulating leptin are no longer recognized by the brain.

In this scenario, there are loads of leptin and stored fat, but the brain believes that leptin levels are low. This causes the brain to think the body is starving, so it stimulates feelings of hunger regardless of how much stored fat there is. Food tastes even better than it ordinarily does, which means that more of it is eaten.

In the Spanish study, the group that regained most of their lost weight all shared a certain physiological signature: circulating leptin levels that remained higher than those in the other study participants. Interestingly, those who'd regained weight did not also have higher levels of insulin, suggesting that it is leptin resistance rather than insulin resistance that most contributes to weight gain, although there may be some connection between the two conditions.

Recently, scientists at Harvard Medical School have found that leptin resistance is due to scrambling of the endoplasmic reticulum (ER)-the protein-making part of the brain cells that produces them, folds them and returns them to the cells. According to Umut Ozcan, a researcher at Children's Hospital Boston, when this protein production becomes faulty-a condition known as 'ER stress'-the brain grows 'deaf' to leptin signals, resulting in a slowing down of protein production.

In earlier researches, Ozcan found that ER stress was linked to type 2 diabetes and insulin resistance. In animal studies, mice fed a high-fat diet developed signs of ER stress in the hypothalamus, the primary region of the brain that receives signals from leptin.7 In yet another study by Ozcan and his team, a protein was removed from the hypothalamus of normal mice. ER function then went awry and the mice began to suffer from ER stress, becoming severely leptin-resistant and obese when fed a high-fat diet.8

As Ozcan puts it, "Most humans who are obese have leptin resistance. Leptin goes to the brain and knocks on the door, but inside, the person is deaf."

According to Tamas Horvath, a neuroscientist at Yale University who is studying the role of leptin in the brain, as the ER is the primary site of construction in the cell, the increased leptin signalling is akin to having architectural instructions to 'overbuild' to the point where the ER is eventually overwhelmed by having too many jobs to do at once.

Leptin also has an important role in maintaining adequate levels of fat in the female body, and this may mean that women are more prone to leptin resistance than men. In fact, in the Spanish study, more women than men who'd regained their weight had high levels of leptin. Medicine now believes that women need adequate levels of leptin to maintain fertility. Leptin also plays a vital role in initiating puberty in girls,9 while having abnormal levels may be related to type 1 diabetes.10

Faulty leptin signalling also causes chronic inflammation in the body, which can eventually lead to cardiovascular disease and a host of other problems. The hormone may also play a role in the development of melanomas, or skin cancer, and is thought to be, together with obesity, the most predictive marker of insulin resistance in children.11

Low levels of ghrelin

As with leptin, levels of ghrelin are abnormal in those who are very overweight. One study found that circulating levels of ghrelin were lower in the persistently obese in two culturally different populations compared with normal-weight individuals, suggesting that ghrelin is downregulated in obesity, possibly due to the accompanying higher-than-normal levels of insulin and leptin. For this reason, the researchers proposed that these lower levels might represent some sort of physiological 'adaptation' to the body's constant oversupply of energy through excess food consumption.12

When dieting, the body often produces more ghrelin than normal, as if the body, sensing that it's starving, is attempting to gain back the weight lost. In one study, dieters were also compared with people who had undergone gastric bypass (bariatric) surgery; the results showed that the latter patients had markedly suppressed ghrelin levels, which most likely contributed to the subsequent weight loss in those who had undergone the procedure.13

But the persistently obese may have a chronic deficiency of ghrelin, resulting in a feeling of never being full. Again, in the Spanish study, although those who initially lost weight showed no evidence of changes in ghrelin levels, the ones who regained their weight were those with lower levels of ghrelin than the others. What's more, men had the biggest changes in ghrelin levels, suggesting that this hormone plays a bigger role in appetite control in men than in women.

Although leptin supplements are sold on the internet as miracle weight-loss pills, leptin itself cannot be taken by mouth as a supplement because it's a protein and, as such, would simply be broken down by the body just like a piece of chicken. In fact, most 'leptin' supplements are composed of a grab-bag of other supplements known to boost thyroid or leptin production, or to generate a feeling of fullness, such as soluble fibre.

Recently, conventional medicine-with its 'pill for every ill' mentality-considered leptin regulation as just a matter of taking a new pill. But the latest evidence suggests that both leptin and leptin resistance are controlled by your lifestyle-in other words, what you eat, how much you exercise, how well you sleep and whether you are able to keep everyday stress in check. Even more important is the fact that leptin resistance is triggered by inflammation of the immune system which, again, may be caused by an unhealthy lifestyle and a chronic deficiency of omega-3 fats.

In the end, the interrelationship between leptin, ghrelin, insulin and other hormone regulators in the body is highly complex and intertwined, suggesting that weight gain and loss are far more complicated than simply a matter of counting calories or energy ingested or taking a 'fat pill' to lose weight. The best approach, as always, is the holistic one: to treat the body as a single interrelated whole and to provide it with the best fuel, the best workout and the best rest.

Under such conditions, your fat thermostat will adjust to normal, giving your body a chance to sort out a healthy weight naturally.

In search of the artificial fat regulator

After leptin was discovered in 1994, the medical industry and academic centres were convinced they had found a solution to obesity: simply administer extra leptin to the obese. These hopes were soon dashed after it was discovered that the overweight are, in fact, leptin-resistant. Those who took hormones lost weight only temporarily and soon yo-yoed back to their normal state of overweight, as the brain became accustomed to the extra levels of hormone and again ignored it.

Researchers are currently working on a method of chemically overcoming leptin resistance. Scientists at Harvard Medical School have confirmed that two agents-4-phenyl butyric acid (4-PBA; Buphenyl) and tauroursodeoxycholic acid (TUDCA)-can prevent the brain from ignoring leptin. Both are ordinarily given as treatments for cystic fibrosis and liver disease.

In a study in which Dr Umut Ozcan and his team gave mice 4-PBA or TUDCA, leptin sensitivity was boosted 10-fold and the mice lost significant weight even when eating a high-fat diet.1 As Ozcan noted, this study was the first to show that leptin could be turned on in mice, despite being fed a high-fat diet.

4-PBA and TUDCA molecules are considered 'chemical chaperones' because they help increase the capacity of the cells' endoplasmic reticulum (ER) to fold proteins. But given the fact that this research is so far only in animals and so may not apply to humans, the real problem is that we don't yet understand the precise mechanism behind ER stress in overweight people who eat a high-fat diet.

At this time, Ozcan's team is still attempting to understand leptin sensitivity more precisely in order to develop drugs that can turn on brain signalling more efficiently than these two agents can. In the meantime, research scientists at the Scripps Research Institute in La Jolla, California, have developed an anti-obesity vaccine, which targets ghrelin by making use of immune-system antibodies that bind to selected targets, thereby stimulating an immune response against them. At least in theory, this is supposed to prevent ghrelin from reaching the central nervous system, so tricking the brain (and the body) into feeling 'full'. So far, the vaccine has been successfully tested in rats, but not yet in humans.2

As another prong of attack, San Diego-based Amylin Pharmaceuticals is carrying out clinical trials of leptin supplementation together with a drug to increase leptin sensitivity. But Tamas Horvath, a neuroscientist at Yale, believes this kind of artificial engineering could be a recipe for disaster, as it might simply encourage the cells to keep on growing. It's also unnecessary, he says, considering the many other proven ways to restore leptin function.

The superfood fat regulators

These superfoods are particularly good as lowering inflammation and restoring your fat regulators.

Vegetables

oCruciferous vegetables
like broccoli and cabbage

oCarrots

oLeeks

oOnions

oSpring onions

oGarlic

oAsparagus

oBell peppers

oArugula

oRomaine lettuce

oSpinach

oTomatoes

Fat-burning herbs

oGinger

oGinseng

oCinnamon

oBilberry

oChamomile

oChasteberry

oGreen tea

oPeppermint

oTurmeric

oDandelion

oAloe vera

oEchinacea

Fruit

oBananas

oApples

oBlueberries

oCherries

oOranges

oGrapefruit

Powering up the fat burners

Although leptin supplements don't work, you can regulate your fat-burning hormones by making a number of important lifestyle choices.

Eat a highly varied, fresh organic diet,with the bulk composed of highly nutritious, colourful fruit and vegetables and good quality fish and and white meat or good animal protein.

Strive to eat nine or 10 fruits and vegetables every day,rather than just the recommended five, says Dr Leo Galland, author of The Fat Resistance Diet (Broadway Books, 2005).

Use herbs and spices liberallyin your food, but avoid chilli.

Pepper your diet with fresh, non-roasted and unsalted nutslike walnuts, linseeds (flaxseeds), sesame seeds and almonds.

Ensure that you have an adequate intake of omega-3 fatty acids;the best animal sources are cold-water fatty fish like salmon and tuna, and plant sources include walnuts, linseeds and pulses (such as soy, kidney and navy beans).

Look to grainswith a lower glycaemic index (GI) such as pasta, brown rice, quinoa, millet, oats and barley.

Indulge in regular sweat-producing exercise,as regular aerobic exercise helps increase leptin production, although the right diet will cause leptin levels to regularize naturally.

Eat organic, good quality protein:fatty and white meat fish (like flounder or cod); chicken and turkey; tofu and, if you eat dairy, organic unsweetened yoghurt. If you eat eggs keep the yoke unbroken, advises Dr Galland; otherwise it oxidizes and produces toxic byproducts that increase inflammation. Eat poached or boiled only or, for scrambled eggs, omelets or frittatas, use egg whites only.

Cut out or cut down on refined sugar-in all its forms.

Watch your carbohydrate intakeand keep off the white stuff by avoiding all processed foods such as white bread, potatoes, white rice, pastries, cakes and the like, and high GI foods like beer.

Take high-quality supplements rich in B vitamins,particularly B12, plus omega-3, magnesium, zinc and coenzyme Q10, which counteracts inflammation.

Avoid fake low-calorie foods,especially artificial sweeteners and diet soft drinks, now found to slow weight loss.1

Eat three good meals a dayand don't snack.

Don't eat late at night.

Include proteinin your breakfast meal.

Get 7 to 8 hours of sleep a night-no more, no less.

Drink plenty of water,green and black teas, and blueberry, cherry, pomegranate and vegetable juices.

References

1

J Clin Endocrinol Metab, 2010; 95: 5037-44

2

J Clin Invest, 2008; 118: 2583-91

3

Nature, 2001; 409: 194-8

4

J Endocrinol, 2009; 202: 191-8

5

J Clin Endocrinol Metab, 2001; 86: 5992

6

Proc Natl Acad Sci U S A, 2004; 101: 10434-9

7

Science, 2004; 306: 457-61

8

Cell Metabolism, 2009; 9: 35-51

9

Pediatrics, 2008; 121 Suppl 3: S208-17

10

J Clin Endocrinol Metab, 2001; 86: 1188-93

11

Int J Obes Relat Metab Disord, 2000; 24: 1265-71

12

Diabetes, 2001; 50: 707-9

13

N Engl J Med, 2002; 346: 1623-30

In search of the artificial fat regulator references

1

Cell Metab, 2009; 9: 35-51

2

Proc Natl Acad Sci U S A, 2006; 103: 13226-31

Sleep your way to a normal fat thermostat references

1

Ann Intern Med, 2004; 141: 846-50

2

Obesity [Silver Spring], 2007; 15: 253-61

Powering up the Fat Burners references

1

JAMA, 2009; 302: 2477-8


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